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.

Drug eruptions are diagnosed mainly from the medical history and clinical examination. However, they can mimic a wide range of other conditions, thus delaying diagnosis (for example, in drug-induced lupus erythematosus, or the acne-like rash caused by erlotinib). A skin biopsy, blood tests or immunological tests can also be useful.

Drug reactions have characteristic timing. The typical amount of time it takes for a rash to appear after exposure to a drug can help categorize the type of reaction. For example, Acute generalized exanthematous pustulosis usually occurs within 4 days of starting the culprit drug. Drug Reaction with Eosinophilia and Systemic Symptoms usually occurs between 15 and 40 days after exposure. Toxic epidermal necrolysis and Stevens-Johnson syndrome typically occur 7–21 days after exposure. Anaphylaxis occurs within minutes. Simple exanthematous eruptions occur between 4 and 14 days after exposure.

TEN and SJS are severe cutaneous drug reactions that involve the skin and mucous membranes. To accurately diagnose this condition, a detailed drug history is crucial. Often, several drugs may be causative and allergy testing may be helpful. Sulfa drugs are well-known to induce TEN or SJS in certain people. For example, HIV patients have an increased incidence of SJS or TEN compared to the general population and have been found to express low levels of the drug metabolizing enzyme responsible for detoxifying sulfa drugs. Genetics plays an important role in predisposing certain populations to TEN and SJS. As such, there are some FDA recommended genetic screening tests available for certain drugs and ethnic populations to prevent the occurrence of a drug eruption. The most well known example is carbamezepine (an anti-convulsant used to treat seizures) hypersensitivity associated with the presence of HLA-B*5801 genetic allele in Asian populations.

DIHS is a delayed onset drug eruption, often occurring a few weeks to 3 months after initiation of a drug. Interestingly, worsening of systemic symptoms occurs 3-4 days after cessation of the offending drug. There are genetic risk alleles that are predictive of the development of DIHS for particular drugs and ethnic populations. The most important of which is abacavir (an anti-viral used in the treatment of HIV) hypersensitivity associated with the presence of the HLA-B*5701 allele in European and African population in the United States and Australians.

AGEP is often caused by antimicrobial, anti-fungal or antimalarial drugs. Diagnosis is often carried out by patch testing. This testing should be performed within one month after resolution of the rash and patch test results are interpreted at different time points: 48 hours, 72hours and even later at 96 hours and 120 hours in order to improve the sensitivity.

Experienced practitioners may make the diagnosis clinically. If the diagnosis is in doubt, tests may be performed to rule out similar conditions such as Lyme disease, ringworm, guttate psoriasis, nummular or discoid eczema, drug eruptions, other viral exanthems.The clinical appearance of pityriasis rosea is similar to that of secondary syphilis, and rapid plasma reagin testing should be performed if there is any clinical concern for syphilis. A biopsy of the lesions will show extravasated erythrocytes within dermal papillae and dyskeratotic cells within the dermis.

A set of validated diagnostic criteria for pityriasis rosea is as follows:

A patient is diagnosed as having pityriasis rosea if:

1. On at least one occasion or clinical encounter, he / she has all the essential clinical features and at least one of the optional clinical features, and

2. On all occasions or clinical encounters related to the rash, he / she does not have any of the exclusional clinical features.

The essential clinical features are the following:

1. Discrete circular or oval lesions,

2. Scaling on most lesions, and

3. Peripheral collarette scaling with central clearance on at least two lesions.

The optional clinical features are the following:

1. Truncal and proximal limb distribution, with less than 10% of lesions distal to mid-upper-arm and mid-thigh,

2. Orientation of most lesions along skin cleavage lines, and

3. A herald patch (not necessarily the largest) appearing at least two days before eruption of other lesions, from history of the patient or from clinical observation.

The exclusional clinical features are the following:

1. Multiple small vesicles at the centre of two or more lesions,

2. Two or more lesions on palmar or plantar skin surfaces, and

3. Clinical or serological evidence of secondary syphilis.

With no particular affinity to any particular ethnic group, seen in all age groups and equally amongst males and females, the precise prevalence is not known.

Dyshidrosis is diagnosed clinically, by gathering a patient's history and making careful observations (see signs and symptoms section). Severity of symptoms can also be assessed using the dyshidrotic eczema area and severity index (DASI). The DASI has been designed for clinical trials and is not typically used in practice.

Antiviral treatment has been tried with some success in a small number of patients.

Schamberg's disease can only be properly diagnosed by a healthcare provider. While reviewing medical history is important to diagnose this condition, it is essential that the purpuric lesions are physically examined. A skin biopsy will be taken to determine capillaritis of dermal vessels. Capillaritis or pigmented purpura is skin condition that has brown-reddish patches on the skin, which is caused by leaky capillaries. The skin biopsy is sent to a laboratory for a pathological examination, where the biopsy is observed under a microscope. In addition to the skin biopsy, dermatologists will perform a dermatoscopy. With the results from the biopsy and from the dermatoscopy, a doctor will be able to identify that the skin lesions are in fact due Schamberg's disease. To ensure that the skin lesions are not caused by other skin conditions or infections, doctors will order a complete blood count (CBC) and other blood tests. Blood tests are usually normal and they are only performed to rule out other bleeding disorders that cause purpura. Since Schamberg's disease is usually asymptomatic, there is not a lot of other tests that can be performed. This condition is easy to diagnose because the appearance of skin lesions on the skin is the first indicator that the lesions are due to Schamberg's disease.

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.

A skin biopsy can be performed to test for EAC; tests should be performed to rule out other possible diseases such as: pityriasis rosea, tinea corporis, psoriasis, nummular eczema, atopic dermatitis, drug reaction, erythema migrans and other rashes.

In many children hydroa vacciniforme (HV) regresses spontaneously by early adulthood. In the 29 patients followed by Iwatuski et al., 11 of the 18 with definite or probable HV were available for follow-up and all were alive without progression of their symptoms. Some had recurrent eruptions of HV. In contrast out of 11 severe patients in this study, 6 had evidence of chronic EBV infection, 5 had hypersensitivity to mosquito bites, 4 had virus-associated hemophagocytic syndrome. 6 of the severe group had natural killer-cell lymphocytosis in the peripheral blood.

A full recovery is expected with treatment. Recurrent id reactions are frequently due to inadequate treatment of the primary infection or dermatitis and often the cause of recurrence is 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.

In all cases of suspected NEH, a skin biopsy should be performed, because the clinical symptoms are non specific, but the histopathological findings on the biopsy are specific. The biopsy shows characteristic changes of the eccrine glands, the major sweat glands of the body.

In NEH, eccrine gland necrosis, and neutrophils surroundings the eccrine glands, are typical findings on biopsy. If the chemotherapy has recently been administered, chemotherapy induced neutropenia may be present, and, as a result, the neutrophils may be absent. But the other characteristic finding, i.e. eccrine gland necrosis, can still be seen. A vacuolar interface dermatitis also is visible in glands and ducts, along with necrosis of the lining cells.

In addition, in patients receiving chemotherapy, keratinocyte atypia can be seen.

Immunoprecipitation, immunoblotting and enzyme-link immunosorbent assay (ELISA)

Poot et al. 2013 determined that immunoprecipitation for antibodies against envoplakin and periplakin or alpha2-macroglobulin-like–1 is the most sensitive test. However, alpha2-macroglobulin-like-1 can also be detected in patients with toxic epidermal necrosis.

Patients with high concentration of antibodies show intercellular, intraepidermal antibodies as well as along the dermoepidermal junction. Patients with low concentration of antibodies only present with them inside the cells (intercellular).

If the results are negative, perform the additional assays regardless. Cases have been confirmed that reported with initial negative DIF and IDIF tests.

Grover's may be suspected by its appearance, but since it has such a characteristic appearance under the microscope a shave skin or punch biopsy is often performed.

Dermatitis herpetiformis is often misdiagnosed, being confused with drug eruptions, contact dermatitis, dishydrotic eczema (dyshidrosis), and even scabies.

The diagnosis can be confirmed by a simple blood test for IgA antibodies against tissue transglutaminase (which cross-react with epidermal transglutaminase), and by a skin biopsy in which the pattern of IgA deposits in the dermal papillae, revealed by direct immunofluorescence, distinguishes it from linear IgA bullous dermatosis and other forms of dermatitis. These tests should be done before the patient starts on a gluten-free diet, otherwise they might produce false negatives. Like in ordinary celiac disease, IgA against transglutaminase disappears (often within months) when patients eliminate gluten from their diet. Thus, for both groups of patients, it may be necessary to restart gluten for several weeks before testing can be done reliably. In 2010, "Cutis" reported an eruption labelled "gluten-sensitive dermatitis" which is clinically indistinguishable from dermatitis herpetiformis but lacks the IgA connection, similar to gastrointestinal symptoms mimicking coeliac disease but without the diagnostic immunological markers.

There are many treatments available for dyshidrosis. However, few of them have been developed or tested specifically on the condition.

- Barriers to moisture and irritants, including barrier creams and gloves.

- Topical steroids - while useful, can be dangerous long-term due to the skin-thinning side-effects, which are particularly troublesome in the context of hand dyshidrosis, due to the amount of toxins and bacteria the hands typically come in contact with.

- Potassium permanganate dilute solution soaks - also popular, and used to 'dry out' the vesicles, and kill off superficial "Staphylococcus aureus", but it can also be very painful. Undiluted it may cause significant burning.

- Dapsone (diamino-diphenyl sulfone), an antibacterial, has been recommended for the treatment of dyshidrosis in some chronic cases.

- Antihistamines: Fexofenadine up to 180 mg per day.

- Alitretinoin (9-cis-retinoic acid) has been approved for prescription in the UK. It is specifically used for chronic hand and foot eczema. It is made by Basilea of Switzerland (BAL 4079).

- Systemic steroids can be taken orally to treat especially acute and severe cases of dyshidrosis.

Treatment is symptomatic.

Treatment does not require a doctor's attention unless the case is severe, with most affected using a topical anti-itch cream (diphenhydramine) and a cortisone solution (hydrocortisone). Do not scratch the area, and avoid any clothing that may irritate the affected area; scratching will result in localized swelling and intense itching.

Upon exiting the water, prompt removal of swim clothing (while it is still wet) followed by a warm sea-water shower largely negates the risk of Seabather's eruption even in endemic areas. A hot freshwater shower with soap (paying particular attention to the hair and areas covered by the suit) is a somewhat less-effective alternative if uncontaminated seawater is unavailable. The contaminated swimsuit should be machine washed with laundry soap and dried in warm air.

Animals can be affected as well, and a cortisone solution for humans can be used on dogs.

No treatment is usually needed as they usually go away anywhere from months to years. The lesions may last from anywhere between 4 weeks to 34 years with an average duration of 11 months. If caused by an underlying disease or malignancy, then treating and removing the disease or malignancy will stop the lesions. It usually doesn't require treatment, but topical corticosteroids may be helpful in reducing redness, swelling and itchiness.

Some supported and not supported methods of having an effect on EAC include:

- Photosensitive so it can be moved/reduced with appropriate sunlight.

- Vitamin D

- Immune system - hence it will increase in size/number when the immune system is low or overloaded.

- Hormone Drugs

- Disulone

- Stress reduction

- Topical calcipotriol - a topical vitamin D derivative has been known to be beneficial

Studies show a moderate neutrophilia (less than 50%), elevated ESR (greater than 30 mm/h) (90%), and a slight increase in alkaline phosphatase (83%). Skin biopsy shows a papillary and mid-dermal mixed infiltrate of polymorphonuclear leukocytes with nuclear fragmentation and histiocytic cells. The infiltrate is predominantly perivascular with endothelial-cell swelling in some vessels, but vasculitic changes (blood clots; deposition of fibrin, complement, or immunoglobulins within the vessel walls; red blood cell extravasation;inflammatory infiltration of vascular walls) are absent in early lesions.

Perivasculitis occurs secondarily, because of cytokines released by the lesional neutrophils. True transmural vasculitis is not an expected finding histopathologically in SS.

The clinical differential diagnosis includes pyoderma gangrenosum, infection, erythema multiforme, adverse drug reactions, and urticaria. Recurrences are common and affect up to one third of patients.

A single case report suggested that oral dapsone may be useful for prevention. However, the efficacy of oral dapsone as prevention has not been demonstrated very clearly until now.

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

Dermatitis herpetiformis generally responds well to medication and changes in diet. However, it is an autoimmune disease, and patients with DH are more likely than others to have thyroid problems and intestinal lymphoma.

Dermatitis herpetiformis does not usually cause complications on its own, without being associated with another condition. Complications from this condition, however, arise from the autoimmune character of the disease, as an overreacting immune system is a sign that something does not work well and might cause problems to other parts of the body that do not necessarily involve the digestive system.

Gluten intolerance and the body's reaction to it make the disease more worrying in what concerns the possible complications. This means that complications that may arise from dermatitis herpetiformis are the same as those resulting from coeliac disease, which include osteoporosis, certain kinds of gut cancer, and an increased risk of other autoimmune diseases such as thyroid disease.

The risks of developing complications from dermatitis herpetiformis decrease significantly if the affected individuals follow a gluten-free diet. The disease has been associated with autoimmune thyroid disease, insulin-dependent diabetes, lupus erythematosus, Sjögren's syndrome, sarcoidosis, vitiligo, and alopecia areata.