Risk factors for drug allergies can be attributed to the drug itself or the characteristics of the patient. Drug-specific risk factors include the dose, route of administration, duration of treatment, repetitive exposure to the drug, and concurrent illnesses. Host risk factors include age, sex, atopy, specific genetic polymorphisms, and inherent predisposition to react to multiple unrelated drugs (multiple drug allergy syndrome).

A drug allergy is more likely to develop with large doses and extended exposure.

In adults, the prevalence of IgE sensitization to allergens from house dust mite and cat, but not grass, seem to decrease over time as people age. However, the biological reasons for these changes are not fully understood.

Corticosteroids: For years, there was no treatment for atopic eczema. Atopy was believed to be allergic in origin due to the patients’ extremely high serum IgE levels, but standard therapies at the time did not help. Oral prednisone was sometimes prescribed for severe cases. Wet wraps (covering the patients with gauze) were sometimes used in hospitals to control itching. However, the discovery of corticosteroids in the 1950s, and their subsequent incorporation in topical creams and ointments, provided a significant advancement in the treatment of atopic eczema and other conditions. Thus, the use of topical steroids avoided many of the undesirable side-effects of systemic administration of corticosteroids. Topical steroids control the itching and the rash that accompany atopic eczema. Side-effects of topical steroid use are plentiful, and the patient is advised to use topical steroids in moderation and only as needed.

Immune modulators: Pimecrolimus and tacrolimus creams and ointments became available in the 1980s and are sometimes prescribed for atopic eczema. They act by interfering with T cells but have been linked to the development of cancer.

Avoiding dry skin: Dry skin is a common feature of patients with atopic eczema (see also eczema for information) and can exacerbate atopic eczema.

Avoiding allergens and irritants: See eczema for information.

Treatment usually involves adrenaline (epinephrine), antihistamines, and corticosteroids.

If the entire body is involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal.

Some examples:

- Allergic asthma

- Allergic conjunctivitis

- Allergic rhinitis ("hay fever")

- Anaphylaxis

- Angioedema

- Urticaria (hives)

- Eosinophilia

- Penicillin allergy

- Cephalosporin allergy

- Food allergy

- Sweet itch

When a medication causes an allergic reaction, it is called an allergen. The following is a short list of the most common drug allergens:

- Antibiotics

- Penicillin

- Sulfa drugs

- Tetracycline

- Analgesics

- Codeine

- Non-steroidal anti-inflammatory drugs (NSAIDs)

- Antiseizure

- Phenytoin

- Carbamazepine

Allergies are caused by an oversensitive immune system, leading to a misdirected immune response. The immune system normally protects the body against harmful substances such as bacteria and viruses. Allergy occurs when the immune system reacts to substances (allergens) that are generally harmless and in most people do not cause an immune response.

- Animal hair and dander

- cockroach calyx

- dust mite excretion

Some people have reported relief of symptoms by following a low-salicylate diet such as the Feingold diet. Aspirin is quickly converted in the body to salicylic acid, also known as 2-Hydroxybenzoic acid. Sommer "et al." reported a multi-center prospective randomized cross-over trial with 30 patients following a low-salicylate diet for 6 weeks. This study demonstrated a clinically significant decrease in both subjective and objective scoring of severity of disease, but made note of the challenge for patients in following what is a fairly stringent diet.

A diet low in omega-6 oils (precursors of arachidonic acid), and high in omega-3 oils, may also help. In a small study, aspirin-sensitive asthma patients taking 10 grams of fish oil daily reported relief of most symptoms after six weeks, however symptoms returned if the supplement was stopped.

The preferred treatment for many patients is desensitization to aspirin, undertaken at a clinic or hospital specializing in such treatment. In the United States, the Scripps Clinic in San Diego, CA, the Massachusetts General Hospital in Boston, MA, the Brigham and Women's Hospital in Boston, MA, National Jewish Hospital in Denver and Stanford University Adult ENT Clinic have allergists who routinely perform aspirin desensitization procedures for patients with aspirin-induced asthma. Patients who are desensitized then take a maintenance dose of aspirin daily and while on daily aspirin they often have reduced need for supporting medications, fewer asthma and sinusitis symptoms than previously, and many have an improved sense of smell. Desensitization to aspirin reduces the chance of nasal polyp recurrence, and can slow the regrowth of nasal polyps. Even patients desensitized to aspirin may continue to need other medications including nasal steroids, inhaled steroids, and leukotriene antagonists.

Leukotriene antagonists and inhibitors (montelukast, zafirlukast, and zileuton) are often helpful in treating the symptoms of aspirin-induced asthma. Some patients require oral steroids to alleviate asthma and congestion, and most patients will have recurring or chronic sinusitis due to the nasal inflammation.

Completely eliminating salicylate from one's diet and environment is virtually impossible and is not a recommended course of action by many immunologists. The range of foods that have no salicylate content is very limited, and consequently salicylate-free diets are very restricted.

Desensitization involves daily administration of progressive doses of salicylate. This process is usually performed as an inpatient, with a crash-cart at the bedside over a six-day period, beginning with 25 mg of I.V. lysine-aspirin and progressing to 500 mg if tolerated.

Montelukast is one form of treatment used in aspirin-intolerant asthma.

Symptoms of an allergic reaction to animals may include itchy skin, nasal congestion, itchy nose, sneezing, chronic sore throat or itchy throat, swollen, red, itchy, and watery eyes, coughing, asthma, or rash on the face or chest.

The culprit can be both a prescription drug or an over-the-counter medication.

Examples of common drugs causing drug eruptions are antibiotics and other antimicrobial drugs, sulfa drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), biopharmaceuticals, chemotherapy agents, anticonvulsants, and psychotropic drugs. Common examples include photodermatitis due to local NSAIDs (such as piroxicam) or due to antibiotics (such as minocycline), fixed drug eruption due to acetaminophen or NSAIDs (Ibuprofen), and the rash following ampicillin in cases of mononucleosis.

Certain drugs are less likely to cause drug eruptions (rates estimated to be ≤3 per 1000 patients exposed). These include: digoxin, aluminum hydroxide, multivitamins, acetaminophen, bisacodyl, aspirin, thiamine, prednisone, atropine, codeine, hydrochlorothiazide, morphine, insulin, warfarin, and spironolactone.

NSAID or nonsteroidal anti-inflammatory drug hypersensitivity reactions encompasses a broad range of allergic or allergic-like symptoms that occur within minutes to hours after ingesting aspirin or other NSAID nonsteroidal anti-inflammatory drugs. Hypersensitivity drug reactions differ from drug toxicity reactions in that drug toxicity reactions result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual (see nonsteroidal anti-inflammatory drugs section on adverse reactions for NSAID-induced toxic reactions); hypersensitivity reactions are idiosyncratic reactions to a drug. Although the term NSAID was introduced to signal a comparatively low risk of adverse effects, NSAIDs do evoke a broad range of hypersensitivity syndromes. These syndromes have recently been classified by the European Academy of Allergy and Clinical Immunology Task Force on NSAIDs Hypersensitivity. The classification organizes the hypersensitivity reactions to NSAIDs into the following five categories:

- 1) NSAIDs-exacerbated respiratory disease (NERD) is an acute (immediate to several hours) exacerbation of bronchoconstriction and other symptoms of asthma (see aspirin-induced asthma) in individuals with a history of asthma and/or nasal congestion, rhinorrhea or other symptoms of rhinitis and sinusitis in individuals with a history of rhinosinusitis after ingestion of various NSAIDs, particularly those that act by inhibiting the COX-1 enzyme. NERD does not appear to be due to a true allergic reaction to NSAIDs but rather at least in part to the more direct effects of these drugs to promote the production and/or release of certain mediators of allergy. That is, inhibition of cellular COX activity deprives tissues of its anti-inflammatory product(s), particularly prostaglandin E2 while concurrently shuttling its substrate, arachidonic acid, into other metabolizing enzymes, particularly 5-lipoxygenase (ALOX5) to overproduce pro-inflammatory leukotriene and 5-Hydroxyicosatetraenoic acid metabolites and 15-lipoxygenase (ALOX15) to overproduce pro-inflammatory 15-Hydroxyicosatetraenoic acid metabolites, including eoxins; the condition is also associated with a reduction in the anti-inflammatory metabolite, lipoxin A4, and increases in certain pro-allergic chemokines such as eotaxin-2 and CCL7.

- 2) NSAIDs-exacerbated cutaneous disease (NECD) is an acute exacerbation of wheals and/or angioedema in individuals with a history of chronic urticaria. NECD also appears due to the non-allergic action of NSAIDs in inhibiting the production of COX anti-inflammatory metabolites while promoting the production 5-lipoxygenase and 15-lipoxygenase pro-inflammatory metabolites and the overproduction of certain pro-allergic chemokines, e.g. eotaxin-1, eotaxin-2, RANTES, and interleukin-5.

- 3) NSAIDs-induced urticarial disease (NEUD) is the acute development of wheals and/or angioedema in individuals with no history of chronic NSAIDs-induced urticaria or related diseases. The mechanism behind NEUD is unknown but may be due to the non-allergic action of NSAIDs in promoting the production and/or release of allergy mediators.

- 4) Single NSAID-induced urticarial/angioedema or anaphylaxis (SNIUAA) is the acute development of urticarial, angioedema, or anaphylaxis in response to a single type of NSAID and/or a single group of NSAIDs with a similar structure but not to other structurally unrelated NSAIDs in individuals with no history of underlying relevant chronic diseases. SNIUAA is due to a true IgE-mediated allergy reaction.

- 5 Single NSAID-induced delayed reactions (SNIDR) are a set of delayed onset (usually more than 24 hour) reactions to NSAIDs. SNIDR are most commonly skin reactions that may be relatively mild moderately severe such as maculopapular rash, fixed drug eruptions, photosensitivity reactions, delayed urticaria, and contact dermatitis or extremely severe such as the DRESS syndrome, acute generalized exanthematous pustulosis, the Stevens–Johnson syndrome, and toxic epidermal necrolysis (also termed Lyell's syndrome). SNIDR result from the drug-specific stimulation of CD4+ T lymphocytes and CD8+ cytotoxic T cells to elicit a delayed type hypersensitivity reaction.

An important salicylate drug is aspirin, which has a long history. Aspirin intolerance was widely known by 1975, when the understanding began to emerge that it is a pharmacological reaction, not an allergy.

It is estimated that 2—3 percent of hospitalised patients are affected by a drug eruption, and that serious drug eruptions occur in around 1 in 1000 patients.

The Arthus reaction involves the in situ formation of antigen/antibody complexes after the intradermal injection of an antigen. If the animal/patient was previously sensitized (has circulating antibody), an Arthus reaction occurs. Typical of most mechanisms of the type III hypersensitivity, Arthus manifests as local vasculitis due to deposition of IgG-based immune complexes in dermal blood vessels. Activation of complement primarily results in cleavage of soluble complement proteins forming C5a and C3a, which activate recruitment of PMNs and local mast cell degranulation (requiring the binding of the immune complex onto FcγRIII), resulting in an inflammatory response. Further aggregation of immune complex-related processes induce a local fibrinoid necrosis with ischemia-aggravating thrombosis in the tissue vessel walls. The end result is a localized area of redness and induration that typically lasts a day or so.

Arthus reactions have been infrequently reported after vaccinations containing diphtheria and tetanus toxoid. The CDC's description:

Arthus reactions (type III hypersensitivity reactions) are rarely reported after vaccination and can occur after tetanus toxoid–containing or diphtheria toxoid–containing vaccines. An Arthus reaction is a local vasculitis associated with deposition of immune complexes and activation of complement. Immune complexes form in the setting of high local concentration of vaccine antigens and high circulating antibody concentration. Arthus reactions are characterized by severe pain, swelling, induration, edema, hemorrhage, and occasionally by necrosis. These symptoms and signs usually occur 4–12 hours after vaccination. ACIP has recommended that persons who experienced an Arthus reaction after a dose of tetanus toxoid–containing vaccine should not receive Td more frequently than every 10 years, even for tetanus prophylaxis as part of wound management.

This is an additional type that is sometimes (especially in the UK) used as a distinction from Type 2.

Instead of binding to cell surfaces, the antibodies recognise and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling.

Some clinical examples:

- Graves' disease

- Myasthenia gravis

The use of Type 5 is rare. These conditions are more frequently classified as Type 2, though sometimes they are specifically segregated into their own subcategory of Type 2.

The Arthus reaction was discovered by Nicolas Maurice Arthus in 1903. Arthus repeatedly injected horse serum subcutaneously into rabbits. After four injections, he found that there was edema and that the serum was absorbed slowly. Further injections eventually led to gangrene.

Hypersensitivity (also called hypersensitivity reaction or intolerance) is a set of undesirable reactions produced by the normal immune system, including allergies and autoimmunity. They are usually referred to as an over- reaction of the immune system and these reactions may be damaging, uncomfortable, or occasionally fatal. Hypersensitivity reactions require a pre-sensitized (immune) state of the host. They are classified in four groups after the proposal of P. G. H. Gell and Robin Coombs in 1963.

Few treatments are fully efficacious once lesions have appeared. The only effective form of treatment is preventitive - i.e. prevent further insect bites - so these techniques will also be discussed here. Treatments generally fall into one of the following categories:

1) Insecticides and Repellents: These may be applied to the horse or its environment. The most commonly used and effective are permethrins. and benzyl benzoate Citronella has been used, with variable effect. Some sources advocate draining of any stagnant water or pools, to reduce the local breeding potential of the insects. Midge numbers are often larger near water sources, for example ponds, bogs, and slow moving water. Moving the horse away from these areas may help to prevent further problems.

2) Barrier Techniques: Rugs etc., that prevent flies and midges settling on the animal's skin to bite. These include "Boett Rugs" and fly masks. In addition, thin screens may be placed over stable doors and windows to exclude biting insects. Stabling the horse at times of day when the midges are most prevalent is also quite effective.

3) Immunotherapy: A wide variety immunotherapy and desensitisation protocols have been trialled in attempts to reduce or modify the immune response, with considerable success rates. So far, there appear to a significant benefit in more than 80% of equine cases. This particular BioEos product is now available through The National Sweet Itch Centre in the UK and ProVet in the EU. The underlying immune modulation is now proven to shift the immune system from a Th2 to a Th1 mode. BioEos is a research and development company with worldwide patents derived from many years of research at University College London and the many applications are being developed for use in both human, agricultural and aquaculture treatments. Current clinical trials for the treatment of pancreatic cancers (Immodulon Therapeutics) and the treatment of other chronic immune deficiency disorders (ActinoPharma) are putting this research into practical effect.

4) Nutritional supplements: Various supplements may be effective in individuals, including fatty acid supplemantation and linseed oil. However, although owners perceived an improvement, this was not bourne out by objective statistical analysis.

5) Symptomatic Control: Control of symptoms to some degree can be achieved with antihistamines (especially hydroxyzine, and with corticosteroids, although the potential side effects (e.g. laminitis, immune suppression) make this a less preferred option. In addition, antibiotics may be required to manage any secondary infection.

6) Alternative Medicines: A wide variety of herbal, homeopathic and other alternative remedies have been suggested. Among the natural remedies suggested are sulfur, wild geranium (as the base for a shampoo), Lavender oil, Aloe vera (to reduce the itching).

Overall, the wide variety of treatments proposed leads to the conclusion that no one method is universally effective.

With discontinuation of offending agent, symptoms usually disappear within 4–5 days.

Corticosteroids, antihistamines, and analgesics are the main line of treatment. The choice depends on the severity of the reaction.

Use of plasmapheresis has also been described.

Avoidance of antitoxins that may cause serum sickness is the best way to prevent serum sickness. Although, sometimes, the benefits outweigh the risks in the case of a life-threatening bite or sting. Prophylactic antihistamines or corticosteroids may be used concomitant with the antitoxin. Skin testing may be done beforehand in order to identify individuals who may be at risk of a reaction. Physicians should make their patients aware of the drugs or antitoxins to which they are allergic if there is a reaction. The physician will then choose an alternate antitoxin if it's appropriate or continue with prophylactic measures.

The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage. Corticosteroids such as prednisolone may help to control symptoms but may produce side-effects.

A hypersensitivity reaction to specific allergens (protein molecules causing an extreme immune response in sensitised individuals) in the saliva of "Culicoides" midges. There are multiple allergens involved, although some workers claim that the larger proteins (of molecular weight 65kDa) are the most important. These allergens appear to be cross-reactive across many species of "Culicoides" - i.e. many different varieties of midges produce similar allergens, giving the same effects upon horses.

The hypersensitivity response is mediated by IgE, an antibody produced by the horse's immune system which binds the allergens, causing a cascade production of histamine and cytokines which make the horse's skin inflamed and itchy. Of these, histamine appears the most important in the initial phase of reaction.

When penicillin is used at high doses hypokalemia, metabolic acidosis, and hyperkalemia can occur. Developing hypernatremia after administering high doses of penicillin can be a serious side effect.