If not treated, pemphigus can be fatal, usually from overwhelming opportunistic infection of lesions. The most common treatment is the administration of oral steroids, especially prednisone, often in high doses. The side effects of corticosteroids may require the use of so-called steroid-sparing or adjuvant drugs. One of the most dangerous side effects of high dosage steroid treatments is intestinal perforations, which may lead to sepsis. Steroids and other medications being taken to treat Pemphigus may also mask the effects of the perforations. Patients on high dosages of oral steroids should closely monitor their GI health. As lesions are usually terribly painful, it is likely that pain medication can complicate and exacerbate the GI issues caused by steroids.

All of these drugs may cause severe side effects, so the patient should be closely monitored by doctors. Once the outbreaks are under control, dosage is often reduced, to lessen side effects.

If skin lesions do become infected, antibiotics may be prescribed. Tetracycline antibiotics have a mildly beneficial effect on the disease and are sometimes enough for Pemphigus Foliaceus. In addition, talcum powder is helpful to prevent oozing sores from adhering to bedsheets and clothes. Wound care and treatment is often akin to that used in burn units, including careful use of dressings that don't stick to the wounds, etc.

If paraneoplastic pemphigus is diagnosed with pulmonary disease, a powerful cocktail of immune suppressant drugs is sometimes used in an attempt to halt the rapid progression of bronchiolitis obliterans, including methylprednisolone, ciclosporin, azathioprine, and thalidomide. Plasmapheresis may also be useful.

Corticosteroids and other immunosuppressive medications have historically been employed to reduce pemphigus symptoms, yet steroids are associated with serious and long-lasting side effects and their use should be limited as much as possible. Intravenous immunoglobulin, mycophenolate mofetil, methotrexate, azathioprine, and cyclophosphamide have also been used with varying degrees of success.

An established alternative to steroids are monoclonal antibodies such as rituximab, which are increasingly being used as first-line treatment. In numerous case series, many patients achieve remission after one cycle of rituximab. Treatment is more successful if initiated early on in the course of disease, perhaps even at diagnosis. Rituximab treatment combined with monthly IV immunoglobulin infusions has resulted in long-term remission with no recurrence of disease in 10 years after treatment was halted. This was a small trial study of 11 patients with 10 patients followed to completion.

Research into using genetically modified T-cells to treat pemphigus vulgaris in mice was reported in 2016. Rituximab indiscriminately attacks all B cells, which reduces the body's ability to control infections. In the experimental treatment, human T cells are genetically engineered to recognize only those B cells that produce antibodies to desmoglein 3.

Topical and intralesional (injected into the affected areas) corticosteroid drugs may be used, such as fluocinonide, clobetasol propionate or triamcinolone acetonide. Oral candidiasis may develop with long term topical steroid use, and sometimes antimycotics such as miconazole gel or chlorhexidine mouthwash are used to prevent this. Topical ciclosporin is sometimes used.

Dapsone is sometimes used as a steroid sparing agent. The dose is often increased very slowly in order to minimize side effects. Systemic steroids, such as prednisone or prednisolone may be needed in severe cases. Many other drugs have been used to treat mucous membrane pemphoid, including azathioprine, cyclophosphamide, methotrexate, thalidomide, mycophenolate mofetil, leflunomide, sulphasalazine, sulphapuridine, sulphamethoxypiridazine, tetracyclines (e.g. minocycline, doxycycline) and nicotinamide.

Many different treatments have been reported for cutaneous lichen planus, however there is a general lack of evidence of efficacy for any treatment. Treatments tend to be prolonged, partially effective and disappointing. The mainstay of localized skin lesions is topical steroids. Additional treatments include retinoids, such as acitretin, or sulfasalazine. Narrow band UVB phototherapy or systemic PUVA therapy are known treatment modalities for generalized disease.

Treatments include class I topical steroids (clobetasol, halobetasol, etc.) which in some studies have proven to be equally effective as systemic, or pill, therapy and somewhat safer. However, in difficult-to-manage or widespread cases, systemic prednisone and powerful steroid-free immunosuppressant medications, such as methotrexate, azathioprine or mycophenolate mofetil, may be appropriate. Antibiotics such as tetracycline or erythromycin may also control the disease, particularly in patients who cannot use corticosteroids. The anti-CD20 monoclonal antibody rituximab has been found to be effective in treating some otherwise refractory cases of bullous pemphigoid.

IgA-mediated pemphigoid can often be difficult to treat even with usually effective medications such as rituximab.

Plasmapheresis appears to help some cases. Sometimes surgical procedures are required to repair scars, prevent complications such as blindness, upper airway stenosis or esophageal stricture.

Reassurance that the condition is benign, elimination of precipitating factors and improving oral hygiene are considered initial management for symptomatic OLP, and these measures are reported to be useful. Treatment usually involves topical corticosteroids (such as betamethasone, clobetasol, dexamethasone, and triamcinolone) and analgesics, or if these are ineffective and the condition is severe, the systemic corticosteroids may be used. Calcineurin inhibitors (such as pimecrolimus, tacrolimus or cyclosporin) are sometimes used.

Keratosis pilaris is medically harmless, but many individuals may seek treatment as the condition can cause emotional distress. Topical creams and lotions are currently the most commonly used treatment for keratosis pilaris, specifically those consisting of moisturizing or keratolytic treatments, including urea, lactic acid, glycolic acid, salicylic acid, vitamin D, or topical retinoids such as tretinoin. Corticosteroid creams can also be used as a treatment for KP. Improvement of the skin often takes months and the bumps are likely to return. Limiting time in the shower and using gentle exfoliation to unplug pores can help. Many products are available that apply exfoliation and alpha or beta hydroxy acids.

Some cases of keratosis pilaris have been successfully treated with laser therapy, which involves passing intense bursts of light into targeted areas of the skin. Depending on the body's response to the treatment, multiple sessions over the course of a few months may be necessary.

Azathioprine is a steroid-sparing agent used in combination with Prednisone. It functions by inhibiting RNA and DNA synthesis.

Ciclosporin is an immunosuppressive agent most often used in organ transplantation that has demonstrated to be effective with skin disorders. It functions by lessening production of autoantibodies and therefore diminishing the development of blisters and erosions. The mechanism of action is by inhibiting the production of T lymphocytes and lymphokines.

Topical steroid preparations often help outbreaks; use of the weakest corticosteroid that is effective is recommended to help prevent thinning of the skin. Drugs such as antibiotics, antifungals, corticosteroids, dapsone, methotrexate, thalidomide, etretinate, cyclosporine and, most recently, intramuscular alefacept may control the disease but are ineffective for severe chronic or relapsing forms of the disease. Intracutaneous injections of botulinum toxin to inhibit perspiration may be of benefit. Maintaining a healthy weight, avoiding heat and friction of affected areas, and keeping the area clean and dry may help prevent flares.

Some have found relief in laser resurfacing that burns off the top layer of the epidermis, allowing healthy non-affected skin to regrow in its place.

Secondary bacterial, fungal and/or viral infections are common and may exacerbate an outbreak. Some people have found that outbreaks are triggered by certain foods, hormone cycles and stress.

In a few cases naltrexone appears to help.

Even though there is no way to cure the disease itself, there are ways to dampen the symptoms. These include medical help in form of pills, and using heavy lotions and oils.

To maintain the good health of the skin after the symptoms have dampened the person with the disease are advised to go on normally with their lives but to take precautions while showering. This is to take shorter, colder baths than usual to not stress the skin. It is also known to help to use bar-soap, instead of a liquid body wash.

The mainstay of treatment for SSSS is supportive care along with eradication of the primary infection. Conservative measures include rehydration, antipyretics (e.g., ibuprofen, aspirin, and paracetamol), management of thermal burns, and stabilization. Parenteral antibiotics to cover "S. aureus" should be administered. Most strains of "S. aureus" implicated in SSSS have penicillinases, and are therefore penicillin resistant. Therefore, treatment with Nafcillin, oxacillin, or vancomycin is typically indicated. Clindamycin is sometimes also used because of its inhibition of exotoxins.

Pemphigoid is usually considered to be mediated by IgG, but IgA-mediated forms have also been described.

IgA-mediated immunobullous diseases can often be difficult to treat even with usually effective medications such as rituximab.

A dermatologist or general physician usually administers combination therapy of drugs used for tuberculosis, such as Rifampicin, Isoniazid and Pyrazinamide (possibly with either streptomycin or ethambutol).

There are a wide range of depigmenting treatments used for hyperpigmentation conditions, and responses to most are variable.

Most often treatment of hyperpigmentation caused by melanin overproduction (such as melasma, acne scarring, liver spots) includes the use of topical depigmenting agents, which vary in their efficacy and safety, as well as in prescription rules. Several are prescription only in the US, especially in high doses, such as hydroquinone, azelaic acid, and koijic acid. Some are available without prescription, such as niacinamide, or cysteamine hydrochloride. Hydroquinone was the most commonly prescribed hyperpigmentation treatment before the long-term safety concerns were raised, and the use of it became more regulated in several countries and discouraged in general by WHO. For the US only 2% is at present sold over-the-counter, and 4% needs prescription. In the EU hydroquinone was banned from cosmetic applications. Treatments that do not involve topical agents are also available, including fraction lasers and dermabrasion.

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.

When no pus is present, warm soaks for acute paronychia is reasonable, even though there is a lack of evidence to support its use. Antibiotics such as clindamycin or cephalexin are also often used, the first being more effective in areas where MRSA is common. If there are signs of an abscess (the presence of pus) drainage is recommended.

Chronic paronychia is treated by avoiding whatever is causing it, a topical antifungal, and a topical steroid. In those who do not improve following these measures oral antifungals and steroids may be used or the nail fold may be removed surgically.

Commonly used dietary supplements include:

- Omega-6 fatty acids (e.g., safflower or sunflower oil)

- Omega-3 fatty acids (e.g., fish oils)

- Vitamin A.

Immunosuppressant and anti-inflammatory therapy serves to stop on-going destruction of the sebaceous glands. Like other inflammatory diseases, most animals receive an initial course to stop the inflammation and treatment is tapered off to the lowest dose that keeps the disease in remission. Oral cyclosporine may be used. Corticosteroids (e.g. prednisone) are used only if pruritus is a major clinical feature.

Bullous pemphigoid may be self-resolving in a period ranging from several months to many years even without treatment. Poor general health related to old age is associated with a poorer prognosis.

As with all types of ichthyosis, there is no cure but the symptoms can be relieved.

- Moisturizers

- Prevention of overheating

- Eye drops (to prevent the eyes from becoming dried out)

- Systemic Retinoids (isotretinoin and acitretin are very effective, but careful monitoring for toxicity is required. Only severe cases may require intermittent therapy.)

Psychological therapy or support may be required as well.

Severe acne usually indicates the necessity of prescription medication to treat the pimples. Prescription medications used to treat acne and pimples include isotretinoin, which is a retinoid. Historically, antibiotics such as tetracyclines and erythromycin were prescribed. While they were more effective than topical applications of benzoyl peroxide, the bacteria eventually grew resistant to the antibiotics and the treatments became less and less effective. Also, antibiotics had more side effects than topical applications, such as stomach cramps and severe discoloration of teeth. Common antibiotics prescribed by dermatologists include doxycycline and minocycline. For more severe cases of acne dermatologists might recommend accutane, a retinoid that is the most potent of acne treatments. However, accutane can cause various side effects including vomiting, diarrhea, and birth defects if taken during pregnancy.