Often a diagnosis of exclusion, skin biopsy shows a neutrophillic inflammatory infiltrate.

Guttate psoriasis can typically be diagnosed by clinical examination alone. If necessary, a skin biopsy can be used to support the diagnosis.

A diagnosis of psoriasis is usually based on the appearance of the skin. Skin characteristics typical for psoriasis are scaly, erythematous plaques, papules, or patches of skin that may be painful and itch. No special blood tests or diagnostic procedures are usually required to make the diagnosis.

The differential diagnosis of psoriasis includes dermatological conditions similar in appearance such as discoid eczema, seborrhoeic eczema, pityriasis rosea (may be confused with guttate psoriasis), nail fungus (may be confused with nail psoriasis) or cutaneous T cell lymphoma (50% of individuals with this cancer are initially misdiagnosed with psoriasis). Dermatologic manifestations of systemic illnesses such as the rash of secondary syphilis may also be confused with psoriasis.

If the clinical diagnosis is uncertain, a skin biopsy or scraping may be performed to rule out other disorders and to confirm the diagnosis. Skin from a biopsy will show clubbed epidermal projections that interdigitate with dermis on microscopy. Epidermal thickening is another characteristic histologic finding of psoriasis lesions. The stratum granulosum layer of the epidermis is often missing or significantly decreased in psoriatic lesions; the skin cells from the most superficial layer of skin are also abnormal as they never fully mature. Unlike their mature counterparts, these superficial cells keep their nucleus. Inflammatory infiltrates can typically be visualized on microscopy when examining skin tissue or joint tissue affected by psoriasis. Epidermal skin tissue affected by psoriatic inflammation often has many CD8+ T cells while a predominance of CD4+ T cells makes up the inflammatory infiltrates of the dermal layer of skin and the joints.

There is no consensus about how to classify the severity of psoriasis. Mild psoriasis has been defined as a percentage of body surface area (BSA)≤10, a Psoriasis Area Severity Index (PASI) score ≤10, and a dermatology life quality index (DLQI) score ≤10. Moderate to severe psoriasis was defined by the same group as BSA >10 or PASI score >10 and a DLQI score >10. The DLQI is a 10 question tool used to measure the impact of several dermatologic diseases on daily functioning. The DLQI score ranges from 0 (minimal impairment) to 30 (maximal impairment) and is calculated with each answer being assigned 0–3 points with higher scores indicating greater social or occupational impairment.

The psoriasis area severity index (PASI) is the most widely used measurement tool for psoriasis. PASI assesses the severity of lesions and the area affected and combines these two factors into a single score from 0 (no disease) to 72 (maximal disease). Nevertheless, the PASI can be too unwieldy to use outside of research settings, which has led to attempts to simplify the index for clinical use.

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 diagnosis of SSSS is made clinically. This is sometimes confirmed by isolation of "S. aureus" from blood, mucous membranes, or skin biopsy; however, these are often negative. Skin biopsy may show separation of the superficial layer of the epidermis (intraepidermal separation), differentiating SSSS from TEN, wherein the separation occurs at the dermo-epidermal junction (subepidermal separation). SSSS may be difficult to distinguish from toxic epidermal necrolysis and pustular psoriasis.

Von Zumbusch observed a male patient, who had had classic psoriasis for several years, and who then went through recurrent episodes of bright [erythema] and [edema], which became studded with multiple pustules. Von Zumbusch observed this patient through nine hospital admissions over 10 years.

Treatments vary widely, and many different drugs have been documented as being successful. Some medications are successful in some patients, while unsuccessful in others. Below is a list of some medications used to treat GPP:

- Enbrel (Etanercept)

- Methotrexate

- PUVA

- Hydroxyurea

- Dapsone

- Systemic corticosteroids

- Cyclosporin A

- Adalimumab

- Etretinate

- Isotretinoin (Accutane)

- Acitretin (Neotigason)

The Nail Psoriasis Severity Index (NAPSI) is a numeric, reproducible, objective, simple tool for evaluation of nail psoriasis. It evaluates several signs separately, each on a 1–3 scale: pitting, Beau's lines, subungual hyperkeratosis and onycholysis. A 2005 study proposed a modified NAPSI scale for persons with psoriasis and named the title of their publication "Modification of the Nail Psoriasis Severity Index". Then, in 2007, a study found that there was a high level of inter-rater variability of the 2003 NAPSI scale and proposed another index which was, like the 2005 article, a modification of the 2003 article, and was named modified NAPSI.

A 2008 study found that Cannavo's qualitative system correlated with NAPSI (P<0.001) and is less time-consuming.

There is a risk of misdiagnosis with onychomycosis.

Eosinophilic folliculitis may be suspected clinically when an individual with HIV exhibits the classic symptoms. The diagnosis can be supported by the finding of eosinophilia but a skin biopsy is necessary to establish it. Skin biopsies reveal lymphocytic and eosinophilic inflammation around the hair follicles.

The causes of a rash are numerous, which may make the evaluation of a rash extremely difficult. An accurate evaluation by a provider may only be made in the context of a thorough history (What medication is the patient taking? What is the patient's occupation? Where has the patient been?) and complete physical examination.

Points to note in the examination include:

- The appearance: "e.g.", purpuric (typical of vasculitis and meningococcal disease), fine and like sandpaper (typical of scarlet fever); circular lesions with a central depression are typical of molluscum contagiosum (and in the past, small pox); plaques with silver scales are typical of psoriasis.

- The distribution: "e.g.", the rash of scarlet fever becomes confluent and forms bright red lines in the skin creases of the neck, armpits and groins (Pastia's lines); the vesicles of chicken pox seem to follow the hollows of the body (they are more prominent along the depression of the spine on the back and in the hollows of both shoulder blades); very few rashes affect the palms of the hands and soles of the feet (secondary syphilis, rickettsia or spotted fevers, guttate psoriasis, hand, foot and mouth disease, keratoderma blennorrhagicum);

- Symmetry: "e.g.", herpes zoster usually only affects one side of the body and does not cross the midline.

A patch test may be ordered, for diagnostic purposes.

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.

The classification of exfoliative dermatitis into Wilson-Brocq (chronic relapsing), Hebra or pityriasis rubra (progressive), and Savill (self-limited) types may have had historical value, but it currently lacks pathophysiologic or clinical utility.

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.

During diagnosis it is important to determine the type of hand eczema and plan specific treatment accordingly. An additional diagnosis of allergies will indicate whether contact allergies or atopy diathesis are the cause of the hand eczema. Discussion concerning frequency of contact with water, irritants, and allergens in private and professional environments will also help evaluate individual stresses on the patient's skin. The hands may also exhibit various other skin illnesses and potential fungal infection or psoriasis must be ruled out. Usually, taking the patient’s personal history into account will help provide an accurate diagnosis.

Patch testing has been found to be helpful in the diagnosis of hand eczema.

First-line therapy for disseminated or localized instances of pyoderma gangrenosum is systemic treatment by corticosteroids and ciclosporin. Topical application of clobetasol, mupirocin, and gentamicin alternated with tacrolimus can be effective.

Pyoderma gangrenosum ulcers demonstrate pathergy, that is, a worsening in response to minor trauma or surgical debridement. Significant care should be taken with dressing changes to prevent potentially rapid wound growth. Many patients respond differently to different types of treatment, for example some benefit from a moist environment, so treatment should be carefully evaluated at each stage.

Papules that begin as small "spouts" can be treated with Dakins Solution to prevent infection and wound clusters also benefit from this disinfectant. Wet to dry applications of Dakins can defeat spread of interior infection. Heavy drainage can be offset with Coban dressings. Grafting is not recommended due to tissue necrosis.

If ineffective, alternative therapeutic procedures include systemic treatment with corticosteroids and mycophenolate mofetil; mycophenolate mofetil and ciclosporin; tacrolimus; thalidomide; infliximab; or plasmapheresis.

There is currently a phase III trial for the use of the IL-1B modulating agent gevokizumab in treating the ulcers of pyoderma gangrenosum.

Puppies are first presented with what appears to be staphylococcal pyoderma. Definitive diagnosis requires cytologic and histopathologic evaluations. Cytologic examination of papulopustular lesions of juvenile cellulitis reveals pyogranulomatous inflammation with no microorganisms and carefully performed cultures are negative. Biopsies of early lesions reveal multiple discrete or confluent granulomas and pyogranulomas consisting of clusters of large epithelioid macrophages with variably sized cores of neutrophils. Cytological analysis of joint fluid often reveals sterile suppurative arthritis.

Guttate psoriasis accounts for approximately 2% of psoriasis cases.

Kogoj's spongiform pustules can be observed via histopathology to confirm acute GPP.

Available studies lack sufficient power to extrapolate a standardized therapeutic regimen.

As of April 2009, an assessment of the evidence for the efficacy and safety of the treatments for nail psoriasis is in progress.

- Infliximab appears to be the most effective treatment for nail psoriasis to date.

- Results from low-dose acitretin therapy show NAPSI score reductions comparable with those studies evaluating biologic drugs for nail psoriasis and suggest that low-dose systemic acitretin should be considered in the treatment of nail psoriasis.

You have to treat the primary cause or the exacerbation may persisist and reincide.

Topical steroids are the primary category of medications used to treat exfoliative dermatitis (ED). A sedative antihistamine may be a useful adjunct for pruritic patients, since it helps patients to sleep at night, thus limiting nocturnal scratching and excoriations. Antimicrobial agents often are used if an infection is suspected to be precipitating or complicating exfoliative dermatitis. Other drugs specifically indicated for management of underlying cause of exfoliative dermatitis may be necessary.

Eosinophilic folliculitis associated with HIV infection typically affects individuals with advanced HIV and low T helper cell counts. It affects both men and women as well as children with HIV and is found throughout the world.

EF may also affect individuals with hematologic disease such as leukemia and lymphoma. It may also affect otherwise normal infants in a self-limited form. HIV-negative individuals can also develop EF — this is more common in Japan.

The prognosis of SSSS in children is excellent, with complete resolution within 10 days of treatment, and without significant scarring. However, SSSS must be differentiated carefully from toxic epidermal necrolysis, which carries a poor prognosis. The prognosis in adults is generally much worse, and depends upon various factors such as time to treatment, host immunity, and comorbidities.

Acute GPP typically requires inpatient management including both topical and systemic therapy, and supportive measures. Systemic glucocorticoid withdrawal is a common causative agent. Withdrawal or administration of certain drugs in the patient's previous medication regimen may be required. Oral retinoids are the most effective treatment, and are considered first line. Cyclosporine or infliximab may be required for particularly acute cases.

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