The most common type of eruption is a morbilliform (resembling measles) or erythematous rash (approximately 90% of cases). Less commonly, the appearance may also be urticarial, papulosquamous, pustular, purpuric, bullous (with blisters) or lichenoid. Angioedema can also be drug-induced (most notably, by angiotensin converting enzyme inhibitors).

Some of the most severe and life-threatening examples of drug eruptions are erythema multiforme, Stevens–Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), hypersensitivity vasculitis, Drug induced hypersensitivity syndrome (DIHS), erythroderma and acute generalized exanthematous pustulosis (AGEP). These severe cutaneous drug eruptions are categorized as hypersensitivity reactions and are immune-mediated. There are four types of hypersensitivity reactions and many drugs can induce one or more hypersensitivity reactions.

Identifying a drug allergy can sometimes be the hardest part. Sometimes drug allergies are confused with nonallergic drug reactions because they both cause somewhat similar reactions. Symptoms of a drug allergy can include, but are not limited to, the following list.

- Hives

- Itching

- Rash

- Fever

- Facial swelling

- Shortness of breath due to the short-term constriction of lung airways or longer-term damage to lung tissue

- Anaphylaxis, a life-threatening drug reaction (produces most of these symptoms as well as low blood pressure)

- Cardiac symptoms such as chest pain, shortness of breath, fatigue, chest palpitations, light headedness, and syncope due to a rare drug-induced reaction, eosinophilic myocarditis

Idiosyncratic drug reactions, also known as type B reactions, are drug reactions that occur rarely and unpredictably amongst the population. This is not to be mistaken with idiopathic, which implies that the cause is not known. They frequently occur with exposure to new drugs, as they have not been fully tested and the full range of possible side-effects have not been discovered; they may also be listed as an adverse drug reaction with a drug, but are extremely rare.

Some patients have multiple-drug intolerance. Patients who have multiple idiopathic effects that are nonspecific are more likely to have anxiety and depression.

Idiosyncratic drug reactions appear to not be concentration dependent. A minimal amount of drug will cause an immune response, but it is suspected that at a low enough concentration, a drug will be less likely to initiate an immune response.

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

The U.S Food and Drug Administration defines a serious adverse event as one when the patient outcome is one of the following:

- Death

- Life-threatening

- Hospitalization (initial or prolonged)

- Disability - significant, persistent, or permanent change, impairment, damage or disruption in the patient's body function/structure, physical activities or quality of life.

- Congenital anomaly

- Requires intervention to prevent permanent impairment or damage

Severity is a point on an arbitrary scale of intensity of the adverse event in question. The terms "severe" and "serious" when applied to adverse events are technically very different. They are easily confused but can not be used interchangeably, requiring care in usage.

A headache is severe, if it causes intense pain. There are scales like "visual analog scale" that help clinicians assess the severity. On the other hand, a headache is not usually serious (but may be in case of subarachnoid haemorrhage, subdural bleed, even a migraine may temporally fit criteria), unless it also satisfies the criteria for seriousness listed above.

Photosensitive drug reaction (or drug-induced photosensitivity) secondary to medications may cause phototoxic, photoallergic, and lichenoid reactions, and photodistributed telangiectasias, as well as pseudoporphyria.

Drugs involved include naproxen and doxycycline.

Types A and B were proposed in the 1970s, and the other types were proposed subsequently when the first two proved insufficient to classify ADRs.

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.

Anticonvulsant/sulfonamide hypersensitivity syndrome is a potentially serious hypersensitivity reaction that can be seen with drugs with an aromatic amine chemical structure, such as aromatic anticonvulsants (e.g. diphenylhydantoin, phenobarbital, phenytoin, carbamazepine, lamotrigine), sulfonamides, or other drugs with an aromatic amine (procainamide). Cross-reactivity should not occur between drugs with an aromatic amine and drugs without an aromatic amine (e.g., sulfonylureas, thiazide diuretics, furosemide, and acetazolamide); therefore, these drugs can be safely used in the future.

The hypersensitivity syndrome is characterized by a skin eruption that is initially morbilliform. The rash may also be a severe Stevens-Johnson syndrome or toxic epidermal necrolysis. Systemic manifestations occur at the time of skin manifestations and include eosinophilia, hepatitis, and interstitial nephritis. However, a subgroup of patients may become hypothyroid as part of an autoimmune thyroiditis up to 2 months after the initiation of symptoms.

This kind of adverse drug reaction is caused by the accumulation of toxic metabolites; it is not the result of an IgE-mediated reaction. The risk of first-degree relatives’ developing the same hypersensitivity reaction is higher than in the general population.

As this syndrome can present secondary to multiple anticonvulsants, the general term "anticonvulsant hypersensitivity syndrome" is favored over the original descriptive term "dilantin hypersensitivity syndrome."

Generally, the areas affected are exposed skin not usually protected by clothing; however it can also occur in areas covered by clothing. Areas constantly subjected to the sun's rays may only be slightly affected if at all. People with extreme cases will also have reactions to light bulbs that emit a UV wavelength (any bulb that is not an LED). Parts of the body only thinly covered can also potentially be subjected to an outbreak.

Life with SU can be difficult. Patients are subject to constant itching and pain, as within minutes of the initial exposure to UV radiation a rash will appear. The urticarial reaction begins in the form of pruritus, later progressing to erythema and edema in the exposed areas of the skin. If vast areas of the body are affected, the loss of fluid into the skin could lead to light-headedness, headache, nausea, and vomiting. Extremely rarely, patients have been reported to experience an increase in heart rate that can cause a stroke or heart attack due to the body cavity swelling. Other rare side effects can be bronchospasm and glucose instability issues. Also, if a large area of the body is suddenly exposed the person may be subject to an anaphylactic reaction. Once free of exposure, the rash will usually fade away within several hours; rare and extreme cases can take a day or two to normalize depending on severity of the reaction.

Polymorphous light eruption (PMLE) is the easiest disease to mistake for solar urticaria because the locations of the lesions are similar (the V of the neck and the arms). However, patients with SU are more likely to develop lesions on the face. Also, a reaction with PMLE will take a greater amount of time to appear than with solar urticaria. Lupus erythematosus has been mistaken for SU; however, lesions from lupus erythematosus will take a longer amount of time to go away. Furthermore, when being tested for the two diseases, patients with SU have a reaction immediately while patients with lupus erythematosus will have a delayed reaction. Patients who have experienced solar urticarial symptoms from a young age could mistakenly be thought to have erythropoietic protoporphyria. However, the main symptom for this disease is pain and patients with have been found to have abnormal levels of protoporphyrin in their blood while these levels are normal in SU patients. Finally, cholinergic urticaria, or urticaria induced by heat, can occasionally appear to be solar urticaria because the heat from the sun will cause a person with the disease to have a reaction.

The reaction to a sting is of three types. The normal reaction involves the area around the bite with redness, itchiness, and pain. A large local reaction occurs when the area of swelling is greater than 5 cm. Systemic reactions are when symptoms occur in areas besides that of the bites.

With insect stings a large local reaction may occur (an area of skin redness greater than 10 cm in size). It can last one to two days. It occurs in about 10% of those bitten.

The histomorphologic appearance of insect bites is usually characterized by a wedge-shaped superficial dermal perivascular infiltrate consisting of abundant lymphocytes and scattered eosinophils. This appearance is non-specific, i.e. it may be seen in a number of conditions including:

- Drug reactions,

- Urticarial reactions,

- Prevesicular early stage of bullous pemphigoid, and

- HIV related dermatoses.

Bullous drug reaction (also known as a "bullous drug eruption", "generalized bullous fixed drug eruption", and "multilocular bullous fixed drug eruption") most commonly refers to a drug reaction in the erythema multiforme group. These are uncommon reactions to medications, with an incidence of 0.4 to 1.2 per million person-years for toxic epidermal necrolysis and 1.2 to 6.0 per million person-years for Stevens–Johnson syndrome. The primary skin lesions are large erythemas (faintly discernible even after confluence), most often irregularly distributed and of a characteristic purplish-livid color, at times with flaccid blisters.

In adverse drug reactions involving overdoses, the toxic effect is simply an extension of the pharmacological effect (Type A adverse drug reactions). On the other hand, clinical symptoms of idiosyncratic drug reactions (Type B adverse drug reactions) are different from the pharmacological effect of the drug.

The proposed mechanism of most idiosyncratic drug reactions is immune-mediated toxicity. To create an immune response, a foreign molecule must be present that antibodies can bind to (i.e. the antigen) and cellular damage must exist. Very often, drugs will not be immunogenic because they are too small to induce immune response. However, a drug can cause an immune response if the drug binds a larger molecule. Some unaltered drugs, such as penicillin, will bind avidly to proteins. Others must be bioactivated into a toxic compound that will in turn bind to proteins. The second criterion of cellular damage can come either from a toxic drug/drug metabolite, or from an injury or infection.

These will sensitize the immune system to the drug and cause a response.

Idiosyncratic reactions fall conventionally under toxicology.

SJS usually begins with fever, sore throat, and fatigue, which is commonly misdiagnosed and therefore treated with antibiotics. SJS and TEN are often heralded by fever, sore throat, cough, and burning eyes for 1 to 3 days. Patients with SJS and TEN frequently experience burning pain of their skin at the start of disease. Ulcers and other lesions begin to appear in the mucous membranes, almost always in the mouth and lips, but also in the genital and anal regions. Those in the mouth are usually extremely painful and reduce the patient's ability to eat or drink. Conjunctivitis of the eyes occurs in about 30% of children who develop SJS. A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and soles of the feet, but usually not the scalp.

A typical allergic reaction to alpha-gal has a delayed onset, occurring 3–8 hours after the consumption of mammalian meat products, instead of the typical rapid onset with most food allergies. After the delayed onset, the allergic response is typical of most food allergies, and especially an IgE mediated allergy, including severe whole-body itching, hives, angioedema, gastrointestinal upset, and possible anaphylaxis. In 70% of cases the reaction is accompanied by respiratory distress and as such is particularly harmful to those with asthma.

Alpha-gal allergies are the first food allergies to come with the possibility of delayed anaphylaxis. It is also the first food-related allergy to be associated with a carbohydrate, rather than a protein.

The most common symptoms of salicylate sensitivity are:

- Stomach pain/upset stomach

- Tinnitus ringing of the ears

- Itchy skin, hives or rashes

- Asthma and other breathing difficulties

- Angioedema

- Headaches

- Swelling of hands, feet, eyelids, face and/or lips

- Bed wetting or urgency to pass water

- Persistent cough

- Changes in skin color/skin discoloration

- Fatigue

- Sore, itchy, puffy or burning eyes

- Sinusitis/Nasal polyps

- Diarrhea

- Nausea

- Hyperactivity

- Memory loss and poor concentration

- Depression

- Pseudoanaphylaxis

Stevens–Johnson syndrome (SJS) is a type of severe skin reaction. Together with toxic epidermal necrolysis (TEN) it forms a spectrum of disease, with SJS being less severe. Early symptoms include fever and flu-like symptoms. A few days later the skin begins to blister and peel forming painful raw areas. Mucous membranes, such as the mouth, are also typically involved. Complications include dehydration, sepsis, pneumonia, and multiple organ failure.

The most common cause is certain medications such as lamotrigine, carbamazepine, allopurinol, sulfonamide antibiotics, and nevirapine. Other causes can include infections such as "Mycoplasma pneumoniae" and cytomegalovirus or the cause may remain unknown. Risk factors include HIV/AIDS and systemic lupus erythematosus. The diagnosis is based on involvement of less than 10% of the skin. It is known as TEN when more than 30% of the skin is involved and an intermediate form with 10 to 30% involvement. Erythema multiforme (EM) is generally considered a separate condition.

Treatment typically takes place in hospital such as in a burn unit or intensive care unit. Efforts may include stopping the cause, pain medication, antihistamines, antibiotics, intravenous immunoglobulins, or corticosteroids. Together with TEN it affects 1 to 2 people per million per year. It is twice as common in males as females. Typical onset is under the age of 30. Skin usually regrows over two to three weeks; however, complete recovery can take months.

AGEP is an acute febrile drug eruption characterized by numerous small, primarily non-follicular, sterile pustules, arising within large areas of red swollen skin.

The eruption follows a self-limiting course and will end before a week provided the causative agent (e.g. medication) is discarded. It is accompanied by fever, a high number of neutrophils and eosinophils in the blood, liver inflammation, and sometimes by facial swelling. The mortality rate is about 5% and the differential diagnosis includes Stevens–Johnson syndrome (SJS). Contrary to SJS, in AGEP, mucosa are not affected, which means that there are no blisters in the mouth or vagina.

It resembles bacterial sepsis and can occur after initiation of antibacterials, such as mild silver protein, penicillin or tetracycline, for the treatment of louse-borne relapsing fever (80–90% of patients) and in tick-borne relapsing fever (30–40%). It usually manifests within a few hours of the first dose of antibiotic as fever, chills, rigor, hypotension, headache, tachycardia, hyperventilation, vasodilation with flushing, myalgia (muscle pain), exacerbation of skin lesions and anxiety. The intensity of the reaction indicates the severity of inflammation. Reaction commonly occurs within two hours of drug administration, but is usually self-limiting. It is observed in 50% of patients with primary syphilis and about 90% of patients with secondary syphilis.

The treatment is (1) stop the offending drug (antibiotics), (2) symptomatic (fever), and (3) for complications (hepatitis).

Salicylate sensitivity, also known as salicylate intolerance, is any adverse effect that occurs when a usual amount of salicylate is ingested. People with salicylate intolerance are unable to consume a normal amount of salicylate without adverse effects.

Salicylate sensitivity differs from salicylism, which occurs when an individual takes an overdose of salicylates. Salicylate overdose can occur in people without salicylate sensitivity, and can be deadly if untreated. For more information, see aspirin poisoning.

Salicylates are derivatives of salicylic acid that occur naturally in plants and serve as a natural immune hormone and preservative, protecting the plants against diseases, insects, fungi, and harmful bacteria. Salicylates can also be found in many medications, perfumes and preservatives. Both natural and synthetic salicylates can cause health problems in anyone when consumed in large doses. But for those who are salicylate intolerant, even small doses of salicylate can cause adverse reactions.

Alpha-gal allergy, also known as meat allergy or Mammalian Meat Allergy (MMA), is a reaction to galactose-alpha-1,3-galactose (alpha-gal), whereby the body is overloaded with immunoglobulin E (IgE) antibodies on contact with the carbohydrate. The alpha-gal molecule is found in all mammals apart from Old World monkeys and the apes, which include humans. Anti-Gal is a human natural antibody which interacts specifically with the mammalian carbohydrate structure Gal alpha 1-3Gal beta 1-4GlcNAc-R, termed, the alpha-galactosyl epitope. Whereas anti-Gal is abundant in humans, apes and Old World monkeys, it is absent from New World monkeys, prosimians and nonprimate mammals.

Bites from certain ticks, such as the lone star tick in the US, which can transfer this carbohydrate to the victim have been implicated in the development of this delayed allergic response which is triggered by the consumption of mammalian meat products. Despite myths to the contrary, an alpha-gal allergy does not require the afflicted to become a vegetarian, as poultry and fish do not trigger a reaction.

The allergy most often occurs in the central and southern United States, which corresponds to the distribution of the lone star tick. In the Southern United States, where the tick is most prevalent, allergy rates are 32% higher than elsewhere. However, as doctors are not required to report the number of patients suffering the alpha-gal allergies, the true number of affected individuals is unknown. While there is no known cure, symptoms of the allergy may recede over time. Some patients report observing symptoms for over 20 years.