Posts Tagged ‘allergic condition’

potassium permanganate Purple crystals, soluble in water. A powerful oxidizing and deodorizing agent used 1:1000 as lotion, 1:10000 to 1:5000 as mouthwash, douche, bladder washout and bath.
povidone-iodine A complex of iodine with an organic carrier. When applied to the skin it slowly releases iodine, and has an extended antiseptic action. Used for local application to the skin and mucous membranes as solution containing the equivalent of 0.75-1 % of iodine.
pralidoxime A reactivator of cholinesterase. Organophosphorus insecticides inhibit that enzyme, and poisoning by such insecticides is an occupational hazard. Their toxicity can be reversed in part by the injection of 2 mg atropine, but the enzyme can be reactivated and muscle power restored by pralidoxime (30 mglkg) given by slow i.v. injection, repeated as required. It is effective only if given within 24 hours of exposure to the insecticide.
pravastatin A blood lipid-lowering agent with the specific enzyme-inhibiting properties of simvastatin, and used in primary hypercholesterolaemia not responding to the other drugs.
Dose: 10 -40 mg daily as a single dose. Side-effects include myalgia, rash and gastrointestinal disturbances. (Lipostat). See page 146 and Table 20.
prazinquantel A schistosomicide of low toxicity, effective against Schistosonia hamratobium, S, mansoni and S. japonicum It is also active against tapeworm. Dose: 10-20nig/kg as a single oral dose. (Biltricide).
prazosin An alpha-adrenoceptor blocking agent and vasodilator used in the treatment of hypertension and congestive heart failure.
Dose: I mg daily initially, increased as required up to a maximum of 20 mg daily. The initial dose may cause marked hypotension, and it should be taken at night, in bed. prazosin is also given in benign prostatic hypertrophy in maintenance doses of 4 mg daily. Side-effects are drowsiness, nausea and postural hypotension. (Hypovase). See page 148 and Table 21.
prednisolone A glucocorticosteroid with the actions and uses of hydrocortisone, but effective in much lower doses. It is often the preferred drug for oral use, and is given in a wide range of conditions including asthma, severe allergic reactions, rheumatoid arthritis, collagen disorders and inflammatory skin conditions. prednisolone is also of value in leukaemia, ulcerative colitis, the nephrotic syndrome, pemphigus, sarcoidosis, myasthenia gravis, haemolytic anaemia, agranulocytosis and other blood dyscrasias. Large doses are given in the immunosuppressive control of transplant surgery. The dose varies with the nature and severity of the condition being treated, and in every case the lowest dose required to evoke an adequate response should be used, after which the dose should be reduced in stages. Dose: in rheumatoid arthritis, 7.5-10 ing daily initially; other conditions may require doses up to 100 mg daily. Dose by i.m. injection 25-100 ing once or twice a week. Asa retention enema, 20 mg to relieve the inflammation of colitis and Crohn’s disease; as eye drops and ear drops, 0.5% solution. The side-effects are those of the corticosteroids generally, and include salt and water retention, hypertension, muscle weakness and peptic ulcer.
prednisone A glucocorticosteroid that is converted to prednisolone in the body, and so has the actions and uses of that drug.
prilocaine A local anaesthetic with the actions, uses and side-effects of lignocaine. (Citanest).
primaquine An antimalarial drug used mainly to prevent a relapse of benign tertian malaria after treatment with chloroquine, as it kills the malarial parasites that may still be present in the liver. Dose: 13 mg daily, for 2-3 weeks after chloroquine treatment. Side-effects are nausea and abdominal pain.

primidone An anticonvulsant used in the treatment of grand mat and psychomotor epilepsy.
Dose: 125nig daily initially, slowly increased as required up to a maximum of 1.5 g daily. Side-effects include drowsiness, nausea, blurred vision and rash. (Mysoline). See page 136 and Table 15.
probenecid A uricosuric agent that
increases the excretion of uric acid, and so is useful in the treatment of gout and hv
I peruncacrina.
Dose: O.5-2 g daily. An adequate fluid intake and an alkaline urine are necessary for the best response. probenecid also delays the excretion of penicillin and sonic cephalosporins, and is given in doses of 2 g daily to raise the plasma level of those antibiotics. Side-effects include occasional nausea, flushing and dizziness. (Benernid). ,See page 140 and Table 17.
procainamide A procaine derivative occasionally of value in the treatment of ventricular arrhythmias.
Dose: till to 50 mg/kg daily. It is also given by slow i.v. injection under E’C.C, control in doses of 25-50 ing/tininute up to a maximum of I g. Side-effects are gastrointestinal disturbances, lever and rash. (Prones(vi).
severe nausea and vomiting, 20 mg orally, or 12.5 mg by deep i.m. injection. It is also used as suppositories of 25 ing. (Stemetil). See page 168 and Table 30.
procyclidine An anticholinergic drug similar to benzhexol, used mainly in the treatment of parkinsonism. Reduces rigidity more than tremor.
Dose: 73-30 mg daily. In acute states it is given by i.m. injection in (loses of-i-10 mg, or 5 mg doses i.v. (Arpicolin; Kernadrin). See page 160 and Table 26.
progesterone The hormone of the corpus luicum, responsible for the preparation of the uterus to receive a fertilized ovum. It is used in dysfunctional uterine bleeding and in the premenstrual syndrome. Dose: 200-400 nig daily per ragina on a cyclic basis. (Cyclogest). Also a constituent of sonic oral contraceptives. See dydrogesteronc and norethisterone.
proguanil hydrochloride A synthetic antimalarial of high potency and low toxicity, used in the prophylaxis and suppressive treatment of malaria, often in association with chloroquine.
Dose: 100-200 rig daily, and continued for 6 weeks after leaving the infected area. (PaILICIrinc).
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procaine A local anaesthetic now largely replaced by lignocaine.
procaine penicillin An old long-acting loan of penicillin, given together with penicillin G to obtain a high initial blood level. It is now used mainly in early syphilis. Dose: 900 mg daily by Lin. injection for 10 days. (Ificillin).
procarbazine A cytotoxic drug used mainly as part of a multi-drug treatment of Hodgkin’s disease. It is also used to treat other lymphomas no longer responding to other therapy.
Dose: 50 ing initially, increasing to a maxiintini of 300 mg daily. Side-effects include nausea, anorexia and bone marrow depression. Alcohol may cause a disulfiram reaction. (Nitulan). See page 122 and Table 8.
prochlorperazine A tranquillizer with the actions, uses and side-effects of chlorpromazine.
Dose: in schizophrenia, 25-100 Tng daily; in severe anxiety, 15-20 mg daily. In
promazine A tranquillizer with the actions, uses and side-effects of chlorpromazine, but less potent. It is used mainly to
control agitation in the elderly, and in other minor conditions of psychiatric disturbance.
Dose: 50-800 ing daily, adjusted to need .111d response; by injection 25-50 mg. (Sparine).
promethazine A long-acting antihistamine with sedative properties. It is used for the relief of a wide range of allergic conditions, in mild insomnia and for preoperative sedation. It is also of value as an antiemetic in the prophylaxis and treatment of travel sickness, vertigo and drug-induced nausea.
Dose: 25-50 mg daily; 25-100 ing by deep i.m. injection. In anaphylaxis, sometimes given by slow i.v. injection in doses up to 100 mg to supplement previously injected adrenaline. The side-effects are those of the antihistamines generally. (Phenergan). See page 110 and Table 2.

propafenone An anti-arrhythmic agent of the lignocaine type, used in the prophylaxis and treatment ofventricular arrhythmias. Dose: under ECG control 450 ing daily initially, after food, increased at 3-day intervals up to a maximum of 900 mg daily. Side-effects are dizziness, gastrointestinal disturbances and postural hypotension. (Arythniol).
propantheline An anticholinergic agent used as a spasmolytic in gastrointestinal disorders, in urinary frequency associated with bladder neck weakness, and in nocturnal enuresis.
Dose: 45-120 mg daily at least I hour before food. Side-effects include dryness of the mouth and blurred vision. (Pro- Banthine). See page 174 and Table 33.
propofol A non-irritant short-acting i.v. anaesthetic for smooth induction and maintenance of general anaesthesia for up to I hour. Dose: 2-2.5 mgft initially, followed by Supplementary doses of 0.1-0.2
ing/kg1min as required but some local pain may occur. Side-effects include mild hypotension, transient apnoea an([ bradycardia. Recovery is normally rapid and uneventful but delayed recovery, convulsions and anaphylaxis have been reported. Care is necessary in cardiovascular, respiratory or renal impairment. (Diprivan).
propranolol A beta-adrenoceptor blocking agent that reduces the cardiac response to circulating adrenaline and noracircrialine. It reduces the load on the heart during
exercise and stress, and is used in the treatment of angina, coronary insufficiency, cardiac arrhythmias, hypertension, and after myocardial infarction. It also ameliorates the tremor and palpitation of transient anxiety and stress, and is useful ill the prophylactic treatment of migraine. Dose: 160-320 mg daily according to need. In arrhythmias and thyrotoxic crisis, propranolol is given by slow i.v. injection in doses of I ing, repeated up to a maximum of 10 ing. Side-effects are bradycardia, bronchospasni and gastrointestinal disturbances. Care is necessary in renal and hepatic deficiency, asthma is a contraindication. (Inderal). See page 146 and’I'able 21.
propylthiouracil A thyroid inhibitor occasionally used as an alternative to carbiniazole in hyperthyroidism. Dose: 300-450 ing daily.
prostacyclin See epoprostenol.
prostaglandin A generic term applied to a series of closely related hormone-like fatty acid derivatives, originally extracted front the prostate gland, but now prepared
synthetically. Prostaglandins are widely distributed in animal tissues, and have a complex and varying range of biological activity.’rhus they may have a smooth muscle stimulating or relaxant action, pressor, vasodilator, inflammatory or other properties. The anti-inflammatory action of aspirin and related drugs is due to an inhibition of prostaglandin synthesis. See alprostadil, carboprost, dinoprostone and genieprost.
protamine sulphate A simple protein obtained from fish sperm. It neutralizes the anticoagulant effect of heparin, and it is used in controlling the haemorrhage i hat may occur during heparin therapy. Dose: 1% solution i.v. according to need; ling will neutralize 80-100 units of heparin.
prothionamide A second-line antitubercular drug that has been used in resistant tuberculosis. See page 170 and Table 31. It has also been used in the treatment of leprosy.
protirelin The thyrotrophin- releasing hormone (TRH) of the hypothalamus. Dose: in the diagnosis of hyperthyroidism, as a single i.v. dose ol’200 pg. It normally induces a rapid rise in the plasma levels of thyrotrophin, but in thyrotoxicosis that rise does not occur. Side-effects include nausea, flushing, a strange taste and urinary urgency.
protriptyline A tricyclic antidepressant with actions and uses similar to amitriptyline. It is used in depression associated with apathy, as it has some stimulant action. Dose: 15-40 mg daily. Side-effects are cardiovascular distu&nce, rash and photosensitivity. (Concordia). See
page 128 and Table 11.
proxymetacaine A local anaesthetic used as 0.5% drops in ophthalmology. (Oplithaine).
pseudoephedrine A drug very closely related to ephedrine, but now used mainly as a respiratory decongestant. It has been used in nocturnal enuresis, but may cause hallucinations in sonic children.

halothane A potent non-inflammable inhalation anaesthetic. It suppresses mucous and bronchial secretions, and reduces capillary bleeding. It has sonic muscle-relaxant properties, but in major surgery, supplementary treatment with a muscle relaxant is necessary. Halothane may cause some cardiac irregularities, but an occasional serious side-effect is severe hepatotoxicity, particularly after further exposure to the drug within periods of 441 weeks. Such susceptibility cannot yet be detected, so great care is necessary in any cases of liver dysfunction.
(Fluothane).
hamamelis An extract of witch hazel leaves referred to as harnarnelis or witch hazel water is used as a soothing application for bruises and sprains.
Hartmann’s solution An electrolyte-replacement solution containing sodium lactate, sodium chloride, potassium chloride and calcium chloride.
heparin The natural anticoagulant obtained front lung and liver tissue. It is widely used in deep-vein thrombosis and pulmonary embolism.
Dose: by i.v. injection 5000 units initially, followed by 1000-2000 units hourly by i.v. infusion, or 15000 units by s.c. injection 12-hourly under laboratory control. Prophylactic dose before surgery 5000 units, then 5000 units every 8-12 hours for 7 days. Overdosage call be controlled by the i.v. injection of prolamine sulphate. Treatment with heparin may be combined with that of oral anticoagulants such as phenindione or warfarin to provide immediate action before the slow-acting oral drugs begin to take effect. Occasional side-effects include hypersensitivity reactions and alopecia. Heparin is a complex polysaccharide, but certain fragments of that large molecule retain sonic anticoagulant activity, and are referred to as low molecular weight heparins. They are used mainly in the prophylaxis of venous thrombo-embolism, as they have a longer
action than standard heparin. They are given by once-daily s.c. injection, and laboratory control of the bleeding time is not necessary. The dose varies to some extent with the product used.
hepatitis A & 8 vaccines Inactivated hepatitis virus antigens for the protection of individuals highly exposed to the infections. Dose: see data sheets. (I iaverix A;
kncigix B; II–B–Vax).
theroin See diamorphine.
hetastarch A soluble modified starch that is used as a 6% solution with 0.9% sodium chloride as a plasma volume expander. Dose: 500-1500 nil daily by i.v. infusion, up to a maximum of 20 mltkg daily. It is excreted by the kidneys, and care must be taken to avoid circulatory overload. Not for use in congestive heart failure or renal insufficiency. Side-effects are vomiting, chills, fever and urticaria. (clol-IAES; Hespan).
hexachlorophene A slow-acting antiseptic used for skin sterilization, and present in sonic medicated soaps.
hexamine (methenamine) A formaldehyde derivative of low toxicity, occasionally used as a urinary antiseptic. Dose: 2 g daily. It is usually given as hexamine hippurate to ensure the necessary acidification ol’the urine. (Iliprex).
histamine A compound present in a bound form in all mammalian tissues; its release is probably the ultimate cause of many allergic conditions.
histamine H,-receptor antagonists See antihistamines. See page 110 and Table 2.
histamine Hz -receptor antagonists Drugs that (litter from conventional antihistamines in having a selective blocking action on receptors ill the gastric cells that secrete acid. They are widely used in the treatment of peptic ulcer and other conditions requiring a reduction in gastric acid secretion. See page 162 and Table 27.
homatropine An atropine derivative with a similar but more rapid mydriatic action (15-30 minutes), but a shorter duration of effect of about 24 hours. Eye drops
(1-2%) sometimes with cocaine.

hyaluronidase A ’spreading’ factor used to increase the absorption of large-volume s.c. injections. The injection of 1500 units of hyaluronidase, either into the injection site or mixed with the injection fluid, will promote the absorption of 500-1000 mL of electrolyte solution by s.c. drip infusion. (Hyalase).
hydralazine A vasodilator that is useful in the supplementary treatment of hypertension.
Dose: 50- 100 nig daily, usually with a IlliaUide diuretic or a beta-blocking agent. Also given in hypertensive crisis by slots, i.v. injection in doses of 5-10 mg; over-rapid injection may cause a marked fall in blood pressure. Side-effects are nausea, tachycardia and fluid retention (less likely with low doses), but a lupus erythematOSLIS- like syndromemay occur with extended high-dose therapy. (Apresoline). See page 148 and “Fable 21.
hydrochlorothiazide A thiazide diuretic that brings about it marked increase in the excretion of salts and water, and is of value in congestive heart failure and other oedematous conditions. It is also of value iii    as it reduces peripheral resistance, and potentiates the action of some other antihypertensive drugs.
Dose: 50-111(1 Ing daily initially in
oedenia; maintenance dose 25-50 mg daily or oil alternate days. III hypertension, 25-30 Ing daily according to need.
I lydrochlorolhiazidc, like other thiazid”, Increases the excretion of potassium as well as sodium, and in extended treatment supplementary treatment with potassium chloride or effervescent potassium tablets may be required. Side-effects include nausea, rash, dizziness and photosensitivity. (I lydroSaluric). See page 148
and ‘I able 21.
acute lyniphoblastic leukaemia and some lymphomas. In common with some other corticosteroids, hydrocortisone inhibits organ-transplant rejection and in high doses it is given to control incipient rejection.
Dose: varies considerably according to need: for replacement therapy, 20-30 mg daily: in shock, 100-300 mg or more by slow i.v. injection, repeated as required. Side-effects are numerous and include hypertension, oedema, mental disturbances, re-activation of peptic ulcer, muscle weakness and diabetes. Cushing’s syndrome may occur with high doses.
I I ydrocortisone, unlike cortisone, is active topically, in(] is used as eye drops 0.3% (usually with an antibiotic), ointment and cream (0.50/o and 11M, often with an antibiotic to control any secondary infection.
hydroflumethiazide A thiazide diuretic N,ith the actions, uses and side-effects of bendrofluazide.
Dose: 25- 100 nig daily in (lie morning; 25-50 Ing daily in hypertension.
ff lydrenox). See page 148.
hydrogen peroxide solution It contains 5-7% of H 02
, equivalent to about 20 volumes oJ oxygen. It has antiseptic and deodorizing properties, and is used mainly for cleaning wounds. It is also used as a mouthwash (diluted 1:7), and as ear drops (1:4 in water or 501% alcohol).
thydromorphone A potent opioid analgesic of the morphine type. Dose: in severe pain 1.3-2.6 Ing 4 t,-hourly. Walladone).
hydrotalcite Aluminium magnesium hydroxide carbonate. An antacid used in dyspepsia and related conditions.
Dose: I g as required.
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hydrocortisone The principal corticosteroid, also known as cortisol, that is secreted by the adrenal cortex. It plays a major role in the metabolism of glucose, protein and calcium, in maintaining the electrolyte balance, and in reducing inflammatory and allergic responses. It is used in all cases of adrenocortical insufficiency, including Addison’s disease and after adrenalectomy. It is also used in anaphylactic shock, asthma, rheumatoid disease and allergic states. It is valuable in
hydroxocobalamin A derivative of eydnu,obdlaniin, and now the preferred form of vitamin B,, as it has a more prolonged action.
Dose: in pernicious anaemia and other vitamin 13, deficiency states, I Ing initially ian. repeated 5 times at intervals of 2-3 days; maintenance dose 1 mg by I’ll’
by )CC- Lion every 3 months. It is also given
prophylactically after total gastrectonly. (Cobalin-H; NCO-Cytalliell). See
page 112.

hydroxyapatite A natural substance with a mineral composition somewhat similar to that of bone. It is used as a source of calcium and phosphorus in osteoporosis and other deficiency states. Tablets of 830 mg are available. (Ossopan).
hypermotility of the gastrointestinal tract, and may be useful in spasmodic dysmenorrhoea.
Dose: 40-80 mg daily; in acute spasm, .10 mg by injection. (Buscopan).
hydroxychloroquine An antimalarial with the actions, uses and side-effects of chloroquine. It is also useful in rheumatoid arthritis in doses of 200-400mg daily, and in lupus erythematosus, but side-effects are numerous, and treatment requires expert supervision. (Plaquenil). See page 165.
hypromellose A cellulose-derivative that dissolves in water to form a viscid, colloidal solution. Such a solution is used as a base for eye drops to extend the action of a dissolved ophthalmic drug; to lubricate contact lenses; and to act as a lubricant in chronic, sore eye conditions.
5-hydroxytryptamine See serotonin.
hydroxurea (hydrocarbamide) A cytotoxic agent sometimes used in chronic myeloid leukaemia.
Dose: 20- 30 mg/kg as a single dose daily or 80 nig/kg every third day. Side-effects are nausea, skin reactions and myelo- suppression. (Hydrea). See page 122 and Table 8.
hydroxyzine A mild tranquillizer with some sedative and antihistaminic properties. It is given in the short-term treatment of anxiety, and in pruritus and dermatoses complicated by emotional tension. Dose: 50-400 mg daily. It has the side-effects of the antihistamines, and is not recommended where some sedation is undesirable. (Atarax; Ucerax). See page 117 and Table 3.
hyoscine (scopolamine) An alkaloid obtained from plants of the belladonna group. It is a powerful hypnotic and is widely used together with papaveretum for premedication before anaesthesia in doses of 300-600 pg by s.c. or i.m. injection. It has some antiemetic properties, and is useful in travel sickness and vertigo. Dose: 300 mg 30 minutes before starting the iourney, followed by up to 3 doses 6-hourly. Scopoderm is a patch of 500 pg. Thc side-effects of mouth dryness and dizziness are those of the anticholinergic drugs generally. It is contraindicated in glaucoma. It is used occasionally in terminal care for bowel colic and excessive respiratory secretions. Dose: 600 pg-2.4 mg daily by s.c. infusion.
hyoscine butylbromide A derivative of hyoscine that differs in lacking any central action. It is given in spasm and
I
ibuprofen A non-steroidal anti-inflammatory agent (NSAID) widely used in rheumatoid and arthritic conditions. It is also given as an analgesic for mild to moderate pain, but not for acute gout. Dose: 1.8 g daily initially; lly; maintenance duos, 600 lllg-L2 daily after food. A 5% cream is available for local use. The sideeflicts are those of the NSAID& generally. (BrUlen; Feribid). See page 165.
ichthammol A thick, dark brown liquid with a characteristic odour, derived from certain bituminous oils. It is a mild antiseptic and is used mainly in chronic eczema as a 100A, ointment or zinc paste. A solution (10% in glycerin) has been used oil ulcers and inflamed areas.
idarubicin A potent cytotoxic agent similar in actions and uses to doxorubicin. It is given orally and i.v. in acute nonlymphocytic leukaemia, breast cancer, and as second-line therapy in acute lymphatic leukaemia. Dose is based on skin area. (Zavedos). See page 122 and Table 8.
idoxuridine An antiviral agent now virtually superseded by acyclovir and related drugs. Used occasionally in herpes zoster skin infection by local application of a 5% solution. See page 144 and Table 19.

fosfamide A derivative of cyclophosphamide with similar actions and uses. It is effective in lung, ovary, breast and soft-tissue tumours, as well as some malignant lymphomas.

Homeopathy
`We believe that a serious effort to research homeopathy is clearly warranted despite its implausibility.’ That was the conclusion of a group of German and American scientific

researchers who, in 1997, looked at every study of homeopathy they could find. This prestigious trans-Atlantic team carefully assessed the scientific validity of each study, and

then considered the data from studies that were of reasonably good quality.
This kind of study, in which all the available research data on a topic are combined, is called a meta-analysis. There were 119 research studies which were good enough to be

included in this meta-analysis and, taken together, these studies suggested that homeopathy does indeed have some real effects. In other words, it produces significantly more

benefits than simple placebo effect – the psychosomatic improvement which tends to occur with any treatment, even a dummy pill (see p. 233).
Some of the most convincing scientific studies included in the meta-analysis were those relating to homeopathic remedies for allergic conditions (see p. 217). But what exactly

does this mean for allergy sufferers? Is homeopathy a treatment that is worth a try? Unfortunately, it is difficult to say.
Firstly, the evidence from the homeopathy meta-analysis is far from overwhelming, as the researchers themselves point out. The observed improvements – the overall differences

between the placebo and the homeopathic remedy – are not huge. Secondly, even if there are some homeopathic treatments that have real effects, it does not mean that every kind

of homeopathic treatment works. Homeopathy is a very broad field, with a multitude of different approaches. The types of homeopathy that have been tested, and appear to help,

may bear little or no relation to the homeopathic remedies that are generally available (see p. 217).
`Let like cure like’
The central idea in homeopathy – often known as the principle of similars – is that a substance which causes a particular set of symptoms can also, if handled in the right way,

cure symptoms of
a similar kind. In the words of Samuel Hahnemann, the German doctor who invented homeopathy at the beginning of the 19th century, ‘Let like cure like.’
The natural substances that form the basis for homeopathic remedies are mostly derived from toxic plants or minerals. (Sometimes extracts from diseased tissue – called nosodes –

are used instead, but this is a relatively recent development. So is the use of allergen extracts, such as pollen, described on p. 217.) Hahnemann himself began with the

standard drugs of his own day, such as belladonna and arsenic compounds. His innovation was to use them in very much smaller doses than his fellow physicians, and to apply them

to entirely different diseases.
Hahnemann worked by first discovering what the effects of the drugs were, when taken by a healthy person (he experimented on himself and his family for this). Then he tried to

match the symptom pattern produced by the drug with the symptoms of a particular disease. For example, he observed that belladonna produces hallucinations and a hot, dry skin –

symptoms that were also seen in children with scarlet fever. He claimed that, by giving belladonna in very small doses, much less than was normally used, he could stimulate the

body to heal itself of scarlet fever.
Hahnemann, unlike his medical contemporaries, also advocated a good diet, fresh air and exercise. And he was heartily opposed to the conventional medicine of his day, a brutal

business that involved a great deal of blood-letting and large doses of very toxic medicines. Considering how useless, and indeed dangerous, the orthodox medicine of the time

frequently was, Hahnemann’s successes were not really surprising.Less is more’
Homeopathy today is the ultimate version of the ‘less is more’ philosophy. A homeopathic remedy is prepared by taking the basic ingredient, dissolving it in water, and then

diluting that solution over and over again. Imagine pouring a bottle of wine into the Pacific Ocean, and you have a rough idea of how dilute homeopathic remedies are. Making

extreme dilutions was an idea introduced by some of Hahnemann’s followers, after his death.
Dilution is only part of the story, however. With each dilution, homeopaths apply a special shaking-and-tapping technique known as percussing. This was originally done by hand,

but now is often done mechanically. Homeopaths believe that percussing makes the active substance more powerful, despite the dilution. The term used by homeopaths is potency,

and a homeopathic remedy of the highest potency is the one that has been most thorDughly diluted and percussed.
In fact, a simple calculation, using the basic laws of physics, shows that there is nothing there at all but water – many homeo pathic remedies are watered down so thoroughly

that not one Jingle molecule of the active substance is likely to remain. It is  which leads medical researchers to use words such as ,nplausibility’ (see p. 216) when talking

about homeopathy.
Nhat homeopaths do
\ homeopath starts by considering all your symptoms (not just allergies, but any other symptoms as well) and various other characteristics that conventional doctors do not

usually consider, including physical appearance and psychological traits. The homeopath then chooses a substance which, if taken at full strength, would produce a comparable set

of symptoms and characteristics. This approach is called classical homeopathy.
In addition, homeopaths often give advice on diet, sleep, exercise and allergen avoidance. As in the early days of homeopathy, this may be the most important part of the

treatment.
Like many other complementary therapists, homeopaths will listen if you need to talk about personal problems and emotional difficulties, and will offer reassurance or advice.

This can be valuable, though not everyone would agree that a homeopath is the best source for such help. There are two distinct traditions within homeopathy – a scientifically

inclined tradition (represented today by experiments with homeopathic immunotherapy – see right) and a highly metaphysical tradition. Among the many ideas floating about within

the metaphysical tradition is the notion that all illness is a result of psychological or moral failings. Attitudes of this kind, which are quite common among complementary

therapists, can be very damaging (see p. 209).
Sometimes homeopaths recommend avoiding certain foods, on the assumption that the patient suffers from food intolerance, though they rarely use an elimination diet (see p. 194),

the only way to achieve accurate diagnosis.
In addition to all this, some homeopaths also give herbal remedies where they think it will help. This approach is called complex homeopathy.
A much more recent development within homeopathy is homeopathic immunotherapy or HIT, which uses an extreme dilution of an allergen (such as pollen or dust mite) to treat people

who are allergic to that substance. While homeopathic immunotherapy was inspired by conventional immunotherapy, the relationship between the two is a very distant one indeed.

The extensive dilution process means that the liquid used for homeopathic immunotherapy is unlikely to contain even one molecule of the allergen. This puts it in a completely

separate realm from conventional immunotherapy, where the presence of the allergen, and the steadily increasing dose with successive injections, is what produces the beneficial

effect (see p. 166).
Does it work for allergy?
Two scientific trials suggest that HIT makes a difference, albeit a small one, for hayfever and pollen asthma. In the meta-analysis described on p. 216, one of these trials was

given a good rating for scientific reliability, and the other was considered fairly good.
Another type of homeopathic treatment that appeared to be effective for patients with allergic asthma was one using a nosode – an extract of the asthmatic airway itself. A small

sample of the airway was taken from each asthmatic patient, diluted and per-cussed, then given to the patient as a treatment. It seemed to work, and the scientific rating of

this trial was very high.
The third homeopathic treatment that appeared to have an effect in valid scientific studies was Galphimia, used for symptoms in the eye caused by pollen allergy.
If you go to a local homeopath, it is very unlikely that you will be given either of the first two treatments – these are only used experimentally, in large research centres.
The Galphimia treatment might be available from a local homeopath, but it will not necessarily be in the same form as the treatment used in the scientific trial.
Note that all the studies described above are trials with a positive outcome. If you are trying to assess homeopathy overall, you should also consider the many trials that found

no effect. For example, a very careful study of homeopathy for children with asthma, carried out at the University of Exeter and published in 2003, found no benefit from

individualised homeopathy treatment.

Drugs for Asthma
The drug treatment of asthma is far more complex than for any other allergic disease. Drugs prescribed for asthma fall into two basic categories: those that open up the airways by relaxing the airway muscles, called relievers, and those that treat the inflammation in the lining of the airways, called preventers. The former offer a ‘quick fix’ - like taking an aspirin when you have a headache. Just as the actual cause of the headache is not treated by an aspirin, so the actual cause of the asthma attack is not addressed by relievers. Preventers, on the other hand, tackle the basic problem - the inflammation that triggers the contraction of the airway muscles (see p. 36).
In the past ten years, there has been a quiet revolution in asthma treatment, with far more people being given preventer inhalers, usually low-dose steroids. The aim is to get the airways in better condition, with the inflammation thoroughly damped down, so that the airway muscles don’t go into spasm. The ultimate objective is to make people far less reliant on reliever inhalers, because the potential hazards of over-using them are now realised.
The details of modern asthma management, and the different approaches used, are described on p. 160, following the discussion of the main types of drug used for asthma treatment.
Beta-2 relievers (beta-agonists)
Our airways open up when we produce adrenaline. This is the body’s natural response to feeling angry or frightened. The adrenaline widens the airways so that we can run faster or fight more vigorously.
Adrenaline (epinephrine), given as a drug, was among the earliest treatments for asthma. However, it also stimulates the heart to beat faster and raises
the blood pressure. While it is useful for emergency treatment (see p. 155) the side effects make it too hazardous for routine use.
The beta-2 relievers work by mimicking adrenaline – they bind to the same receptors in the airways, the beta-2 receptors. Binding to these receptors stimulates the airway muscles to relax, so that the airways open up.
In other respects, the beta-2 relievers are not like adrenaline. Clever chemical manipulation has made them sufficiently different from adrenaline to have little effect on the heart and other organs, when taken at normal doses.
Beta-2 relievers are best taken by inhalation. Although tablets and syrup are available these are far more likely to bring on side effects, because the dose needed is so much bigger.
Inhaled beta-2 relievers target the drug directly on the airways, so the dose can be smaller. They also have the great advantage of taking effect soon after being inhaled, and giving full relief from airway narrowing within 10-15 minutes.
There are two different kinds of beta-2 relievers:
•    the traditional short-acting beta-2 relievers whose effects last for 3-6 hours (usually about four). The modern consensus is that these should be used only when needed, not taken routinely.
•    the newer long-acting beta-2 relievers, which last up to 12 hours. These drugs are prescribed for more severe forms of asthma (see p. 154), and are generally used routinely, twice a day.
A key question for asthma sufferers is: How often can short-acting beta-2 relievers be used? Ideas about this have changed considerably over the last 20 years, and no doctor would now want to have patients using a Ventolin inhaler five, six or more times a day - something that was quite common in the past. This level of need for beta-2 relievers indicates that the asthma is poorly controlled and requires treatment with a preventer, to quell the inflammation in the airways.
Detailed policy on beta-2 relievers still varies from one part of the world to another. British guidelines state that anyone who needs to use a short-acting beta-2 reliever more than once a day, or who suffers from nocturnal asthma, should be given a preventer as well. The international guideline is more stringent: if a short-acting beta-2 reliever is needed more than three times a week, a preventer should also be prescribed.
How safe are these drugs in the long term? The cause of the big re-think on beta-2 relievers was an epidemic of asthma-related deaths in New Zealand between 1976 and 1988. The death rate from severe asthma attacks was 2-4 times its previous level for a while, and over a thousand New Zealanders died in the epidemic.
There has been a huge controversy over what exactly caused these deaths. Most researchers now agree that the main cause was a new brand of inhaler that delivered a double dose of the drug fenoterol, a short-acting beta-2 reliever with a very powerful effect on the airways and quite high levels of side effects involving the heart. The same brand of inhaler may have been linked to increased death rates in Canada and Germany.
Research suggests that the problem was greatest in New Zealand because sales of the new inhaler were highest there, and because many patients got their inhalers through repeat prescriptions. As a result, people whose asthma was deteriorating badly were not seen by a doctor and were using large amounts of beta-2 reliever, rather than taking preventer drugs. This is now believed to be a major cause of asthma deaths. There are three separate factors involved:
•    The beta-2 reliever covers up the effects of the severe inflammation of the airways. People feel reasonably well, because the reliever is opening up their airways, and don’t realise just how bad their asthma really is. The untreated inflammation in the airways can eventually lead to a very serious, and potentially fatal, asthma attack.
•    The short-acting beta-2 reliever, used regularly, makes the airways more sensitive to exercise, and to allergens such as dust mite or pollen. This means that an asthmatic who is already allergic to these allergens reacts to them at much lower levels in the air.
•    The airways become less and less responsive to the beta-2 reliever itself, so that when a serious attack occurs, requiring hospital treatment, huge doses of beta-2 reliever are needed to open up the airways. These massive doses carry a risk of serious side effects involving the heart.
The details of the New Zealand epidemic still evoke controversy. Was fenoterol itself, which is stronger than other beta-2 relievers, the cause of the deaths? Or was it just that the inhaler delivered a double dose - would any short-acting beta-2 reliever be dangerous at twice the normal dose? Or was it over-use of all beta-2 relievers and lack of preventer drugs?
Some common brand names
Common brand names include:
short-acting beta-2 relievers in inhalers - Aerolin, Airomir, Bricanyl, Ventolin short-acting beta-2 relievers in tablets - Bambec, Bricanyl, Volmax short-acting beta-2 relievers in syrup - Monovent, Ventolin
long-acting beta-2 relievers in inhalers - Bambec, Foradil, Oxis, Serevent
Until this is resolved, safety-conscious asthmatics may want to assume that any of these possibilities could be correct. An ultra-cautious approach would include:
•    Avoiding fenoterol (it is no longer available in Britain, except in the Duovent inhaler, combined with an anti -choli nerg ic drug)
•    Not using double-dose inhalers of any beta-2 reliever (i.e. inhalers that deliver 200mcg/ micrograms per puff)
•    Not routinely taking two puffs of a single-dose inhaler (check with your doctor if you have been told to take two puffs)
•    Using any short-acting beta-2 reliever only I as needed’ – which should be once a day or less according to British guidelines. Note that, with this level of use, there is absolutely no risk from these drugs: it is only regular over-use that is damaging and dangerous.
•    Using a peak-flow meter and ensuring that you are assessed regularly by your doctor
•    Always taking your preventer medication as prescribed.
Since about 1990, the death rate from asthma has been falling, particularly in countries with a policy of reducing use of beta-2 relievers, and increasing inhaled steroids. The death rate in New Zealand is now the lowest it has been for 50 years, and at the same level as in other Western countries.
Unnecessary alarm
While investigating the causes of the New Zealand epidemic, medical researchers discovered that patients inhaling a short-acting beta-2 reliever four times a day had more irritable airways after just two weeks. Their airways were also less responsive to the drug, even after this brief period of use.
Some researchers began to ask if the asthma epidemic itself – the increasing number of cases of asthma – could actually be due to these drugs. Maybe children with mild wheezing, which might have cleared up if left untreated (and which would have gone untreated in the past) were becoming full-blown asthmatics because they were now using beta-2 inhalers?
Many doctors became very concerned about these questions, and a leading medical journal
published an article with the provocative title: ‘Worldwide worsening wheezing – is the cure the cause?’ That was in 1992. Since then, much more research has been done, and it is clear that this particular fear about beta-2 relievers was unfounded.
Unfortunately, there are a few books and other publications around that are spreading unnecessary alarm about these drugs by reporting the debate as it was in 1992. They have taken up that question ‘Is the cure the cause?’, assumed that the answer is ‘yes’, and ignored all the subsequent research, which shows the opposite.
Beta-2 relievers in severe asthma
A few patients with severe asthma remain breathless and wheezy, even though they are inhaling moderate doses of a steroid preventer every day. Increasing the dose of inhaled steroids does not make a huge difference to their symptoms, and it substantially raises the risk of steroid side effects.
Taking a long-acting beta-2 reliever often works wonders for such patients. These relatively new drugs relax the airway muscles, and go on working for 12 hours or more.
There has obviously been concern about long-acting beta-2 relievers having the same sort of insidious side effects as their short-acting colleagues (see p. 153), and so increasing the likelihood of deaths from asthma. However, studies of people taking these drugs suggest that the risks are minimal. Certainly, long-acting drugs taken twice a day are very much safer than short-acting drugs taken four times a day.
Other studies show that the chemical differences of the long-acting drugs, as well as prolonging their effects, also give them a more complex set of actions in the body. For example, they improve the effect of steroids in calming inflammation, and may even have some small anti-inflammatory effect of their own.
Doctors believe that, for patients with troublesome asthma, the benefits of long-acting beta-2 relievers greatly outweigh the risks. But they should only be used in combination with inhaled steroids. Various other options, such as allergen avoidance and the new anti - leukotriene drugs (see p. 159), should probably be investigated as well.
If you are taking long-acting beta-2 relievers, do use them regularly, once every 12 hours – the good effect gradually builds up with consistent use.
Generally speaking, you should not take additional doses in between. These are not intended for use if you have a sudden asthma attack – your doctor will prescribe a short-acting beta-2 reliever for this. This limitation on the use of long-acting beta-2 relievers is certainly appropriate for salmeterol (which was the first of the long-acting beta-2 relievers to be developed) because it is very slow to take effect on the airways. However, one of the newer long-acting beta-2 relievers, called formoterol, begins to work just as quickly as a short-acting beta-2 reliever. Formoterol could, in theory, be used on an ‘as-needed’ basis to combat asthma attacks. You may want to discuss this possibility with your doctor.
Finally, don’t stop taking your preventer drug (e.g. inhaled steroid or cromoglycate), even if you feel a lot better. Long-acting beta-2 relievers are not a substitute for preventers.
Some patients with very severe asthma need to take regular doses of short-acting beta-2 relievers as well as long-acting beta-2 relievers. You should obviously follow the advice of your asthma specialist closely if you are on this kind of drug regime, and not change anything without approval. However, it might be worth discussing other options, such as anti -leukotriene drugs. In addition, do all you can to combat your asthma in other ways – by reducing allergen exposure, avoiding asthma triggers (see p. 39), and employing various other self-help measures (see p. 41).
Immediate side effects of beta-2 relievers
Minor immediate side effects of these drugs include:
•    headache
•    nervousness, trembling, restlessness, anxiety; children may become more excitable, and some are badly behaved or even aggressive.
•    flushing
•    dry mouth
•    muscle cramps.
These side effects – all of which are due to the resemblance of beta-2 relievers to adrenaline – usually wear off relatively quickly. Some long-acting beta-2 relievers may cause nausea and vomiting.
A pounding heart is usually a relatively minor side effect, but it can be more serious, and should be reported to your doctor.
A few asthmatics find that their airways tighten up when these drugs are inhaled, rather than opening. This is called paradoxical bronchoconstriction. If this happens, stop using the inhaler and see your doctor as soon as you can.
Even more rarely, asthmatics can develop allergic reactions to the drugs, or suffer hallucinations or seizures. Obviously you should stop using the inhaler immediately if you experience side effects of this kind, and should see your doctor.
There can be an interaction between beta-2 relievers and other drugs or medical conditions. Should you need a diuretic, tell the doctor or pharmacist that you are also taking a beta-2 reliever, and ask which diuretics are safe. If you have high blood pressure, a heart problem, or a thyroid condition, make sure the doctor remembers this when prescribing beta-2 relievers.
Adrenaline inhalers
Adrenaline inhalers are for use in emergencies. Technically, they are not available in Britain, but they can be imported under special licence, and your doctor may be persuaded to obtain one for you if he or she thinks it might be useful. They are given to people who have asthma and have sometimes had attacks of anaphylaxis (see p. 58), for example in reaction to food, latex or an insect sting. The inhaler provides prompt emergency treatment for the kind of severe asthma attack that you may experience during anaphylaxis.
You should probably be carrying an adrenaline auto-injector as well, as you may need to use both (see p. 98). Those who usually have fairly mild reactions to their allergen can use the inhaler first, to treat symptoms in the mouth, throat and airways. If other symptoms develop, such as faintness or widespread nettle rash,
Asthma alert
If you ever find that your short-acting beta-2 reliever has no effect within ten minutes, or is needed more than once every four hours, this indicates a serious asthma attack and you need urgent medical help (see p. 100).
During a severe asthma attack, while getting to hospital or waiting for a doctor to arrive, up to 30 puffs of a short-acting beta-2 reliever should be taken as an emergency treatment, to get the airways open. There is a risk of death if you don’t use the reliever fully in this situation. (This emergency dose is safe for almost everyone, but there may be risks if you have a heart condition – get detailed advice from your doctor in advance.)
then the adrenaline injector can be used. Those with a history of more severe reactions should start with the adrenaline injector and then use the inhaler if there are still symptoms in the mouth or airways.
Don’t exceed the maximum number of puffs stated on the canister, as the propellant can cause problems. If you have a heart condition, your doctor will advise you about using this kind of treatment safely - adrenaline can affect the heart.
Ephedrine
Ephedrine and orciprenaline (brand name Alupent) belong to the previous generation of reliever drugs. They are chemically very similar to adrenaline and therefore cause a lot of side effects, especially involving the heart.
These drugs are no longer recommended, and will soon be phased out completely. Some older asthmatics may still be using them, just because they have been on them for years and no one has reviewed their treatment.
If you are taking such drugs, ask your doctor about switching to a newer form of reliever - it will be more effective in treating your asthma, as well as having fewer side effects.
Anti -cho linerg ics
These drugs, also known as anti-muscarinics, are relievers. However, they work in a completely different way from the beta-2 relievers. They block the action of the parasympathetic nervous system, a set of nerves that are the biological equivalent of auto-pilot - working without the intervention of conscious thought. The parasympathetic nervous system has many effects on the body, including keeping the airway muscles nicely toned (see box on p. 235). By blocking the parasympathetic, anticholinergics help the airway muscles to relax.
Anti-cholinergics are taken by inhaler, and require 30-90 minutes to achieve their full effects. They should continue working for 3-6 hours.
Some common brand names
Common brand names of anti-cholinergics include: inhalers – Atrovent, Oxivent
nasal spray - Rinatec
For most asthmatics, especially those with a strong allergic component to their asthma, anti-cholinergics are generally less effective than beta-2 relievers. But they are useful to children under one year, who may not respond to beta-2 relievers. They also have a role where asthma is combined with chronic bronchitis -here the anti -choli nerg ics can sometimes be more effective than beta-2 relievers - and they are particularly useful for asthma with a lot of mucus, because blocking the parasympathetic tends to reduce mucus production. For severe asthmatics, anticholinergics may be combined with beta-2 relievers.
Anti -choli nerg ics should be taken only when needed, not regularly several times a day. If used regularly, they can make the airways more sensitive, just as short-acting beta-2 relievers can (see p. 153).
Side effects
Minor side effects of anti-cholinergics may include a dry mouth, blurred vision, constipation, and irritation of the mouth and throat. A few people suffer nausea or difficulty in passing urine.
Serious side effects are rare. Any increase in the stickiness of the sputum coughed up may be a cause for concern, especially in children. If there is an increase in wheezing or coughing, stop taking the drug and see your doctor.
If you already have glaucoma or prostate problems you should be monitored carefully by your doctor, as these conditions can get worse with anti -choli nerg ic drugs.
When anti -choli nerg ics are used in a nebuliser, it is vital that the mask fits well (see p. 163).
Anti-cholinergics for the nose
Another use for anti-cholinergics is in nasal sprays, for the treatment of vasomotor rhinitis, a non-allergic condition that is frequently mistaken for allergic rhinitis (see p. 29). In this disorder, the constant flow of mucus is caused by a malfunction of the parasympathetic nervous system, which is why anti-cholinergics work well.

Various anti-allergy drugs
An allergic reaction is a lengthy, complex process, and the various anti-allergy drugs all work on different stages of that process. That is why it often makes sense to use several different drugs for the same allergic condition: they each tackle the problem in their own way.
Steroids (see p. 140) intervene at a very late stage, quelling the inflammation that follows on from an allergic reaction. Using a steroid is rather like calling the fire brigade to put out a fire, whereas using an antihistamine (see p. 138) is like having fire-proof doors, to prevent the fire spreading at an early stage. Cromoglycate-type drugs (see below) intervene at an even earlier stage. They are like basic fire prevention - teaching children not to play with matches, or fitting smoke detectors.
Anti - leukotnene drugs (see p. 149) work at roughly the same stage of the process as anti-histamines but tackle an entirely different aspect of the allergic reaction.
Cromoglycate-type drugs
These drugs are also referred to as mast-cell stabilisers or mast-cell Mockers.
There are three drugs in this group, sodium cromoglycate (also spelled cromoglicate), nedocromil sodium, and lodoxamide. All operate at an early stage of the allergic reaction, stopping it before it actually starts. They stabilise the outer membrane of the mast cells (see box on p. 12), which prevents the allergic response from occurring.
Some common brand names
Common brand names of cromoglycate-type drugs include:
inhalers - Cromogen Easi-Breathe, Intal, Tilade
eye drops - Hay-Crom, Opticrom, Rapitil, Vividrin, Viz-on nose sprays - Rynacrom, Vividrin
capsules - Nalcrom
This is a far more satisfactory way of dealing with an allergic reaction than trying to tackle it after the reaction has occurred. But from a purely practical point of view, it has a drawback. I order to work at all, these drugs must reach the mast cells in advance of the allergen. They are of very little use if taken after the allergic reaction has begun.
For those who are taking cromoglycate-type drugs on a regular schedule, several times a day, it is very important to be conscientious about taking them on time. This maintains the protective effect of the drug, without any gaps.
If you are using these drugs on an ‘as-needed’ basis, you should take them 30 minutes before an allergen is encountered. or 30 minutes before a bout of exercise, if they are being prescribed for exercise-induced asthma. (Note that children sometimes respond differently, getting protection from these drugs immediately.)
The effect of these drugs takes time to build up. You should take them regularly for at least four weeks before deciding whether they are helping you or not.
One point in favour of cromoglycate-type drugs is that they are extremely safe, with few or no side effects in most people. Sadly, they do not work for everyone. A fairly high percentage of children respond well to them, but the response rate is much lower for adults. Nevertheless, adult allergy sufferers, especially those who need steroids to control their symptoms, should always be given the opportunity to try out these drugs. When cromoglycate-type drugs do work, they are very effective and almost always trouble-free, so they are a good alternative to steroids.
Both sodium cromoglycate and nedocromil sodium are available in inhaler form for asthma (see p. 157). Sodium cromoglycate is also available as nose drops for hayfever and other nasal allergies.
All three drugs are available as eye drops. Recent evidence suggests that sodium cromoglycate drops are less effective than the other two, particularly for the treatment of severe allergic conjunctivitis (inflammation of the eye).
Sodium cromoglycate is available in capsule form for food allergy. Note that these capsules are of very limited value in food allergy, and are certainly not a substitute for food avoidance. They do reduce sensitivity a little and can sometimes be helpful for those with multiple food allergies (see p. 67).
Side effects
There are no serious side effects at all for nedocromil sodium. cromoglycate can, very rarely, cause joint pain and swelling. An allergic reaction to the drug itself is even more uncommon. Stop taking the drug and see your doctor promptly if either of these occurs.
The only other side effects that have occasionally been reported are headache, nausea and vomiting. None of these indicates any damaging effect by the drugs – they are all minor side effects.
Eye drops containing these drugs may cause stinging and burning when inserted, but this is a minor side effect and usually wears off. Flushing and dizziness have sometimes been reported with lodoxamide eye drops.
Nose drops may also cause local irritation. This could be due to the drug itself, in which case it is a minor side effect. Alternatively, the irritation may be due to the preservative used or some other non-drug ingredient (see box on p. 33).
Occasionally cromoglycate nose drops cause bronchospasm – contraction of the airway muscles – but this tends to wear off quite quickly. Bronchospasm can also occur when cromoglycate-type drugs are inhaled (see p. 157).
Anti - leu kotriene drugs
These drugs, which have a set of very specific effects (see p. 159), were originally designed to treat asthma. Their potential for treating other allergic diseases is currently being explored:
•    Several studies show that they work well for perennial allergic rhinitis brought on by allergens such as house-dust mite. They also have some effect on hayfever, but standard treatment (such as antihistamines plus a steroid spray for the nose) is more effective.
•    They are especially useful for both rhinitis and asthma in patients suffering from triad (see box on p. 28). Research shows that they also reduce asthmatic reactions to very small test doses of aspirin, but they don’t give protection against anaphylaxis brought on by normal doses.
•    They have also been used successfully in cases of chronic urticaria and for some patients with delayed pressure urticaria. It seems plausible that they would also be helpful for chronic urticarla linked to aspirin sensitivity.
•    Preliminary trials suggest that these drugs might be useful in atopic eczema. Some studies show a very good response that allows a reduction in steroid creams.
•    Montelukast works very well for eosinophilic gastroenteritis and eosinophilic oesophagitis (see p. 72), according to some new studies.
For side effects of these drugs see pp. 159-60.
Anti-IgE drugs
Since the antibody IgE (see box on p. 12) is such a crucial player in allergic reactions, developing drugs that disable this antibody should help allergy sufferers. The first such drug is omalizumab (brand name Xolair) which was licensed for use in the United States in 2003. It is expected to become available in Britain some time in the next few years.
Omalizumab binds to IgE antibodies and stops them from interacting with mast cells, so blocking any allergic reaction. The drug is given as a ‘depot injection’, just under the skin, every 2-4 weeks. It is gradually released from the injection site and moves around the body in the blood, mopping up IgE molecules.
At present, omalizumab is used for severe hayfever and for people with asthma who are not responding well to the usual treatments. It is only worth using if there is clear evidence that allergies play a part in the asthma. Patients who use omalizumab are often able to reduce their dose of inhaled steroids – and they suffer fewer serious asthma attacks and have better lung function. Some patients can even stop using steroids completely.
Other anti-IgE drugs are in the pipeline. Pilot studies show that one works very well for peanut allergy: after just four injections, sensitivity to the allergen falls sharply, reducing the risk of anaphylaxis from traces of peanut eaten accidentally.
More powerful anti-allergy drugs
Occasionally people with severe allergies, who are on constant high doses of steroid tablets, or who fail to respond to steroids, need treatment with powerful anti-inflammatory drugs, such as methotrexate or cyclosporin. These suppress the immune system, and extremely careful monitoring for side effects is needed.
Adrenaline (epinephrine)
Anyone who has suffered anaphylactic shock (see p. 58) should be carrying a special syringe, called an auto-injector, loaded with adrenaline. The injector is very simple to operate and is designed for emergencies. Most allergy sufferers, even children, can give themselves the injection – or a parent or other adult can give it.
Some asthmatics, and those with food allergy who suffer swelling of the throat, may be given adrenaline in inhaler form as well (see pp. 155-6). This can be useful as an additional treatment but it’s definitely not a substitute for an injector.
See pp. 98-9 for instructions on using adrenaline in a crisis.
Wherever you go, take your injector with you. Always keep it close at hand: you need to be able to use it within minutes of the allergic reaction starting. You may be unable to speak (and therefore unable to ask someone else to fetch it) quite soon after the attack begins. The injector must never be refrigerated. It can also be damaged by sunlight and excess heat.
If you live in the countryside or in an area with a poor ambulance sevice, or if you are going camping or hiking somewhere remote, ask your doctor for a second injector, or one that can deliver multiple injections. Also ask about the maximum number of injections that can be given, and never exceed this total. Some doctors believe everyone should have two injectors, just in case the first dose doesn’t do the trick and help is slow in coming.
It is vital that you are shown exactly how to use the auto-injector. Canadian researchers discovered that only one in four
Some common brand names
Common brand names of adrenaline preparations include: auto-injectors – Anapen, EpiPen
inhalers – AsthmaHaler Mist, Bronkaid, Epiphrine
health professionals got the technique correct when demonstrating how to use an auto-injector In this study, pharmacists were much the best as regards accurate instructions. Dummy injectors are useful for training purposes and most pharmacies have them.
When the adrenaline auto-injectors expire, they can be very useful for practising with, or for showing a new baby-sitter or teacher – practise on an orange or grapefruit.
If you are taking beta-blockers (e.g. for a heart condition or anxiety), adrenaline may not have much effect.
Heavy daily use of beta-2 relievers for asthma (see p. 152) will also make adrenaline less effective when you need it.
Side effects
The important side effects of adrenaline involve the heart. Anyone with a heart condition should be given special advice in advance by their doctor about using adrenaline. The same goes for people with diabetes, hyperthyroidism or high blood pressure, and anyone taking tricyclic anti-depressants. There are quite a few minor side effects from adrenaline, such as anxiety, trembling, nausea. sweating, dizziness and cold extremities. These soon wear off.
Drugs that can make you worse
Aspirin and its relatives have a very bad effect on some people with rhinitis and/or asthma (see box on p. 151). Unfortunately, recent research shows that paracetamol is not safe either. It makes asthma more likely to develop in those who do not yet have the disease, and increases the severity of asthma symptoms for those who do. Unlike aspirin, paracetamol affects everyone, because it lowers the levels of a natural antioxidant, called glutathione, which the body makes to protect the lungs from oxidants. The greatest effects are seen in people who take paracetamol regularly (once a week or more), but even an occasional dose makes some difference.
All the other drugs that can make you worse are prescription drugs, and your doctor should be alert to the dangers. But doctors are overworked and sometimes forget, so it is sensible to know about the risks for yourself. If you have any doubt about the drugs you are taking, ask a pharmacist.
Beta-blockers are a major hazard for people with allergies. They can make the airways contract, and can bring on a serious asthma attack. They also make anaphylaxis more likely in someone who already has allergic reactions (see p. 59) and they increase the risk of a severe reaction to
immunotherapy (see p. 166) or skin-prick tests (see p. 91). Beta-blockers are prescribed for high blood pressure, angina and other heart problems, migraine and thyroid disease. There are alternative drugs in all cases. Sometimes asthma develops in people who have been taking beta-blockers for years. The beta-blockers are not responsible for this, but once asthma has begun, they will make symptoms worse. Eye drops for the treatment of glaucoma may also contain beta-blockers and can have a bad effect on asthmatics.
ACE inhibitors, used for heart conditions, may cause a cough and airway narrowing. They may also increase the risk of a severe reaction to immunotherapy.
Female hormones affect asthmatics, so taking the contraceptive pill or hormone replacement therapy (HRT) may make asthma worse. Progesterone-only contraceptive pills tend to cause fewer problems.
The drug isoniazid (INH), prescribed for tuberculosis, makes the body far more susceptible to histamine in foods (see p. 200).
An allergic reaction to a specific drug (e.g. penicillin) can also occur in some people, resulting in urticaria, or even anaphylactic shock.
Aspirin sensitivity
Aspirin sensitivity is not an allergic reaction, because neither IgE nor mast cells are involved. What causes this problem is a metabolic abnormality — a malfunction in one aspect of the body’s chemistry. The details of this are very complicated: you may want to skip the next three paragraphs and
simply read about how to cope with the problem.
The exact nature of aspirin sensitivity is still far from clear, but it seems to involve a relatively poor production of prostaglandins, combined with a plentiful production of leukotrienes. Both these substances are messenger chemicals which, broadly speaking, promote inflammation. But the details of their pro-inflammatory activities differ. It seems that, ideally, the body should have a harmonious balance between the two, and an imbalance produces problems.
Both prostaglandins and leukotrienes are manufactured from certain fats that are found in the diet. These fats, the raw materials, are worked on initially by two different enzymes — one that leads to the production of prostaglandins and another that leads to the production of leukotrienes.
If one of these enzymes is defective, it may mean that the other is oversupplied with raw materials, resulting in a serious imbalance between prostaglandins and leukotrienes. In those with aspirin sensitivity, or at risk of developing aspirin sensitivity, the enzyme that produces prostaglandins seems to be defective.
Even in the absence of aspirin, this imbalance in the production of prostaglandins and leukotrienes causes problems. It leads to symptoms such as chronic urticaria (see p. 51) or rhinitis, nasal polyps and asthma (a cluster of symptoms that is commonly called triad — see box on p. 28).
Taking aspirin can make the imbalance between prostaglandins and leukotrienes even worse in a person with this underlying abnormality. Aspirin exerts its painkilling effects by disabling the main prostaglandin-making enzyme — the enzyme that is already defective.
When someone with aspirin sensitivity takes aspirin, they may suffer worsening asthma, a severe asthma attack or — the worst-case scenario —collapse. This is a potentially fatal reaction, similar to anaphylaxis, requiring emergency medical treatment (see p. 101).
The greatest puzzle about aspirin sensitivity is why it often takes so long to develop in someone who already has the symptoms of triad —indicating the basic metabolic abnormality. It may be as much as 20 years from when someone has their first triad symptoms to when they begin reacting badly to aspirin.
If you have triad symptoms already, but no aspirin sensitivity yet, what should you do? Unfortunately, there are no safe tests for aspirin sensitivity at present — taking a small dose of aspirin and seeing what happens is very hazardous. It is probably best to assume that you are going to become sensitive to aspirin at some stage, and avoid all aspirin and aspirin-like drugs. Caution is the best plan here because aspirin sensitivity can come on very suddenly, and be life-threatening the very first time it occurs. Note
that some triad sufferers have polyps and rhinitis but no asthma until they actually develop aspirin sensitivity — a dose of aspirin suddenly brings on their first asthma attack plus other symptoms of aspirin sensitivity.
Avoiding aspirin itself is not difficult, but aspirin-like drugs pose more of a problem. Every year there are a number of deaths from these drugs. Some cases occur because a busy doctor momentarily forgets that a patient should not take these drugs. The drugs that need to be avoided are all known as non-steroidal anti-inflammatory drugs (NSAIDs), COX-1 inhibitors or COX-2 inhibitors. However you will not see any of these names on the packet. These drugs are very widely used for pain relief (e.g. in headache and backache remedies such as Nurofen), for the treatment of arthritis, and for several other inflammatory diseases.
There are dozens of non-steroidal anti-inflammatory drugs available, and many are sold under several different brand names. The list grows every year, as new drugs or new brands are launched. The only way to avoid these drugs is to be very cautious:
•    When buying any cold- or flu-remedies, painkillers, medicines for sprains or sports injuries (including those you apply directly to the skin), headache tablets or migraine tablets, always buy them at a chemist’s shop rather than a supermarket, and check with the pharmacist that they do not contain aspirin or aspirin-like drugs.
•    Be cautious also about remedies for an upset stomach. A few (e.g. Alka-Seltzer) contain aspirin.
•    Don’t take any drugs unless you are 100% sure of what they contain. Remember that the ingredients of a familiar brand name can sometimes change — read the label every time.
•    When a doctor prescribes any new drug, always mention that you are sensitive to aspirin, or that you have triad symptoms. Alternatively, check with the pharmacist when the prescription is filled.
•    Aspirin-free painkillers almost always contain paracetamol, a drug which can cause a severe reaction (similar to the collapse induced by aspirin itself) in about 5% of those with aspirin sensitivity. If you are taking paracetamol for the first time, start with half a tablet. Be sure that, for the next 2-3 hours, you have a way of getting to hospital quickly should you start to feel ill. (Note that paracetamol has another entirely separate effect, increasing the severity of asthma, and it is best not to take it too often — see box on p. 150.)
Avoiding all aspirin-like drugs will prevent you having anaphylaxis or severe attacks of asthma. Unfortunately, triad symptoms will not go away however careful you are about avoiding aspirin.
It is well worth trying the new anti-leukotriene drugs (see p. 149), especially if you have aspirin-induced asthma. They seem to help with triad symptoms by curtailing the activities of leukotrienes and so redressing the balance between leukotrienes and prostaglandins.