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Allergy Non

Food Allergy: An Overview

FOOD ALLERGY: AN OVERVIEW

MEENAKSHI BHARKATIYA*, KAMAL SINGH RATHORE, ANKUR MAHESHWARI, SUNITA PANCHAWAT, R.K.NEMA

B.N.GIRLS' COLLEGE OF PHARMACY, UDAIPUR-RAJ. 31002

INTRODUCTION

Food allergy is recognized as a common worldwide problem, and, like other atopic disorders, its incidence seems to increase. In the past years, investigations of allergic food proteins and related immunological responses have moved to the molecular level, and the newly-found knowledge might provide novel experimental strategies for the laboratory diagnosis and the immuno-modulatory control of food-induced allergic reactions (1, 2).

Approximately 20% of the population alters their diet for a perceived adverse reaction to food, but the application of double-blind placebo-controlled oral food challenge, the "gold standard" for diagnosis of food allergy, shows that questionnaire-based studies overestimate the prevalence of food allergies. The clinical disorders determined by adverse reactions to food can be classified on the basis of immunologic or no immunologic mechanisms and the organ system or systems affected (3, 4, 5).

The true prevalence of food allergy is lower and seems to range from 1% to 4% of the general population and about 6% of the general population and about 6% of the paediatric population, but does occur in as much as 25% of children with eczema6. Allergic hypersensitivity simply put, is an adverse immune reaction to a protein (or allergen) in our environment, which is normally harmless to the non-allergic person. It may present as mild itching of the skin, tissue swelling and wheezing or even progress to full-blown anaphylaxis and death. 18 million allergy sufferers live in the UK where 4% of the populations also have a food allergy.

Allergy develops after repeated exposure to the causative allergen. Sensitization takes place on initial exposure (a process that may take up to six weeks to develop) and no adverse reaction appears to occur during initial sensitization (6).

(A) DEFINITION

A food allergy is an immunologic response to a food protein and caused by allergens in the food that are a kind of protein in the food. These proteins resist the cooking process, the acid in the stomach and the enzymes in the stomach and intestines and enter the blood stream and they cause the allergy reaction after they enter the blood stream.

(B) SIGNS AND SYMPTOMS

Symptoms of food allergies are: -

1. Anaphylaxis: - a severe, whole-body allergic reaction that can result in death. Leads to vasodilation and, if severe, symptoms of life-threatening shock.

2. Angioedema: - rapid swelling (edema) of the skin, mucosa and submucosal tissues, especially of the eyelids, face, lips, and tongue.

3. Eczema is a form of dermatitis, or inflammation of the upper layers of the skin.

(a). Atopic eczema (aka infantile e., flexural e., atopic dermatitis) is believed to have a hereditary component, and often runs in families whose members also have hay fever and asthma. Itchy rash is particularly noticeable on face and scalp, neck, inside of elbows, behind knees, and buttocks.

(b). Contact dermatitis is of two types: allergic (resulting from a delayed reaction to some allergen, such as poison ivy or nickel), and irritant (resulting from direct reaction to a solvent, for example). Some substances act both as allergen and irritant (e.g. wet cement). Other substances cause a problem after sunlight exposure, bringing on phototoxic dermatitis.

(c). Xerotic eczema (aka asteatotic e., e. craquele or craquelatum, winter itch, pruritus hiemalis) is dry skin that becomes so serious it turns into eczema. It worsens in dry winter weather, and limbs and trunk are most often affected. The itchy, tender skin resembles a dry, cracked, river bed. This disorder is very common among the older population.

(d). Seborrhoeic dermatitis (aka cradle cap in infants, dandruff) causes dry or greasy scaling of the scalp and eyebrows. Scaly pimples and red patches sometimes appear in various adjacent places. In newborns it causes a thick, yellow crusty scalp rash called cradle cap which seems related to lack of biotin, and is often curable.

4. Skin rashes, such as nettle rash (also called urticaria or hives). Some of these longer lasting rashes are called atopic dermatitis. 

5. Itching of the mouth, throat, eyes, skin, or any area

6. Nausea, vomiting, diarrhoea, stomach cramps, or abdominal pain

7. Running nose or nasal congestion

8. Wheezing, scratchy throat, shortness of breath, or difficulty swallowing

9. Mood swings, depression: The symptoms of an Immunoglobulin E (IgE) allergic reaction can take place within a few minutes to an hour. The process of eating and digesting food affects the timing and location of a reaction. IgG reactions build over a period of hours to days, and therefore symptoms can be difficult to notice as allergy-related (7). 

 TYPES OF ALLERGENIC FOOD

There are a number of groups of foods that are responsible for causing the majority of food allergies (6).  Rice allergy is more common in East Asia where rice forms a large part of the diet.  In Central Europe, celery allergy is more common. The top allergens vary somewhat from country to country but milk, eggs, peanuts, tree nuts, fish, shellfish, soy, wheat and sesame tend to be in the top ten in many countries (8).

The most common food allergies are: -

1. Milk allergy:-

Two out of a hundred infants under one year old suffer from cow's milk allergy, making it the most common food allergy of childhood. In general children lose this sensitivity as they grow up with nine out of ten losing it by the age of three; it is unusual for adults to suffer from this allergy. Symptoms are frequently vomiting and diarrhoea in children, with 30-50% also having skin rashes of some type. A small number of children have an anaphylactic reaction to milk which tends to be life-long.

The major allergens in milk are the caseins and the protein b-lactoglobulin. People are usually allergic to more than one kind of milk protein. The proteins from cow's milk are very similar to those from goats and sheep. Thus goat's or sheep's milk cannot be used as a cow's milk substitute in allergic individuals (8). 

A report about 22-year-old Female patient is described who was repeatedly hospitalised on account of severe asthmatic attacks presumably due to the ingestion of cow's milk or milk-containing products. There were no signs of gastrointestinal disturbance, but some urticaria and angioedema occurred. Strongly positive RASTs (radioallergosorbent test) were observed in the blood serum against the proteins in cow's milk, bovine serum, egg white, cod fish, and house dust. The symptoms were successfully controlled by rigorous dietary measures (8). 

2. Eggs:-

Allergy to eggs is usually observed in young children rather than adults, and like cow's milk allergy, fades with time. Occasionally children suffer from a severe form of allergy which is not outgrown.

The main allergens are the egg white proteins ovomucoid, ovalbumin, and ovotransferrin. The eggs of other poultry, such as ducks, are very similar to those of hens and can cause reactions in egg-allergic individuals (8). 

3. Peanut allergy:-

Peanuts are one of most allergenic foods and frequently cause very severe reactions, including anaphylaxis. Allergy to peanuts is established in childhood and usually maintained throughout life. Peanut allergy can be so severe that only very tiny amounts of peanut can cause a reaction. Thus the traces of nuts found in processed oils, or the carryover of materials on utensils used for serving foods, can be enough in some individuals, to cause a reaction. The main allergens in peanuts and Soya are the proteins used by the seed as a food store for it to grow into a seedling. One of the allergens in Soya bean is very similar to a major allergen from dust mites, a common environmental allergen. We aren't sure yet whether this means there is a link between dust allergy and Soya allergy.

A large number of children who develop peanut allergy have their first reaction the first time they are given a peanut-containing product (usually a dab of peanut butter). A large number of children who develop peanut allergy have their first reaction the first time they are given a peanut-containing product (usually a dab of peanut butter). Peanut protein could pass into breast milk Twenty-three lactating women; aged 21 to 35 years ate 50 grams of dry roasted peanuts (about 60 peanuts or 1/3 cup). Breast milk samples were collected at hourly intervals. Peanut protein was found in the breast milk of 11 of the mothers. In 10 mothers, it was detected within two hours after she ate peanuts, in one mother it was detected six hours later.

That peanut protein is secreted into breast milk, thus sensitizing the baby who is at risk for developing an allergy. This may explain why up to 85 percent of children have a peanut allergy reaction the first time they eat a peanut-containing product. A baby born into a family with allergies.

[Note: - Milk, eggs, and wheat have previously been shown to pass into breast milk. The mothers from allergic families eliminate peanuts and tree nuts (e.g., almonds, walnuts, etc.) and consider eliminating eggs, milk, fish, and perhaps other foods from their diets while nursing. If you choose to do this, be sure to speak with a registered dietitian to be sure your diet is well-balanced (8).

4. Tree Nut Allergy:-

This group includes true tree nuts, such as Brazil nuts, hazelnuts, walnut and pecan. Whilst not as intensively studied as peanuts, indications are that tree nuts can cause symptoms as severe which can occasionally be fatal. Children who become sensitised to tree nuts tend to remain allergic throughout life. Hazelnut and almond allergies are more like those people get to fruit, and are linked to pollen allergies. Nut allergens can be both destroyed by, and resistant, to cooking and we think that roasting may actually create new allergens. The allergens can be the seed storage proteins, or other molecules which are also found in pollen.

5. Fish and shellfish allergy:-

Allergies to shellfish are unusual in children, mostly being experienced by adults. Reactions to fish are found in children and adults. The incidence of seafood allergy is higher in those countries with a high consumption of fish and shellfish. Severe reactions are more frequently found with these foods, including anaphylaxis. Cooking does not destroy the allergens in fish and shellfish, and some individuals maybe allergic to the cooked, but not raw, fish. The major allergens in fish are flesh proteins called parvalbumins which are very similar in all kinds of fish. Shellfish allergens are usually found in the flesh and are part of the muscle protein system, whilst in foods such as shrimps, allergens have also been found in the shells.

If pregnant or trying to be, avoid seafood and shellfish. Some believe that it may cause your child to develop food allergy.

6. Fruits allergy:-

In general allergic reactions to fruits and vegetables are mild, and are often limited to the mouth, and are called the oral-allergy syndrome (OAS). Around four out of ten people having OAS are also allergic to tree and weed pollens. Thus people who are allergic to birch pollen are much more likely to be allergic to apples. There allergens in fruits and vegetables are not as complicated as other foods. Many of them are very like the allergens in pollens, which is why people with pollen allergies are also allergic to certain fruits.

Many fruit allergens are destroyed by cooking, and thus cooked fruits are often safe for fruit allergic people to eat. Allergies to latex gloves, especially amongst health professionals, are increasing. As many of the latex allergens are like those found in certain tropical fruits, such as bananas, these people can get an allergic reaction to handling or eating these foods (8). Tomato Allergy: - Reported on four cases (two adults with throat constriction, one child with gastro esophageal reflux disease [GERD], one child with atopic dermatitis) with IgE-mediated reactions to tomatoes.

Using extracts prepared from the skin, seeds, and fleshy fruit of the tomato, specific IgE antibody in the sera of patients was detected by ELISA. After characterizing the extracts for their antigen profile and reactivity with IgE, proteins were separated by SDS-PAGE (sodium dodecyl sulfate-polyacrylamide gel electrophoresis). Of the four patients, one adult showed higher IgE against tomato skin extract. Western blot tests of the patient's scrum with tomato skin extract also revealed reaction with a protein band in the 42-45kD region. Tomato allergy can be manifested as atopic dermatitis, laryngeal angioedema, and even gastroesophageal reflux.

7. Cereals allergy:

Suffered by children and adults alike, wheat allergy appears to be particularly associated with exercise-induced anaphylaxis. The more of a cereal (wheat, rye, barley, oats, maize or rice) we eat the more likely we are to suffer an allergy. Thus rice allergy is found more frequently in populations eating ethnic diets. Seed storage proteins (such as wheat gluten) and other proteins present in grain to protect it from attack by moulds and bacteria, have been found to be major allergens.

8. Penicillin's allergy reaction:

Frequently manifestations are – rash, itching, urticaria and fever. Wheezing, angioneuritis, edema, serum sickness and exofolliative dermatitis are less common. Anaphylaxis is rare but may be fatal. Fear of anaphylactic shock has several restricted the use of injPnG in general practice.  All form of penicillin (natural or semi synthetic) can cause allergy but it is more commonly seen after parenteral administration.

 Penicillin produce hypersensitivity – urticaria, angioedema, bronchiospasm, anaphylaxis or serum sickness. If earlier reaction had been only a rash, penicillin may be given cautiously – often no untoward effect is seen. History of penicillin allergy must be elicited before injection it. A scratch test on intradermal test (with 2 – 10 u ) may be performed first. On occasion, his it has caused fatal anaphylaxis. Testing with benzyl-penicilloyl – polylysine is safer. However a negative intradermal test does not rule out delayed hypersensitivity. It should also be released that presence of antibodies to penicillin does not mean allergy to it, because practically everyone who receives penicillin develop antibodies to it.

For the development of antibodies, penicillin or a product of it (mostly penicilloyl moiety – major determent) act as a hapten. Topical use of penicillin is highly sensitizing (contact dermatitis and other reaction). Therefore, all topical preparation of penicillin (including eye ointment) have been banned, except for use in eye as solution in case of gonococcal opthalmia (9).

CLASSIFICATION OF FOOD ALLERGY

1. IMMEDIATE REACTION TYPE (SKIN-SENSITIVE OR WHEAL TYPE)

Antibody: Skin sensitizing:-

A. Hereditary: spontaneous, abrupt, obvious, often severe symptoms,     Involving all major systems of body Portal of entry:                                                                                                               

 (a) Alimentary mucosa causes: food by ingestion

(b) Respiratory mucosa causes: Inhaled dusty airborne food dusts and volatile food odours by inhalation (rare)

(c) Skin causes: food by percutaneous absorption (rare)

(d) By parenteral injection causes: Therapeutic agent containing food excitants

B. Nonhereditary: Induced, anaphylactic, often severe symptoms involving all major system of body

Portal of entry: By parenteral injection causes: sensitizers such as organ extracts, virus vaccines (egg media)

2. DELAYED REACTION TYPES   (SKIN-NEGATIVE OR NON- WHEALTYPE)

Antibody: unknown:-

A. Hereditary: Deliberate, obscure symptoms involving all major systems  

    Of body

Portal of entry: Alimentary mucosa causes: Foods by ingestion

B. Nonhereditary: - Induced (contact dermatitis), rare, involving respiratory and cutaneous systems

Portal of entry: Intact oral, and buccal mucosa, and skin causes: Foods, essential oils of foods and spices (10).

PATHOPHYSIOLOGY

A food allergy is an immunologic response to a food protein Food allergy is type 1 hypersensitivity reaction. Type I Hypersensitivity is characterised by excessive activation of mast cells and basophils by IgE, resulting in a systemic inflammatory response that can result in symptoms as benign as a runny nose, to life-threatening anaphylactic shock and death.

Exposure to an allergen activates B cells to form IgE secreting plasma cells   . The secreted IgE Molecules bind to IgE specific Fc Receptor on mast cells. Second Exposure to allergen leads to cross linking of the bound IgE triggering release of pharmacologically active mediators vasoactive amines (11).

Immunoglobulin E (IgE):

The potent biological activity of IgE allowed it to be identified in serum despite its extremely low average serum concentration (0.3microgram/ml).IgE antibodies mediate the immediate hypersensitivity reaction that are responsible for the symptoms of hay fever, asthma, hives and anaphylactic shock. When the appropriate antigen was later injected at the same site, a wheal and flare reaction developed there .this reaction, called the p-k reaction was the basis for the first biological assay for IgE activity.

IgE binds to Fc receptors on the membranes of blood basophils and tissue mast cells, Cross-linkage or receptor bound IgE molecules by antigen (allergen) induces basophils and mast cells to translocation their granules to the plasma membrane and release their contents to the extracellular environment, a process known as degranulation.  As a result, a variety of pharmacologically active mediators are released and given rise to allergic manifestations.

Fc Receptors:

Many cells feature membrane glycoproteins called Fc receptors (FcR) that have an affinity for the Fc portion of the antibody molecule.  These receptors are essential for many of the bioligocal functions of antibodies.  An FcR binds IgE like: - The cytoplasmic domains of the chains of FcRI are associated with protein tyrosine kinase (PTKs). Crosslinkage of the FcRI receptors activates the associated PTKs, resulting in the phosphorylation of tyrosines within the ITAMs of the subunit as well as phosphorylation of residue on the  subunit and on phospholipace C.  These phosphyrylation events incduce the producton of a number of second messengers that mediate the process of degranulation.

Within 15 s after crosslinkage of FcRI, methylation of various membrane phospholipids is observed, resulting in an increase in membrane fluidity and the formation of Ca2+ channels.  An increase of Ca2+ reaches a peak within 2 min. of FcRI crosslinkage.  This increase is due both to the uptake of extracellular Ca2+ and to a release of Ca2+ from nitracellular stores in the endoplasmic reticulum.  The Ca2+ increase eventually leads to the formation of arachidonic acid, which is converted into two classes of potent mediators: prostaglandins and leukotrienes.  The increase of Ca2+ also promotes the assembly of microtubules and the contraction of microfilaments, both of which are necessary for the movement of granules to the plasma membrane.  The importance of the Ca2+ increase in mast-cell degranulation is highlighted by the use of drugs, such as disodium cromoglycate (cromolyn sodium), that block this influx as a treatment for allergies (11).

Concomitant with phospholipid methylation and Ca2+ increase, there is a transient increase in the activity of membrane-bound adenylate cyclase, with a rapid peak of its reaction product, cyclic adenosine monophosphate (cAMP), reached about one min. after crosslinkage of FcRI.  The effect of cAMP is exerted through the activation of cAMP-dependent protein kinases, which phosphorylate proteins on the granule membrane, thereby changing the permeability of the granules to water and Ca2+.  The consequent swelling of the granules facilitates their fusion with the plasma membrane, releasing their contents.  The increase in cAMP is transient and is followed by a drop in cAMP to levels below baseline.  This drop in cAMP appears to be necessary for degranulation to proceed; when cAMP levels are increased by certain drugs, the degranulation process is blocked.  Histamines are the main mediator of food allergy (11).

IgE Crosslinkage Initiates Degranulation

The biochemical events the mediate degranulaton of mast cells and blood basophils have many features in common.  For simplicity, this section presents a general overview of mast-cell degranulation mechanisms without calling attention to the slight differences between mast cells and basophils.  Although mast-cell degranulation generally is initiated by allergen crosslinkage of bound IgE, a number of other stimuli can also initiate the process, including the anaphylatoxins (C3a, C4a, and C5a) and various drugs.  This section focuses on the biochemical events that follow allergen crosslinkage of bound IgE as follows

 Receptor Crosslinkage

IgE-mediated degranulation begins when an allergen cross links IgE that is bound (fixed) to the Fc receptor on the surface of a mast cell or basophil.  In itself, the binding of IgE to FcRI apparently has no effect on a target cell.  It is only after allergen crosslinks the fixed IgE-receptor complex that degranulation proceeds.  The importance of crosslinkage is indicated by the inability of monovalent allergens, which cannot crosslink the fixed IgE, to trigger degranulation.

Genetic basis

There is much evidence to support the genetic basis of allergy, as allergic parents are more likely to have allergic children, and their allergies are likely to be stronger than those from non-allergic parents. However some allergies are not consistent along genealogies with parents being allergic to peanuts, but having children allergic to ragweed, or siblings not sharing the same allergens. Ethnicity has also been shown to play a role in some allergies. Interestingly, in regard to asthma, it has been suggested that different genetic loci are responsible for asthma in people of Caucasian, Hispanic, Asian, and African origins. It has also been suggested that there are both general atopy genes and tissue-specific allergy genes that target the allergic response to specific mucosal tissues. Potential disease associated alleles include both coding region variation and SNPs. Caucasian people seem to have the most asthma (11).

DIAGNOSIS OF FOOD ALLERGY

Diagnosis of food allergy is based on clinical history, skin prick tests, and     laboratory tests to detect serum-food specific IgE, elimination diets and challenges (12).

1. History: - The physician interviews the patient to determine if the facts are consistent with a food allergy. . The doctor asks such questions as: What was the timing of the reaction? Did the reaction come on quickly, usually within an hour after eating the food? Was treatment for allergy successful? For example, if hives stem from a food allergy, antihistamines should relieve them. Is the reaction always associated with a certain food? Did anyone else get sick? For example, if the person has eaten fish contaminated with histamine, everyone who ate the fish should be sick. In an allergic reaction, however, only the person allergic to the fish becomes ill. 

2. Dietary Diary: - To keep a record of the contents of each meal and whether reactions occurred that are consistent with allergy. The dietary diary provides more details than the oral history, so that the doctor and patient can better determine if there is a consistent relationship between a food and the allergic reactions.

3. Elimination Diet: - The next step is an elimination diet. The patient does not eat a food suspected of causing the allergy, for example, eggs, and substitutes another food, in this instance, another source of protein. If after the patient removes the food, the symptoms go away, the doctor almost always can make a diagnosis of food allergy. This technique is also not suitable if the allergic reactions have been infrequent13.

4. Skin Prick Tests: - The skin prick is easy to do and results are available in minutes. Different allergists may use different devices for skin prick testing. Some use a "bifurcated needle", which looks like a fork with two prongs. Others use a "multi-test", which may look like a small board with several pins sticking out of it (14).

In a scratch-the-skin test, a dilute extract of the suspected food is placed on the skin of the forearm or back. This portion of the skin then is scratched with a needle and observed for swelling or redness, which would signify a local allergic reaction to the food. A positive scratch test indicates that the patient has the IgE that is specific for the food being tested on the skin's mast cells. In some highly allergic patients, however, especially if they have had anaphylactic reactions, skin tests should not be done because they could provoke another dangerous reaction. Skin tests also cannot be done in patients with extensive eczema (13).

It is good for quickly learning if a person is allergic to a particular food or not, because it detects allergic antibodies known as IgE. Skin tests cannot predict if a reaction would occur or what kind of reaction might occur if a person ingests that particular allergen. They can however confirm an allergy in light of a patient's history of reactions to a particular food. This almost painless procedure allows the tested protein to interact with food-specific IgE on the surface of skin mast cells (12).

A device, such as a lancet, plastic probe or tip of a small gauge needle, is pressed through a commercial extract of food and a positive (histamine) and negative (saline-glycerine) controls into the epidermis. Allergens eliciting within 15 min a wheal at least 3 mm larger than that produced by the negative control are considered positive, indicating the possibility that the patients have symptomatic reactivity to the specific food, with strongly positive results implying a greater likelihood of clinical reactivity. When evaluating allergy to fruits and vegetables, commercially prepared extracts are often inadequate because they are prone to degradation, and therefore the fresh food might be used for prick-by-prick test. A number of investigators have examined the use of the "atopy patch test" in addition to skin prick test for the diagnosis of non-IgE-mediated food allergy, with delayed reactions to food, but at this time, there are no standardized reagents or methods of application and interpretation. Thus, its diagnostic accuracy remains still controversial, especially in older children (12).

In Eosinophilic gastroenteritis associated with food allergy and bronchial asthma. A skin prick test and RAST (radioallergosorbent test) to causative food allergens showed a negative result. A fiber-optic endoscopic biopsy from the gastric mucosa showed an intense eosinophilic infiltration. The fiber-optic endoscopic biopsy might be needed to identify coexisting EG if an allergic patient with blood eosinophilia complains of severe gastrointestinal symptoms (14).

5. Blood Tests:- Blood tests such as the RAST (radioallergosorbent test) and the ELISA (enzyme-linked immunosorbent assay). These tests measure the presence of food-specific IgE antibodies in the blood of patients, but they cost more than skin tests, and the results are not available immediately (13).

In RAST, blood is drawn and sent to a lab for testing to determine "predictive values" for certain foods. These predictive values can be compared to the RAST blood test results. If a person's RAST score is higher than the predictive value for that food, then there is over a 95% chance the person will have an allergic reaction (limited to rash and anaphylaxis reactions) if they ingest that food. Currently, predictive values are available for the following foods: milk, egg, peanut, fish, soy, and wheat. Blood tests allow for hundreds of allergens to be screened from a single sample, and cover food allergies as well as inhalants. However, non-IgE mediated allergies cannot be detected by this method. Blood testing methodologies currently available that can measure antibodies of IgG are not acceptable as a method of allergy evaluation. IgG-type anitbodies are not implicated in food allergy reactions15.

(A)       In vitro IgE food allergen-specific assays:-

The in vitro IgE assay is less sensitive, however, then the epicutaneous skin test. The in vitro IgE assay uses the same commercial food extract16.

1. Redioallergosorbeny (RAST):- The first test using this new technology was the redioallergosorbent test (RAST). The first step requires coupling the allergen (e.g., cow's milk protein) to solid support (e.g., a paper disk). When this disk is placed in a test tube with patient serum, the coupling of antibodies directed against milk or that were anti- cow's milk in nature (this includes IgE, M, A, or E class) occurs. After washing, the third  step is the addition of radio-labelled (I125) rabbit antihuman IgE antibodies .these antibodies will attach themselves only to the IgE antimilk antibodies( which in turn are coupled to the cow's milk protein in the paper disk). Then the amount of radioactivity can be measured, and thus the amount of cow's milk-allergen-anti-IgE cow's milk antibody can be quantities (16).

2. Enzyme-Linked Immunosorbent Assay (ELISA) :- This is more recent type of test, but is just like the RAST test except for two factors. First, allergen is usually coupled to the inner surface of small plastic walls (into which the patient's serum and other ingredients of the test are placed). The second, and more important, difference is the final quantitative factor. In the ELISA system, an enzyme coupled to the antihuman IgE denatures a substrate, which either change color or becomes fluorescent. Then the amount of color or fluorescence can be measured(16).

 (B) The production of interferon-gamma in response to a major peanut allergy, Ara h II correlates with serum levels of IgE anti-Ara h II.

To examine the potential role of T cells in the pathogenesis of peanut allergy. Peripheral blood mononuclear cells (PBMCs) from patients with peanut allergy, patients with asthma, and nonatopic normal control subjects were assessed for proliferation after stimulation with a 17 kd major peanut allergen (Ara h II), ovalbumin, casein, soy, and Candida albicans. That Ara h II and C. albicans induced significantly higher levels of proliferation than ovalbumin, casein, and soy. Because interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) play critical roles in IgE regulation, the production of these cytokines after stimulation with C. albicans and Ara h II. C. albicans stimulated similar levels of IFN-gamma in all three study groups. In contrast, after stimulation with Ara h II, culture supernatants from PBMCs of subjects with peanut allergy contained significantly lower levels of IFN-gamma than did the PBMCs of the two control groups (p = 0.02). More important, there was a significant (p = 0.05) inverse correlation between the serum IgE anti-Ara h II levels and IFN-gamma production by PBMCs from the respective peanut-allergic patients. IL-4 protein was not detected in culture supernatants of PBMCs stimulated with Ara h II. However, amplification of cytokine gene transcripts by polymerase chain reaction did demonstrate IL-4 expression in Ara h II-stimulated PBMCs from both patients with peanut allergy and control subjects. Conclusion is that the level of IFN-gamma production in response to Ara h II may be an important factor in determining the development of peanut-specific IgE responses (17).

(6). Other Laboratory Tests:- When evaluating patients with gastrointestinal symptoms, suspecting food hypersensitivities, a number of other standard laboratory studies might be useful. Patients with allergic eosinophilic esophagitis and allergic eosinophilic gastroenteritis have peripheral eosinophilia, and patients with severe allergic eosinophilic gastroenteritis might have anaemia, blood in the stool, and decreased serum protein, albumin and IgG levels (with preservation of IgM and IgA). Endoscopy and biopsy are the most definitive approaches for diagnosing many of the gastrointestinal food hypersensitivities and might help the differential diagnoses. Greater than 10-20 eosinophils per 40 × high-power field in the esophagus is diagnostic of allergic eosinophilic esophagitis, especially if the pH probe is normal and there is lack of responses to antireflux medication. Eosinophils are normally present in the gastric and intestinal mucosa, and therefore eosinophil number must be greater to make the diagnosis of allergic eosinophilic gastroenteritis.

(7). Food Challenge:- The double-blind, placebo-controlled oral food challenge (DBPCFC) with gradually increasing amounts of the suspected food under observation over hours or days, is considered the "gold standard" test for the diagnosis of food allergy.

 In this test, various foods, some of which are suspected of inducing an allergic reaction, are placed in individual opaque capsules. Both the patient and the doctor are blinded, so that neither of them knows which capsules contain the suspected allergens. (Another medical person prepared the capsules.) The patient swallows a capsule and the doctor then observes whether an allergic reaction occurs. This process is repeated with each capsule. The advantage of a food challenge is that if the patient has an allergic reaction only to the suspected foods and not to the other foods tested, the diagnosis of food allergy is confirmed. Just as with a rechallenge after the elimination diet and with the skin tests, however, someone having a history of severe reactions should not be tested with a food challenge because of the danger of inducing another severe reaction. In addition, this procedure is expensive because it is difficult and requires a lot of time, especially for patients with multiple food allergies. Consequently, double-blind food challenges are done infrequently (13.)

Hypotension might occur in about 15% of these challenges, especially in patients affected by acute IgE-mediated reactions, enterocolitis syndrome, and severe atopic dermatitis, and therefore intravenous hydration therapy and supplies for resuscitation should be immediately available (12).

Genetic Basis for Food Allergy

The R576 allele occurred with less frequency in nonatopic subjects than in patients with food allergy. Investigation of the prevalence of the glutamine to arginine (Q to R) mutation at position 576 of IL4R alpha (a position formerly shown to segregate with atopy) was conducted in 22 patients with a history of adverse food reactions, positive skin tests, and/or RAST. Eleven patients had positive food challenges. This was compared with a reference group of 57 nonatopic subjects.

In food allergy patients, allele frequency of the Q576 was 68% (30/44) and of the R576 was 32% (14/44), compared with 81% (92/114) and 19% (22/114) in the control group. Half of the patients (11) carried the R576 allele, 13% (3) of whom were homozygous, compared with prevalence in the general population of 20%. The high occurrence of the R576 allele in atopic patients was associated with a susceptibility to food allergy. Atopy, in general, has been known to be genetically determined, yet evidence for a genetic link to specific allergies has been lacking. This study demonstrates a significant association between the Q576R allele and the development of food allergy. Extension of this work may lead to a specific test for prediction of food allergy (13).

TREATMENT OF FOOD ALLERGY

(A). ORAL DESENSITIZATION & TOPICAL TREATMENT:- Various medications can provide relief for certain aspect of food-induced disorders. The primary therapy for food allergy is to avoid the responsible food.1 Only two specific treatments are available to the allergic patient - allergen avoidance and allergen-specific immunotherapy (SIT) given either orally or by injection (13).

(1). Treatment for Milk Allergies:-  It is total avoidance of milk proteins. Initially if the infants are breastfed, the lactating mothers are given an elimination diet. If symptoms are not relieved or if the infants are formula-fed, milk substitute formulas are used to provide the infant with a complete source of nutrition. Milk substitutes include hypoallergenic formulas based on hydrolyzed protein (such as nutramigen, alimentum, and pregestemil) or free amino acids. Soy milk should not be used in milk protein allergy as there is a 40-50% rate of cross-antigenicity of soy and cow protein.

(2.) Treatment for Nut allergy:-  It is usually treated with an exclusion diet and vigilant avoidance of foods that may be contaminated with tree nuts or nut particles and/or oils. The most severe nut allergy reaction is called anaphylaxis and is an emergency situation requiring immediate attention and treatment with Epinephrine.

(3).Treatment for fruits allergy:- An OAS (Oral Allergy Syndrome) sufferer should avoid foods to which they are allergic. Peeling or cooking the foods have shown to reduce the effects of the allergy in the throat and mouth, but may not relieve reactions in the gastrointestinal tract. Antihistamines may also relieve the symptoms of the allergy. Persons with severe reactions may consider carrying injectable medication (such as an EpiPen) to relieve themselves if necessary. Allergy immunotherapy has improved or cured OAS in many patients.

(4).Antihistamines:- The older sedating type antihistamine tablets or syrup such as Piriton will reduce itching especially at night. Newer long acting anti-histamines such as Cetirizine have also proved to be very good for reducing skin inflammation if used for extended periods of up to 6 months.22 Antihistamines might partially relieve oral allergy syndrome and IgE-mediated skin symptoms, i.e. itching and rash, but they do not block systemic reactions (12).

(5).Cortisone or Steroid:- Systemic corticosteroids are generally effective in treating chronic IgE-mediated disorders (atopic dermatitis). A course of corticosteroids can be used to reverse severe inflammatory symptoms, but the side effects of protracted use are unacceptable. These produce rapid relief and are used for short periods to settle eczema flare-ups. They may also be used for longer periods when diluted in an emollient in which case treatment should be tapered off slowly. However, their long-term use may lead to thinning of the skin. Cortisone tablets or injections are very rarely, if ever, used in eczema (11).

(6). Sublingual Immunotherapy - the procedure:- Grazax oral tablet desensitisation immunotherapy is now available for adults as a treatment for grass pollen induced hay fever and allergic rhino-conjunctivitis.  This oral treatment is called Sublingual Immunotherapy or SLIT.  Each tablet contains an extract of Timothy Grass (Phleum Pratense) 75000SQ-T.  The procedure is very safe and far less likely than injection immunotherapy to cause any adverse reaction (SLIT side-effects include headache and oral itching). The treatment involves taking one tablet daily and allowing it to dissolve under the tongue over one minute before swallowing.  Treatment should commence two months before the grass pollen season and continued throughout the grass pollen season for maximal benefit. The treatment is stopped in the autumn/winter and then recommences two months prior to each subsequent grass pollen season (11).

(7). Emollients:- These skin moisturising creams and ointments, the mainstay of eczema treatment, are completely safe and should be applied liberally at least three or more times per day to hydrate and protect the skin. Different emollients include Emulsifying Ointment (HEB), White Soft Paraffin, Aqueous cream (UEA), Diprobase or Lipobase with Cetomacrogol, Epaderm, and Oilatum cream. Sometimes coal tar is applied to treat thickened skin. Oilatum Plus is an excellent bath emollient. Aveeno is an oatmeal based emollient for very dry skin while Balneum is Soya oil based11.

(8). Wet Wraps:- These are applied at night to keep moisture in the skin, aid absorption of creams and to protect against scratching. First of all, emollients and steroid creams are applied to the eczematous areas. Elasticated cotton-based tubular dressings are soaked in luke-warm water and then cut to size so that they cover the affected areas. These can be applied overnight to the limbs, trunk, neck and even face (holes are cut in the dressing to allow apertures for eyes, ears, nose and mouth). This treatment is highly successful for severe weepy eczema, which is non-responsive to emollients and steroid creams.

(9). Other Therapies:- Evening Primrose oil (or gamolenic acid) has been tried with minimal success in the past.  Extracts of Chinese herbal teas seem to reduce inflammation although they are quite unpalatable.  Tacrolimus (Protopic) and Pimecrolimus (Elidel) cream has just become available and results so far have been very encouraging, although chronic use has been associated with skin cancers in animals (11).

Multicenter Study of Emergency Department Visits for Food Allergy  

  1. This study showed that although guidelines exist for the emergency management of food allergy, "adherence to these guidelines appears low (18).

Prevention

The high-risk infants (both parents and siblings atopic) be exclusively breast-fed, that lactating mothers avoid peanuts and nuts to avoid sensitization through breast milk, that the introduction of solid be delayed until six mo of age, and major allergens, such as peanuts, nuts and seafood, be introduced after three years of age (11).

(B) VACCINES, IMMUNOTHERAPY & INJECTION:-

  1. If the food is accidentally ingested and a systemic reaction occurs, then epinephrine (best delivered with an autoinjector of epinephrine such as an Epipen) or Twinject should be used. It is possible that a second dose of epinephrine may be required for severe reactions (14). Epinephrine is the mainstay of treatment for anaphylaxis. Intramuscular injection allows more efficient absorption than the subcutaneous route (12).                                                                                                                                                                                                                                                                                                                                                                                                        

Novel therapies for IgE-mediated food allergy have been evaluated. Subcutaneous injections of humanized IgG anti-IgE antibodies (TNX-901), that recognize and mask an epitope in the CH3 region of IgE responsible for the binding to the high affinity Fc epsilon receptor I (FC?RI) on basophils and mast cells, for the treatment of patients affected by peanut allergy, showed a long-term increase in the average amount of peanut tolerated, but 25% of subjects showed no improvement.

Another anti-IgE preparation (Omalizumab) has been approved for the treatment of persistent allergic asthma in patients who are poorly controlled with inhaled corticosteroids, but has not yet been evaluated for its efficacy in treating patients with peanut allergy. Theoretically, anti-IgE antibody therapy should be protective against multiple food allergens, although it would have to be administered indefinitely to maintain its protective effects. Other immunotherapeutic strategies include use of engineered proteins lackink IgE-binding sites, immunomodulatory sequences being effective in reversing IgE-mediated sensitization, and engineered chimeric molecules forming complexes with allergen-specific IgE bound to mast cells and basophils, inhibiting their functions.

Some recent studies suggested that probiotics, commonly defined as live micro organisms (bacteria from the genera Lactobacillus, Bifidobacterium, Escherichia, Enterococcus, Bacillus and Saccharomyces), administered in adequate amounts, which confer a beneficial health effect on the host, might be useful in the treatment and prevention of food allergy. They might provide maturational signals for the gut-associated lymphoid tissue, balance the generation of pro- and anti-inflammatory cytokines, reduce the dietary antigen load by degrading and modifying macromolecules, reverse the increased intestinal permeability, characteristic of children with food allergy, normalization of the gut microecology, and enhance specific IgA responses frequently defective in children with food allergy. Among the therapeutic option, currently under investigation, there are peptide immunotherapy, traditional Chinese medicine, mutated protein immunotherapy, DNA immunization, and immunization with immuno stimulating sequences (ISSs) and anti-immunoglobulin E (anti-IgE) Therapy. These novel forms of treatment for allergic disease hold promise for the safe &effective treatment of food allergic individuals & the prevention of food allergy in the future.

Traditional therapies:-

Although injection immunotherapy has traditional been employed in the treatment of inhalant allergies, such as allergic rhinitis, it has also been used with success in the treatment of food allergy when a young child was successfully to fish. In patient with allergic rhinitis experiencing oral allergy syndromes with the ingestion of cross-reacting allergens in fruits, nut, & vegetables,  traditional injection immunotherapy has been also been successful in many cases in ameliorating the oral allergy symptoms with minimal adverse reaction. Traditional injection immunotherapy for food allergy is currently not recommended because of the allergic side effects of the therapy. Studies have been conducted of a double-blind, placebo-controlled trial of rust immunotherapy for the treatment of anaphylactic hypersensitivity to peanuts. Patients in the treatment group were able to tolerate increased amounts of peanuts in post-treatment food challenges. The actual peanut immunotherapy produced so many side effects of treatment that it would be practically impossible to perform on a routine basis.

While food desensitization in the oral allergy syndrome has been generally successful & well tolerated with cross-reacting pollen immunotherapy. The practice of injection immunotherapy for food allergy has been largely abandoned, due to the associated risk of serious systemic reaction. Since Traditional immunotherapy has been largely impractical for the treatment of most food allergies, several noval therapies are being explored13.

THERAPY    TYPES OF ALERGY          ROUTES (s)  IMMUNOLOGIC MECHANISM  RISK(s)

  1. Traditional injection immunotherapy  oral allergy syndrome  Subcutaneous  Increased IgE-blocking antibodies,decrease specific IgE         Safe when performed properly
  2. peptide immunotherapy          IgE-mediated food allergy     Subcutaneus    Immune deviation from Th2 to Th1      Appear safe
  3. Traditional Chinese medicine IgE-mediated food allergy (asthma)   Subcutaneous  Immune deviation from Th2 to Th1      Appear safe
  4. Fusion proteins            IgE-mediated (all type)           Subcutaneous  Blocks IgE-mediated  Unknown
  5. Mutated protein immunotherapy        IgE-mediated food allergy     Subcutaneous & oral   Immune deviation from Th2 to Th1(3)     Appear safe
  6. DNA immunization,   IgE-mediated food allergy     Subcutaneous & oral   Immune deviation from Th2 to Th1(oral) increase levels of allergen specific secretory IgA in the gut & systemic IgG         Unknown long-term
  7.  Immunostimulating sequences (ISSs)            IgE-mediated food allergy     Subcutaneous  Immune deviation from Th2 to Th1          Appear safe
  8. Anti-IgE Therapy        IgE-mediated food allergy     Subcutaneous  Deplete IgE, blocks IgE from binding to high affinity IgE-receptor(FC?RI):down-regulation IgE receptors productions       Appear safe
  9. Sodium cromoglycate in a dosage of 800 mg a day for 1 week, or a single dose of 1.0 g by mouth, did not block any of the reactions. By inhalation it blocked the asthmatic reactions which developed within a few sec of challenge (19).

(c).COMPLEMENTARY TREATMENTS OF FOOD   ALLERGY:-

1. Enzyme Potentiated Desensitization:- It involves mixing the alleged allergen with beta-glucuronidase (a common enzyme in the body) and applying it to the skin in very low doses. It has been used to treat hay fever and alleged food allergies. Double blind studies have failed to show any significant benefit with this regime (13).

2. Ionization:- Ionizing machines emit negative electric charges into the air, and this supposedly causes airborne allergens to cluster and fall to the ground. These machines have been claimed to help hay fever and asthma sufferers by decreasing the allergen load on the nasal mucosa and lungs.

3. Ozone Therapy:- In treating allergy is a new addition to complementary medical treatment. The allergic patient's blood be exposed to ozone gas and then re-injected or ozone is directly insufflate rectally or vaginally. This practice could have serious adverse results, as ozone is a very well documented trigger for allergy and asthma.

4. Homeopathy:- It is based on the law of similar - "like cures like". Treatments are usually individualized for the specific patient and not the disease. But a well designed study published in the Lancet by Reilly and Taylor from Glasgow(4) did however show significant improvement in hay fever symptoms, as did Kleijnen's review of clinical trials in homeopathy published in the.

5. Acupuncture:- Acupuncture is an ancient Chinese form of treatment that involves inserting tiny needles into specific meridians or areas of the body A small but temporary improvement in wheezing when acupuncture was employed.

6. Herbal medicine:- An herbal remedy such as the Ma Huang plant (Ephedra sinica) which contains ephedrine has been used to treat asthma for 5000 years. One recently noted exception is the use of traditional Chinese herbal tea in the treatment of atopic eczema. Ling zhi (Reishi Mushroom) is another eastern herbal preparation with steroid like properties used to treat allergies. Butterbur has been advocated in hay fever.

7. Nampudripad's Allergy Elimination Technique (NAET):- It consists of combination of discredited methods of diagnosing and treating allergy such as kinesiology, Vega testing and acupuncture. The premise is that allergy contrary to our current understanding, is due to some form of internal energy blockage triggered by abnormal energy fields in the brain and Nampudripad proposed that after 20 or so treatments she can reprogram the brain and body energy flow and eradicate all allergies and many other diseases affecting mankind. However the whole issue of energy flow and electrical fields in the body being the cause of allergies has not ever been proven13.

MEDICINE - HERB/FOOD INTERACTIONS

Herbs and Foods May Lead to Complications If You Take Them with Drugs. Herbs and foods may interact with medications you normally take that result in serious side reactions. It is always a good practice to tell your doctor or health practitioners what you are taking so that they can advise you of possible complications, if there is any. You should also keep an eye for unusual symptoms. Very often, this may foretell the symptoms of a drug interaction (19). Experts suggest that natural does not mean it is completely safe. Everything you put in your mouth has the potential to interact with something else. The medication that is taken by mouth travels through the digestive system in much the same way as food and herbs taken orally do. So, when a drug is mixed with food or another herb, each can alter the way the body metabolizes the other. Some drugs interfere with the body's ability to absorb nutrients. Similarly, some herbs and foods can lessen or increase the impact of a drug (20).

Alcohol is a drug that interacts with almost every medication, especially antidepressants and other drugs that affect the brain and nervous system. Some dietary components increase the risk of side effects. Theophylline, a medication administered to treat asthma, contains xanthines, which are also found in tea, coffee, chocolate, and other sources of caffeine. Consuming large amounts of these substances while taking theophylline increases the risk of drug toxicity. Certain vitamins and minerals impact on medications too. Large amounts of broccoli, spinach, and other green leafy vegetables high in vitamin K, which promotes the formation of blood clots, can counteract the effects of heparin, warfarin, and other drugs given to prevent clotting. Dietary fiber also affects drug absorption. Pectin and other soluble fibers slow down the absorption of acetaminophen, a popular painkiller. Bran and other insoluble fibers have a similar effect on digoxin, a major heart medication. As more and more people discover new herbs, there is more and more potential for the abuse of these herbs and the patients may end up in serious problems.

Ginseng, according to research, can increase blood pressure, making it dangerous for those trying to keep their blood pressure under control. Ginseng, garlic or supplements containing ginger, when taken with the blood-thinning drug, Coumadin, can cause bleeding episodes. Coumadin is a very powerful drug that leaves little room for error, and patients taking it should never take any medication or otherwise before consulting a qualified health professional. In rare cases, ginseng may overstimulate resulting in insomnia. Consuming caffeine with ginseng increases the risk of overstimulation and gastrointestinal upset. Long tern use of ginseng may cause menstrual abnormalities and breast tenderness in some women. Ginseng is not recommended for pregnant or lactating women.

Garlic capsules combined with diabetes medication can cause a dangerous decrease in blood sugars. Some people who are sensitive to garlic may experience heartburn and flatulence. Garlic has anti-clotting properties. You should check with your doctor if you are taking anticoagulant drugs. Goldenseal is used for coughs, stomach upsets, menstrual problems and even arthritis. However, the plant's active ingredient will raise blood pressure, complicating treatment for those taking antihypertensive medications, especially beta-blockers. For patients taking medication to control diabetes or kidney disease, this herb can cause dangerous electrolyte imbalance. High amount of consumption can lead to gastrointestinal distress and possible nervous system effects. Not recommended for pregnant or lactating women.

Guarana, an alternative remedy being used as a stimulant and diet aid, contains 3 percent to 5 percent more caffeine than a cup of coffee. So, if you are taking any medication that advises you against taking any drink with caffeine, you should avoid taking this stimulant. It may cause insomnia, trembling, anxiety, palpitations, urinary frequency, and hyperactivity. Avoid during pregnancy and lactation period. Long term use of Guarana may lead to decreased fertility, cardiovascular disease, and several forms of cancer. Kava, a herb that has antianxiety, pain relieving, muscle relaxing and anticonvulsant effects, should not be taken together with substances that also act on the central nervous system, such as alcohol, barbiturates, anti depressants, and antipsychotic drugs.

St. John's Wort is a popular herb used for the treatment of mild depression.

The active ingredient of St. John's Wort is hypericin. Hypericin is believed to exert a similar influence on the brain as the monoamine oxidase (MAO) inhibitors such as the one in major antidepressants. Mixing MAO inhibitors with foods high in tyramine, an amino acid, produces one of the most dramatic and dangerous food-drug interactions. Symptoms, which can occur within minutes of ingesting such foods while taking an MAO inhibitor, include rapid rise in blood pressure, a severe headache, and perhaps collapse and even death. Foods high in tyramine include aged cheese, chicken liver, Chianti (and certain other red wines), yeast extracts, bologna (and other processed meats), dried or pickled fish, legumes, soy sauce, ale, and beer.

Some patients report that Saint John's Wort caused excessive stimulation and sometimes dizziness, agitation and confusion when taken with other antidepressants or over-the-counter medications like Maximum Strength Dexatrim and Acutrim. It also caused their blood pressure to shoot up. White Willow, an herb traditionally used for fever, headache, pain, and rheumatic complaints may lead to gastrointestinal irritation, if used for a long time. It exhibits similar reactions as aspirin (aspirin is derived from white willow). Long term use may lead to stomach ulcers.

Drug Interaction and Food

Drug interaction risk isn't limited to herbal supplements. Certain foods can interact with medications.  People taking digoxin should avoid Black licorice (which contains the ingredient glycyrhizin). Together, they can produce irregular heart rhythms and cardiac arrest; licorice and diuretics will produce dangerously low potassium levels, putting a patient at risk for numbing weakness, muscle pain and even paralysis. Licorice can also interact with blood pressure medication or any calcium channel blockers. Aged cheese (brie, parmesan, cheddar and Roquefort), fava beans, sauerkraut, Italian green beans, some beers, red wine, pepperoni and overly ripe avocados should be avoided by people taking MAO antidepressants. The interaction can cause a potentially fatal rise in blood pressure. And because Saint John's Wort contains the same properties as these MAO antidepressants, it stands to reason that people ingesting the herb should avoid these same foods.

Grapefruit juice interacts with calcium channel blockers (including Calan, Procardia, Nifedipine, and Verapamil), cholesterol control medications, some psychiatric medications, estrogen, oral contraceptives and many allergy medications (Seldane, Hismanal). The juice modifies the body's way of metabolizing the medication, affecting the liver's ability to work the drug through a person's system. Orange juice shouldn't be consumed with antacids containing aluminum. 'The juice increases the absorption of the aluminum. Orange Juice and milk should be avoided when taking antibiotics. The juice's acidity decreases the effectiveness of antibiotics, as does milk.

Milk also doesn't mix with laxatives containing bisacodyl (Correctol and Dulcolax). You might find the laxative works a little "too well" in the morning. Large amounts of oatmeal and other high-fiber cereals should not be eaten when taking digoxin. The fiber can interfere with the absorption of the drug, making the act of swallowing the pill a waste of time. However, don't stop eating your cereal right away, because that could cause digoxin levels in your system to soar to toxic levels. A professional should make the dietary changes after carefully examining the digoxin levels.

Leafy green vegetables, high in vitamin K, should not be taken in great quantities while taking Coumadin. These vegetables could totally negate the affects of the drug and cause blood clotting. Caffeinated beverages and asthma drugs taken together can cause excessive excitability. Those taking Tagament (Simetidine), quinolone antibiotics (Cipro, Penetrex, Noroxin) and even oral contraceptives should be aware these drugs may cause their cup of coffee to give them more of a Java jolt than they expected. Grilled meat can lead to problems for those on asthma medications containing theophyllines. The chemical compounds formed when meat is grilled somehow prevent this type of medication from working effectively, increasing the possibility of an unmanageable asthma attack.

Regularly consuming a diet high in fat while taking anti-inflammatory and arthritis medications can cause kidney damage and can leave the patient feeling, drowsy and sedated. Alcoholic beverages tend to increase the depressive effects of medications such as benzodiazepines, antihistamines, antidepressants, antipsychotics, muscle relaxants, narcotics, or any drug with sedative actions. It's a good idea to not consume any alcoholic beverages, or at least scale way back, when taking prescription medications. Antioxidant and beta-carotene intensify alcohol's effect on the liver. Other commonly used over-the-counter medications can cause interaction problems also.

Aspirin can modify the effectiveness of arthritis medications, strong prescription steroids and diuretics. Combining aspirin with diabetic medications can drop blood sugars to dangerous levels. Aspirin can also cause toxicity when taken with glaucoma and anticonvulsant (anti-seizure) drugs and cause bleeding episodes when combined with a blood thinner, like Coumadin. Acetaminophen can also cause interaction complications when overused. Heavy drinkers who take acetaminophen for hangover relief risk liver damage. Taking high doses of acetaminophen with Coumadin can cause bleeding episodes.

Antacids taken with antibiotics, heart and blood pressure or thyroid medications can decrease drug absorption by up to 90 percent. Over-the-counter antihistamines - sold under the names Actifed, Theraflu, Dimetapp, Benadryl and Comtrex should be avoided if you are taking antianxiety or antidepressant medications. Oral contraceptives are less effective when taken with barbiturates, antibiotics, anti-fungal or tuberculosis drugs.

Turnips contain two goitrogenic substances, progoitrin and gluconasturtin, which can interfere with the thyroid glands ability to make its hormones. Although moderate consumption of goitrogens is not a hazard for healthy people, they can promote development of a goiter (an enlarged thyroid) in persons with thyroid disease. Tomato contains small quantities of a toxic substance known as solanine that may trigger headaches in susceptible people. They are also a relatively common cause of allergies. An unidentified substance in tomatoes and tomato-based products can cause acid reflux, leading to

indigestion and heartburn. Individuals who often have digestive upse

About the Author

Sr.Lecturer, B.N.Girls College of Pharmacy, Udaipur

Allergy Non
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