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Clemastine, Clindamycin, Clonazepam

Sunday, August 2nd, 2009

Generic Name
Clemastine (KLEH-mas-tene) A
Brand Names
DayHist-1    Tavist-1
Tavist    Tavist Allergy
Combination Pr(3dUtj
Generic Ingredients: Acetaminophen + Clemastine + Pseudoephedrine
Tavist Allergy/Sinus/Headache
Type of Drug  Antihistamine.
Prescribed For
Sneezing, stuffy and runny nose, itchy eyes, and scratchy throat caused by seasonal allergies and for other symptoms of allergies such as rash, itching, and hives.
General Information
Antihistamines generally work by blocking the release of naturally occuring histamine (a chemical released by body tissue during an allergic reaction) from cells at the H, histamine receptor site, drying up secretions of the nose, throat, and eyes. Clemastine fumarate is less sedating than most antihistamines, but not less sedating than astemizole, cetirizine, or loratadine.
Cautions and Warnings
Clemastine should not be taken if you are allergic or sensitive to any of its ingredients.
People with asthma or other deep-breathing problems, heart disease, high blood pressure, diabetes, enlarged prostate, glaucoma, stomach ulcers or other stomach problems, and hyperthyroidism should use clemastine with caution because its side effects can aggravate these problems.
Possible Side Effects
✓    Most common: drowsiness; headache; weakness; nervousness; stomach upset; nausea; vomiting; cough; stuffy nose; diarrhea; constipation; sore throat; nosebleeds; and dry mouth, nose, or throat.
✓    Less common: allergic reaction (symptoms include rash, itching, hives, and breathing difficulties), sleeplessness, menstrual irregularities, muscle aches, sweating, tingling in the hands or feet, frequent urination, visual disturbances, and ringing or buzzing in the ears.
Drug Interactions
•    Cbrnbining clemastine with alcohol, sedatives, sleeping pills, or other nervous system depressants may increase the depressant effects of clemastine. Do not combine these drugs.
•    The effects of oral anticoagulant (blood-thinning) drugs may be decreased by clemastine. Do not take this combination without your doctor’s knowledge.
Monoamine oxidase inhibitor antidepressants may increase the drying and other effects of clemastine. This combination can also worsen urinary difficulties.
e When taking antihistamines on a regular basis, notify your doctor if you are taking large amounts of aspirin. Effects of too much aspirin may be masked by the antihistamine.
Food Interactions
Clemastine is best taken on an empty stomach at least 1 hour before or 2 hours after eating; it may be taken with food if it upsets your stomach.
Usual Dose
Adult and Child (age 12 and over): 1.34 mg twice a day up to 8.04 mg of the syrup or 2.68 mg of the tablets in 24 hours.
Child (age 6-12) (syrup only): 0.67 mg twice a day or up to 4.02 mg a day.
Overdosage
Overdose is likely to cause severe side effects. Overdose victims should be given ipecac syrup—available at any pharmacy—to induce vomiting and should then be taken to a hospital emergency room for treatment. ALWAYS bring the prescription bottle or container.
Special Information
Clemastine may make it difficult for you to concentrate or perform complex tasks such as driving a car. Be sure to report any unusual side effects to your doctor
Antihistamines may occasionally produce excitability, particularly in children.
If you forget to take a dose of clemastine, take it as soon as you remember. If it is almost time for your next dose, skip the one you forgot and continue with your regular schedule. Do not take a double dose.
Special Populations
PregnancylBreast-feedj(IV. DO not take any antihistamines without WU ‘Obtlor’s knowledge if you are or might be pregnant—especially during the last 3 months of pregnancy, because newborns may have severe reactions to antihistamines.
Small amounts of clemastine pass into breast milk. Nursing mothers who must take clemastine should use infant formula.
Seniors: Seniors are more sensitive to side effects.

Generic Name
Clindamycin (klin-duh-MYE-sin)
Brand Names
Cleocin    Clindesse
Cleocin T    Clindets
Clinda-Derm    Evoclin Clindagel
Type of Drug  Antibiotic.
Prescribed For
Serious bacterial infections. The vaginal cream is used to treat bacterial vaginosis. Topical clindamycin is used to treat acne and rosacea.
General Information
Clindamycin is one of the few oral drugs that is effective against anaerobic bacteria, which grow only in the absence of oxygen and are often found in infected wounds, lung abscesses, abdominal infections, and infections of the female genital tract. It also works against bacteria usually treated with penicillin or erythromycin, including serious respiratory tract infections. Clindamycin may be useful for treating certain skin or soft tissue infections. It kills the bacteria that frequently cause acne.
Clindamycin is not used to treat vaginal fungus or yeast infections.
Cautions and Warnings
Do not take clindamycin if you are allergic or sensitive to any of its ingredients or to lincomycin, another antibiotic.
People with asthma or a history of allergies should use clindamycin capsules with caution.
Clindamycin can cause a severe intestina(kmkation called colitis, which can be fatal. Signs of colitis are diarrhea, blood in the Stool, and abdominal cramps. Any form of this drug, including products applied to the skin and the vaginal cream, can provoke colitis. Because of this, clindamycin should be reserved for serious infections or those that cannot be treated with other drugs.
Clindamycin should be used with caution if you have gastrointestinal disease or kidney or liver disease.
Possible Side Effects
Capsules
✓    Most common: stomach pain; nausea-, vomiting-, diarrhea,
in up to 20% of people; and pain when swallowing.
♦    Less common: itching; rash; signs of serious drug sensitivity, such as difficulties breathing and yellowing of the skin or the whites of the eyes; colitis, (see “Cautions and Warnings”); effects on blood components; and joint pain.
Topical Lotion
♦    Most common: dry skin, redness, burning, peeling, oily skin, and itching.
♦    Less common: diarrhea, abdominal pain, upset stomach, and colitis (see “Cautions and Warnings”).
Vaginal Cream
♦    Most common: vaginal itching or irritation; thick, white vaginal discharge; and pain during intercourse.
♦    Less common: nausea, vomiting, diarrhea, constipation, abdominal pain, dizziness, headache, vertigo, and colitis (see “Cautions and Warnings”).
Drug Interactions
•    Do not combine clindamycin and erythromycin.
•    The absorption of clindamycin capsules into the bloodstream is delayed by Kaolin-Pectin Suspension (prescribed for diarrhea). Separate these drugs by at least 1 hour.
•    clindamycin should be used with caution by people also using neuromuscular agents.
Food Interactions
Take the oral medication with a full glass of water or with food to prevent irritation of the stomach and intestine.
Usual Dose
Capsules
MUIV ) 50-450 mg every 6 hours.
Child (under age 16): 3.5-11 mg per lb. of body weight a day, in 3-4 doses. For severe infections, at least 37.5 mg 3 times a day, regardless of weight.
Foam: Dispense enough to cover the affected area(s) onto a cool surface (the foam will melt on contact with warm skin). Use fin-gertips to massage small amounts into the affected area(s) until the foam disappears.
Suppositories: Insert 1 suppository a day for 3 consecutive days.
Topical Lotion: Wash the skin and pat dry before application. Apply enough to cover the affected area(s) with a thin coat twice a day.
Vaginal Cream: Insert 1 applicator’s worth at bedtime for 7 consecutive days, except for Clindesse, which requires one applicator’s worth once at any time of day.
Overdosage
clindamycin overdose may lead to severe diarrhea and other drug side effects. Do not treat this diarrhea on your own. Discontinue use of this drug and call your local poison center for information. If you go to an emergency room for treatment, ALWAYS bring the prescription bottle or container.
Special Information
Prolonged or unsupervised use of clindamycin may lead to secondary infections from susceptible organisms. such as fungi. Take this drug for the full course of therapy as indicated by your physician.
If you develop severe diarrhea or abdominal pain, call your doctor at once. Call your doctor immediately if you experience breathing difficulties or jaundice (yellowing of the skin or whites of the eyes).
Women using the vaginal cream should not have vaginal intercourse or use other vaginal products such as tampons or douches until treatment is complete.
Use of latex condoms or diaphragms within 72 hours following treatment with the vaginal creams or suppositories is not recommended. These products may decrease the efficacy of condoms or diaphragms.
The topical lotion is for external use only. Avoid contact with your eyes or mucous membranes.
If you miss a dose of oral clindamycin, take it as soon as you rememlae~. SSW19 almost time for your next dose of clindamycin, double that dose and go back to your regular dosage schedule.
Special Populations
Pregnancy/Breast-feeding: This drug crosses into fetal blood circulation. When the drug is considered crucial by your doctor, its potential benefits must be carefully weighed against its risks.
clindamycin passes into breast milk. Nursing mothers who must take oral clindamycin should use infant formula.
Seniors: Seniors with other illnesses may be unable to tolerate diarrhea and other clindamycin side effects.

Generic Name
Clonazepam (klon-A-zeh-pam)
Brand Name  Klonopin
Type of Drug  Anticonvulsant.
Prescribed For
Petit mal and other seizures and panic attacks; also prescribed for periodic leg movements during sleep, speaking difficulty associated with Parkinson’s disease, acute manic episodes, nerve pain, and schizophrenia.
General Information
Clonazepam is a benzodiazepine drug. Clonazepam is not used as a sedative or hypnotic. It is used only for the uses described above in people who have not responded to other drug treatments. Tolerance to the effects of clonazepam commonly develops within about 3 months of use. Your doctor may raise your clonazepam dosage periodically to maintain the drug’s effect.
Cautions and Warnings
Do not take clonazepam if you are allergic or sensitive to any of its ingredients or any other benzodiazepine.
When stopping clonazepam treatments, the drug must be discontinued gradually. Abrupt discontinuance of clonazepam may lead to drug withdrawal symptoms including severe seizures, tremors, abdominal or muscle cramps, vomiting, whet increased sweating.
IJSIF,l OfMazeparn with caution if you have a chronic respiratory illness, since the drug tends to increase salivation and other respiratory secretions and can make breathing more labored.
Avoid using clonazepam if you have severe depression, severe lung disease, sleep apnea (intermittent cessation of breathing during sleep), liver disease, alcoholism, or kidney disease. These conditions may exacerbate the depressive effects of benzodiazepines, and such effects may be detrimental to your overall
condition.
Clonazepam can aggravate narrow-angle glaucoma, but if you have open-angle glaucoma, you may take it.
Possible Side Effects
♦    Most common: drowsiness, poor muscle control, and behavioral changes.
✓    Rare: Rare side effects can occur in almost any part of the body but are most likely to affect mental function, stomach and intestines, urinary function, blood, and liver. Contact your doctor if you experience any side effect not listed above.
Drug Interactions
•    The depressant effects of clonazepam are increased by sedatives, sleeping pills, narcotic pain relievers, antihistamines, alcohol, monoamine oxidase inhibitor antidepressants, tricyclic antidepressants, and other anticonvulsants.
•    Mixing valproic acid and clonazepam may produce severe petit mal seizures.
•    Smoking, phenobarbital, phenytoin, carbamazapine, and rifampin may reduce clonazepam’s effectiveness.
•    Clonazepam may increase the requirement for other anticonvulsant drugs in people who suffer from multiple types of seizures.
•    The effects of clonazepam may be prolonged when it is taken with cimetidine, contraceptive drugs, disulfiram, fluvoxamine, isoniazid, oral antifungal medications (e.g. ketoconazole), metoprolol, probenecid, propoxyphene, or propranolol.
•    Theophylline may reduce clonazepam’s sedative effects.
•    Separate antacids from y<3kwc_%1Dnazepam dose by at least 1 bZldi %prevent them from interfering with clonazepam being absorbed into the bloodstream.
•    Clonazepam may increase blood levels of digoxin and the risk of digoxin toxicity.
•    Clonazepam may decrease the effect of levodopa + carbidopa.
Food Interactions
Clonazepam is best taken on an empty stomach but may be taken with food if it upsets your stomach.
Usual Dose
Clonazepam is available in either tablets or orally disintegrating tablets, called wafers. Wafers should not be opened until immediately before the dose is to be taken. Do not push the wafer through the foil. Use dry hands to remove the wafer. The wafer will disintegrate quickly in saliva.
Seizures
Adult and Child (age 10 and over): starting dose    0.5 mg 3 times a day. The dose is increased by 0.5-1 mg every 3 days until seizures are controlled or side effects develop. The maximum daily dose is 20 mg.
Panic attacks
Adult and Child (age 10 and over): starting dose-0.25 mg twice daily. The dose is increased to 1 mg a day after 3 days. Most people do not require a higher dose.
Child (under age 10 or below 66 Ms.): starting dose-0.0220.066 mg per lb. of body weight a day in divided doses. Dosage can be increased gradually to a daily dose of 0.22-0.44 mg per lb. of body weight.
Other uses for clonazepam involve doses from 0.5-16 mg a day, depending on the condition and its severity. Clonazepam dosage must be reduced in people with impaired kidney function.
Overdosage
Overdose may cause confusion, coma, poor reflexes, sleepiness, low blood pressure, labored breathing, and other depressive effects. If the overdose is discovered within a few minutes and the victim is still conscious, it may be helpful to induce vomiting with ipecac syrup—available at any pharmacy. Overdose victims must be taken to a hospital emergency room. ALWAYS bring the prescription bottle or contai”iaT.
Special Information
Clonazepam may interfere with your ability to drive or perform other complex tasks because it can cause drowsiness and difficulty in concentrating.
Your doctor should perform periodic blood counts and liver function tests while you are taking this drug to check for possible
side effects.
Do not suddenly stop taking clonazepam—severe seizures may result. The dosage must be discontinued gradually by your doctor.
If you miss a dose by 1 hour or less, take it right away. Otherwise, skip the dose you forgot and go back to your regular schedule. Do not take a double dose.
Carry identification or wear a bracelet indicating that you have a seizure disorder for which you take clonazepam.
Special Populations
Pregnancy/Breast-feeding: Clonazepam crosses into the fetal circulation and can affect the fetus. Women who are or might be pregnant should avoid it. When the drug is considered crucial by your doctor, its potential benefits must be carefully weighed against its risks.
Some reports suggest a strong link between anticonvulsant drugs and birth defects, though most of the information pertains to phenytoin and phenobarbital, not clonazepam. It is also possible that the epileptic condition itself or genetic factors common to people with seizure disorders may figure in the higher incidence of birth defects.
Clonazepam may pass into breast milk. Nursing mothers who must take this drug should use infant formula.
Seniors: Seniors, especially those with liver or kidney disease, are more sensitive to the effects of this drug—especially dizziness and drowsiness—and may require smaller doses.

Celecoxib

Saturday, August 1st, 2009

Celecoxib (sel-eh-KOX-ib)
Brand Name
Celebrex
Type of Drug
Cyclooxygenase-2 (COX-2) inhibitor nonsteroidal anti-inflammatory
drug (NSAID).
Prescribed For
Osteoarthritis, rheumatoid arthritis, juvenile rheumatoid arthritis, acute pain, some colon polyps (FAR), menstrual pain, and arthritis of the spine (ankylosing spondylitis).
General Information
Traditional NSAIDs work primarily by blocking the effects of COX-2, a body enzyme that plays an important role in regulating pain and inflammation. But these NSAIDs also have an unwanted effect: They interfere with cyclooxygenase-1 (COX-1), a related enzyme that helps to maintain the stomach’s protective lining. NSAIDs that block the effects of this enzyme may produce side effects such as stomach irritation, gas, and stomach ulcers.
COX-2 inhibitors such as celecoxib are a class of NSAIDs that work about as well as the older NSAIDs. In fact, both 200 mg a day and 400 mg a day of celecoxib work as well as naproxen 500 mg twice a day. They interfere primarily with COX-2, leaving the stomach-protecting COX-1 relatively unaffected. This means that COX-2 inhibitor NSAIDs can relieve pain and inflammation just like traditional NSAIDs but are less likely to cause gastrointestinal (GI) side effects. Another advantage of celecoxib is that it does not cause thinning of the blood or affect blood platelets as can happen with older NSAIDs. Celecoxib is broken down in the liver.
Black patients absorb about 40% more celecoxib than Caucasians; its importance is unclear. Celecoxib is the first drug proven effective in reducing the number of intestinal polyps in people with the rare genetic disorder FAR
Cautions and Warnings
Do not take celecoxib if you are allergic or sensitive to any of its ingredients or to sulfa drugs. NSAIDs should not be taken by people with asthma or by those who have had a” allergic reaction to aspirin or another NSA13.1hey can develop a group of sympWMS V1Jnny nose with or without nasal polyps and a severe bronchial spasm) known as the aspirin triad.
COX-2 inhibitors, including celecoxib, have been associated with high blood pressure, kidney damage, heart attacks, and stroke. It should not be used to treat pain associated with heart bypass surgery. Two other COX-2 inhibitors were taken off the market because of safety concerns. Rofecoxib was removed because safety issues were noted after people had taken it for 18 months or more. Valdecoxib was taken off the market because of the lack of safety data, severe skin rashes, and concerns raised in people taking the drug after having had heart surgery.
NSAIDs can cause GI bleeding and ulcers and stomach perforation. This can occur at any time, with or without warning, in people who take NSAIDs regularly. Celecoxib should be used with caution by people who have had stomach ulcers or GI bleeding. Minor upper GI problems, such as upset stomach, are common and may occur at any time during NSAID therapy. People who develop bleeding or ulcers and continue NSAID treatment should be aware of the risk of developing more serious side effects. Risk of GI bleeding and ulcers is increased with longer duration of therapy as well as treatment with oral corticosteroids and anticoagulants, smoking, alcoholism, older age, and general poor health.
Children taking celecoxib may be more likely to vomit blood, suffer acute kidney failure, or develop rashes.
Celecoxib has not been studied in people with severe kidney disease. They should not use this drug unless their doctors closely monitor their kidney function.
Celecoxib can cause liver irritation and should be used with caution by people with hepatitis or cirrhosis. People with moderate liver disease can have twice as much celecoxib in their blood and require a reduced dosage. The effect of celecoxib in people with severe liver failure is not known.
Possible Side Effects
Side effects are similar to those of traditional NSAIDs. Stomach and intestinal side effects are about half as common.
♦    Most common: headache.
✓    Common: diarrhea, upset stomach, sinus irritation, and respiratory infection.
♦    Less common: abdominal pain, gas, nausea, back pain, swelling in the legs m arms, accidental injuries, sleeplessness, dizziness, sore throat, runny nose, and rash.
✓    Rare: Rare side effects can occur in almost any part of the body. Contact your doctor if you experience any side effect not listed above.
Drug Interactions
•    Alcohol may increase the risk of serious GI-related side ef-
fects. Avoid alcohol.
•    Combining celecoxib with an aluminum and magnesium antacid slightly reduces the amount of drug absorbed. Separate doses of these antacids and celecoxib by 1-2 hours.
•    Fluconazole and lithium may raise celecoxib blood levels and increase the risk of side effects.
•    While celecoxib may be combined with low dosages of as-
pirin, taking these drugs together can increase the risk of
stomach or intestinal ulcers or other complications. The ulcer
risk associated with this combination is less than that posed
by single-drug therapy with a traditional NSAID.
•    Celecoxib can reduce the blood-pressure-lowering effect of angiotensin-converting enzyme (ACE) inhibitors and diuretic drugs. This combination can also increase the risk of kidney damage after chronic celecoxib use.
•    Celecoxib may affect lithium blood levels.
•    NSAIDS can reduce the effect of furosemide and thiazidetype diuretics.
•    Celecoxib should be used cautiously with warfarin. Concurrent use of these drugs may cause an increased risk of bleeding complications.
Food Interactions
Celecoxib can be taken without regard to Food or meals. For optimal effectiveness, avoid taking this drug with high-fat meals.
Usual Dose
Adult (age 18 and over): arthritis-100-200 mg once or twice a day. FAP-400 mg twice a day.
Child (age 2 and over): juvenile rheumatoid arthritis-22-55 lbs: 50 mg twice a day; over 55 lbs: 100 mg twice a day.
Child (under age 2): not recommended.
Overdosage
Overdosage symptoms include Mnargy, drowsiness, nausea, vomitiR(;, 16M Stomach pain. Stomach or intestinal bleeding or severe allergic reactions can occur. High blood pressure, kidney failure, breathing difficulties, and coma are rare.
The victim should be taken to a hospital emergency room. ALWAYS bring the prescription bottle or container.
Special Information
Call your doctor if you develop rash, itching, unexplained weight gain, nausea, fatigue, jaundice (yellowing of the skin or whites of the eyes), flu-like symptoms, lethargy, swelling, black stools, severe stomach pain, persistent headache, or any bothersome or persistent side effect.
If you forget a dose and remember within 1 or 2 hours of your scheduled time, take it right away. If you do not remember until later, skip the forgotten dose and continue with your regular schedule.
Special Populations
Pregnancy/Breast-feeding: celecoxib has caused birth defects in animal studies. Any NSAID may affect fetal heart development during the second half of pregnancy. Pregnant women should not take celecoxib without their doctor’s approval. When this drug is considered crucial by your doctor, its potential benefits must be carefully weighed against its risks.
NSAIDs may pass into breast milk. There is a possibility that a nursing mother taking celecoxib could affect her baby’s heart or cardiovascular system. Nursing mothers who must take this drug should use infant formula.
Seniors: Generally, seniors can take this drug without special precaution. Those who weigh less than 110 lbs. should begin with the lowest possible dosage.

Principal Drugs A-Z (dimethicone - dopamine)

Friday, June 26th, 2009

dimethicone Activated dimethicone is an antifoaming agent, said to reduce flatulence and protect mucous
membranes. It is a constituent of many antacid preparations. It is also present in some water-repellent skin creams.
dipipanana A rapidly acting morphine-like analgesic of value in the sever rain 4 to -1 dk–
Dose: 30-3450 mg (fail),, but it is usually• given in association with cyclizine as Diconal. The side-effects are similar to those of morphine.
dipivefrine A pro-drug that is converted into adrenaline after absorption. It is used
in chronic open angled- glaucoma as eye
drops (0.1%). (Propine). See page 138 and Table 16.
dimethylsulphoxide (DMSO) An organic liquid, it has been used for the symptomatic relief of interstitial cystitis
(Hunner’s ulcer) by the bladder instillation of 50 ml of a 50% solution. (Rimso-50).
dinoprost Prostaglandin F,.. It has actions and uses similar to dinoprostone.
(Prostin 112).
dinoprostone A synthetic form of prostaglandin E,. It has been used to initiate contractions of the pregnant uterus. Dose: 500 pg orally to induce labour, repeated if necessary at hourly intervals; as vaginal tablets or gel, 3 mg. Side-effects are nausea, diarrhoea, shivering and dizziness. (Prostin E2; Prepidil).
dioctyl sodium sulphosuccinate See dOCUSalC.
diodone injection A solution of a complex organic iodine compound, used as a contrast agent in X-ray examination of kidneys and ureters.
diphenhydramine One of the early antihistamines, with a more sedative action, and use(] in the temporary relief of insomnia. Dose: 10-25 trig. (Medinex. Nytol). It is also present in some cough preparations and nasal decongestants.
diphenoxylate A derivative that resembles codeine III reducing intestinal activity. It is used for the symptomatic relief of diarrhoea, and is usually given with a small dose of atropine to discourage excessive dosage and to reduce the risk of dependence. Dose: 10 mg initially, then 5 nig every 6 hours as required. (Lomotil;’Fropergen).
diphenylpyraline An antihistamine used as .I decongestant in colds and sinusitis. Present in Eskornadc.
dipyridamole An inhibitor of thrombus formation by reducing the adhesiveness of blood platelets in the arterial circulation. Dose: 300-600 mg daily before food. s I
ide-effects include nausea, diarrhoea and headache. (Persantill).
disodium cromoglycate See sodium cromoglycatc.
disodium etidronate See etidronate. disodium pamidronate See pamidronate.
disopyramide A quinidine-like drug used in the treatment of cardiac arrhythmias especially after myocardial infarction. Dose: 300-800 mg daily; dose by slow i.v. injection under ECG cover, 2 nig/kg up to 150 mg, followed by oral therapy as soon as possible. By its anticholinergic action care is necessary in glaucoma and prostatic enlargement. Contraindicated in heart block. (Dirythmin; Rythmodan). See page 1;6 and “fable 24.
distigmine An inhibitor of cholinesterase similar to neostigmine but with a longer action.
Dose: in the control of myasthenia gravis 5-20 mg as a single morning dose before breakfast; in urinary retention after surgery, 5 trig daily. It is sometimes used in neurogenic bladder disorders. Side-effects are nausea, abdominal cramp, diarrhoea and weakness. (Ubretid).
disulfiram When taken with even small amounts of alcohol, disulfiram permits the accumulation of acetaldehyde in the body, with side-effects such a flushing, giddiness, vomiting and headache that may be severe. Distilfiram is used in chronic alcoholism, but prolonged treatment and co-operation of the patient are essential.

Dose: after at least 24 alcohol free hours: 800 nig on the first day, falling over 5 days to 100-200 mg daily. Acute confusion may occur if given at the same time as tucLro-
llidazole. (Antabuse).
dithranol Synthetic compound used locally in the treatment of psoriasis. It is a powerful irritant, and treatment should be commenced with a simple ointment or zinc paste containing 0.1% ofdithranol, gradually increased to 1% if well tolerated. Higher concentrations are sometimes used in ’short -contact -time’ therapy.
Dose: 100 mg/m’ by i.v. infusion over
I hour. Rapid and severe hypersensitivity reactions (hypotension, bronchospasm) may occur, and treatment must be irrnediat4y available. Reaction risks may be reduced by premedication with jexalnetha&one given the day before treatment and continued for 5 days. Rash, pruritus and neutropenia may occur, and blood counts and liver function tests are necessary. (Taxotere). See page 122 and Table 8.
docusate A surface-active agent used as a faeces -softening laxative.
Dose: ill, to 500 nig daily. (Dioctyl).
diuretics The most widely used group of diuretics is the thiazides, represented by bendrofluazide (see page 14I ). They act mainly by increasing the excretion of
sodium by inhibiting its re-absorption by the distal tubule of the kidney, and evoke a rapid response which may persist over 12-24 hours, although some, such as chlorthalidone, have a still longer action. They are given in mild cardiac failure, oedema and in hypertension, but in more severe conditions, and in pulmonary occlema, the more powerful ‘loop’ diuretics, such as frusemide, which act at a different point, are preferred. A side-effect of some thiazides is an increase in the excretion of potassium which may require the use of potassium supplements or a change to a potassium sparing diuretic such as trianiterene. Spironolactone, an aldosterone antagonist, is a more powerful diuretic, of value in resistant oedema. Osmotic diuretics such as mannitol are used mainly in cerebral oedema. Simple diuretics such as potas slum citrate arc mainly used to alkalize the urine and promote diuresis in cystitis and similar conditions. See page 141 and Table 18.
dobutamine A sympathomimetic agent similar to isoprenaline, but with a more selective stimulant action on the beta, receptors in the heart. It increases cardiac contractility but is less likely to cause tachycardia. Useful in acute heart failure and cardiogenic and septic shock. Dose: 2.5-5 pg/kg/min by i.v, infusion, carefully adjusted to need. (Dobutr= Posiject). See page 141 and Table 18.
docetaxel A potent cytotoxic agent derived from the Pacific Yew. Used in advanced breast cancer resistant to other therapy.
domperidone An antiemetic that functions as a dopamine antagonist, as it prevents dopamine from reaching the receptors in the chemoreceptor trigger zone (see antiemetics). It is mainly of value in the severe nausea and vomiting caused by cytotoxic drugs, and is also useful in fum clonal dyspepsia. It is of little value in postoperative and travel sickness.
Dose: 10-20 mg 4-8-hourly; 30-60 nig by suppository. Sedative side-effects are infrequent, as domperidone does not cross the blood-brain barrier. (Motilium). See page 77.
donepezil A reversible inhibitor of anti-cholinesterase. Alzheimer’s disease is linked with a deficiency of acetylcholine in the brain, and donepezil may relieve sonic of the symptoms of that disease by increasing brain acetylcholine.
Dose: 5-10 mg at night. Diarrhoea and muscle cramps are side-effects. (Aricept ).
dopamine A sympathomimetic agent with actions and uses similar to dobutamine. Dose: 2.5-10 pg/kg/min by slow i.v. infusion. Careful control ofdose is essential, as dopamine may cause vasoconstriction with higher doses and increase the risk of heart failure. (Intropin). Dopamine is also a central neurotransinifter, and a deficiency is associated with parkinsonism. See levodopa, page 141 and “table 18.
dopexamine A short-acting drug of the dopamine type but with a more powerful action on the 0,-receptors. It is used in heart failure during cardiac surgery.

Egg-Free Diets

Tuesday, May 26th, 2009

Egg-Free Diets
Tempura-style vegetables
There is nothing quite like an egg, especially when it comes to baking. Egg protein is the magical

ingredient that holds together a pancake, and creates the light and delicate structure of sponge cakes,

batter, souffles, mousses and meringues.
Unfortunately, egg protein is also a potent allergen for some people, and a source of intolerance

reactions for others.
Egg replacers, designed mainly for cake making, are one answer. They can be purchased from specialist

suppliers (see p. 255) or ordered via your local health-food shop. These are protein-rich mixes which

aim to simulate the structural properties of eggs, not the flavour. Recipes are usually supplied with

the replacer, and it is best to follow these recipes at first, for guaranteed results. Once you have

got the feel of using the egg replacer, you can experiment with substituting it for eggs in other cake

recipes.
Note that these egg replacers make no attempt to simulate the richness and characteristic taste of

eggs. You may need to add extra butter or other fats to your cake mix if using egg replacers. Vanilla

extract can also improve the flavour of an egg-free cake.
Can cooking make eggs safe?
Cooking changes proteins, as eggs illustrate vividly. When a hot oven turns liquid egg white into a

hard meringue, or a sloppy cake mix into a firm sponge, the visible effect is due to the egg protein

being fundamentally changed.
Heating changes the basic molecular structure of the egg protein, in a process called denaturing.

Whereas natural egg protein is liquid, denatured egg protein is solid.
Denaturing egg protein has subtle effects, as well as these obvious ones. When the structure of the

molecule changes, some of the epitopes (the key features recognised by allergy antibodies — see box on

p. 15) are obliterated. For a few allergy sufferers — those who react only to the epitopes affected by

denaturing — thorough heating can therefore turn the egg allergen into a harmless substance.
If eggs are hard-boiled, the denaturing process occurs to the fullest possible extent. Consequently,

some people with egg allergy can eat hard-boiled eggs without ill-effects. However, the same people

still react badly to lightly cooked eggs, such as those in a souffle or omelette because, with partial

cooking, the denaturing process is incomplete.
Cakes made with eggs pose an interesting question — given that the cooking process for cakes is

prolonged and at a high temperature, could they too be safe? This is something that allergists have not

so far investigated.
If you want to test your response to hard-boiled eggs, you must do so under full medical supervision

with resuscitation equipment available. Those who find that they can tolerate hard-boiled eggs might

then want to test their reaction to cakes made with eggs. Again, there must be medical supervision for

the test, in case of severe life-threatening reactions. You will, of course, have to convince your

allergist that such a test is worthwhile.
Egg protein is not unique in being susceptible to denaturing — most proteins can be denatured, some by

heat, some by other means. But only in a few cases (tuna fish, and fresh fruits and vegetables — see p.

110) does denaturing tend to destroy the allergenic epitopes.
Very rarely, changing the structure of a protein by cooking may actually create an allergenic epitope

where none exists in the raw protein. There have been cases of individuals with an allergy to cooked

fish but not raw fish, and to pecan nuts in
biscuits but not uncooked pecans. Roasting peanuts makes them much more allergenic.
Tempura-style vegetables
Beer is a good alternative to eggs for making a batter and gives this Japanese batter a wonderfully

light crisp texture. Have all the vegetables ready prepared so you can cook and eat the tempura as

quickly as possible.
PREPARATION TIME: about 45 minutes MAKES: 4-6 servings
400-500g (14oz-11b 2oz) prepared vegetables cut into bite-sized pieces -choose from red pepper,

asparagus, broccoli, spring onion or red onion, carrot, courgette, baby corn, button mushrooms,

aubergine
150g (5/oz) self-raising flour, sieved,
plus extra for coating vegetables
1 tsp salt
2 tbsp sesame seeds
250ml (9fl oz) lager or Japanese beer vegetable oil for deep-frying
To serve:
equal quantities soy sauce and dry sherry
mixed together, or sweet chilli sauce
Toss the prepared vegetables in flour until lightly coated then shake off the excess. Heat the oil in a

large saucepan over medium heat until a cube of bread dropped in turns brown in 30 seconds.
Mix the measured flour, salt and sesame seeds and quickly stir in the beer - don’t worry if the mixture

is slightly lumpy. Dip the vegetables in the batter, a few pieces at a time, and then immediately into

the hot oil. Cook until crisp and golden.
Drain on kitchen paper and keep warm in a hot oven. Continue in the same way until all the vegetables

are cooked.
Serve with a dipping sauce made of soy sauce and dry sherry, or dip in sweet chilli sauce.
Caramelised onion tart
Caramelised onion tart
This makes a good substitute for quiche and other egg-based flans. The long, slow cooking of the onions

is important to bring out their natural sweetness.
PREPARATION TIME: 45 minutes COOKING TIME: 30 minutes MAKES: 6-8 servings
1 k (21b 4oz) onions, halved then thinly sliced
4 tbsp olive oil
125g (41/2oz) streaky bacon, finely chopped
1 tsp caraway seeds
salt and freshly ground black pepper 350g (1 2oz) bread dough or puff pastry
Place the onions in a very large saucepan with the oil, bacon and caraway seeds and cook over medium

heat, stirring occasionally, for about 30 minutes until the onions are softened and lightly

caramelised. Season generously.
Roll out the dough thinly and use to line a deep 24cm (91/2in) fluted flan tin. Prick the base with a

fork then fill with the onion mixture. Cook on a baking sheet in a preheated oven at 230°C/450°F/gas

mark 8 for 30 minutes until the dough or pastry is crisp and golden.
Feta in a crisp polenta jacket
Variations: replace the bacon with 125-1758 (41/2-6oz) crumbled goat’s cheese or 125-175g (4/,2-6oz)

diced smoked tofu, for a vegetarian version; or add a handful of pitted olives.
Feta in a crisp polenta jacket
The oil must be really hot to ensure a crisp crust for these delicious cheese croquettes.
PREPARATION TIME: 15 minutes MAKES: 4 servings
vegetable oil
200g (7oz) feta cheese, cut in 8 fingers 40g (I Y2oz) cornmeal
To serve:
salad of your choice, e.g. tomato, cucumber, red onion and flat-leaf parsley, or skinned and charred

red peppers with rocket
Pour the oil into a saucepan and set over a high heat. Meanwhile, dip the cheese fingers in Iced water

for about 1 minute then roll in the cornmeal until evenly coated. Deep-fry for 1-2 minutes until crisp

and golden. Drain on kitchen paper and serve at once on top of the salad.
Egg-free pancakes
Tofu filling for a savoury flan
This very simple savoury flan filling makes an egg-free, milk-free substitute for quiche. This recipe

makes enough filling for a 20cm (Bin) pastry case.
PREPARATION TIME: 5 minutes COOKING TIME: about 25 minutes
250g (9oz) tofu, natural or smoked 1 tbsp wine vinegar or lemon juice 1 tbsp dried mixed herbs
200ml (7fi oz) soya milk
Combine all the ingredients in a blender and pour into a pre-baked flan case. Cook in a preheated oven

at 190′C/375′F/gas mark 5 for about 25 minutes until set.
Variations., add either sauteed chopped onion; chopped cooked ham with spring onion; roasted

vegetables, such as carrot, peppers and tomatoes; or cooked spinach, beetroot or broccoli.
Tofu mayonnaise
This mayonnaise can be flavoured with chopped herbs, roasted garlic puree or tomato puree. It will

keep, covered, in the fridge for 3-4 days.
PREPARATION TIME: 5 minutes MAKES: approx. 250ml (9fl oz)
Lemon cake
100g (3%oz) soft tofu
100g (3%zoz) Greek yoghurt
1 tsp English mustard
1 tbsp Dijon or wholegrain mustard
iced water
salt and pepper
Blend all the ingredients except the water, salt and pepper in a liquidiser. Season to taste and thin

as required with iced water.
Avocado dressing
This dressing is delicious with tomato salads, prawns or grilled steak. Keep it tightly covered

otherwise it will discolour quickly.
PREPARATION TIME: 5 minutes MAKES: approx. 250ml (9fl oz)
1 medium-sized ripe avocado
4 tbsp vegetable oil
2 tbsp white wine vinegar or lemon or lime juice
iced water
salt and pepper
Halve, stone, peel and chop the avocado and blend in a liquidiser with all the remaining ingredients

except the water, salt and pepper until smooth. Season to taste and thin as required with iced water.
Egg-free pancakes
These pancakes can be served with either savoury or sweet fillings.
PREPARATION TIME: 25 minutes MAKES: 10
100g (3V2oz) plain flour
2 tbsp arrowroot powder
300ml (V2 pint) milk
vegetable oil or melted butter for frying
To serve:
golden syrup, jam or lemon juice and caster sugar
Mix the flour and arrowroot, then stir in the milk to give a smooth batter. Leave to rest, ideally for

20 minutes.
Heat 1 tsp oil in an 18cm (7in) nonstick frying pan and pour in 2-3 tbsp batter, enough to just cover

the base of the pan, swirling it as it falls into the pan to give a thin layer. Cook until golden on

one side then carefully turn and cook the other side. Repeat until all the batter is used up. To ensure

a crisp result every time, make sure the fat is hot.
For a sweet pancake, serve with golden syrup, jam, or lemon juice and caster sugar.
For savoury pancakes, fill with a white sauce flavoured with smoked fish and prawns, or ham and

parsley, or ratatouille and cheese.
Raspberry and sherry syllabub trifle
Syllabub makes an unusual topping for this trifle with its egg-free shortbread base, but if you prefer,

make a custard with custard powder and top with whipped cream. Vary the fruit with the seasons -

poached pears, fresh orange, and cooked cranberries are all suitable.
PREPARATION TIME: 15 minutes MAKES: 6-8 servings
I 75g (6oz) butter shortbread
6 tbsp medium or sweet sherry
225g (8oz) fresh or frozen raspberries 284ml carton whipping cream
50g (13/4oz) caster sugar
To serve:
25g (1oz) toasted flaked almonds
Roughly break the shortbread and put in the bottom of a trifle bowl or any decorative serving bowl.

Sprinkle with 2 tbsp sherry then top with the raspberries. Whip the cream and sugar with the remaining

sherry until it holds its shape, then pile on top of the raspberries. Chill until required, then, just

before serving, sprinkle the top with flaked almonds.
Lemon cake
This cake has a tangy lemon flavour and a slightly dense texture. Serve it plain or with fresh berries

and whipped cream or creme fraiche. Try replacing the lemon with orange.
PREPARATION TIME: 15 minutes
COOKING TIME: about 1 hour
MAKES: 1 x 19-20cm (71/2-8in) cake
100g (3112oz) butter, melted
200g (7oz) caster sugar
250g (9oz) self-raising flour, sieved 1 tbsp baking powder
250g (9oz) natural yoghurt
finely grated zest and juice of 1 small unwaxed lemon
1-2 tbsp milk (optional)
To serve:
icing sugar
Butter a 19-20cm (71/2-8in) spring-release tin and line the base with greaseproof paper. Place all the

ingredients in a large bowl and beat well to a firm dropping consistency. You may need to add 1-2 tbsp

milk, depending on the type of yoghurt you have used. Transfer to the prepared tin, level the surface

then bake in a pre-
heated oven at 180′C/350′F/gas mark 4 for 50-60 minutes until risen and just firm to the touch. Cool in

the tin for about 30 minutes, then transfer to a cooling rack until completely cold. Dust with icing

sugar.
Fig, orange and pear shortcake
PREPARATION TIME: 20 minutes COOKING TIME: 45 minutes MAKES: 8-10 servings
250g (9oz) chopped dried figs
finely grated zest and juice of 1 medium
unwaxed orange 1 ripe pear, chopped
250g (9oz) plain flour, sieved
1758 (6oz) butter
100g (3112oz) light muscovado or soft brown sugar
1 tsp ground cinnamon To serve:
icing sugar (optional)
Place the figs, orange zest and juice and the chopped pear in a saucepan and cook over medium heat

until the figs and pear are soft and all the juice has been absorbed. Place the flour, butter, sugar

and cinnamon in a food processor and blend. Alternatively, rub in by hand until the mixture resembles

fine crumbs. Add 1 tbsp cold water and stir until the mixture forms rough lumps. Press half the cake

mixture onto the oiled base of a 19cm (71/2in) spring-release tin. Spread the fruit mixture on top,

then finish with the remaining cake mixture, pressing it down lightly.
Cook in a preheated oven at 180°C/350°F/gas mark 4 for 45 minutes. Cool in the tin. Dust with icing

sugar, if wished, and serve in wedges.
Variations: replace the figs and pear with dried apricots and an apple; or replace the figs with

prunes, dried pineapple or dried mango.
Date and walnut loaf
Dates give this egg-free cake a wonderfully moist texture that is even better after a day or two. Store

in a cool place in an airtight container.
PREPARATION TIME: 15 minutes COOKING TIME: about 45 minutes MAKES: 1 large loaf
250g (9oz) chopped dried dates
100g (3′12oz) light muscovado or soft
brown sugar 25g (1 oz) butter
2 tsp ground mixed spice
1 tsp bicarbonate of soda
275g (93/4oz) self-raising flour, sieved
1008 (3′12 oz) walnut pieces
To serve:
butter (optional)
Place the dates in a large bowl with the sugar, butter, spice and bicarbonate of soda. Mix well, then

pour on 250ml (9fl oz) boiling water. Leave to cool slightly then beat in the flour followed by the

walnuts. Transfer the mixture to an oiled and base-lined 900g (21b) loaf tin. Level the surface and

cook in a preheated oven at 180°C/350°F/gas mark 4 for about 45 minutes, until risen and just firm to

the touch.
Cool in the tin for about 30 minutes, then transfer to a wire rack to cool completely. Serve in slices,

with or without butter.

Allergy: Avoiding Milk and Lactose

Tuesday, May 26th, 2009

Avoiding Milk and Lactose
Fruit lassi
There are two quite distinct reasons for avoiding milk: either to avoid milk proteins or to avoid

lactose, the sugar found in milk. It is important not to confuse these two because the details of the

avoidance diet required are different. Only a few people need to avoid both milk proteins and lactose.
Diarrhoea and wind in response to drinking milk, but few other symptoms, usually indicates a reaction

to lactose — but a reaction to milk proteins could be an alternative explanation. If it is a reaction

to lactose, this may be due to either primary lactase deficiency or secondary lactase deficiency — your

doctor can order tests to make an exact diagnosis (see p. 79). Note that a bout of diarrhoea, however

caused, often produces a temporary lactose intolerance (secondary lactase deficiency).
Any symptoms other than (or in addition to) diarrhoea and wind strongly suggest a reaction to milk

proteins. This might be a true allergy, another type of immune reaction to milk (see pp. 72-3), or an

idiopathic intolerance reaction (see pp. 76-7). In theory, skin tests should identify true allergic

reactions to milk proteins. Unfortunately, skin tests are not infallible, and it is possible to have a

genuine allergy or other immune reaction to milk proteins, but give negative skin tests. This is

especially common with babies (see p. 65 and p. 69). There are no accurate tests that can confirm

intolerance reactions to milk proteins.
It is possible to have sensitivity to both milk proteins and lactose.
If tests do not give you a definitive answer, you may have to try both types of diet and see which one

works. Remember that lactose intolerance may be only temporary.
Avoiding milk proteins
If you have a sensitivity reaction to cow’s milk proteins, then you need to avoid:
•    milk and all milk-based drinks, including lactose-reduced milk (if you need to avoid lactose as

well, drops and tablets to reduce lactose — see Using lactase replacers, p. 183 — are safe and could be

used with a tolerated milk, e.g. goat’s milk)
•    cream, yoghurt, creme fraiche
•    all kinds of cheese, cottage cheese and cream cheese (some people may be able to tolerate

Norwegian brown cheese, called Gjetost, which is made with milk whey)
•    white sauce, bechamel sauce and other creamy sauces
•    custard, rice pudding and other milk-based puddings
•    almost all home-made cakes, biscuits, cookies, pancakes and pastry
•    some bread, rolls, waffles
•    almost all chocolate
•    casein, casemate, and lactalbumin in packaged foods (see p. 173); you may be able to tolerate

whey but experiment cautiously.
Unless your sensitivity is fairly mild, you will also need to avoid:
•    butter, except clarified butter (ghee)
•    most kinds of margarine (they generally contain milk derivatives, but
some are milk-free — health-food shops are a good source of these).
As long as you do not have a severe allergy to milk, you should be able to tolerate clarified butter.

Make this by melting butter over a low heat, pouring it into a glass jar, and leaving it to cool in the

refrigerator. The milk proteins will settle to the bottom, and be visible as whitish granules — only

eat the clear butter above this level.
Alternatively, put olive oil into a wide-necked container and place in the freezer. It will solidify,

and can be used as a spread in place of butter.
A few of those with cow’s-milk allergy can tolerate sheep’s milk, and possibly (but less commonly)

goat’s milk. However, most people must avoid these as well. (There are also rare individuals who are

allergic to goat’s and sheep’s milk but not to cow’s milk.) Ass’s milk, if you can get it, is tolerated

by most with cow’s-milk allergy. There are many substitutes for cow’s milk now available, such as soya

milk, almond milk, rice milk and hazelnut milk. Try a health-food shop for these. All can be used in

place of ordinary milk when cooking.
Margarine or clarified butter can be used in recipes that call for butter. Soya yoghurt and cream make

reasonable substitutes for ordinary yoghurt and cream.
Avoiding lactose
If you have lactose intolerance, you must avoid:
•    milk and all milk-based drinks, unless lactose-reduced
•    cream, creme fraiche
•    most kinds of yoghurt, especially mild yoghurt. A very strong, acidic yoghurt may contain

little lactose. The bacteria that make yoghurt turn lactose into lactic acid, so the more acidic it is,

the less lactose it contains.
•    cottage cheese and Norwegian brown cheese, or Gjetost. Other kinds of cheese are usually so low

in lactose that they are tolerated. Only those people with extreme lactose intolerance need to avoid

all cheeses.
•    white and bechamel sauce, custard, rice and other milk-based puddings
•    almost all home-made cakes, since milk is generally used for baking. Items cooked with butter

but not milk, such as biscuits, cookies and pastry, are usually tolerated, as is butter itself, and all

margarine.
•    lactose in medicines. Lactose powder is used in many tablets and capsules, just to bulk out the

drugs. The amount used can be sufficient to evoke symptoms in some people with lactase deficiency.

Certain asthma inhalers also contain lactose (see p. 162), and a small amount may be swallowed. The

lactose from inhalers will affect you only if you have severe lactase deficiency.
Soya-based products, and all other nut- or grain-based milk substitutes, are lactose-free. Sheep’s

milk, goat’s milk and other animal milks (including human breast milk) all contain lactose.
Using lactase replacers
Many people with lactose intolerance are able to eat a more varied diet by using lactase replacers.

These provide a temporary supply of the missing enzyme, lactase (see p. 79), which helps out by

digesting the lactose in milky foods. Lactase replacers must be taken at the same time as the milky

food, and are only effective for that one meal. The more lactose there is in the meal or snack, the

more of the lactase replacer you need – trial and error is the only way of working out how much you

need for a particular food. There are a number of different brands of lactase replacer now available,

and it is worth trying out several. Some people find that they are sensitive to an added ingredient in

some brands. Sources of lactase replacers include health-food shops and specialist suppliers – these

can be located through the Internet (see p. 255).
Savoury white sauce
Savoury white sauce is the base of many dishes. Here the flavour of the wine and stock goes well with

chicken, vegetables or fish.
PREPARATION TIME: 7-8 minutes MAKES: approx. 600ml (1 pint)
50g (13/4oz) milk-free baking margarine 50g (1314oz) plain flour
200ml (7fl oz) dry cider or dry white wine 400ml (14f1 oz) vegetable or chicken stock 1 bay leaf, salt

and pepper
Melt the margarine in a small saucepan and stir in the flour. Cook, stirring, over a low heat for
1 minute then stir in the cider or wine, followed by the stock. Add the bay leaf and simmer, stirring

occasionally, for 5 minutes until thickened. Season to taste.
Variations. add approx. 6 tbsp finely chopped herbs, e.g. parsley, chives, tarragon or chervil; or add

English or French mustard; or add lemon juice.
Sweet white sauce
PREPARATION TIME: 5 minutes MAKES: approx. 300ml (’/?pint)
2 tbsp cornflour
25g (1 oz) caster sugar
300ml (V2 pint) apple or white grape juice 4 tbsp soya cream
25g (1oz) milk-free margarine
In a saucepan, mix the cornflour and sugar with a little of the juice to give a smooth paste then

gradually stir in the rest of the juice and bring to a simmer over a low heat. Simmer for 1-2 minutes

until thickened, stirring all the time. Finally, add the soya cream and margarine.
Variations: melt in 1008 (3-/2oz) or more of milk-free chocolate; or add rum or brandy to taste; or add

4-6 pieces finely chopped stem ginger together with 1-2 tbsp of their syrup.
Pancakes
Soya milk has a slightly thicker consistency than cow’s milk and therefore more is used in this pancake

recipe than would be needed in a traditional one.
PREPARATION TIME: 25 minutes MAKES: approx. 16 small pancakes
150g (5V2oz) plain flour, sieved 2 large eggs
pinch salt
450ml (16f1 oz) soya milk
oil or milk-free margarine for frying To serve:
lemon juice and caster sugar or golden syrup
Combine the flour, eggs, salt and soya milk in a liquidiser until smooth. Alternatively place the

flour, eggs and salt in a bowl and slowly whisk in the soya milk to form a thin batter.
Heat approx.1 tsp oil or margarine in an 18cm (7in) non-stick frying pan and swirl until hot. Pour in

sufficient batter to just cover the base of the pan and cook until golden. Turn and cook on the other

side until golden.
Serve with lemon juice and caster sugar or with golden syrup.
Apple and frangipane tart
An alternative to a milk-based custard tart. The combination of apple and almond is delicious. Serve

freshly baked. It can also be eaten cold, but if possible, warm it a
little before serving.
PREPARATION TIME: 30 minutes COOKING TIME: 1-11/4 hours MAKES: 8 servings
Pastry:
175g (6oz) plain flour, sieved
1008 (3 V2oz) milk-free baking margarine, softened
25g (1 oz) caster sugar
Filling:
50g (13/4oz) milk-free sunflower margarine 1008 (3112oz) ground almonds
100g (3112oz) plus 1 tbsp caster sugar 2 egg yolks
2 tbsp dark rum, brandy or orange juice 2 large dessert apples
4 tbsp apricot jam
Work the flour, margarine and sugar together with 1 tbsp cold water to make a soft dough. Roll out and

use to line a deep 20cm (8in) fluted flan tin. Chill this while you prepare the filling.
Preheat the oven to 190′C/375′F/gas mark 5. Beat together the margarine, ground almonds, 100g (3Y2oz)

caster sugar, egg yolks and rum. Peel, core and roughly chop one apple and stir into the mixture.

Spread this in the pastry case. Core and thinly slice the remaining apple and arrange the slices on

top. Sprinkle with the remaining sugar and bake for 1-1′/’4 hours until risen and golden. Cool slightly

then brush the surface with the apricot jam (warm this gently in a saucepan first).
Coconut rice pudding with mango
This pudding is based on a Thai recipe. The rice pudding will become thicker the longer it cooks and

also as it cools. Make sure the mango is ripe.
COOKING TIME: 30-40 minutes MAKES: 6 servings
175g (6oz) pudding rice, rinsed 50-75g (131-2314oz) sugar
1 litre (13/4 pints) carton rice milk 400ml (14f1 oz) coconut milk To serve:
1 extra-large ripe mango, peeled and diced
toasted coconut shreds
Place the rice in a large saucepan with 50g (13/4oz) of the sugar and the rice milk and coconut milk.

Bring to a simmer, stirring. Simmer gently for 30-40 minutes, stirring occasionally, until the rice is

cooked and the milk absorbed. Add the extra sugar if wished. Serve warm or cold, topped with mango and

toasted coconut.
Baked strawberry creams with strawberry sauce
The riper the strawberries the better, to give intensity to both the creams and the sauce.
PREPARATION TIME: 30 minutes COOKING TIME: 20-25 minutes MAKES: 6
1008 (3112oz) caster sugar
4 tbsp Muscat wine
1 tsp lemon juice
350g (12oz) strawberries, hulled and sliced
4 large eggs, beaten Sauce:
225g (Boz) strawberries, hulled and chopped
2 tbsp icing sugar 2 tbsp Muscat wine To serve:
a few whole strawberries
Preheat the oven to 1 70′C/325′F/gas mark 3. Set six 1 50ml (Y4 pint) ramekins in a small roasting tin.

If you plan to unmould the creams, oil the ramekins lightly.
Place the sugar, wine, lemon juice and strawberries in a saucepan and heat gently to dissolve the

sugar. Bring to the boil and cook, uncovered, for 5 minutes. Cool slightly then puree in a liquidiser

and whisk into the beaten eggs. Pass through a sieve then pour into the ramekin dishes.
Pour hot water from a kettle around the ramekins and cook in the centre of the oven for 20-25 minutes

until lightly set.
Remove the dishes from the tin and allow to cool. Chill, if wished.
Combine all the sauce ingredients and liquidise until smooth. Pass through a fine sieve.
Serve the creams in the ramekins with a little sauce poured on top and decorated with a whole

strawberry, or carefully unmould, pour a little sauce over, then decorate with a whole strawberry.
Variation: oil the ramekins. Dissolve 100g (31/2oz) caster sugar in 4 tbsp water in a small saucepan

over gentle heat, then cook to a rich caramel without stirring. Pour a little caramel into each oiled

ramekin then continue as above. Pour the wine for the sauce into the pan used to make the caramel and

warm gently to dissolve any leftover caramel, then continue with the sauce as above.
Frozen vanilla dessert
This is a cross between a sorbet and an ice cream.
PREPARATION TIME: 30 minutes, plus freezing MAKES: 4-6 servings
1 vanilla pod, split
150g (51/2oz) caster sugar 500g carton soya yoghurt
Place the vanilla pod and sugar in a saucepan with 300ml (1/2 pint) water. Dissolve over gentle heat

then bring to a simmer and simmer for 20 minutes. Leave to cool then remove the pod, scraping all the

seeds from it and returning them to the syrup. Beat in the soya yoghurt and freeze.
You will get the best texture by using an ice-cream machine. Alternatively, freeze in a plastic

container then remove from the freezer and beat the mixture well until smooth (you can do this in a

food processor). Return to the freezer. Repeat this process once or twice.
Baked strawberry cream with strawberry sauce
Variations: add 100g (31/2oz) melted plain chocolate; or add 2 tbsp instant espresso coffee dissolved

in 2 tbsp hot water. Alternatively, dissolve 100g (3/2oz) caster sugar over a gentle heat in a small

saucepan until it turns to a rich caramel; then add 100g (31/2oz) unblanched almonds and stir with a

metal spoon until they start to pop. Transfer to an oiled tray and leave to set. Crush roughly and add

to the basic mixture.
Fruit lassi
This refreshing Indian drink can also be made with frozen fruit, in which case don’t use iced water –

cold will do.
PREPARATION TIME: 10 minutes
MAKES: approx. 1.35 litres (21/4 pints)
500g carton soya yoghurt
50-75g (1314-231aoz) sugar
225g (8oz) berries such as raspberries, strawberries, blackberries or blueberries or the equivalent

weight of chopped fruit such as mango, peach or papaya
600ml (1 pint) iced water
Place all the ingredients in a liquidiser and blend until smooth.
Frozen vanilla desert
Banana and strawberry shake
A special treat for a child who cannot have milk.
PREPARATION TIME: 5 minutes MAKES: 600ml (I pint)
2 large, very ripe bananas
150g (5112oz) strawberries
1112 tbsp olive oil
a little nutmeg or other spice, if liked 200ml (7fl oz) water
Peel the bananas and roughly chop the fruit. Combine all the ingredients in a blender until very

smooth. Serve immediately, or cover tightly and store in the refrigerator.
Variations: use a nectarine or a skinned peach instead of strawberries; use coconut milk (available in

tins) instead of olive oil, and the flesh of a small mango, or half a large mango, instead of

strawberries.

Immune reactions to food

Tuesday, May 19th, 2009

Immune reactions to food
`When I finally found someone who could say what was wrong with me, it was such a relief. I can’t tell you how much ill-health and pain and misery I’d had up to that point. I’m immensely grateful to the doctor who sorted the problem out for me. My life has been transformed.’
Richard has eosinophilic gastroenteritis, one of the rarer immune reactions to food. Like all rare diseases, it can escape diagnosis for a long time. IgE (the allergy antibody – see box on p. 12) is sometimes involved in eosinophilic gastroenteritis, but it is not an essential part of the reaction. Those who, like Richard, do not make IgE antibodies to the problem food will not give positive skin-prick tests. For them, the possibility of food being responsible for their symptoms may well be overlooked*.
Another difficulty for patients such as Richard is that most of the non-IgE immune reactions to food affect babies and children exclusively. A few of them can also occur in adults, but this is very rare, so it’s not something that automatically springs to mind when the doctor is searching for a diagnosis.
Eosinophilic diseases
The key event in these diseases is the arrival of large numbers of immune cells called eosinophils (see p. 19) in the walls of the digestive system. If the eosinophils converge on the tube leading down to the stomach (the oesophagus) the disease is called eosinophilic oesophagitis, and the symptoms include reflux (regurgitation) of food, occasional vomiting, refusing food (in babies), stomach pain and disturbed sleep.
If the stomach is the focus for the eosinophils, this is eosinophilic gastritis, and there is vomiting, pain, poor appetite and therefore poor growth. There can also be obstruction of the stomach outlet which may, in a few babies, produce pyloric stenosis (the main symptom is projectile vomiting).
When eosinophils flock to the intestines as well as to the stomach, the disease is called eosinophilic gastroenteritis. In
terms of symptoms, the picture is not much different from the previous condition, but there can be diarrhoea as an additional symptom, and babies may be irritable and puffy in appearance.
These conditions are most common in babies, but sometimes they continue through childhood. Very occasionally they occur in adults too.
Heiner’s Syndrome
This disease affects babies only, and is very rare. It is a severe form of cow’s milk sensitivity leading to wheezing and haemosiderosis (bleeding into the lungs). The child usually seems sickly, growth is slow, and there may be recurrent bouts of pneumonia. A full diagnosis requires blood tests to check for anaemia, examination of sputum under the microscope, and a biopsy or lavage (see p. 92) from the lung. The only effective treatment is to remove cow’s milk from the diet completely. Needless to say, this must be done under full medical supervision.
Other reactions to food
The cause of these diseases is not fully understood, but the immune system is clearly involved.
Dietary protein entero-colitis syndrome
In babies, the symptoms begin with general irritability and vomiting between one and three hours after a feed. Unless the offending food – usually cow’s milk – is withdrawn promptly, there will be bloating, diarrhoea (usually containing blood), anaemia, and poor growth. Older children have similar symptoms, while adults suffer terrible nausea, plus stomach pains and vomiting.
Nickel in food
Nickel and other metals in food may cause immune reactions for those with sensitivity to such metals (see pp. 55-6). The symptoms are usually in the skin, but there can be a few digestive symptoms too.
Dietary protein enteropathy
The main symptom here is diarrhoea, usually very severe. Often babies vomit their feed as well. Most have little appetite, and if the offending food is not withdrawn they suffer from poor growth, anaemia and other signs of malnutrition. This is because damage to the lining of the gut prevents nutrients from being absorbed properly. Older children show similar symptoms.
Dietary protein proctitis
This is a far less severe problem. The babies with this disorder look healthy, but there is inflammation in the bowel and small amounts of blood are passed with the faeces.
Diagnosis
There are two aspects to diagnosis:
• what kind of disease is it?
• what food or foods are causing the reaction?
Your doctor will probably try to answer the first question by looking inside the digestive tract with special equipment (endoscopy) and by taking a small sample – a biopsy (see p. 92).
A blood sample may also be taken to look for raised levels of immune cells and antibodies. Skin-prick tests or RAST tests (see pp. 91-2) will be tried to rule out the possibility of true food allergy – and because IgE may play a small part in these other forms of food sensitivity (in the eosinophilic diseases, for example).
Often the tests yield no very clear answers, especially in babies, and an exact diagnosis is not possible. But failure to answer the first question does not mean that the second question should be ignored. Pinpointing the culprit food or foods is vital.
Identifying the food is easier the younger the child, simply because the range of foods eaten is so much smaller. Cow’s milk is the most common offender when the disease affects young children – particularly bottle-fed babies, since standard infant formula is made with cow’s milk. Your doctor will prescribe an alternative formula (see box on p. 66) for you to try. For older children and adults, an elimination diet will probably be required to identify the food concerned. Among young children, likely offenders include soya, egg, wheat, rice, chicken or fish. A simple elimination diet, similar to that used for atopic eczema (see p. 198) may be adequate. You must have full medical supervision for this.
In the case of eosinophilic reactions, skin-prick tests may help identify the foods concerned, but are usually of limited value, so an elimination diet is again necessary. Where adults are affected by eosinophilic diseases, sensitivity to several different foods is likely, so identifying the offending foods usually requires the most exacting form of elimination diet, using an elemental diet for the exclusion phase (see box on p. 196). The symptoms are very slow to disappear: it can take up to eight weeks of avoiding the foods before your ailing digestive tract recovers. Don’t give up too soon.
Treatment
Avoidance is the only way here. Special infant formula (see box on p. 66) is required for cow’s milk sensitivity in babies.
In the case of eosinophilic reactions, some doctors may use steroid tablets as an additional treatment, just for a few weeks, to get the inflammation under control. Some new studies show that the anti-leukotriene drugs (see p. 149) are very effective for eosinophilic gastroenteritis.
Controversial topics
According to some doctors, a reaction to food may, on rare occasions, produce vasculitis (inflammation of the blood vessels).
Vasculitis itself is a well-recognised condition. The blood vessels are damaged by inflammation, and become more leaky. Symptoms often begin with a general swelling (angioedema), and an outbreak of small red blotches deep in the skin — especially on the legs — where small amounts of blood have escaped. These blotches later turn purplish, then yellow, before fading. This type of rash is known as purpura. Sometimes there are larger emissions of blood, resulting in spontaneous bruising.
Many different conditions can cause vasculitis, but only a few doctors would agree that food sensitivity is one of them. The inflammation could be caused by circulating immune complexes containing food antigens bound to antibodies (see p. 13). There is evidence, in some patients, of a direct effect on the cells called platelets that cause blood to clot.
Equally controversial is the suggestion that food sensitivity can be the cause of trouble for some children with kidney disorders. Some research groups have found that a few children with certain kinds of kidney disease recover on an elemental diet (see box on p. 196). All those affected have a classical allergic disease such as asthma or atopic eczema as well, and they tend to be sensitive to several different foods, plus pollen or other airborne allergens. Circulating immune complexes might be involved here, but no one is sure.
Some cases of food-related rheumatoid arthritis and palindromic rheumatism (see p. 76) could be due to immune complexes involving food molecules becoming deposited in the joints, but it is not the mechanism in all, or even most, of those affected.

Coeliac Disease

Tuesday, May 19th, 2009

Coeliac Disease
During World War 11, there was no bread to be had in the Netherlands and people were forced to eat tulip bulbs. ‘My mother roasted them,’ one survivor recalls, ‘and they tasted delicious then, because we were so hungry I suppose. I cooked some years later, just to taste them again, and they were absolutely disgusting.’
While most of the population was thin and unwell on this starvation diet, a few children were actually healthier than before. An observant Dutch doctor noted that these were the children who, before the war, had suffered from constant diarrhoea, fatigue, poor growth and muscle wasting. They were suddenly stronger and, his enquiries revealed, their diarrhoea had vanished. But when the food situation improved at the end of the war, all their old problems returned. By carefully experimenting with the diet of these patients, the doctor discovered that eating wheat and rye caused the symptoms. Subsequent research has revealed that both contain a collection of proteins, referred to as gluten, which are the source of coeliac disease.
Belly disease
Coeliac disease (or celiac disease) is an old name which simply means ‘belly disease’. It is derived from the Greek word for’belly’ — koilia. Once the cause of the symptoms became understood, a new name was devised — gluten-sensitivity enteropathy — but it has not really caught on. Other terms that you may come across are non-tropical sprue and coeliac sprue, based on the close resemblance of the symptoms to those of tropical sprue. This disease, found in those who live or have lived in the tropics, is probably caused by bacterial infection. There is no causal link with coeliac disease.
Symptoms
The symptoms of coeliac disease are:
• diarrhoea, with pale, bad-smelling stools
• in a few patients, constipation rather than diarrhoea, but this is very rare
• bloating and wind
• damage to the lining of the intestine. This is of a characteristic type: the complex folded structures (the villi) of the intestinal lining are destroyed. Additionally, huge numbers of immune cells are present.
• the loss of the villi results in failure to absorb nutrients from food (malabsorption) causing poor growth in babies, and weakness and weight-loss in adults.
• poor appetite, especially in babies. This can greatly reduce the diarrhoea.
Coeliac disease usually appears in babies during weaning, a few weeks after cereals are introduced, but it can also begin for the first time in adults. The tendency to coeliac disease is genetically inherited, so it runs in families.
Where coeliac disease runs in the family, another disease, dermatitis herpetiformis, is also likely to occur. Dermatitis herpetiformis has the same basic mechanism as coeliac disease but very different symptoms:
• an intensely itchy rash, sometimes with tiny blisters; the rash is symmetrically distributed on the buttocks, shoulders, scalp, and the outer surfaces of the knees and elbows
• the same characteristic damage to the lining of the intestine as seen in tests for coeliac disease, though generally less severe
• diarrhoea, in some cases, but not all. About 5% of those with coeliac disease actually go on to develop dermatitis herpetiformis. Most people have either one or the other.
Both diseases are caused by the same gene, which results in sufferers developing antibodies against one of their own proteins, an enzyme called tissue-transglutaminase. The job of this enzyme, which is found in the intestines, is to assist with the breakdown of gluten.
If no gluten is present, the enzyme does not arouse the interest of the immune system. It is the process of gluten digestion, in which a particular peptide is produced from gluten, that provokes the autoimmune reaction. (A peptide is any short length of protein chain, obtained from the complete protein chain by digestion.)
What seems to trigger the autoimmune reaction is this enzyme–peptide combination: the offending peptide, newly produced and still attached physically to the enzyme. There is something about the particular ‘chemical picture’ that this combination makes which outrages the immune system of individuals with a particular genetic make-up.
The impact of this autoimmune reaction on the intestinal lining is severe in coeliac disease, less so in dermatitis herpetiformis. What causes dermatitis herpetiformis is a particular type of antibody, called dimeric IgA, which is transported by the bloodstream from the gut to the skin. It is deposited in the skin all over the body, but for some reason only provokes inflammation in certain areas.
In rare cases, an IgE-mediated food allergy to wheat can co-exist with coeliac disease, making reactions more severe.
Secondary problems
Paradoxically, while the damaged gut lining of untreated coeliac disease makes a poor job of absorbing specific nutrients (e.g. iron and vitamins) in a form that the body can use, it also lets through far more intact, or partially digested, food molecules. These get into the bloodstream in such numbers that they can lead to idiopathic food intolerance (see p.74). Sensitivity to soya is a common problem, because it is so heavily used in gluten-free bread and other prepared food. Those with coeliac disease who have not improved fully, despite a strict gluten-free diet, often benefit from an elimination diet (see p. 194). This must be done under medical supervision.
Another possible effect of the intestinal damage is lactose intolerance (see p.79), producing a sensitivity to milk.
The frequency of schizophrenia is higher among those with coeliac disease than among the general population. Coeliacs not following a strict gluten-free diet are also vulnerable to other psychological problems. These might be linked to the effects of food-derived exorphins (see pp. 76-7) and other peptides on the brain. The increased permeability of the gut could play a part in this, allowing more exorphins to reach the bloodstream.
Diagnosis
A biopsy (see p. 92) is the only really reliable form of diagnosis. It is crucial that this is done before removing gluten from the diet, because the damage is repaired if gluten is avoided and the healing process is fairly rapid for some people (though in others it takes many months). If the intestinal lining reverts to a normal appearance quite quickly, an accurate diagnosis is never obtained, which can have serious consequences: if you or your child are coeliac, you need to know.
New blood tests can also be helpful in diagnosis, but they do not give the unequivocal result obtained with a biopsy.
Research from the United States suggests that coeliac disease is under-diagnosed in some countries compared to others – for example, Italy screens children routinely but the States does not. Some authorities suspect that there is a great deal of ‘hidden’ coeliac disease in the States, and this could be true in other countries as well. There is no routine screening of children in Britain.
The symptoms of coeliac disease are not always distinctive. Many cases are first detected when patients with rather non-specific symptoms are discovered, by a blood test, to be anaemic.
Treatment
There are no drug treatments for coeliac disease and avoiding gluten religiously is the only way to remain well. Those who are lax about their gluten-free diet may be more vulnerable to certain cancers of the digestive tract.
A strict gluten-free diet is not easy to follow (see p. 177). The most severely affected coeliacs are so sensitive to gluten that they react violently to even a tiny amount: this is known as coeliac shock and can be fatal.
A gluten-free diet is also the treatment for dermatitis herpetiformis, but at the outset the rash can be controlled with the highly effective drug dapsone.

Food Intolerance in Allergy

Monday, May 18th, 2009

Food Intolerance
The comments of those who have recovered from food intolerance after many years of ill-health are always memorable. ‘It’s like getting my life back again,’ said one woman. ‘I had actually forgotten what it felt like to be well,’ said another, ‘the effect of cutting out certain foods was just amazing.’
For most of those with food intolerance, the disease begins very subtly and gradually – first one symptom (persistent and unexplained diarrhoea, perhaps) then, some years later, another (migraine or headaches) and then, when a few more years have passed, another symptom (such as joint pain or muscle aches). Steadily increasing levels of irritability, `fuzzy-headedness’ or inexplicable tiredness may accompany this decline in health.
Most patients have no idea that all these symptoms are connected until they try an elimination diet, and everything clears up at once, quite dramatically. As one former sufferer described it: `Some of the stuff that got better – well, I’d been like that so long I thought it was just the way I was –grumpy and exhausted, and feeling terrible if I didn’t eat meals on time. It was an absolute revelation to feel completely OK again.’
What does ‘food intolerance’ mean?
In this book, food intolerance means any reaction to food where the immune system has no proven central role.
All the people I have described so far have idiopathic food intolerance, which means, food intolerance with no established mechanism – in other words, doctors can’t say exactly how it is caused. This is a highly controversial area.
The definition of food intolerance used in this book means that it also includes metabolic abnormalities, which do have a well-established cause. These are due to defective enzymes (see upper box on p. 75).
The question of what words mean is a key part of the debate over idiopathic food intolerance. At one extreme, you may come across doctors who call this problem ‘food allergy’, using the original meaning of the word ‘allergy’ (see p. 6). (Some of these doctors use terms such as delayed food allergy and masked food allergy, to point up the distinction from true food allergy, but not all do.) Using the word ‘allergy’ in this context causes a lot of aggravation and confusion, so the term ‘food intolerance’ has, for a long time, been widely accepted as a useful one that avoids unnecessary conflict.
You will also hear the term ‘food intolerance’ used to mean idiopathic food intolerance only – this is probably the most common usage. When the term is used in this way, metabolic abnormalities are being thought of as a separate entity altogether.
A new twist has recently been added to this long-standing wrangle over meanings. When mentioning food intolerance in their literature, some of the major medical organisations (those who dispute the very existence of idiopathic food intolerance) now say simply ‘food intolerance e.g. lactase deficiency’. To anyone familiar with this field, it looks suspiciously like an attempt to redefine ‘food intolerance’ so that it means nothing more than ‘metabolic abnormalities’. The idea seems to be that, if you deny a disease a name, it will go away!
In the medical wilderness
The main text of this article is about idiopathic food intolerance, a disease with a distinctly dubious reputation among doctors. Because it is so controversial, few doctors actually look at the evidence that it exists – which is in fact quite strong (see box on p. 77). Such evidence is simply ignored in most of what is written by the major medical organisations debunking idiopathic food intolerance.
This lack of medical recognition is very unfortunate for patients with idiopathic food intolerance, whose debilitating symptoms could be eliminated, rather than simply being treated (usually to little effect) with drugs.
This prejudiced attitude to idiopathic food intolerance also plays into the hands of those offering bogus diagnostic tests and phoney treatments, often at a very high price. These practitioners
– who have moved in to fill the gap left by conventional medicine
– are a considerable part of the problem, helping to give idiopathic food intolerance a bad name.
The waters are muddied even more by the fact that some people who believe themselves to have food intolerance are actually suffering from psychological problems, which they prefer to attribute to food. Many more have picked up on food intolerance as something rather glamorous to suffer from, inspired by all the media reports about food intolerance among celebrities. All these patients are a good source of revenue for the less scrupulous fringe practitioners and are unlikely, therefore, to be discouraged from their beliefs.
Fortunately there are enough conventional but open-minded doctors, often GPs, who have come to realise, through experience with their own patients, that elimination diets have a remarkable curative effect for some people. The ones who benefit are often the doctor’s ‘old faithfuls’ – those with long-term multiple symptoms, who have been referred to innumerable specialists and treated with all kinds of drugs, but who never get much better. The conventional view of such patients is that they have psychological problems that are being expressed as physical symptoms. This may well be true for some – but others have idiopathic food intolerance.
One of our enzymes is missing
Metabolic abnormalities are a distinct type of food intolerance. Unlike other kinds of food intolerance, metabolic abnormalities have a clearly understood cause: an enzyme that carries out a crucial task in the body’s metabolism is either missing or inept. The problem is generally caused by a defective gene and is therefore inherited.
The most common metabolic abnormality is lactase deficiency leading to lactose intolerance (see p. 79) — this may or may not be inherited. Other metabolic abnormalities include:
trehalase deficiency, lack of the enzyme which breaks down a substance in mushrooms and most other fungi, including yeast. galactosaemia, a defect in the enzyme which processes galactose, one of the sugars found in milk (cow’s or human). This is a serious disease and sufferers must avoid milk scrupulously.
fructose intolerance, which is extremely rare. Those affected have an unpleasant taste in the mouth on eating fruit and other sources of fructose, so avoidance is no particular problem.
phenylketonuria, also very rare. Those affected are usually identified early in life, by a routine blood test.
Is it just placebo effect?
Doctors who doubt the very existence of idiopathic food intolerance will say that people who recover on an elimination diet are just experiencing placebo effect — a psychological response that operates with any treatment, whether effective or ineffective, simply because people believe that the treatment will work. But this is to ignore certain facts:
• Placebo effect produces a fairly small improvement in most people — you have to be very suggestible to feel enormously better. By contrast, when people respond to an elimination diet (the standard method for diagnosing idiopathic food intolerance —see p. 194) they usually have a sudden and dramatic improvement.
• Most of those with idiopathic food intolerance have had it for years and tried all sorts of treatments. They have often experienced some small benefit from these, probably placebo effect. When they try an elimination diet, they have a response that is in a completely different league.
• The idea that all the different symptoms are linked has never occurred to many people who try an elimination diet — they are often trying it for just one symptom, and are staggered when everything clears up. Placebo effect relies on expectation.
• Placebo effect doesn’t last very long — it fades over the ensuing weeks and months. Avoiding the culprit food usually produces a lasting improvement for those with idiopathic food intolerance.
Symptoms
The symptoms of idiopathic food intolerance come on slowly after eating the offending food, and the foods to blame are often those eaten very regularly, such as wheat or milk. Consequently, the symptoms from one meal tend to overlap with those from the previous meal and people with idiopathic food intolerance are more-or-less unwell for most of the time. It Is usually not obvious that food is at fault.
All the symptoms of idiopathic food intolerance are common ones that can be caused in other ways. And no two patients have exactly the same set of symptoms.
(As far as doctors are concerned, neither of these attributes gives the disease a respectable air.)
These are some of the symptoms commonly reported:
• headache or migraine
•diarrhoea, sometimes with bloating and wind; this is often diagnosed as irritable bowel syndrome (IBS)
• in children, stomach aches
• occasionally constipation
• nausea and indigestion
• joint pain
• aching muscles
• a constantly runny or blocked nose (this could be perennial allergic rhinitis linked to food – see p. 68)
• glue ear (see p. 29)
• fatigue and a general feeling of vague ill-health.
Asthma and eczema, triggered by specific foods (see p. 68), can also be part of the picture.
In babies, colic is often caused by food intolerance, including foods the mother is eating which come through into the breast milk in tiny amounts (see p. 202).
Less common symptoms include:
• recurrent mouth ulcers
• stomach or duodenal ulcers
• chronic urticaria (see pp. 50-53)
• swelling (angioedema).
The following diseases have also been linked to idiopathic food intolerance in some patients:
• Crohn’s disease
• palindromic rheumatism (intermittent episodes of joint inflammation)
• rheumatoid arthritis.
Psychological problems such as depression, anxiety, or hyperactivity in children can sometimes be due to food (see p. 80) but it is rare for such psychological effects to occur without any physical symptoms.
Remember that every single one of these symptoms and conditions can be caused in some other way. However, the constellation of migraine/headache, joint pain and diarrhoea is highly characteristic of idiopathic food intolerance.
How might intolerance be caused?
No one knows how idiopathic food intolerance is caused. There are probably many factors involved, with a slightly different mix of factors in each patient. This would help to explain why the symptoms are so extraordinarily varied, with no two sufferers exactly alike.
Although symptoms accumulate over the years, some people can in fact pinpoint the moment when their problems began. ‘I had this terrible bout of diarrhoea from eating too much melon. I lived near a farm and they were free, because of a glut, so I just gorged myself on them. Although I was over the diarrhoea in a couple of days, I was never what you’d call “regular” after that, and the least thing would upset me. Eventually the doctor said it was irritable bowel syndrome. When the other problems began, ages afterwards – headaches and hypoglycaemia and fatigue – it seemed like something quite separate. I never associated them in my mind with the diarrhoea.’
Bad diarrhoea can clear the intestines of their beneficial bacteria, known collectively as the gut flora (see p. 204), and this is probably what initiates food intolerance in such cases. Large doses of antibiotics (as are sometimes given before an operation, e.g. a hysterectomy), or prolonged and repeated courses of antibiotics, given for glue ear or acne, can also disrupt the gut flora and lead to food intolerance. A study of hysterectomy patients has shown that antibiotic treatment before the operation tends to result in irritable bowel syndrome – a common symptom of idiopathic food intolerance – afterwards.
A few interesting observations suggest that minor metabolic abnormalities – a defect in certain detoxification enzymes – may sometimes play a part in idiopathic food intolerance. This is especially likely where there is intolerance to food additives, or where there are behavioural symptoms (such as hyperactivity) or symptoms involving the nervous system (such as migraine).
A third factor that could play a part for some patients are food-derived exorphins. These are fragments of proteins (called peptides) produced by the digestion of food proteins. They happen, probably by pure coincidence, to resemble the substances called endorphins that we all produce for ourselves. Endorphins
are our internal painkillers. They modify nerve impulses in the body and brain, reducing sensations of pain, and improving the sense of well-being. The receptors to which they bind are the same receptors that bind morphine and heroin - it is the intensive stimulation of these receptors that makes these drugs so effective.
Food-derived exorphins may sound like the stuff of science fiction, but they have actually been demonstrated in the digestion products of wheat and milk. They may exist for other foods as well. They are nowhere near as strong as morphine, but do seem to improve mood.
These exorphins may explain the strange observation (made repeatedly, by a great number of initially sceptical doctors) that patients with idiopathic food intolerance often eat huge amounts of their offending food, and ‘can’t live without it’. Often they eat the food several times day, sometimes at every meal. With a ubiquitous ingredient like wheat or milk, this is not particularly difficult - wheat cereal and milk for breakfast, a cheese sandwich at lunchtime, pasta with a creamy sauce for supper, a milky drink and biscuits at bedtime.
Any of these abnormalities is likely to be just one factor in a multi-factorial disease.
Diagnosis
Unfortunately there are no simple accurate tests for idiopathic food intolerance. The kind of tests you may see offered commercially (in advertisements in health magazines for example) are very inaccurate, and a waste of money. Consequently, the only way to diagnose idiopathic food intolerance is through an elimination diet, in which you cut out all the foods you commonly eat, and then -if you get better - test them one by one.
It sounds easy but it isn’t, so make sure you read all the instructions for doing the diet before you start (see pp. 194-7). You should also see your doctor and get his or her approval. Some symptoms - such as severe diarrhoea or headaches -should be investigated by conventional methods first, in case there is some serious underlying cause.
The first step in diagnosis is to decide if a food really is the cause of the symptoms, and the second step is to identify the food or foods concerned.
The first step is crucial. One of the problems with the diagnostic tests that are advertised - such as those using samples of hair or blood - is that they begin with the second step. In other words they assume that food is the problem (see p. 93).
When it comes to the second step, remember that although common foods are often the culprits, almost anything that is eaten can cause idiopathic food intolerance. Every patient with this problem is different in the foods they react to.
Treatment
Avoidance of the food is usually the best treatment for idiopathic food intolerance - however most people do not have to avoid their problem foods for ever. After a while - it could be six months or it could be three years - you can usually go back to eating it again, but in moderation. You must never start eating the food in large amounts again, and it is best not to eat it every day - certainly not at almost every meal, which is the usual pattern for cow’s milk and wheat in the Western diet.
If you find the restrictive diet too difficult, you could try desensitisation treatment (see pp. 210-13). This can work very well.
The patients who should avoid the culprit food indefinitely are those with Crohn’s disease and rheumatoid arthritis: a severe and irreversible relapse can occur otherwise.
The evidence
The evidence for idiopathic food intolerance is more substantial than its opponents would have you believe.
One very well-conducted and interesting study involved children with severe migraine who were investigated by a research team at Great Ormond Street Hospital in London. These are children who are very difficult to treat successfully by normal means. On an elimination diet, 88% of those children got better — an astonishing number. Not just their migraine, but all sorts of other symptoms as well, including aching limbs, runny noses, asthma, eczema, diarrhoea, wind, mouth ulcers and hyperactivity. Some of these children also had epileptic fits, and even this symptom cleared up on the diet, recurring when culprit foods were tested.
A notable feature of this study is that, of the five researchers involved, four were deeply sceptical at the outset. Their report notes that they ‘embarked on this study believing that any favourable response, such as that claimed to substantiate the dietary hypothesis, could be explained as a placebo response. The positive double-blind controlled trial… provides clear evidence that a placebo response was not the explanation.’
Other studies with good scientific credentials have demonstrated a role for idiopathic food intolerance in adults with migraine, and for sufferers from irritable bowel syndrome and Crohn’s disease. There are also good studies of individual patients with rheumatoid arthritis and palindromic rheumatism (an episodic form of inflammatory arthritis) who have responded dramatically to avoidance of a particular food. Some of these patients were given several double-blind challenges and showed changes in certain immunological tests, as well as joint symptoms, when challenged with the offending food. This suggests that the immune system could be playing some part in these food reactions.

Atopic Eczema

Monday, May 18th, 2009

Atopic eczema
A Greek word meaning ‘to boil over’ or ‘to erupt’ is the source of the medical term ‘eczema’. It refers, of course, to the way in which the skin erupts into a rash, but it could equally well describe the eruption of controversy around this disease. No other allergic disease is quite such a cauldron of dissent - indeed, even the question of whether it is an allergic disease remains unresolved. These controversies directly affect the treatment of atopic eczema, so it is useful to understand them if you or your child have eczema.
The disagreement begins with the question of what causes atopic eczema.
Let’s start with the one point that everyone agrees on: dry skin plays a fundamental role. Those with atopic eczema have dry skin, not just in the eczematous areas, but in other parts as well, sometimes all over the body. The skin cells are less efficient than normal skin cells at retaining water.
Everyone would also agree that there is inflammation of the skin – a reaction that is produced by the immune system. But when it comes to the question of what starts off the inflammation there are huge differences of opinion among specialists treating atopic eczema – these specialists include dermatologists, allergists and paediatricians.
Since people with atopic eczema are atopic (allergy-prone), and most have
huge amounts of the allergy antibody, IgE, going round in their blood, it might
seem plausible that an allergic reaction to some external item kicks off the
inflammation. And when skin-prick tests (see p. 91) to common allergens such
as house-dust mite are tried, there are usually a large number of positive results.
But many of these turn out to be false positives – when tested more directly,
the allergen concerned does not actually play a part in causing the skin symptoms.
This has led some specialists working with eczema, mainly dermatologists, to
What the words mean
Eczema is not a disease in itself. The word refers to a certain type of reddish rash — a rash which can be caused in a variety of ways. The type of eczema that affects people of an allergic disposition (atopics), is called either atopic eczema or atopic dermatitis.
The word dermatitis just means inflammation of the skin. Most doctors consider it to be synonymous with eczema, but some give it a slightly broader meaning.
believe that allergic reactions play little part in either initiating or perpetuating atopic eczema. In their view, the basic cause of atopic eczema is dry skin and a generally overwrought immune system, not specific allergic reactions.
To some of these doctors, positive skin-prick tests are all false positives in atopic eczema – that is, irrelevant to the disease process. A positive skin-test result, in their opinion, simply indicates that the skin of atopic eczema sufferers is in a highly sensitive state, not that the allergen concerned plays any causative role.
Allergists tend to take a different view of this, as you might expect. And recent research shows that they are correct – allergens often do play a significant part in provoking atopic eczema.
Research using direct challenge tests (see p. 90) has identified some of the things that could provoke such sensitivity reactions:
• house-dust mites, pollen or moulds
• cats, dogs, rabbits and other furry pets
• cow’s milk or other food – a prime suspect in babies and young children (see p. 68). The response to food is usually delayed, occurring some hours after the item is consumed.
With mite, pollen and pet allergens, the eczema symptoms can be provoked either by allergens falling on the skin, or by direct contact (e.g. mite allergens in the bed, skin contact with pets, or lying on grass for those with grass-pollen allergy).
The rash tends to occur on skin not covered by clothes, as you would expect. But it can sometimes occur only on particular exposed areas – usually the most sensitive areas of skin. For example, there are people who react to house-dust mite but have eczema on the eyelids only.
Additionally, experiments show that even when an airborne allergen is only inhaled it can sometimes provoke eczema symptoms. The allergen probably reaches the skin in the bloodstream. (Alternatively, it might provoke an immune reaction in the airways which generates chemical messages of the kind that promote inflammation – these then reach the skin in the blood.) This means that the skin reaction could occur anywhere on the body, not just on exposed skin.
In the case of food, the molecules of food that cause the trouble are probably being absorbed from the stomach without being completely broken down. They then reach the skin via the blood to provoke a reaction there. (Or, again, it could be an inflammatory messenger chemical travelling from the gut to the skin in the blood.)
When food gets directly onto the skin – which it frequently does with small children, of course – it can provoke a reaction that way too. This may be a slow eczema-causing reaction, or a much faster reaction known as contact urticaria (see pp. 50-51). Reacting to food with contact urticaria is quite common in children with atopic eczema – but the same food doesn’t necessarily provoke atopic eczema when it is eaten. (However, eating these foods can sometimes trigger anaphylaxis – see pp. 58-9. They should therefore be treated with great caution.)
At the same time as all this research – which shows for sure that allergens play a part in atopic eczema – others have been asking what actually happens when skin reacts to an allergen. Their studies have turned the accepted understanding of allergies upside-down. They show that when something like egg or pollen provokes atopic eczema, what is occurring isn’t necessarily an allergic reaction of the usual sort, with IgE and mast cells (see
box on p.12). Instead, other immune cells are causing the trouble. Sometimes IgE is involved, but without mast cells. Sometimes neither is involved. These revolutionary discoveries are described in more detail on pp. 18-19. One interesting realisation from this research is that in different eczema sufferers, different immune reactions may be producing the rash – even if they are reacting to the same allergen! This helps to explain why the results of skin tests are so inconsistent and puzzling.
The wandering rash
For a baby with atopic eczema, the face, and especially the cheeks, are commonly affected, but there may be a rash all over the legs, the backs of the arms, and the back. As the months go by, the rash settles on the lower legs, and spreads to the fold of the elbow, and then the fold at the back of the knees — by about three years of age, this flexure eczema is the main problem for most children.
In adults, eczema is often found in quite restricted areas, such as the hands, scalp, lips, eyelids or chest. It may be located around the nipples — a sensitive spot where rubbing by clothing is enough to initiate a rash.
Atopic eczema is always in a process of change, and different parts of the body may display different stages of the rash:
• The rash is red and usually dry at first, and there may be not a great deal to see. In this early stage the visible signs may be minimal, while the itchiness can be colossal. Sometimes there is oozing of clear fluid.
• Occasionally the first phase is more marked, with dense patches of small red bumps or tiny blisters. On the hands, these may merge to form larger blisters.
• Infections tend to change the appearance of the rash (see p. 44).
• With time the skin becomes thicker, paler and scaly. It may form leathery patches (called lichenification), especially if there is habitual scratching or rubbing. This is chronic eczema.
• When the eczema clears, there may be an area of skin that is lighter in colour, or darker, than the surrounding skin.
The next step
Whatever causes atopic eczema, it provokes the most horrendous itching, as every eczema sufferer knows. The itch cries out to be scratched, and scratching is the major cause of the visible rash. If left untouched, the skin does not erupt into eczema, although it may well turn red, and there are still distinct changes in the skin that can be seen with a microscope.
Once eczema has erupted, the skin is no longer an intact protective layer that neatly separates ‘in-here’ from ‘out-there’. The skin becomes more permeable and loses its own natural moisture far more readily, so the dryness gets worse. At the same time allergens and irritants penetrate far more easily, causing yet more inflammation.
Something else compounds the damage: once atopic eczema is established, the immune system starts making IgE antibodies to the body’s own proteins, especially those found in skin cells. This helps explain why atopic eczema can become so severe and so entrenched.
Infections — another vicious circle
When eczema erupts and the skin barrier is breached, infections often become a problem. A regular source of trouble is the bacterium Staphylococcus aureus, a cause of the infection impetigo. This microbe invades eczematous skin far more readily than healthy skin, causing a prolific ooze with golden-yellow crusting.
Staphylococcus aureus produces a toxin known as a ’super-antigen’ which revs up the immune system to even more furious effort. This effort does not, unfortunately, oust the bacteria, but it does make the skin inflammation even worse. To add to their woes, many who are afflicted with atopic eczema start making IgE antibodies against Staphylococcus aureus toxins.
Infection with fungi (yeasts and moulds) is also a problem in atopic eczema (see p. 49), and there may be sensitivity reactions to these fungi.
The herpes virus, responsible for causing cold sores, can also invade eczematous skin, though this is much rarer. It worsens the eczema and produces fever and general weakness. There may also be flocks of small red bumps, each with a tiny dimple or blister at the centre. Any symptoms of this kind indicate that the patient needs urgent treatment.
Irritants and stress
People with atopic eczema are far more susceptible to everyday irritants such as wool and rough synthetic fabrics, soap, and traces of detergent left behind in clothes. Chlorinated water, either in swimming pools or from the tap, can also aggravate the skin, and even ‘hard’ water (found in areas with chalk or limestone bedrock) may be a factor.
Some air pollutants may play a part in atopic eczema. Researchers in Germany have found that children living close to busy trunk roads, or in homes with a gas cooker and no extraction hood (see pp. 128-9), were more likely to develop eczema. Formaldehyde fumes, often found in modern houses (see p. 129), are sometimes a factor when eczema affects the face and hands.

Sinusitis in Allergy.

Monday, May 18th, 2009

Sinus cavities are something that most people just don’t know they have. It’s only when they start to

hurt that you find out where they are. ‘There is this terrible throbbing pain above and around my eyes,

and in my cheeks. It’s the most unpleasant feeling, but it’s hard to describe to anyone who hasn’t felt

it,’ says Gina, who suffers from chronic sinusitis (long-term inflammation of the sinus cavities).

There are no figures, but chronic sinusitis seems to be increasingly common.
A sinus cavity has no function, it is just empty space without which our skulls would be much heavier.

In other words, these airy spaces seem to have evolved simply to help us feel more ‘light-headed’. If

you have sinusitis, unfortunately, you feel just the opposite. ‘I had sinusitis for years,’ says Dr

Wellington S. Tichenor, a New York allergist who now specialises in treating chronic sinusitis. ‘I kept

working but felt like I wanted to die.’
Sinus cavities are lined with a membrane which is essentially similar to that lining the nose. It

contains immune cells and can produce mucus when necessary. Most of the time it doesn’t need to produce

much, because relatively few microbes or foreign particles get into the sinus cavities.
Any mucus that is produced should escape from the sinus cavities through narrow drainage channels,

called Ostia, leading to the nose. Unfortunately, the Ostia are very narrow – the diameter of a

pin-head – and U-shaped, making them prone to blockage. And that is not the only problem. These

drainage channels are situated at the top rather than the bottom of the main sinus cavities – this

arrangement was fine for our ancestors who walked on all fours, and therefore did not have to fight

gravity when clearing their sinuses. Sadly for
us, natural selection has not got around to reorganising things yet. It would be a completely hopeless

arrangement if not for the tiny hairs known as cilia, which lie like a carpet across the membranes

lining the sinus cavities. The cilia beat rhythmically. 18 times a second, to waft the mucus upwards to

the top of the sinus cavity.
This is a far-from-perfect system, and it is hardly surprising that it sometimes goes wrong. Chronic

sinusitis can begin in at least three different ways:
• The sinus membranes become inflamed due to an allergic reaction – 28 for likely airborne

allergens.
• The drainage channels from the sinus cavities become blocked due to events in the nose

(infection or allergy) or due to the growth of polyps (non-cancerous jelly-like lumps that can block

the drainage channels). When mucus cannot drain away, it stagnates in the sinus cavities encouraging

infection by bacteria or fungi. These infections cause inflammation.
• A bout of acute sinusitis (see box on p. 31), due to bacterial infection, never really goes

away and the persistent infection causes longterm inflammation. Note that this is unlikely: it is rare

for acute sinusitis not to clear up.
Whether the problem begins through allergy or blockage or infection, once it has begun a vicious circle

can be set up all too easily. Mucus output increases when there is inflammation, blocking the drainage

channels even more, so the sinus cavities become clogged up and increasingly uncomfortable. More mucus

pooling in the sinus cavities perpetuates any existing infections and fosters new ones.
All this infection results in more severe inflammation, causing the membranes which line the sinus

cavities to swell up. Inflammation also makes polyp growth more likely. The cilia may be lost or

severely depleted, and the mucus gets thicker. All this means yet more blockage. To cap it all, there

can be allergic reactions to some of the microbes involved (see right), fuelling the inflammation

further.
The body’s own attempts to clear the sinuses are defeated, and the problem is also very resistant to

medical treatment. This may make depressing reading, if you have chronic sinusitis, but don’t despair.

Understanding the complexities of the problem is a large part of the battle. Chronic sinusitis is not

invincible, if you have a good doctor to help you - that means a doctor who also understands these

complexities.
The symptoms of sinusitis are:
• pain and a sense of swelling or unpleasant fullness around the cheeks, or over and between the

eyes
• earache or headache; pain around the teeth
• reduction in the senses of smell and taste
• sore throat
• coughing, particularly at night
• post-nasal drip (mucus from the back of the nose running into the throat and airways)
• bad-smelling breath
• feverishness
• for some people, severe fatigue, poor concentration and even (but very rarely) psychiatric

symptoms
• irritability, especially in children.
Note that any of these symptoms can be caused in other ways, and even if you have several of them, you

may not necessarily have sinusitis. On the other hand, sinusitis can go unrecognised - to some people

it may seem like nothing more than a lingering cold.
Acute or chronic?
In medical terms, ‘acute’ means short-lived, while ‘chronic’ means long-lasting.
Acute sinusitis — a short, sharp dose of it, lasting less than 3-4 weeks - usually follows on from a

cold. Colds are caused by viruses, but a bacterial infection can follow, and it is the bacteria that

move into the sinus cavities and cause trouble. Some people are far more susceptible than others and

have an attack of sinusitis after every cold.
Chronic sinusitis means symptoms lasting more than three months, according to some authorities, but the

time point is a little arbitrary. This article deals with chronic sinusitis.
If your sinusitis has been going on for between four weeks and three months you will obviously be

asking ‘Is this acute or chronic?’ At this point, no one can say, but you would certainly be wise to

seek some expert medical treatment now, on the basis that it could be the start of chronic sinusitis.

Tackling chronic sinusitis before the problem becomes
entrenched and complex is a good plan.
Allergy and chronic sinusitis
Chronic sinusitis is not necessarily an allergic disease, but it can be connected with allergies (or

other forms of immune sensitivity) in various ways:
• Allergic reactions can occur in the sinuses, usually in conjunction with allergic reactions in

the nose.
• Even if the allergic reaction does not affect the sinuses directly, allergic reactions in the

nose can block the drainage channels from the sinuses, causing an accumulation of mucus there. This may

lead to sinus infections.
• Once sinusitis has begun, infectious fungi (moulds) in the sinuses may provoke allergic

reactions, or other forms of immune sensitivity. This allergy to ‘the enemy within’ fuels more

inflammation and more mucus production. Right now, allergic fungal sinusitis (as it is known) is a

source of heated debate - 32. Allergic reactions to some of the bacteria that are present may also

occur.
• Chronic sinusitis - however caused - can contribute to asthma. Research on children with both

sinusitis and asthma found that 80% no longer needed asthma drugs once their sinusitis had been

treated, and 85% no longer wheezed. The link may be due to post-nasal drip, increased mouth-breathing,

or to a nerve-connection between the sinuses and the airways (the sinobronchial reflex) which can

stimulate airway inflammation. Alternatively, the sinusitis may simply fire up the immune system with

messenger chemicals in the bloodstream, resulting in more powerful responses throughout the body.
• Chronic sinusitis can also be the root cause of long-standing nettle rash (chronic urticaria),

and treating the sinusitis can result in a prompt and remarkable clearance of the skin symptoms.
• Some people who have chronic sinusitis are sensitive to aspirin (see box on p. 28) - a

sensitivity which is also linked with asthma, nasal polyps, rhinitis and chronic urticaria. Avoiding

aspirin and all other aspirin-like drugs (151) may substantially improve the sinusitis.
Diagnosis
Because so many different factors can play a part in chronic sinusitis, diagnosis should, ideally,

consider the problem from several different angles:
• The sinuses are viewed using X-rays and CT scans (computed tomographic scans - they use X-rays

but give a much more precise picture). These reveal how badly swollen the sinus membranes are, which

sinus cavities are blocked, and how much mucus has collected in the sinuses.
• Endoscopy (92) may be used to look inside the sinus cavities. Polyps are best located by this

method.
• Where allergies seem to be part of the picture, the doctor may employ skin-prick tests (91) to

identify allergies to airborne allergens (from house-dust mites, moulds, pets, pollen, cockroaches,

etc.)
• Laboratory tests on samples taken from your sinus cavities will be used to show which bacteria

and/or fungi have set up home there. There may also be a hunt for the immune cells known as eosinophils

(19) or the typical debris which they generate. The presence of large numbers of eosinophils is one

indication of allergic fungal sinusitis (see below).
• Skin testing with fungi (moulds) found growing in the sinus cavities may also be tried if

allergic fungal sinusitis is suspected.
• In severe cases, there may be tests of immune function, to see whether this is depressed in any

way.
• Children may be tested for an inherited disorder affecting the cilia, or for cystic fibrosis -

mild forms may escape detection, and can produce both chronic sinusitis and wheezing.
The enemy within
The biggest controversy in sinusitis research at the moment concerns allergic fungal sinusitis. The

orthodox view of this condition is that:
• It affects a small minority of chronic sinusitis patients -fewer than 10%.
• There is a true IgE-mediated allergic reaction to the fungus (mould) growing in the sinus

cavities. This allergic reaction is detectable with a skin-prick test (91). Immune cells known as

eosinophils (19) are also key players in the inflammatory reaction to the fungus, but it is an

IgE-response to the fungus that draws the eosinophils into the sinuses.
• There is clear evidence of fungal infection in the mem- banes of the sinus cavities.
• There may also be ‘fungus balls’ - a solid mass of fungus inside the sinus cavity. Or there may

be ‘allergic mucin’, a dark sticky mucus containing fragments of the fungus.
A rare complication
In rare cases, the fungi involved in allergic fungal sinusitis can be invasive, spreading from the

sinuses to the surrounding bone. This problem needs prompt and thorough treatment with anti-fungal

drugs.
In 1996, researchers at the Mayo Clinic in Rochester, Minnesota, USA, caused a rumpus by claiming to

have identified a different form of allergic fungal sinusitis which is overlooked by standard

diagnostic techniques, and which affects 96% of patients with chronic sinusitis.
This is a staggering figure - 96% means, in effect, that they are claiming to have found the

fundamental cause of virtually all chronic sinusitis. ‘Up to now, the cause of chronic sinusitis has

not been known. Our studies indicate that, in fact, fungus is the likely cause of nearly all of these

problems,’ states Dr David Sherris, one of the researchers.
According to the Mayo Clinic team:
• The fungi (moulds) are growing in the mucus of the sinus cavities, not generally in the

membrane itself. They are not detected by normal diagnostic methods which tend to ignore the mucus. A

special method of collecting the mucus is required to detect the fungi.
• The immune reaction to the fungi is not usually an IgEmediated reaction, so skin-prick tests

are often negative.
• Finding evidence of unusual numbers of eosinophils is adequate for diagnosis of allergic fungal

sinusitis because the eosinophils are the prime movers in this sensitivity reaction to the fungi, as in

several other diseases (19).
‘We can now begin to treat the cause of the problem instead of the symptoms,’ says Dr Eugene Kern, head

of the research team. There is a lot of scepticism about these claims among other sinusitis

specialists, and so far no new treatment for chronic sinusitis has emerged.
The Mayo Clinic researchers say that they are in the process of developing a drug treatment, but that

it will take several more years before it is generally available. Existing anti-fungal drugs (taken in

capsule form) could not work on this particular form of allergic fungal sinusitis (if it exists)

because the drug does not get into the mucus. Any new treatment would probably involve inserting an

anti-fungal drug directly into the sinus cavities, which is far from easy.
All we can do for now is wait and see what emerges from the ongoing research. The current treatment for

allergic fungal sinusitis involves all the usual methods (see right) with special emphasis on steroids

to calm the inflammation, plus anti-fungal drugs where fungal infection is detectable in the membrane.

In some countries, immunotherapy is also used to reduce the immune reaction to the fungus, but this is

difficult to obtain in Britain (164).
Clearing moulds from your home may help (34). So may reducing the humidity in the house (119), as humid

conditions seem to be linked with allergic fungal sinusitis.
Treatment
Sinusitis can be very hard to treat, particularly if it has been going on for a long time. You need a

really committed attitude if treatment is to be successful.
All these treatments should be given at the same time:
1 Antibiotics for 2-3 weeks minimum (it takes this long because the antibiotic has such trouble getting

into the sinus cavities – if you are offered a shorter course, this suggests that the doctor does not

have enough expertise with chronic sinusitis, so you might be better off with someone else). It must be

the right antibiotic – commonly used ones such as penicillin, tetracycline and erythromycin are

unlikely to work because the bacteria are usually resistant to them.
2 Steroid drops in the nose to combat the inflammation. It is important to put these in correctly, so

that they have maximum effect (144) especially if you have polyps.
3 Irrigating the nose and sinus cavities daily with sterile salt water (saline). Your doctor will show

you how to do this.
4 Tablets that reduce the congestion in the nose.
5 Nose drops that reduce congestion, but for three days only (29).
6 Steam inhalations to loosen the mucus. There are special steam vaporisers on sale (ask at a

pharmacy), but you can just inhale steam from a bowl of boiling water, with a towel over your head to

keep the steam in. Adding eucalyptus oil to the water may help. For a quick-and-easy version, warm up a

damp flannel in the microwave and place it over your nose. Some doctors recommend having a steam

vaporiser beside the bed at night, when nasal blockage is most likely to occur, but if you have

allergies to house-dust mite or moulds this is not a good idea in the long term, as a damp bedroom will

favour both (and could encourage allergic fungal sinusitis).
7 A drug called guaifenesin which thins the mucus is used in some countries but rarely in Britain.

Alpha-methyl-cysteine is another drug that breaks up mucus. It is mainly used in chronic bronchitis but

some doctors also find it valuable in chronic sinusitis. If steam inhalations didn’t work – suggesting
that the mucus is too solid to be shifted – these drugs may be worth trying.
8 Anti-fungal drugs (taken by mouth) if allergic fungal sinusfis is suspected. Sometimes these have a

dramatic effect on chronic sinusitis that has previously resisted treatment.
You may also be given other drugs, such as steroid tablets. The new anti-leukotriene drugs (149) are

also being tried, with some success. As well as being taken by mouth, they can be applied directly to

the nose in an irrigation fluid, and may be helpful for those with nasal polyps.
Problems with nose drops
Nasal drops and washes contain preservatives and other non-drug ingredients. Some of these may act as

irritants – or the pH (acidity or alkalinity) of the preparation might cause problems. If you

experience burning or irritation after inserting drops or irrigating the sinuses, ask your doctor or

pharmacist about trying a different preparation.
Antibiotic resistance
Bacteria are becoming resistant to the effects of antibiotics: it is probably the biggest headache

facing modern medicine.
This is emerging as a particular problem in chronic sinusitis because many patients have been dosed

very regularly with antibiotics. Although most of the bacteria have been killed each time, the fact

that the sinus cavity is so clogged up with mucus, and so badly accessed by the bloodstream anyway,

means there is always some nook or cranny where a few bacteria survive because they have not been

exposed to the full lethal dose of the antibiotic. As you might expect, these survivors tend to be the

‘tough ones’ – those bacteria that are not just well hidden but also the least sensitive to the

antibiotic.
Repeat this process many times, with frequent courses of antibiotics (separated by intervals during

which the hard-to-kill bacteria multiply in numbers) and what happens? Eventually you breed a race of

bacteria that are completely resistant to one or more of the antibiotics taken.
If you ever get to this point with your sinusitis, treatment is going to be extremely difficult. That’s

why it is so important to treat infections really thoroughly, and get rid of them completely. Expert

medical help is essential for this treatment campaign.
Too many people with chronic sinusitis are careless about taking their antibiotics regularly, or feel

ambivalent about them and stop the course before it’s complete, or don’t see the doctor again when the

tablets are used up. This is courting disaster.
Don’t start antibiotic treatment for chronic sinusitis until you are sure you can see it through. If

you have doubts about taking antibiotics, try all the other treatments and self-help measures first.

They may be sufficient, especially if you find you have an allergy underlying the chronic sinusitis and

can tackle this successfully.
Should there be no improvement, you could then go on to the antibiotic programme: delaying this

treatment for a few months will do no harm. What is hazardous is starting the antibiotic programme and

then stopping, or not taking the drugs consistently.
Antihistamines may be prescribed to treat any allergic reactions, but some specialists feel that they

can also aggravate the problems. In their experience, antihistamines dry out the mucus so that it

sticks to the walls of the sinus cavities, rather than being ushered out by the cilia. Drying out the

mucus may make you feel better initially, by reducing the pressure inside the sinus cavities, but it

makes matters worse in the long run.
Anti-chollnergic drugs (156) are sometimes prescribed for chronic sinusitis, but they too can dry up

the mucus and should be used cautiously.
After three weeks, if the sinusitis has not improved substantially, a different antibiotic is given. If

there are any bacteria resistant to the first antibiotic infesting your sinus cavities, the new

antibiotic is intended to kill them off.
Should you still have sinusitis after another three weeks, you will be given yet another antibiotic.

Changing the antibiotic, and taking prolonged courses, is the best way of exterminating the bacteria

completely, which prevents the development of antibiotic-resistant bacteria (see box at left).
It is crucial that you always see the doctor promptly at the end of each course, so that there is no

gap between the courses – do not give the bacteria any opportunity to build up their numbers again. The

last antibiotic treatment should continue for at least a week after symptoms clear up.
Dealing with allergic reactions is also important:
• If you cannot get allergy tests, try to work out for yourself if an allergen is playing a part.

Ask yourself if there were any changes in your life before the sinusitis began, such as getting a new

pet, moving house, increased exposure to moulds or house-dust mite, or starting a new job with exposure

to allergens. When thinking about this, remember that allergies to newly encountered allergens do not

develop immediately – it may take up to two years. Try avoiding the allergen concerned and seeing if

you improve.
• Should you discover that an allergen is at the root of the problem, but have difficulty

reducing your exposure to the offending item, try to obtain immunotherapy (164) or another form of

desensitisation treatment (210).
• If you suspect allergic fungal sinusitis (32), it is well worth eliminating any mould growth in

your home (120). One research study showed that the moulds growing in a patient’s sinus cavities were

often the same as those growing in the patient’s house. It is possible that, by inhaling the mould

spores from moulds in their houses, sinusitis sufferers are continually reinfecting their sinuses.
Various other self-help measures can be valuable during this medical treatment:
• Reduce your exposure to cigarette smoke (including other people’s) to an absolute minimum.

Cigarette smoke acts as an irritant to the nose and sinuses, but, more importantly, it paralyses the

cilia, preventing them from shifting mucus out of the sinus cavities.
• Avoid breathing other irritants, especially ozone (130). Think about the chemicals you use both

at work and at home – could any of these be irritants that are aggravating your sinusitis?
• Don’t drink too much alcohol – it dries out the sinus membranes and makes matters worse.
• Drink plenty of water, to keep your mucus from becoming too dry and therefore hard to shift.
• Try to breathe through your nose as much as possible. The amount of oxygen in your sinus

cavities drops drastically if you breathe through your mouth, and the low oxygen level probably fosters

the growth of certain bacteria. Devices, such as nose clips, that help keep the nose open at night may

be worth trying.
• Spicy food can help to clear nasal and sinus congestion, so try eating chilli or hot curry

regularly.
• Some people find that garlic helps – either eaten or sniffed.
• If you suspect that your sinusitis might be related to food sensitivity (68) consider trying an

elimination diet to identify the culprit food.
• Observe your reactions immediately after eating – some foods, such as yeast and red wine, can

cause an immediate swelling of the nasal membranes in certain people. So can sulphite food additives.

Avoid such items if you are affected.
• Treating gastro-oesophageal reflux (acid regurgitation from the stomach after meals) can

improve sinusitis.
• See an osteopath. By gently manipulating parts of your face, a good osteopath may be able to

improve the drainage from the sinus cavities.
• Some patients experience good effects from acupuncture although there are no observable changes

on CT scans. Other alternative therapies, such as homeopathy or Chinese herbal medicines, have not been

investigated scientifically, but some patients report good results.
Prolonged courses of antibiotics destroy many of the beneficial bacteria in the intestine, and may

cause long-term bowel problems. It makes sense to take a bacterial replacer (205).
Surgery for sinusitis
Chronic sinusitis sufferers may be offered surgery to remove polyps, or to correct anatomical problems

such as a deviated septum (the central division of the nose).
These operations can be very useful, but if you have asthma try all other options first, because

surgery to the nose can sometimes make asthma much worse.
Surgery on the sinus cavities themselves is also a possibility, when sinusitis does not respond to

medical treatment. The operation enlarges the natural drainage channels, so that mucus drains away more

easily. This rarely cures chronic sinusitis completely, but it usually makes it much easier to manage.

Once the drainage channels are larger, antibiotics can be put directly into the sinus cavities, for

example, avoiding the need for antibiotic tablets.
Don’t agree to surgery unless other forms of treatment, such as allergen avoidance or immunotherapy,

have been tried to the full. Patients for whom surgery seemed to be the only answer have sometimes

found they did not need an operation once their allergies were treated.
If you decide on having an operation, make sure your surgeon has a proven track-record with this type

of surgery. Don’t be afraid to ask searching questions about how many operations of this kind the

surgeon has done, how many he or she carries out per year, and the complication rates (how often things

go wrong). It’s a delicate job, and you want a real expert.