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 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.

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.

Many suspected aetiologic factors have been reported to cause EM.

- Infections: Bacterial (including Bacillus Calmette-Guérin (BCG) vaccination, haemolytic "Streptococci", legionellosis, leprosy, "Neisseria meningitidis, Mycobacterium, "Pneumococcus, "Salmonella" species, "Staphylococcus" species, "Mycoplasma pneumoniae), "Chlamydial.

- Fungal (Coccidioides immitis)

- Parasitic ("Trichomonas" species, "Toxoplasma gondii), "

- Viral (especially Herpes simplex)

- Drug reactions, most commonly to: antibiotics (including, sulphonamides, penicillin), anticonvulsants (phenytoin, barbiturates), aspirin, antituberculoids, and allopurinol and many others.

- Physical factors: radiotherapy, cold, sunlight

- Others: collagen diseases, vasculitides, non-Hodgkin lymphoma, leukaemia, multiple myeloma, myeloid metaplasia, polycythemia

EM minor is regarded as being triggered by HSV in almost all cases. A herpetic aetiology also accounts for 55% of cases of EM major. Among the other infections, "Mycoplasma" infection appears to be a common cause.

Herpes simplex virus suppression and even prophylaxis (with acyclovir) has been shown to prevent recurrent erythema multiforme eruption.

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

The cause of erythema toxicum is thought to be an activation of the immune system. Some neonates are more sensitive than others and develop erythematous spots all over the body. Another theory is hypersensitivity to detergents in bedsheets and clothing is sometimes suspected, but the connection remains unproven.

It is thought to be a benign condition that causes no discomfort to the infant. The rash will generally disappear spontaneously in about 2 weeks.

Zirconium granulomas are a skin condition characterized by a papular eruption involving the axillae, and are sometimes considered an allergic reaction to deodorant containing zirconium lactate. They are the result of a delayed granulomatous hypersensitivity reaction, and can also occur from exposure to aluminum zirconium complexes. Commonly, zirconium containing products are used to relieve toxicodendron irritation. The lesions are similar to those from sarcoidosis, and commonly manifest four to six weeks after contact. They appear as erythrematous, firm, raised, shiny papules. Corticosteroids are used to ease the inflammation, but curative treatment is currently unavailable.

Acute generalized exanthematous pustulosis (AGEP) (also known as "pustular drug eruption" and "toxic pustuloderma") is a rare skin reaction that in 90% of cases is related to medication administration. AGEP is characterized by a sudden skin eruption that appears on average five days after the medication is started.

It is mediated by T cells.

The cause of pityriasis rosea is not certain, but its clinical presentation and immunologic reactions suggest a viral infection as a cause. Some believe it to be a reactivation of herpes viruses 6 and 7, which cause roseola in infants.

In most patients, the condition lasts only a matter of weeks; in some cases it can last longer (up to six months). The disease resolves completely without long-term effects. Two percent of patients have recurrence.

The cases of this condition are most common between the spring and autumn months in the northern hemisphere.

Typically, 5-20% of fair skinned populations are affected, but it can occur in any skin type. It is more common in females than in males. The condition can affect all ethnic groups and research suggests that 20% of patients have a family history of the complaint. Those suffering from PLE usually do so by age 30.

The cause of PLE is not yet understood. It is thought to be due to a type IV delayed-type hypersensitivity to an allergen produced in the body following sunlight exposure. It can be provoked by UVA or UVB rays. Some progression to autoimmune disease has been observed.. It is also thought that skin microbiome or microbial elements could be involved in pathogenesis of the disease

In cases of cutaneous Porphyria alcohol consumption has been found to be a strong trigger. Consumption of alcohol inhibits certain portions of Porphyrin synthesis which creates the excess enzymatic intermediaries. These compounds, upon circulation in the blood stream and oxidized by light are responsible for the itchy blisters and plaques.

Because the eruption is transient and self-limiting, no treatment is indicated.

It can be treated with systemic antiviral drugs, such as aciclovir or valganciclovir. Foscarnet may also be used for immunocompromised host with Herpes simplex and acyclovir-resistant Herpes simplex.

The overwhelming majority of neutrophilic eccrine hidradenitis (NEH) is seen in people with cancer, especially leukaemia, who receive chemotherapy with a cytotoxic drug. These include: Bleomycin, chlorambucil, cyclophosphamide, cytarabine, doxorubicin, lomustine, mitoxantrone, topotecan, and vincristine.

NEH was first described in 1982 in a patient with acute myeloid leukaemia (AML) who had received cytarabine as chemotherapy.

Cancer itself, infections, and other medicinal drugs also can lead to NEH. NEH has been reported in patients with cancer who have not received any form of chemotherapy (i.e., as a paraneoplastic syndrome), in patients with HIV and/or AIDS, and after the use of paracetamol (acetaminophen). Also the use of targeted agents can lead to NEH, e.g. imatinib, a tyrosine kinase inhibitor.

NEH has also been described without any known reason (idiopathic cases), including idiopathic cases in children.

The exact cause of NEH is unknown. In patients receiving chemotherapy, it has been postulated that a high concentration of the cytotoxic drug in sweat has a direct toxic effect on the eccrine glands.

Erythema multiforme is frequently self-limiting and requires no treatment. The appropriateness of glucocorticoid therapy can be uncertain, because it is difficult to determine if the course will be a resolving one.

This reaction occurs mainly in the tropics and in Florida, due to the proximity of the Gulf Stream to the U.S. state. It has been identified in other locations as well.

The cause for actinic prurigo is unknown, however researchers believe that protein in our bodies may be a cause to the condition also:

•UV-A and UV-B light seem to be the main provoking agents. This observation is supported by the fact that most patients live at high altitudes (>1000 m above sea level), and the condition improves in many patients when they move to lower altitudes. However, some patients who are affected already live at sea level.18,19,27 •Some authors are considering a food photosensitizer or a nutritional selective deficiency as a cause; however, no evidence proves this theory.27

Urticarial allergic eruption is a cutaneous condition characterized by annular or gyrate urticarial plaques that persist for greater than 24 hours.

At certain times of the year this can be a problem in some areas of the Bahamas particularly around New Providence.

This infection affects multiple organs, including the eyes, brain, lung, and liver, and can be fatal.

Infantile acropustulosis (also known as "Acropustulosis of infancy") is an intensely itchy vesicopustular eruption of the hands and feet.

Involvement of scabies has been suggested.

infantile acropustulosis is characterized by itchy papules and vesicles that are similar to those found in scabies "mosquito like bites" but there is absence of the typical burrowing with S like burrows on the skin and can occur in small babies as opposed to scabies mostly found on children and young adults.

The cause of NME is unknown, although various mechanisms have been suggested. These include hyperglucagonemia, zinc deficiency, fatty acid deficiency, hypoaminoacidemia, and liver disease. The pathogenesis is also unknown.

Schamberg's disease is caused by leaky blood vessels near the surface of the skin, capillaries, which allow red blood cells to slip through into the skin. The red blood cells in the skin then fall apart and release their iron, which is released from hemoglobin. The iron causes a rust color and this accounts for the orange tint of the rash that can be seen on the skin. The underlying cause of the leaky blood vessels is not known, but researchers are suggesting that there could be some potential triggers. Some possible triggers include viral infection, a hypersensitivity to some agent, and interaction of some medications, such as thiamine and aspirin. Even though there is no correlation with genetics, there have been a few cases where few people in a family had this condition.

Although the cause of capillary inflammation is unknown, certain preventive measures can be taken. Doctors may prescribe medications that enhance the circulation of blood, which can keep blood vessels strong and healthy. Daily intake of vitamin C has proven to be a natural home remedy that can prevent the onsite of any disease or infection. Doctors always recommend that their patients monitor what they eat because their diet could be a possible factor that contributes to this condition. A healthy body that receives nutritious meals is more likely to have a healthy life that does not revolve around a lot of health problems.

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."