Sweating causes lesions to form, but lesions aggravated by sweat usually return to "normal" fairly quicklyavoiding sweat is not a reason to avoid exercise. Minor outbreaks can be controlled with prescription strength topical cortisone creams. More severe eruptions usually clear up after treatment for one to three months with Accutane or tetracycline. If these fail or the outbreak is severe, PUVA phototherapy treatments, antifungal pills and cortisone injections are alternatives.

Some research has suggested a correlation of Grover's disease with mercury toxicity in which case Dimercaptosuccinic acid might help.

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.

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.

There is no standard treatment for PLC. Treatments may include ultraviolet phototherapy, topical steroids, sun exposure, oral antibiotics, corticosteroid creams and ointments to treat rash and itching.

One study identified the enzyme bromelain as an effective therapeutic option for PLC.

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.

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.

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.

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.

Treatment is predominantly preventive. Avoidance of topical phenols and diets low in tyrosine may help. Replacement and repair of damaged tissue is also possible.

DPN lesions are benign and no treatment generally is indicated unless lesions are cosmetically undesirable. Surgical options including curettage, cryotherapy and laser therapy are options Scarring, postoperative skin discoloration or keloid formation are potential complication. Therefore, conservative dpn treatment is advisable.

Antibiotic creams are the preferred treatment for mild cases of impetigo, despite their limited systemic absorption. Such prescribed ointments include neosporin, fusidic acid, chloramphenicol and mupirocin. More severe cases of impetigo however (especially bullous impetigo) will likely require oral agents with better systemic bioavailability, such as cephalexin. Cases that do not resolve with initial antibiotic therapy or require hospitalization may also be indicative an MRSA infection, which would require the use of agents specifically able to treat it, such as clindamycin.

Antibiotic treatment typically last 7–10 days, and although highly effective some cases of methicillin resistant S. aureus (MRSA) may require longer therapy depending on the severity of infection and how much it has spread.

It is self limiting condition

1.reassurence

2.steriod cream for local application

3.moisterizer lotion

The most accepted way to treat PG is with the use of corticosteroids, i.e. prednisone; and/or topical steroids, i.e. clobetasol and betamethasone. Suppressing the immune system with corticosteroids helps by decreasing the number of antibodies attacking the skin. Treating PG can be difficult and can take several months. Some cases of PG persist for many years. In the" post partum" period, if necessary, the full range of immunosuppressive treatment may be administered for cases unresponsive to corticosteroid treatments, such as tetracyclines, nicotinamide, cyclophosphamide, ciclosporin, goserelin, azathioprine, dapsone, rituximumab, or plasmaphoresis, or intravenous immunoglobulin may sometimes be considered when the symptoms are severe.

There is no cure for PG. Women who have PG are considered in remission if they are no longer blistering. Remission can last indefinitely, or until a subsequent pregnancy. PG usually occurs in subsequent pregnancies; however, it often seems more manageable because it is anticipated.

Since the common pathogens involved with impetigo are bacteria naturally found on the skin, most prevention (especially in children), is targeted towards appropriate hygiene, wound cleaning, and minimizing scratching (i.e. by keeping nails trimmed and short). Avoiding close contact and sharing of items such as towels with potentially infected individuals is also recommended.

No treatment of seborrheic keratoses is necessary, except for aesthetic reasons. Since a slightly increased risk of localized infection caused by picking at the lesion has been described, if a lesion becomes itchy or irritated by clothing or jewelry, a surgical excision is generally recommended.

Small lesions can be treated with light electrocautery. Larger lesions can be treated with electrodesiccation and curettage, shave excision, or cryosurgery. When correctly performed, removal of seborrheic keratoses will not cause much visible scarring except in persons with dark skin tones.

Systemic corticosteroids such as (prednisone) can produce rapid improvement and are the “gold standard” for treatment. The temperature, white blood cell count, and eruption improve within 72 hours. The skin lesions clear within 3 to 9 days. Abnormal laboratory values rapidly return to normal. There are, however, frequent recurrences. Corticosteroids are tapered within 2 to 6 weeks to zero.

Resolution of the eruption is occasionally followed by milia and scarring. The disease clears spontaneously in some patients. Topical and/or intralesional corticosteroids may be effective as either monotherapy or adjuvant therapy.

Oral potassium iodide or colchicine may induce rapid resolution.

Patients who have a potential systemic infection or in whom corticosteroids are contraindicated can use these agents as a first-line therapy.

In one study, indomethacin, 150 mg per day, was given for the first week, and 100 mg per day was given for 2 additional weeks. Seventeen of 18 patients had a good initial response; fever and arthralgias were markedly attenuated within 48 hours, and eruptions cleared between 7 and 14 days.

Patients whose cutaneous lesions continued to develop were successfully treated with prednisone (1 mg/kg per day). No patient had a relapse after discontinuation of indomethacin.

Other alternatives to corticosteroid treatment include dapsone, doxycycline, clofazimine, and cyclosporine. All of these drugs influence migration and other functions of neutrophils.

There are no specific treatments for this problem, other than using ice or numbing medicines to ease the pain.

What happens after your child is diagnosed with CRMO/CNO?

Find a doctor who has experience with patients with CRMO/CNO. CRMO/CNO in children is generally treated by a pediatric rheumatologist. Ask your doctor for a referral.

Why do we treat CRMO/CNO?

- Reduce inflammation

- Prevent bone damage and bone deformities

- Decrease pain

How is CRMO/CNO treated?

CRMO/CNO is different for each patient. Not every child responds to every treatment. Your doctor may need to try several medications before finding the one that works for your child. In severe cases, doctors may combine medications to treat the disease. Your doctor will work with you and your child to help find the best treatment.

For some CRMO/CNO patients, the disease can be managed with non-steroidal anti-inflammatory drugs (NSAIDs). NSAIDs are the first line treatment. However, if NSAIDs are not effective, or if your child does not tolerate NSAIDs well, second line treatments are available.

First line treatments include Naproxen (Aleve), Celecoxib (Celebrex) Meloxicam (Mobic), Piroxicam (Feldene), Indomethacin (Indocin), Diclofenac (Voltaren).

Second line treatments include corticosteroids (Prednisone/Prednisolone), Methotrexate (Otrexup, Rasuvo, Trexall), Sulfasalazine (Azulfidine), Pamidronate (Aredia), Zolendronic Acid (Zometa), Adalimumab (Humira), Etanercept (Enbrel), Infliximab (Remicade).

These medications are also used in children with other inflammatory and/or bone conditions. Side effects may occur while taking these medications. Your physician will have a discussion with you prior to starting any new treatment.

Grover's disease (GD) is a polymorphic, pruritic, papulovesicular dermatosis characterized histologically by acantholysis with or without dyskeratosis. Once confirmed, most cases of Grover's disease last six to twelve months, which is why it was originally called "transient". However it may last much longer. Nevertheless, it is not to be confused with relapsing linear acantholytic dermatosis.

DPN is not a premalignant condition nor is it associated with any underlying systemic disease. DPN lesions show no tendency to regress spontaneously, and often increase in size and number as an individual ages.

Mycosis fungoides can be treated in a variety of ways. Common treatments include simple sunlight, ultraviolet light (mainly NB-UVB 312 nm), topical steroids, topical and systemic chemotherapies, local superficial radiotherapy, the histone deacetylase inhibitor vorinostat, total skin electron radiation, photopheresis and systemic therapies (e.g. interferons, retinoids, rexinoids) or biological therapies. Treatments are often used in combination.

In the “Stanford technique” of Total skin electron therapy the patient stands about 10 meters from a radiation source, with a large acrylic sheet in between to scatter the electrons across a broad area. Then the patient carefully assumes six different positions. In severe cases that progress to Sézary disease

Stanford University has been pioneering low-dose radiation (1/3 of the standard), followed by stem-cell transplantation without chemo, as a potential cure with promising results.

In 2010, the U.S. Food and Drug Administration granted orphan drug designation for naloxone lotion, a topical opioid receptor competitive antagonist used as a treatment for pruritus in cutaneous T-cell lymphoma.

Erythema dyschromicum perstans (EDP) (also known as ashy dermatosis, and dermatosis cinecienta) is an uncommon skin condition with peak age of onset being young adults, but it may also be seen in children or adults of any age. EDP is characterized by hyperpigmented macules that are ash-grey in color and may vary in size and shape. While agents such as certain medications, radiographic contrast, pesticides, infection with parasites, and HIV have been implicated in the occurrence of this disease, the cause of this skin disease remains unknown.

EDP initially presents as grey or blue-brown circumferential or irregularly shaped macules or patches that appear. While the lesions of EDP are generally non-elevated, they may initially have a slight raised red margin as they first begin to appear. These lesions usually arise in a symmetric distribution and involve the trunk, but also commonly spread to the face and extremities. EDP does not usually have symptoms beside the macules and patches of discolored skin; however, some itching in these areas may occur.

Because EDP is an uncommon disease of the skin, it is important to consider other skin diseases that may resemble erythema dyschromicum perstans, such as infectious diseases (i.e. leprosy or pinta), reaction to drugs, post inflammatory hyperpigmentation, or lichen planus pigmentosus.

There is no cure for EDP. While multiple various topical and systemic therapies have been tried, none have been consistently successful. In children, spontaneous resolution of EDP over the course of months to years is possible; however, this outcome is less likely if EDP presents in adulthood.

Hydroquinone-induced exogenous ochronosis is an avoidable dermatosis that is exceedingly difficult to treat.

However, some studies show that treatment may be possible with a Q-switched alexandrite (755 nm) laser.

It is recommended that individuals with this disorder stop using hydroquinone-containing compounds. It is important to be aware of this as dermatologists may think the symptoms a patient is exhibiting are a melasma, and prescribe a hydroquinone-containing cream.

Linear IgA bullous dermatosis is frequently associated with medication exposure, especially vancomycin, with men and women being equally affected. It was first described by Tadeusz Chorzelski in 1979. Linear IgA dermatosis is a rare immune-mediated blistering skin disease that may be divided into two types:

- "Adult linear IgA disease" is an acquired, autoimmune blistering disease that may present with a clinical pattern of vesicles indistinguishable from dermatitis herpetiformis, or with vesicles and bullae in a bullous pemphigoid-like appearance. This disease can often be difficult to treat even with usually effective medications such as rituximab.

- "Childhood linear IgA disease" (also known as "Chronic bullous disease of childhood") is an acquired, self-limited bullous disease that may begin by the time the patient is age 2 to 3 and usually remits by age 13.

Many other conditions can lead to localized scaling or hyperpigmentation.

This condition should firmly be distinguished from dermatitis artefacta, which is the "factitious" creation of a skin lesion, whereas dermatosis neglecta results from unconscious avoidance of cleaning due to pain or immobility.

Other skin conditions which should not be mistaken for dermatosis neglecta include: terra firma-forme dermatosis (in which there is no history of inadequate cleaning); confluent and reticulated papillomatosis of Gougerot and Carteaud; several forms of ichthyosis; acanthosis nigricans; and Vagabond's disease.