Diagnosis is based on visual examination and the presence of itching. A skin biopsy is often performed to exclude other diseases. Lesion biopsies will typically show a high level of eosinophils in PN. A culture of at least one lesion will rule out staphylococcus infection, which has been significantly linked to atopic dermatitis.

Lichen planus has a unique microscopic appearance that is similar between cutaneous, mucosal and oral. A Periodic acid-Schiff stain of the biopsy may be used to visualise the specimen. Histological features seen include:

- thickening of the stratum corneum both with nuclei present (parakeratosis) and without (orthokeratosis). Parakeratosis is more common in oral variants of lichen planus.

- thickening of the stratum granulosum

- thickening of the stratum spinosum (acanthosis) with formation of colloid bodies (also known as Civatte bodies, Sabouraud bodies) that may stretch down to the lamina propria.

- liquefactive degeneration of the stratum basale, with separation from the underlying lamina propria, as a result of desmosome loss, creating small spaces (Max Joseph spaces).

- Infiltration of T cells in a band-like pattern into the dermis "hugging" the basal layer.

- Development of a "saw-tooth" appearance of the rete pegs, which is much more common in non-oral forms of lichen planus.

The differential diagnosis for OLP includes:

- Other oral vesiculo-ulcerative conditions such as Pemphigus vulgaris and Benign mucous membrane pemphigoid

- Lupus erythematosus, with lesions more commonly occur on the palate and appear as centrally ulcerated or erythematous with radiating white striae. In contrast, OLP and lichenoid reactions rarely occur on the palate, and the striae are randomly arranged rather than radial.

- Chronic ulcerative stomatitis

- Frictional keratosis and Morsicatio buccarum (chronic cheek biting)

- Oral leukoplakia

- Oral candidiasis

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.

Bullous Pemphigoid, Cicatricial Pemphigoid, Drug Eruptions. Epidermolysis Bullosa, Epidermolysis Bullosa Acquisita, Erythema Multiforme, Lichen Planus, pemphigus vulgaris, Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis.

PNP is most commonly mistaken for pemphigus vulgaris, due to the extreme similarities of the lesions that develop. However, the difference lies in the specificity of the autoreactive antibodies in each case.

The disease often goes undiagnosed for several years, as it is sometimes not recognized and misdiagnosed as thrush or other problems and not correctly diagnosed until the patient is referred to a specialist when the problem does not clear up.

A biopsy of the affected skin can be done to confirm diagnosis. When a biopsy is done, hyperkeratosis, atrophic epidermis, sclerosis of dermis and lymphocyte activity in dermis are histological findings associated with LS. The biopsies are also checked for signs of dysplasia.

It has been noted that clinical diagnosis of LS can be "almost unmistakable" and therefore a biopsy may not be necessary.

There is no effective treatment for this condition. It has been reported that clearance of lesions can be done with melphalan and cyclophosphamide alone or in combination with prednisone. Both isotretinoin and etretinate have also been shown to improve the conditions. All medications listed can cause adverse symptoms, with isotretinoin and etretinate particularly dangerous since they are both teratogens. Other attempted treatments include interferon-alpha, cyclosporine, PUVA photochemotherapy, electron-beam therapy, IVIg, and dermabrasion. However, the overall prognosis for the disease is poor. There are reported instances of remission of the disease when treated with a combination of Revlimid and Dexamethasone over a 24-month period.

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.

Prurigo nodularis is very hard to treat, but current therapies include steroids, vitamins, cryosurgery, thalidomide and UVB light. In the event that staphylococcus or other infection is present, antibiotics have proven effective, but tend to cause more harm than good for this particular disease.

A physician may administer a strong dose of prednisone, which will almost immediately stop the itch/scratch cycle. However, cessation of steroids allows relapse to occur, usually within a few weeks. Horiuchi "et al" recently reported significant improvement in PN with antibiotic therapy.

Another drug a physician may administer is Apo-Azathioprine. Azathioprine, also known by its brand name Imuran, is an immunosuppressive drug used in organ transplantation and autoimmune diseases and belongs to the chemical class of purine analogues.

For the diagnosis of lupus 4 out of 11 signs must be present.

Testing may include:

- Antinuclear antibody (ANA)

- CBC with differential

- Chest x-ray

- Serum creatinine

- Urinalysis

Scleroderma in pregnancy is a complex situation; it increases the risk to both mother and child. Overall scleroderma is associated with reduced fetal weight for gestational age. The treatment for scleroderma often includes known teratogens such as cyclophosphamide, methotrexate, mycophenolate, etc. and hence careful avoidance of such drugs during pregnancy is advised. In these cases hydroxychloroquine and low-dose corticosteroids might be used for disease control.

Verrucous lupus erythematosus (also known as "Hypertrophic lupus erythematosus") presents with non-pruritic papulonodular lesions on the arms and hands, resembling keratoacanthoma or hypertropic lichen planus.

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.

Papular mucinosis affects adults of both sexes equally and appears between ages 30 and 80. Recently, it has been reported in patients infected with the HIV/AIDS virus.

Typical scleroderma is classically defined as symmetrical skin thickening, with about 70% of cases also presenting with Raynaud's phenomenon, nail-fold capillary changes and antinuclear antibodies. Affected individuals may or may not experience systemic organ involvement. There is no single test for scleroderma that works all of the time and hence the diagnosis is often a matter of exclusion. Atypical scleroderma may show any variation of these changes without skin changes or with finger swelling only.

Laboratory testing can show antitopoisomerase antibodies, like anti-scl70 (causing a diffuse systemic form), or anticentromere antibodies (causing a limited systemic form and the CREST syndrome). Other autoantibodies can be seen, such as anti-U3 or anti-RNA polymerase.

Lupus erythematosus may manifest as systemic disease or in a purely cutaneous form also known as "incomplete lupus erythematosus". Lupus has four main types:

- systemic

- discoid

- drug-induced

- neonatal

Of these, systemic lupus erythematosus (also known as SLE) is the most common and serious form.

A more thorough categorization of lupus includes the following types:

- acute cutaneous lupus erythematosus

- subacute cutaneous lupus erythematosus

- discoid lupus erythematosus (chronic cutaneous)

- childhood discoid lupus erythematosus

- generalized discoid lupus erythematosus

- localized discoid lupus erythematosus

- chilblain lupus erythematosus (Hutchinson)

- lupus erythematosus-lichen planus overlap syndrome

- lupus erythematosus panniculitis (lupus erythematosus profundus)

- tumid lupus erythematosus

- verrucous lupus erythematosus (hypertrophic lupus erythematosus)

- cutaneous lupus mucinosis

- complement deficiency syndromes

- drug-induced lupus erythematosus

- neonatal lupus erythematosus

- systemic lupus erythematosus

LSC is typically diagnosed by careful observation and history taking. It is easily recognized (see "signs and symptoms", and "gallery"). Biopsies are not necessary, and cannot be used to distinguish LSC from psoriasis.

Generally, lichen nitidus is asymptomatic and self-limited; therefore, no treatment is required. However, if persistent pruritus is present, or the appearance “...interferes with daily activities or outlook...” topical glucocorticoids may be tried. If the disease process is symptomatic, generalized and extensive, oral glucocorticoids may be indicated. Other reported treatments include PUVA, UVA/UVB phototherapy, astemizole, acitretin, and etretinate.

When appears with sun/humidity; air conditioning (cool dry air) reduces swelling and discomfort.

The disease can last for a considerably long time. Occasionally, "spontaneous cure" may ensue, particularly in young girls.

Lichen sclerosus is associated with a higher risk of cancer. Skin that has been scarred as a result of lichen sclerosus is more likely to develop skin cancer. Women with lichen sclerosus may develop vulvar carcinoma. Lichen sclerosus is associated with 3–7% of all cases of vulvar squamous cell carcinoma. In women, it has been reported that 33.6 times higher vulvar cancer risk is associated with LS. A study in men reported that "The reported incidence of penile carcinoma in patients with BXO is 2.6–5.8%".

The diagnosis is confirmed by a skin biopsy and a positive culture for acid-fast bacilli. A PPD test may also result positive.

The term pustular psoriasis is used for a heterogeneous group of diseases that share pustular skin characteristics.

Nodular lichen myxedematosus is a cutaneous condition characterized by multiple nodules on the limbs and trunk, with a mild or absent papular component.

The differential diagnoses are: acrodermatitis enteropathica, erythema infectiosum, erythema multiforme, hand-foot-and-mouth disease, Henoch–Schönlein purpura, Kawasaki disease, lichen planus, papular urticaria, papular purpuric gloves and socks syndrome, and scabies.

Pustular psoriasis is classified into two major forms: localized and generalized pustular psoriasis. Within these two categories there are several variants:

The histology of lichen nitidus is significant for a "...localized granulomatous lymphohistiocytic infiltrate in an expanded dermal papilla with thinning of overlying epidermis and downward extension of the ridges at the lateral margin of the infiltrate, producing a typical 'claw clutching a ball' picture..."