Posts Tagged ‘nasal allergies’

flumazenil A benzodiazepine antagonist used in anaesthesia to reverse the sedative effects of benzodiazepines.
Dose: 200µg initially by i.v. injection, with subsequent doses of 100 pg at I -minute intervals, up to a maximum of I mg. Further doses may be given by i.v. infusion if drowsiness returns, as the action of flumazenil is brief. ( Anexate).
flunisolide A potent corticosteroid used locally in the more severe forms of hay fever and other nasal allergies.
Dose: 1)), nasal inhalation, 50pg (2 sprays), 2 or 3 times a day, continued for 2-3 weeks, or longer if required. (Syntaris).
flunitrazepam A benzodiazepine with a hypnotic action used for the short-term treatment of insomnia.
Dose: 0.5-2 nig. Side-effects include drowsiness, ataxia and visual disturbances. (Rohypnol). See page 152 and Table 22.
fluocinolone A topically active potent corticosteroid. Used as cream, ointment or gel (0.00625-0.025%) in severe, inflamed, corticosteroid-responsive skin disorders. Excessive application should be avoided. (Synalar).
fluocino”ide A potent locally effective anti-inflammatory steroid similar to fluocinolone, used as cream, ointment or lotion (0.05%). (Metosyn).
fluocortolone A locally acting corticosteroid used as cream or ointment (0.25%) in severe, inflamed skin conditions. (Ultralanum).
fluorouracil A cytotoxic agent used in the palliative treatment of carcinoma of the breast and gastrointestinal tract and other solid tumours.
Dose: 15 ingft orally or by i.v. infusion weekly, up to a total dose of 12-25 g. Side-effects include alopecia and dermatitis, but haeniatotoxicity, severe gastrointestinal disturbance and haemorrhage may limit treatment. Fluorouracil is used locally as a 5% cream (Efudix) in malignant skin lesions.
fluoxetine An antidepressant that acts by selectively inhibiting the uptake of serotonin. Given in single daily doses of 20 mg. Dose: 60 mg daily are given in bulimia nervosa. Side-effects are gastrointestinal disturbances, dizziness and anorexia; rash is an indication of withdrawal. It should not be used with other drugs that influence serotonin uptake. (Prozac). See page 128 and Table 11.
flupenthixol A tranquillizer similar to fluphenazine and used in the treatment of schizophrenia with apathy and withdrawal. It also has an antidepressant action.
Dose: 6-18 ing daily initially, with subsequent adjustment according to need. It may cause some restlessness and insomnia. Dose by deep i.m. injection, 20-40 mg every 2-4 weeks. Dose in depression: 500 pg 31ngdaily.The side-effects are similar to those of chlorpromazine. (Depixol; Fluanoxol). See page 168 and Table 30.
fluphenazine An antipsychotic drug with the actions and uses of chlorpromazine, but with reduced sedative and anticholinergic side-effects, although extra-pyramidal symptoms may be increased. Dose: 2- 10 mg initially in schizophrenia adjusted up to 20 ing daily. In severe anxiety states 1-4 mg. For depot treatment, 12.5-100 ntg of the decanoate by deep i.m. injection every 12-14 days according to response. (Modecate; Moditen). See page 168 and Table 30.
fluorescein An orange-red dye; solutions have a strong green fluorescence. Used as eye drops (1-2%) for detecting corneal lesions, as areas of cornea denuded of epithelium stain green.
fluorometholone A corticosteroid used as eye drops (0.10%) for inflammatory conditions of the eye. (FML).
flurandrenolone A potent locally acting corticosteroid used as a cream or ointment (0.0125%) in severe skin disorders not responding to other therapy. (Haelan). An adhesive tape is used for small resistant dermatoses.
flurazepam A benzodiazepine hypnotic for
the short-term treatment of insomnia.

flurbiprofen A non-steroid anti-inflammatory drug with the actions, uses and side-effects of naproxen. It is used in the relief of pain and inflammation in rheumatoid and arthritic conditions, and in other
nitisculoskeletal disorders.
Dose: 150 mg daily, after food, increased tip to 300 mg daily if necessary. Suppositories of 100 nig are available. Care is necessary in peptic ulcer and in aspirin-sensitive asthmatic patients. (Froben). See page 165 and’I'able 29.
flutamide An androgen blocking agent that inhibits the action of androgens on target organs. It is used in advanced prostatic cancer not responding to other drugs, usually in association with goserelin or related agents.
Dose: 750 mg daily. Side-effects include gynacconiastia, and liver function should be checked. (Drogenil). See page 122 and Table 8.
folic acid A constituent of the vitamin B group. It is essential for cell division and the growth and development of normal red blood cells. The main therapeutic use is in the treatment of megaloblastic anaemias due to folic acid deficiency. Dose: 5 ing daily for 4 months initially;
ing weekly may be adequate after the haematological response has been obtained. Sometimes given with anti-epileptic drugs, as long-term therapy may cause a folic acid deficiency. Small doses are present in many iron preparations to prevent the inegaloblastic anaemia that may occur in later stages of pregnancy. It must not be used alone in pernicious anaemia, as it cannot prevent the degeneration of the central nervous system associated with that disease.
folinic acid A methotrexate antidote. It is given ai the end of a course of methotrexate to reduce the toxic effects on normal cells and in methotrexate-overdose. Dose: up to 120 mg over 24 hours by i.m. injection (or i.v.), with 60 mg orally for another 48-72 hours.
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fluticasone A corticosteroid of increased potency. Used as a metered dose pump for the prophylaxis and treatment of seasonal allergic rhinitis and hay fever.
Dose: 100 pg (2 sprays) into each nostril mice a day in the morning. Maximum reliefmay not be obtained for 3-4 days. Systemic absorption extremely low. (Nixonaw.
fluvastatinV An inhibitor of the enzyme I I N46-CoA-reductase used in the treatment of hyperlipidaemia.
Dose: 20-40 ing daily in the evening. (Lescol). See page 146,’I'able 20 and atorvastatin, provastatin and ‘inivastatin.
fluvoxamine An antidepressant that acts by inhibiting the central re-uptake of serotonin. It is used mainly for maintenance treatment during depressive illness. Dose: 100-300 mg, daily in the evening; a steady plasma level is normally reached within 10-14 days. Side-effects after initial nausea may include somnolence, constipation and agitation. It should not be used with other drugs that increase scrotonin uptake, or with aminophylline or theophylline. (Faverin). See page 128 and Table 11.
follitropin A recombinant form of the follicle stimulating hormone used in some forms of infertility. It is given by injection in doses dependent on the degree of ovarian response. (Puregon).
formaldehyde A powerful but toxic germicide used mainly in the disinfection of rooms, and as’formalsaline’ (5% in normal saline) for the preservation of pathological specimens. Warts have been treated with a 3% solution.
formestane An inhibitor of aromatase, the enzyme that converts androgens to oestrogens. It is used in advanced postmenopausal breast cancer, as it has a cytotoxic action mediated by causing an oestrogen deficiency state.
Dose: 250 mg by deep intragluteal injection at intervals of 2 weeks, with variations of the injection site. Side-effect are rash, pruritus and occasional vaginal bleeding. Mentaron). See page 122 and Table 8.
foscarnet An antiviral agent for the treatment of sight-damaging cytomegalovirus retinitis in AIDS patients as an alternative to ganciclovir.
Dose: 60 mg/kg daily by i.v. infusion for 2-3 weeks, with subsequent infusion at a rate dependent on renal function. (Foscavir). See page 144 and,ribic ig.
fosfestrol A water-soluble derivative of stilboestrol. It is metabolized by the enzyme acid phosphatase to liberate stilboestrol in tissues rich in that enzyme, and so it is of value in prostatic carcinoma.
Dose: 1)), slow i.v. injection, 600-1200 rni, daily for 5 days or more. Oral maintenance dose: 120-360 nig daily. perinea) pain is a side-effect. (I lonvan). See page 122 and Table 8.
fosfomycin A phosphorus-containing antibiotic used mainly for infections of the lower urinary tract.
Dose: 3 g nightly after voiding the
bladder. Also used prophylactically before prostatectomy. Rash, nausea and diarrhoea are side-effects. (Monuril).
fosinopril An ACE inhibitor indicated in hypertension when standard therapy is ineffective or unsuitable.
Dose: 10 mg daily initially, adjusted after •1 weeks up to 40 nig according to need. It is eliminated by the liver as well as the kidneys, and may have some advantages in renal impairment. (Staril). See ACE inhibitors, page 148 and Table 21.
framycetin An antibiotic resembling neomycin in general properties. Used in eye infections as drops or ointment 0.5%. (Soframycin).
friar’s balsam Contains benzoin, storax, aloes, balsam of tolu. Official name Compound Tincture of Benzoin. See benzoin.
frusemide A loop diuretic with a powerful and intense action of short duration. Often effective in conditions no longer responding to thiazide diuretics.
Dose: 20-40 mg daily or on alternate days, or 20-50 mg i.ma or i.v. Much larger oral doses, varying front 250 nie, up to a single maximum dose of 2g may be required in renal failure and oliguria. Side-effects include nausea, diarrhoea and cramp. Masix). See page 141 and’Fable 18.
fusidic acid See sodium fusidate.
gabapentin An anticonvulsant used in the L11111101 of the partial seizures of epilepsy, although the mode of action is not yet clear. Dose: 300 mg initially, slowly increased to 1.2 g daily according to need. Drowsiness, tremor and weight gain are some side-effects. Withdrawal is with slowly reduced doses over 2-3 weeks. (Neurontin). See page 136 and Table I5.
gallamine A synthetic non-depolarizing (competitive) muscle relaxant.
Dose: 80-120 mg initially i.v. with small subsequent doses according to need and response. The action of the drug may be terminated by the injection of neostigmine, 2.5-5 mg, together with atropine, 0.5-1 mg. (Flaxedil). Now used less frequently as tachycardia is a side-effect.
gamolinic acid A derivative of linoleic acid present in evening primrose oil. It is said to be of value in atopic eczema.
Dose: 320-480 mg daily. It is also used in mastalgia (breast pain) in doses of
240-320 mg daily, but the response is slow (8-12 weeks). (Epogam; Ffarnast).
gammaglobulin See immunoglobulin.
ganciclovir An antiviral agent similar to aciclovir, but more toxic. It is used only in sight- and life- threatening infections with cytomegalovirus (CMV) in immunocompromised patients.
Dose: by i.v. infusion, 5 mg/kg every 12 hours for 14-21 days, with mainte nance (lose of 5 mg/kg daily. Later oral dose 3 g daily. The solution is very alkaline, and injection requires care. Regular blood counts are essential. (Cvnievene). See page 144 an(Frable 19.
G-CSF human urnan granulocyte colony stimulating factor. See filgrastim and lenograstim.
fusafungine An antibiotic with anti-inflammatory properties used for upper respiratory tract infections.
Dose: as aerosol spray 123 jig 5 boles  day. (Locabiotal).
Gee’s linctus A soothing cough linctus containing camphorated tincture of opium, oxymcl of squill and syrup of tolu.

Allergies and Pregnancy
Great care is taken in prescribing drugs during pregnancy. This is something that doctors are now exceedingly cautious about, but do tell the doctor as soon as you decide to try for a baby. The foetus is most vulnerable to damage by drugs during the first three months, and especially the first few weeks after conception.
Your prescription will be changed if the drugs you are currently taking could pose any threat to the unborn child. A drug that has not had sufficiently rigorous testing for safety during pregnancy, or lacks a long track record, will probably be withdrawn. New drugs are generally considered to be slightly more risky than the tried-and-true older drugs: rare side effects may not come to light during the testing which precedes release of a drug, but they do become apparent once the drug is in widespread use for a long time (see pp. 136-7).
If you are already pregnant as you read this, don’t worry too much. With a few notable exceptions – certain antihistamines and antibiotics – most of the drugs used for allergic diseases do not pose any major risk to the unborn child. There is probably nothing to worry about, but see your doctor as soon as you can – and talk to a pharmacist, in the meantime, if you are concerned. Don’t panic, and don’t stop taking your drugs unless you are absolutely sure that you can do without them. Do not stop taking your drugs if you have asthma.
Some non-prescription medicines are best avoided during pregnancy. Read the packet carefully, and talk to your pharmacist if you have any doubts.
From the moment you start trying for a baby, remember to tell any medical personnel who treat you, and any pharmacist you buy medicines from, that you could be pregnant.
Immunotherapy and skin testing
Immunotherapy should not begin during pregnancy, because of the risk of anaphylaxis (see below), but pregnant women who are already undergoing immunotherapy can continue.
The safety procedures described on p. 166-7 should be followed with meticulous care.
Most doctors continue immunotherapy at a steady ‘maintenance dose’ because there is always a small risk of anaphylaxis with immunotherapy when the dose is increased. Some doctors are even more cautious and reduce the maintenance dose during pregnancy, but give more frequent injections – this minimises the chance of bad reactions.
Many doctors do not give skin tests for allergy during pregnancy, as these also carry a very small risk of anaphylaxis. If you do have skin tests, there must be resuscitation equipment available. Intradermal tests (see p. 92) are best avoided.
Severe allergic reactions (anaphylaxis)
Special care should be taken to avoid anaphylaxis during pregnancy as this may increase the chance of a miscarriage.
Injecting adrenaline during the first three months of pregnancy may carry some small risk of malformation of the baby. But the evidence here is uncertain, whereas the danger to your own life, if you don’t use adrenaline when you need it, is both certain and substantial. If you have an adrenaline self-injection kit, talk to your doctor now about what you should do in an emergency. The best policy is to be ultra-careful about avoiding your allergen, so that anaphylaxis does not happen.
Women who suffer from exercise-induced anaphylaxis (see p. 59) generally play safe by exercising less strenuously while pregnant. The problem can get worse during pregnancy, but it does not usually do so. Labour itself is very strenuous of course, but problems during the birth are uncommon. If anaphylaxis does occur, the reaction is usually quite mild – nettle rash only – and the baby is delivered alive and well. However, many women find that the attacks of exercise-induced anaphylaxis are more frequent and severe when they start exercising again after the baby is born. It is best to resume exercise very gradually.
Eczema and other skin problems
Atopic eczema may improve during pregnancy, probably because the body produces slightly more of its own natural steroid, hydrocortisone. Contact dermatitis may either improve or flare up.
Stretch marks often itch a great deal, and widespread itchy skin, with or without a rash, is a common problem during pregnancy. These are not usually allergic reactions, and no cause can be identified in most cases. The skin tends to recover a few days after the birth.
If there is itching in the vulva) area, this could be due to a Candida infection (your doctor can prescribe a safe treatment) or it might be just another of those unexplained itches of pregnancy.
Hayfever and other nasal allergies
The natural hormone changes of pregnancy affect the nose, which can become more blocked. If you have allergic rhinitis this will add to your woes. See your doctor and make sure that your drug treatment is adequate (see p. 29). The nose-clearing exercises on pp. 230-31 might also help.
Asthma
Severe asthma can be bad for both the pregnant mother and the unborn child. Uncontrolled asthma increases the risk of the baby being born prematurely – and premature babies are more likely to develop asthma themselves. The death rate for newborn babies is also higher if the mother has poorly controlled asthma.
Treating a severe asthma attack promptly helps to prevent any damage to the baby, so don’t hesitate to call an ambulance –and tell the operator you are pregnant. The ambulance should be carrying oxygen which is particularly important for helping the unborn baby through the attack.
If you have asthma, don’t stop using your drugs or reduce the dose unless advised to do so by a doctor. Because it is so important to keep asthma under control during pregnancy, your doctor may want to add, or increase, preventer drugs such as inhaled corticosteroids or sodium cromoglycate (see p. 148). It
also makes sense to monitor your peak flow twice a day (see p. 97) so that you have advance warning of serious attacks.
Unfortunately, some asthmatics – usually those who have severe asthma to begin with – get much worse during their pregnancy. In such cases, careful monitoring and increased use of preventer medicines are essential. The symptoms usually increase from week 24 to week 36 of the pregnancy. The last four weeks tend to be much better, and things are back to normal by about three months after the birth.
Some women with asthma have fewer symptoms while they are pregnant, and for others their asthma stays about the same.
Asthma can also appear for the first time during pregnancy, and may be quite severe. However, a relatively mild breathlessness can be due simply to the fact that, as the pregnancy advances, the chest cavity, and therefore the lungs, become compressed. This is not necessarily asthma.
This simple physical effect can also add to the difficulties experienced by women who were already asthmatic before they became pregnant.
GER (acid reflux) – see p. 38 – can contribute to asthma during pregnancy, and treating this problem may help.
Asthma attacks during the birth
Severe asthma attacks very rarely occur during labour, but it is still important that all the medical staff in attendance know you have asthma. They should also be told if you have taken steroid tablets during the previous two years. A record of when you took steroids, how long for, and at what dose, will be valuable. You may need a low dose of steroid to get you through the physical stress of labour (see p. 142). Some doctors believe that patients who have been using high-dose inhaled steroids should be treated in the same way.
Smoking
Smoking is a bad idea if you have allergies or any allergic tendency in the family. Smoking is a very bad idea indeed if you are pregnant, or a parent. This is the moment, if ever there was one, to give up.
Enlist your doctor’s help, and ask if counselling, psychotherapy or other forms of support are available. If you have tried all this before, and failed, then talk to your doctor about the possibility of using nicotine patches. Some doctors believe that, for pregnant women who smoke 20 cigarettes or more a day, the advantages of nicotine patches outweigh the risks to the foetus. Nicotine levels in the blood are lower with patches than with heavy smoking, and your baby is not enduring the hundreds of other toxins found in cigarette smoke.

Allergy and Your Immune System
`The summer used to be such a miserable time for me because I’m allergic to grass pollen. For most of

my life I have had dreadful hayfever, and my asthma would get worse during the summer as well.

Antihistamines knocked me for six, and although there were nose drops that helped a little, they

certainly did not resolve the problem completely. Exam time was always a nightmare when I was a student

- then, as now, it coincided exactly with the pollen season.’
‘Getting a job in Chicago was a turning point in my health. My colleagues were amazed to see me

snuffling through the summer and just accepting that nothing could be done to improve matters. The

whole approach to treating allergies is different there. Eventually someone marched me off to see her

allergist, who said that I should have “allergy shots” and that my health insurance would cover it. The

process was very time-consuming at first, and it took a while to work, but the change is remarkable.

I’ve never regretted having the treatment. Summer is a time I can actually enjoy now.’
Not everyone responds this well to immunotherapy, but for those allergy sufferers who do benefit, this

is an excellent treatment. It tackles allergies right at their source, by teaching the immune system to

react differently to the allergen.
Also known as Specific Immunotherapy (SIT), Incremental Immunotherapy (11T) or simply as

hyposensitisation, this form of treatment was devised by two English medical researchers, Leonard Noon

and John Freeman, who reported their successes with hayfever patients in 1911. Ironically, their

treatment is now less readily available in Britain than in any other industrialised nation. Only a

small minority of British allergy patients receive immunotherapy. The cause of this strange situation

is a ruling made in 1986 by the Committee on the Safety of Medicines (CSM). This states that

immunotherapy must only be given where there is resuscitation equipment available, and that all

patients must wait for an hour after each injection, in case of
side effects. In addition, immunotherapy cannot be used for severe asthma.
The requirement for resuscitation equipment rules out most GP surgeries, and this effectively puts

immunotherapy beyond the reach of many allergic individuals in Britain, owing to the extreme shortage

of allergists and hospital allergy clinics (see p. 89). (In the past, the lack of allergy specialists

meant that most immunotherapy in Britain was given by GPs.)
The CSM ruling was triggered by a number of deaths due to immunotherapy: there were eleven fatalities

between 1980 and 1986, with five of these in the eighteen months just before the report. But almost all

these deaths were due to very basic errors in the way the injections were given – tragic as the deaths

were, the official response to them was inappropriate. Fatal reactions to immunotherapy can be avoided

with close attention to ordinary safeguards (see p. 166-7).
Allergen immunotherapy is still freely available elsewhere in the world, and is regarded as a key part

of allergy treatment. Britain is now out of step with all other developed countries, and most doctors

feel that British restrictions are far too strict.
There are hopes that this situation may change within the next few years, and that more allergy

sufferers may be able to take advantage of this valuable treatment. This could be achieved, in part, by

investing more National Health Service money in allergy clinics and allergy specialists. In addition,

there should be a relaxation of the regulations, so that properly trained GPs can give immunotherapy to

patients who are not at high risk of a fatal reaction. For people whose lives are affected by

allergies, the reintroduction of this treatment (with appropriate safeguards) would be a huge boon.
The uses of immunotherapy
Immunotherapy is mainly used for airborne allergens such as pollen, house-dust mite and mould spores.

Allergies to animals can also be treated with immunotherapy, but the treatment cannot work miracles –

if a cat-allergic person decides to keep the cat, the high dose of allergen inhaled every day limits

the impact of immunotherapy treatment.
People with straightforward allergic reactions affecting the nose and eyes (allergic rhinitis and

conjunctivitis) respond well to immunotherapy. In patients with hayfever, for example, the success rate

(patients showing some degree of improvement) is about 80-90%. When nasal allergies are complicated by

chronic sinusitis or nasal polyps, the chance of success is a little lower.
Some studies of the long-term effects of immunotherapy suggest that, if it is given to children with

hayfever or perennial rhinitis, those children are less likely to develop asthma.
The benefits of using immunotherapy to treat established asthma are less certain. Asthma is a more

complex disease than hayfever, and allergies are only one factor among many (see p. 36), which may

limit the impact that immunotherapy can make. Experience suggests that immunotherapy can be a great

help for an asthmatic with a strong allergic reaction to a single airborne allergen, such as grass

pollen or house-dust mite, but not for other asthmatics. Asthmatics with aspirin sensitivity or chronic

sinusitis are unlikely to benefit.
The value of immunotherapy to children with asthma is a subject of great debate among doctors in the

United States. Some studies suggest that it is of little real benefit, while others are more positive.

One interesting study, that followed asthmatic children for 15 years or more, found that if they were

given a full five-year course of immunotherapy when young, they tended to have fewer asthma symptoms

and need less medication in their late teens and early twenties.
Chronic urticaria (nettle rash) is occasionally due to airborne allergens, in which case immunotherapy

may help. However, immunotherapy is not recommended for atopic eczema. When people with both eczema and

rhinitis try immunotherapy for their nasal allergies, some find that their eczema gets worse.
Insect-sting allergy is a prime candidate for immunotherapy (see pp. 167-8) but food allergy is a

different matter, and is not treated with immunotherapy at present (see p. 168).
Who can get immunotherapy?
As a result of the CSM ruling (see p. 164) remarkably few allergy sufferers in Britain receive

immunotherapy.
Those with insect-sting allergy, who have suffered anaphylaxis (see p. 58), are the most likely to be

offered this treatment. However, even with this frightening and life-threatening problem, which can be

treated with almost 100% success by immunotherapy (see p. 167-8), such treatment is not automatically

available.
A few people with severe hayfever that does not respond well to drug treatment may also be given

immunotherapy. It is worth asking your doctor about such treatment if you feel you would benefit.
How immunotherapy works
Immunotherapy consists of a series of small injections, just under the skin. The liquid that is

injected contains an extract of the offending allergen, for example house-dust mite. The injections are

given at regular intervals, usually once a week, although other schedules are possible (see p. 167-8).
At the outset, a very dilute version of the allergen extract is used, way below the threshold for an

allergic reaction. People who seem highly sensitive, on the basis of their skin tests, start on an

extract that is even more dilute.
For the next injection, a slightly higher concentration of the allergen extract is used, and the

concentration goes on increasing with each successive injection. The idea is to habituate the immune

system to the offending allergen, by very gradually raising the dose. Eventually, when the dose reaches

a level which generally gives beneficial effects, no further increases are made.
If an allergy sufferer reacts badly to immunotherapy injections (see p. 166) on several successive

occasions, the dose may be levelled off before the ideal maximum dose is reached. However, a good

allergist will persist for some time in trying to increase the dose because stopping at a lower level

often results in the treatment being ineffective.
The first stage of immunotherapy, when the concentration of allergen is being increased week by week,

is referred to as the build-up stage. The second stage, when the dose is being kept at the same level,

is called maintenance therapy, and the dose used is the maintenance dose.
There is sometimes an obvious improvement by the time the build-up stage is complete, but not always.

The benefits of the treatment generally appear within six months of reaching the maintenance dose, but

some people have to wait a year or even two before things improve. As the immunotherapy begins to take

effect, symptoms decline and there is often less need for drugs.
A great deal of research effort has gone into finding out what lies behind these changes – in other

words, what is actually happening to the immune system when immunotherapy is effective. The answer is

that a surprising number of different changes may occur and no two allergy sufferers react to

immunotherapy in quite the same way. Frequently there is a shift in the kinds of antibodies the body

produces against the offending allergen. Levels of IgG antibodies (which help to block the allergic

reaction) go up, while levels of the allergy antibody, IgE, tend to stabilise and eventually go down.

The numbers of mast cells (see box on p. 12) may also decline, and they can become less responsive to

the allergen. The balance of power between Th1 cells and Th2 cells may also shift, with the pro-allergy

Th2 cells (see p. 11) becoming less influential.
What can go wrong
The secret of safe immunotherapy is to go at exactly the right speed for the immune system of the

individual being treated. The doctor should look for feedback from the immune system – signs that show

how well it is coping with the steadily increasing dose of allergen – and use these to pace the

immunotherapy schedule.
Going too fast – getting ahead of the immune system’s ability to cope – is hazardous. A major allergic

reaction, called anaphylaxis (see p. 58), can occur, and this is the cause of deaths during

immunotherapy. However, as long as there is injectable adrenaline (see p. 150) and resuscitation

equipment available, even such an extreme crisis can be dealt with safely.
Serious reactions to immunotherapy usually occur:
•    during the initial build-up phase; maintenance therapy is much safer
•    during the pollen season, for those with pollen allergy
•    when a new vial of allergen extract is first being used, because of variations in concentration

(see p. 168-9).
Those most vulnerable to severe reactions are:
•    people with asthma, especially severe or unstable asthma
•    those who have experienced systemic allergic reactions in the past
•    anyone who appears to be extremely allergic, on the basis of skin tests
•    anyone taking beta-Mockers (see box on p. 150).
With care, these fatalities can be avoided. Patients who are given immunotherapy can ensure their own

safety by being well informed about the procedure (see p. 167).
The timing of immunotherapy
There are various different approaches to the timing of immurotherapy. The basic method (which has a

good safety record in the United States where it is very commonly used) starts with injections once a

week. After the maintenance dose has been reached, maintenance injections are given once every 2-4

weeks. The frequency of these may be increased during the pollen season, for people with pollen

allergies.
It is the regularity of the injection schedule that gradually creates, and then sustains, immune

tolerance, so the treatment is only of value to patients who can reliably keep their appointments.
When immunotherapy is successful, it can eventually be discontinued without any reappearance of the

allergic reaction. It usually takes 4-5 years of regular therapy, from the time of the first injection,

to get to this point. The benefits then persist for many years, perhaps indefinitely in some people,

even without any further injections.
Rush immunotherapy
Trying to speed up the process of immunotherapy greatly increases the risk of a severe reaction

(anaphylaxis). However, there are some situations where fast results are needed, and in such cases rush

immunotherapy, also called accelerated immunotherapy, may be used.
During the build-up stage of rush immunotherapy, injections are given every day, or even several times

a day. All the usual safety procedures (see below) are observed with particular care, to reduce the

chance of a severe reaction.
In semi-rush immunotherapy, the build-up injections are given twice a week, and the risks are lower

than with daily injections, but still higher than with weekly injections.
Minimising the risks
If you are lucky enough to be offered immunotherapy treatment under the National Health Service, you

should not feel concerned about accepting the offer. There is very little risk of a bad reaction

because safety procedures are now so stringent.
To minimise the risk of suffering a severe reaction, the doctor will ask you, at each visit, about any

reactions that occurred after your previous injection. Reactions might include redness, itching or

swelling around the injection site, or (more seriously) symptoms elsewhere on the body, such as nettle

rash (urticaria), itchy skin, sneezing, a runny nose, red or itchy eyes, tightness in the throat or

chest, coughing or wheezing. Always make a note of such symptoms, so that you don’t forget to mention

them at the next visit. This is crucially important, as such reactions can indicate that the immune

system is being hurried along too fast.
The doctor will also ask if you have an infection of any kind, as this can alter your reaction. You

should also tell the doctor about any new medicines being taken, as some, such as betablockers (see box

on p. 150), can make a bad reaction to the injection more likely to occur.
Asthmatics can expect the doctor to ask about current asthma symptoms, and to check their peak flow

both before and after an injection. If there are any symptoms, or if the peak flow is less than 70% of

the best-ever value, the injection won’t be given.
Severe reactions can sometimes begin several hours after the injection, so stay within reach of a phone

for about 24 hours. Among United States allergists (who don’t require their patients to wait after the

injection for more than 20-30 minutes) there are some who believe that everyone undergoing

immunotherapy should carry an adrenaline (epinephrine) auto-injector (see p. 150) on the day an

injection has been given, for use in the event of a severe reaction. Anyone who has suffered

anaphylaxis in response to an insect sting will probably have an adrenaline auto-injector anyway, and

this can certainly be used to treat anaphylaxis following immunotherapy. Note, however, that using the

adrenaline is just the first step in treating anaphylaxis (see p. 98) and you must then go back to your

allergist, or to the nearest hospital emergency department, without any delay.
It is sensible to avoid exercise for two hours after an injection. Be extra-cautious during the pollen

season if you are receiving immunotherapy for pollen allergies.
Immunotherapy for insect-sting allergy
`Our daughter has had two really bad reactions from being stung by a wasp. After the second one, the

doctor at the accident and emergency department told us that she nearly died. We got so anxious about

it that we worried every time we left the house in the summer, and it was even worse if she went out

without us. My wife got so upset about it that she wasn’t sleeping well. It was affecting the whole

family badly.
‘Then we heard about desensitisation treatment, and asked our GP, but he said he couldn’t do it.

According to him, they might be able to do it at the hospital, but it might not work, and it was risky

too. We accepted that at first, but then I started doing some research on the Internet, and discovered

that in America and Germany this treatment is absolutely standard – someone like our daughter would

automatically be given it. We felt very angry when we found this out, and went back to the doctor.

Eventually Ann was referred to the allergy department at a hospital, and now she is getting this

desensitisation treatment. I’m pleased about that, obviously, but I still think it shouldn’t have been

such a fight to get it.’
Immunotherapy provides highly effective protection for those with insect-sting allergy, and should be

given to anyone who has had a severe systemic reaction (see p. 60). Some United States allergists also

recommend it for adults who have had a cutaneous systemic reaction (see p. 60), on the basis that they

may well progress to a severe systemic reaction with the next sting.
Studies of people who have suffered severe systemic reactions, and are then treated with immunotherapy,

show that 97% have no systemic reaction to future insect stings. For the 3% who are not fully

protected, the severity of the reaction is much reduced and far less likely to be life-threatening. In

other words, this is an excellent treatment which can save lives.
Targeting the treatment
Choosing the right venom for immunotherapy can sometimes be difficult. Not everyone with insect-sting

allergy sees the insect that caused the reaction. Skin tests may not give the answer either, because

there are often positive reactions to several different venoms. Some of these may be false positives

(see box on p. 91) and it is impossible for the allergist to say which one(s) are actually relevant.

Most allergists will recommend immunotherapy for all of them, using a mixture of venom extracts.
Where the guilty insect was seen and identified, but other venoms also give positive skin tests, a more

difficult decision has to be made. Many allergists carry out immunotherapy for all the venoms that gave

a positive skin test, on a ‘better safe than sorry’ basis. Since there are cross-reactions between

venoms (see box on p. 113), there is some sense in this. Other allergists just give immunotherapy for

the insect that did the deed.
Will immunotherapy against one insect protect against a related insect? With two closely related

insects such as wasps and hornets, which have many allergens in common, it might do – but there is no

guarantee. The problem is that, as well as the shared allergens, each venom also has its own unique

ingredients. It’s impossible to say, with the kind of tests available at present, if an allergic

reaction was to shared allergens or unique ones. So immunotherapy against wasp venom may give

protection against hornet venom, but it will not necessarily do so – and vice versa.
In the case of bumblebee allergy (seen almost exclusively in those, such as horticulturalists, whose

work involves handling bumblebees) a more definite answer can be given – honeybee immunotherapy does

not work. Immunotherapy with bumblebee venom does work, fortunately. The bumblebee extract has to be

obtained from specialist sources.
Injections are given weekly during the build-up phase, unless protection is needed urgently, as with

work-related sting allergy, in which case rush immunotherapy may be used. Once the maximum dose has

been reached, a maintenance injection is needed every four weeks. After a year, this maintenance dose

can be given every 6-8 weeks.
After 3-5 years of immunotherapy, skin tests with insect venoms are usually tried again. If the results

are negative, the immunotherapy will stop. Research now shows that, even if skin tests are still

positive when immunotherapy ends, there’s an 8090% chance that no systemic reaction will occur to

future stings. Some people are not reassured by this, and prefer to continue with immunotherapy for

their own peace of mind. Indeed, research shows that a near-fatal systemic reaction has a long-lasting

psychological impact, and that many people continue to feel anxious despite completing immunotherapy

and reacting negatively to skin tests.
At one time, challenge stings with live insects were given to check whether immunotherapy had actually

worked. Few doctors do this now, but your allergist may be prepared to do a challenge test if you ask.

Adrenaline and resuscitation equipment would be available if a challenge test were used, so any severe

reaction could be dealt with promptly and effectively. The fact that the psychological consequences of

insect-sting allergy are so persistent suggests that challenge tests with live insects may have a

particular value, in demonstrating that immunotherapy has worked. Challenge tests are also helpful for

those who work with stinging insects, such as honeybees and bumblebees, and who need to be sure that

they can go back to work safely.
Immunotherapy for food allergy?
Attempts to use standard immunotherapy for food allergy have been made repeatedly, but without success.

The process of giving the injections is nerve-racking because of the constant risk of a severe

reaction. The risks prevent the dose of allergen being increased very much, so the beneficial effects

are small. While there may be some reduction insensitivity, it is not enough – or not reliable enough –

to be of any practical value.
What doctors are aiming for here, incidentally, is simply to protect against the effects of

accidentally eating a tiny amount of the food – no one is expecting that someone with peanut allergy

will be able to eat peanut butter sandwiches as a result.
Some of the new developments in immunotherapy may be useful for food allergy, as described in the next

section.
The future of immunotherapy
Many different research teams are working on ways of improving immunotherapy – making it more

effective, safer to give, and less time-consuming.
One approach involves altering the allergen, so that it only interacts with those parts of the immune

system whose job is to control allergic reactions (and therefore bring about tolerance). The changes

made to the allergen are designed to make it ‘invisible’ to the parts of the immune system that

actually attack the allergen. The idea is to inject something that can’t cause a bad reaction, and is

therefore 100% safe.
The modified allergens are called allergoids. Another term often used is peptide immunotherapy – this

describes a technique in which the allergens are chopped up into small pieces to make them safe

(allergens are proteins, and a fragment of a protein is called a peptide).
Already, researchers in Germany have made an allergoid from birch pollen that can reduce hayfever

symptoms with a series of just seven injections given before the pollen season.
Meanwhile, a research team in London is working on peptides made from cat allergen, with encouraging

results so far. In a group of asthmatics who were allergic to cats, a series of 4-10 injections, over a

period of 2-8 weeks, produced benefits in about half those treated. The researchers believe that they

can improve on this and help the majority of people with cat allergy, at least enough to survive

temporary exposure to cat allergen (when visiting cat-owning friends, for example). They hope to refine

the treatment sufficiently to enable some cat-allergic people to keep their pet, rather than finding it

a new home. This is a relatively safe treatment that might be given by a GP, rather than only by

specialists. The research team hopes the treatment will be available by about 2009.
Could this kind of technique work for food allergy? Doctors believe that it can, and a great deal of

research work is being done, in both Britain and the United States. A major focus of this effort is

peanut allergy, since this puts so many young lives at risk. Even if the research is successful, It

will be several years before such treatments become available.
Researchers are also working hard to produce standardised allergen extracts – in other words, allergen

extracts that always contain a standard amount of the allergen. The aim is not only to reduce the

number of treatment failures (which can occur if the extract does not contain enough allergen) but also

to avoid mishaps when a new vial of allergen extract is used (differences in strength, between one vial

and another, are sometimes a cause of anaphylactic reactions).
Standardisation is difficult, because the starting materials –skin particles from horses, for example,

or dust-mite droppings –are natural materials and therefore variable. Some samples contain far more of

a particular allergenic ingredient than others.
One way around this problem is to develop accurate methods of measuring the amount of allergen in the

extract. Another approach is to abandon the whole business of making extracts, and produce allergens

artificially, in a laboratory. This is done by inserting the gene for the allergen – the gene for the

Der p1 allergen of house-dust mite, for example – into bacteria. These bacteria then act as production

units, manufacturing large amounts of the allergen every day. With this high-tech approach, the exact

content of the allergen preparations can be controlled.
These high-tech allergen preparations are extremely pure, and therefore very effective – as long as the

person receiving immunotherapy really is sensitised to the particular allergen that is included.

Unfortunately, most natural allergenic materials contain two, three or even more separate allergens. In

house-dust mite droppings, for example, while Der p1 is the allergen that affects most people, there is

also an allergen called Der p2, and a few people are more sensitive to this than to Der pl.
Artificially produced allergen preparations usually include the main allergen only. For the minority of

people who are more severely allergic to one of the other allergens, this extract will not work.

Eventually this problem will no doubt be circumvented by means of more precise skin testing before

immunotherapy begins – skin tests with individual allergens, rather than with allergen extract

containing a mix of allergens.
A third approach is to change from injections to oral immunotherapy – giving the allergen extracts by

mouth. The best results are obtained when the allergen is held under the tongue for a while and then

swallowed. This is known as Sub-lingual immunotherapy or SLIT, and has become very popular in Italy and

France, where it is a common treatment for hayfever. A recent pilot trial among GPs in Britain suggests

that it may be useful, but is not a miracle cure. Overall, the group treated with SLIT had fewer

symptoms during the pollen season, but antihistamines were still needed. There is some evidence from

Italy that SLIT might reduce the likelihood of children with hayfever going on to develop asthma, and

reduce the chance of new sensitivities.
Side effects are unusual with this treatment, and those that do occur are mostly mild – itching in the

mouth, for example. The treatment is safe enough for routine use in children.
Might oral immunotherapy work for food allergy? Other Italian studies suggest that it could. The

objective of these studies is to reduce the risk to children with cow’s-milk allergy from accidental

encounters with ‘hidden milk’ in prepared food or drink. The immunotherapy treatment begins with

miniscule amounts of milk – the doctors start with a single drop diluted in water, each day for a week

– and increase the dose extremely slowly. Antihistamines are given to minimise the risk of a reaction.
The whole process requires enormous patience, but after seven months, the majority of the children

involved can tolerate some milk – between three tablespoonfuls and a small cupful each day.
This is a very encouraging study that should be repeated by doctors in Britain. Because of the risks of

anaphylaxis – which can, of course, be fatal – it does require full medical supervision, and you should

not attempt it at home. Whether this method would work for allergens other than milk is something that

nobody has yet investigated.
A great many other approaches to immunotherapy are currently being tried for food allergy. Many of the

new techniques are highly experimental, and some show great promise, but it will be many years before

they are in use.
One innovation that is closer to being in general use in the United States involves giving the anti-IgE

drug omalizumab (see p. 149) alongside immunotherapy injections. The drug maximises the benefits from

the immunotherapy, and may make the build-up stage (see p. 165) safer, by lowering the risk of

anaphylaxis. For British allergy sufferers, who cannot yet get omalizumab, and whose chances of getting

immunotherapy are vanishingly small, it may seem unkind even to mention such treatments, but we can

only hope that things will improve here in the near future. You might take some comfort from the

thought that, by the time immunotherapy is available again in Britain, there will be a whole host of

highly effective new techniques available for doctors to try.
All the methods described above are forms of specific immunotherapy – they treat an allergy to dust

mites or to grass pollen or some other specific allergen.
A far more radical and ambitious approach to immunotherapy is now the aim of some medical researchers:

blocking the tendency to allergies as a whole.The underlying idea here is to reverse the basic shift in

the immune response, from Th1 cells to Th2 cells. It is this shift to Th2 cells which produces the

allergic tendency (see pp. 11 –13).
Some interesting findings have already been made in this area, including the surprising discovery that

the balance of Th1 cells and Th2 cells can be adjusted even in people with longstanding allergies.

Inspired by discoveries about hygiene and allergy (see p. 21), British researchers have made a vaccine

containing inactivated cells of a harmless bacterium found in the soil, Mycobacterium vaccae. This is

given as a single injection just under the surface of the skin. It has been used for adult patients

with asthma, and for children with severe atopic eczema, with some improvement in both groups. If the

treatment proves as useful as the preliminary studies suggest, this could be a common treatment in a

few years’ time.

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.

A blocked or runny nose in Allergy
THAT LASTS ALL YEAR
`Everyone has heard of hayfever, but it’s news to most people that you can have this sort of problem all year round,’ complains Elizabeth. ‘Before we got the treatment sorted out, Benny was “the kid with the constant cold”, and I did notice other mothers looking less than enchanted at the prospect of his coming over to play.’
Benny suffers from allergic reactions to house-dust mites and cats which cause hayfever-style symptoms (26) all year round. This condition doesn’t even have a common name – the medical one is perennial allergic rhinitis – yet it is one of the most common allergic diseases.
Any airborne allergen that is found in the air all year round can cause perennial allergic rhinitis:
• House-dust mite is the number one suspect in most parts of the world. Particles from other insects, such as midges and mosquitoes outdoors, and cockroaches, house flies, bloodworms (used for fish food) or carpet beetles indoors, can also cause nasal allergies.
• Mould spores can be the problem: they are found both indoors and out.
• In some regions, certain types of pollen are airborne all year round (27).
• All pets other than fish produce allergenic particles (even snakes).
• Allergens encountered at work (133) can also produce symptoms in the nose. This is a warning sign gn you should not ignore – it often means that occupational asthma is on its way (132).
Occasionally, the offending substance is being eaten not inhaled. This is less common, so you should investigate inhaled allergens first, before trying an elimination diet (29).
Skin-prick tests (91) will help to identify any airborne allergens that are responsible, but where food is the culprit, skin-prick tests are often negative (69)
Triad and NARES
Diagnosis of perennial allergic rhinitis is complicated by the fact that there are two other conditions – called triad and NARES – which produce similar symptoms and involve the immune system but are not, strictly speaking, allergies.
Triad is so called because it involves three distinct symptoms:
• perennial rhinitis
• polyps in the nose – little fleshy growths that can kill your sense of smell
• asthma.
People with triad tend to collect all three symptoms gradually, in no fixed order, over a period of years or even decades. Many are sensitive to aspirin and related drugs, and almost everyone with triad develops this sensitivity eventually.
Aspirin sensitivity can come on very suddenly and produces a reaction akin to anaphylaxis (101). This can be fatal, so it is probably best to avoid all aspirin-like drugs if you have triad, even though you have not reacted to aspirin in the past Aspirin-like drugs are found in painkillers, arthritis drugs and cold remedies – check with a pharmacist before you buy (151).
If you have asthma, think twice about operations on the nose to remove polyps – they can make the asthma much worse.
The initial letters of Non-Allergic Rhinitis with Eosinophilia have been stretched a bit to get NARES. (This is a medical joke –the Latin word Hares means nostrils.) The problem is caused by eosinophils (19), which flock into the nose and cause severe inflammation. Some people with NARES go on to develop triad.
Collateral damage
Having the nose swamped with mucus can lead to knock-on problems in the ears, sinuses and airways.
If the tube that leads from the ear to the nose (the Eustachian tube) becomes blocked, then fluid cannot drain away from the middle ear. This is called secretory otitis media, or glue ear - it dulls the hearing and causes an unpleasant ‘popping’ sensation. The ears may also feel blocked and itchy, but if children have had this problem since they were tiny they may not complain because they assume that’s just the way ears are supposed to feel. Deafness is often the first sign anyone notices.
Sinusitis is another possible complication, because fluid from the sinuses should also drain into the nasal cavity. With the ouflow blocked, mucus builds up in the sinuses and can become infected by bacteria (30).
Post-nasal drip can also occur with perennial allergic rhinitis. The over-abundant mucus runs down the back of the nose, into the throat and then the airways. This produces a persistent phlegmy cough, which may occasionally be mistaken for asthma.
When the rhinitis is treated effectively, all these problems should sort themselves out, although additional treatment is usually necessary in the case of persistent sinusitis (33).
Treatment
Where an allergen such as house-dust mite or mould spores has been identified as the source of the problem, eradicating it from your house (see Chapter 4) will make a huge difference, and may avoid the need for drugs. If the allergen is unavoidable, immunotherapy (see pp. 164-8) or some alternative form of desensitisation (see pp. 210-13) could be very helpful.
Where drugs are needed, nose drops are best. They get the drugs right to the target so doses are minimal, which means very few side effects. The drugs used are:
• cromoglycate to prevent the allergic reaction before it starts (148)
• antihistamines to block the allergic reaction before it produces inflammation (138)
• steroids to calm down inflammation (144). Steroid nose drops are also useful for NARES and triad. If you are taking steroid drops continuously, your doctor should check the membranes inside your nose every six months. Make sure you put the drops in correctly, especially if you have polyps (144).
If you suffer stinging, burning or dryness, it might be due to preservatives in the drops, not the drug itself (see box on p. 33), so talk to your doctor about a different formulation.
Don’t use over-the-counter decongestant drops: they do nothing to treat the allergy or inflammation, and are little more than a ‘chemical crowbar’ to open up the nose. Your nose gets addicted to them in a few days, and when you stop using them you get ‘rebound congestion’ - absolute and total blockage. It does wear off eventually, but is unpleasant meanwhile. If you are suffering this problem at this very moment, don’t put more decongestant drops in - your nose needs to go ‘cold turkey’ to recover, not have its addiction fed!
If none of the anti-allergy drugs work, but decongestant drops do, then you probably have a non-allergic disease called vasomotor rhinitis. The symptoms are very similar to allergic rhinitis, but without the sneezing and itching. See your doctor again, because there is an effective treatment that uses anticholinergic drugs (see box on p. 156). Acupuncture (see below) can also be helpful.
An elimination diet (194) will diagnose any food reactions. It works wonders for some people with severe and unexplained perennial rhinitis, Including people with such a flood of mucus that they can scarcely work or live normally. You should certainly give this diagnostic diet a try if there are clues that suggest food is the culprit (69) or if no airborne allergen can be identified. Yeast - found in bread, beer and B-vitamin tablets -is quite often the culprit in rhinitis, but it could be any food.
Acupuncture is worth trying, to reduce the blockage in the nose and stem the flow of mucus, because the autonomic nervous system (see box on p. 235) plays some part in the symptoms of allergic rhinitis (and is the sole cause of the symptoms for those with vasomotor rhinitis). For those with severe sinusitis, osteopathy can be good for draining mucus from the sinuses.
Very occasionally, psychological or emotional reactions play a part in perennial allergic rhinitis, with symptoms getting significantly worse during stressful events. One possible manifestation of this is post-coital rhinitis, where sex brings on rhinitis (and sometimes asthma as well). In such cases, psychotherapy should be considered. (But check you are not just allergic to the dust mites in your bed first…)
A nose by any other name…
Rhinitis means inflammation (-itis) of the nose (rhin-). The same Greek word gives us rhinoceros - ‘nose-horn’.