It is not contagious and currently there is no cure for the disease, although the lesions can be treated with ultraviolet therapy as well as topical steroids and antibiotics.

Treatment often involves multiple therapies that address the immune system and bacterial, viral, or dermatological causes.

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.

The condition usually resolves on its own, and treatment is not required. Oral antihistamines or topical steroids may be used to decrease itching. Steroids do provide relief from itching, and improve the appearance of the rash, but they also cause the new skin that forms (after the rash subsides) to take longer to match the surrounding skin color. While no scarring has been found to be associated with the rash, scratching should be avoided. It's possible that scratching can make itching worse and an itch-scratch cycle may develop with regular scratching (that is, you itch more because you scratch, so you scratch more because you itch, and so on). Irritants such as soaps with fragrances, hot water, wool, and synthetic fabrics should be avoided. Lotions that help stop or prevent itching may also be helpful.

Direct sunlight makes the lesions resolve more quickly. According to this principle, medical treatment with ultraviolet light has been used to hasten resolution, though studies disagree whether it decreases itching or not. UV therapy is most beneficial in the first week of the eruption.

Oral erythromycin was effective in treating patients in one early trial, but a later study could not confirm these results. Since Human Herpes Virus 6 or Human Herpes Virus 7 has been hypothesized to be the cause, the antiviral drug Acyclovir may reduce length of duration and severity.

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

Usually, a common form of treatment for the condition is a type of hand cream which moisturises the hard skin. However, currently the condition is incurable.

No curative treatment against EV has been found yet. Several treatments have been suggested, and acitretin 0.5–1 mg/day for 6 months’ duration is the most effective treatment owing to antiproliferative and differentiation-inducing effects.

Interferons can also be used effectively together with retinoids.

Cimetidine was reported to be effective because of its depressing mitogen-induced lymphocyte proliferation and regulatory T cell activity features. A report by Oliveira "et al." showed that cimetidine was ineffective. Hayashi "et al." applied topical calcipotriol to a patient with a successful result.

As mentioned, various treatment methods are offered against EV; however, most importantly, education of the patient, early diagnosis, and excision of the tumoral lesions take preference to prevent the development of cutaneous tumors.

No treatment is required and the patches in time will settle.

The redness, scale and itch if present may be managed with simple emollients and sometimes hydrocortisone, a weak steroid, is also used.

As the patches of pityriasis alba do not darken normally in sunlight, effective sun protection helps minimise the discrepancy in colouration against the surrounding normal skin. Cosmetic camouflage may be required.

Tacrolimus has been reported as speeding resolution.

In exceptionally severe cases PUVA therapy may be considered.

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.

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.

Treatments for tinea versicolor include:

- Topical antifungal medications containing selenium sulfide are often recommended. Ketoconazole (Nizoral ointment and shampoo) is another treatment. It is normally applied to dry skin and washed off after 10 minutes, repeated daily for two weeks. Ciclopirox (Ciclopirox olamine) is an alternative treatment to ketoconazole, as it suppresses growth of the yeast "Malassezia furfur". Initial results show similar efficacy to ketoconazole with a relative increase in subjective symptom relief due to its inherent anti-inflammatory properties. Other topical antifungal agents such as clotrimazole, miconazole, terbinafine, or zinc pyrithione can lessen symptoms in some patients. Additionally, hydrogen peroxide has been known to lessen symptoms and, on certain occasions, remove the problem, although permanent scarring has occurred with this treatment in some sufferers. Clotrimazole is also used combined with selenium sulfide.

- Oral antifungals including ketoconazole or fluconazole in a single dose, or ketoconazole for seven days, or itraconazole can be used. The single-dose regimens, or pulse therapy regimens, can be made more effective by having the patient exercise 1–2 hours after the dose, to induce sweating. The sweat is allowed to evaporate, and showering is delayed for a day, leaving a film of the medication on the skin.

The most common method of treatment includes radiotherapy and/or surgical excision .

Treatment consists of topical application of dandruff shampoo, which contains selenium sulfide, over the skin. Topical antifungal imidazoles may also be used, such as ketoconazole. This is the same treatment plan for tinea or pityriasis versicolor.

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.

If the cradle cap is not severe, it could simply be combed out gently after bathing. The softened scales can then be brushed away with a soft brush, comb or cloth, but if not done very gently, this could worsen the condition and bring about temporary hair loss. Applying petroleum jelly (e.g., Vaseline) liberally overnight is another popular treatment. The softened scales either fall off during the night, or can be brushed off in the morning. Making a paste from sodium bicarbonate (baking soda) and leaving it on the affected area for 10 minutes can also help lift the scales. There have been no studies done on these treatments.

There is broad disagreement regarding the role of shampoos. Some sources warn against frequent shampooing, others recommend it. Mild baby shampoo is often recommended, but the exact denotation of the label "mild" in this context is not quite clear. Baby shampoos often contain detergent surfactants, perfumes, quaternium-15 and other eczemagenic irritants. Again, no studies have been performed on non-prescription shampoos.

In stubborn cases some doctors may recommend keratolytic (dandruff) shampoos (e.g. with sulfur, selenium, zinc pyrithione, or salicylic acid) while others warn against the use of medicated shampoos in newborns due to systemic absorption. Dandruff shampoos often contain sodium dodecyl sulfate, a noted skin irritant.

Steroid and tar preparations have also been used but may have drawbacks. Immunomodulators (tacrolimus/Protopic, pimecrolimus/Elidel) have not been approved for babies under two years.

Ketoconazole shampoos and creams are currently shown to be the most effective medical treatment of moderate to serious cradle cap. Research indicates that this anti-fungal medication is not absorbed into the bloodstream.

Typical medical advice is to use diluted baby shampoo on a cotton swab to cleanse the eyelid. There is no agreement on the dilution, which ranges from a few drops to a half cup warm water, to a 50/50 mix.

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.

Antihistamines are not effective in treating the hives in this condition. It may respond to immunosuppressant drugs such as corticosteroids, cyclooxygenase inhibitors, interferon alpha, interleukin 1 receptor antagonists (Anakinra), perfloxacin, colchicine, cyclosporine or thalidomide. The hives may respond to treatment with PUVA, and the bone pain may respond to bisphosphonates.

Because Schnitzler's syndrome is so rare, the efficacy of different treatments cannot be compared using statistics. Nevertheless, case studies provide evidence that anakinra (otherwise known as kineret) is much more effective for Schnitzler's syndrome than any other drug, and that the improvement in symptoms associated with this treatment is dramatic. For example, Beseda and Nossent (2010) reviewed the literature concerning IL1-RA treatment (i.e. anakinra) for Schnitzler's syndrome. They concluded that, “Twenty-four patients with Schnitzler's syndrome... have been successfully treated with anakinra.” They add that “seven out of seven patients [with Schnitzler’s syndrome], that either interrupted or used anakinra every other day, had relapse of their symptoms within 24-48 h; anakinra was restarted in all patients with the same clinical efficiency.” Kluger et al. (2008) investigated the effectiveness of anakinra for a range of conditions. They searched MEDLINE for English-language trials of anakinra and abstracts from rheumatologial scientific meetings. They conclude that, “Over the last few years it has become increasingly evident that anakinra is highly effective and safe in patients with ... Schnitzler’s syndrome”. The year before, De Koning et al. (2007) reviewed the disease characteristics of Schnitzler syndrome and collected follow-up information to gain insight into long-term prognosis and treatment efficacy. They used data from 94 patients, and their conclusions about treatment for the condition are that, “There have been promising developments in therapeutic options, especially antiinterleukin-1 treatment, which induced complete remission in all 8 patients treated so far.”

Reports of individual patients treated with anakinra illustrate its effectiveness. Beseda and Nossent (ibid.) report treating a longstanding multidrug resistant Schnitzler’s syndrome patient with anakinra: “Within 24 h after the first injection, both the urticaria and the fever disappeared and have not recurred. For the past 6 months, the patient has been in clinical and biochemical remission.” Other authors report “a complete resolution of symptoms” (Dybowski et al., 2008). Crouch et al. (2007) report the effective treatment of a 52-year-old man who had been diagnosed with Schnitzler’s syndrome 8 years earlier: “On review, one week later, the patient’s systemic symptoms had resolved, and his previously elevated white cell count and inflammatory markers had normalised. The use of anakinra in our patient resulted in resolution of symptoms and has enabled cessation of oral prednisolone. Our patient remains symptom free on anakinra after 14 months of follow-up”. Similar stories are reported by Frischmeyer-Guerrerio et al. (2008), Wastiaux et al. (2007), and Eiling et al. (2007), Schneider et al. (2007). De Koning et al. (2006) treated three patients with Schnitzler’s syndrome with thalidomide and anakinra. Thalidomide was only effective for one of the three patients and was discontinued because of polyneuropathy. In contrast, for all three patients, anakinra “led to disappearance of fever and skin lesions within 24 hours. After a follow-up of 16-18 months, all patients are free of symptoms”. The authors concluded that anakinra as a treatment for Schnitzler’s syndrome “is preferable to thalidomide... as it has fewer side effects”.

As well as being more effective, anakinra is safer than the other treatments available for Schnitzler's syndrome. The Cochrane review entitled, ‘Anakinra for rheumatoid arthritis’ (Mertens and Singh, 2009 ) evaluates the (clinical effectiveness and) safety of anakinra in adult patients with rheumatoid arthritis, using data from 2876 patients, from five trials which constituted 781 randomized to placebo and 2065 to anakinra. The authors conclude, “There were no statistically significant differences noted in most safety outcomes with treatment with anakinra versus placebo - including number of withdrawals, deaths, adverse events (total and serious), and infections (total and serious). Injection site reactions were significantly increased, occurring in 1235/1729 (71%) versus 204/729 (28%) of patients treated with anakinra versus placebo, respectively”. These injection site reactions last for no more than four months, and are trivial compared to the very debilitating symptoms of Schnitzler's syndrome.

Localized demodectic mange is considered a common puppyhood ailment, with roughly 90% of cases resolving on their own with no treatment. Minor, localized cases should be left to resolve on their own to prevent masking of the more severe generalized form. If treatment is deemed necessary Goodwinol, a rotenone-based insecticide ointment is often prescribed, but it can be irritating to the skin. Demodectic mange with secondary infection is treated with antibiotics and medicated shampoos.

In more severe generalized cases, Amitraz is a parasiticidal dip that is licensed for use in many countries (the only FDA approved treatment in the USA) for treating canine demodicosis. It is applied weekly or biweekly, for several weeks, until no mites can be detected by skin scrapings. Demodectic mange in dogs can also be managed with avermectins, although there are few countries which license these drugs, which are given by mouth, daily, for this use. Ivermectin is used most frequently; collie-like herding breeds often do not tolerate this drug due to a defect in the blood–brain barrier, though not all of them have this defect. Other avermectin drugs that can be used include doramectin and milbemycin.

Recent results suggest that the isoxazolines afoxolaner and fluralaner, given orally, are effective in treating dogs with generalised demodicosis.

Cats with "Demodex gatoi" must be treated with weekly or bi-weekly sulfurated lime rinses. "Demodex cati" are treated similarly to canine demodicosis. With veterinary guidance, localized demodectic mange can also be treated with a topical keratolytic and antibacterial agent, followed by a lime sulfur drip or a local application of Rotenone. Ivermectin may also be used. Generalized demodectic mange in cats is more difficult to treat. There are shampoos available that can help to clear dead skin, kill mites and treat bacterial infections. Treatment is in most cases prolonged with multiple applications.

Because of the possibility of the immune deficiency being an inherited trait, many veterinarians believe that all puppies with generalized demodex should be spayed or neutered and not reproduce. Females with generalized demodex should be spayed because the stress of the estrus cycle will often bring on a fresh wave of clinical signs.

It can be treated with systemic antiviral drugs, such as aciclovir or valganciclovir. Foscarnet may also be used for immunocompromised host with Herpes simplex and acyclovir-resistant Herpes simplex.

Courses of treatment for children with is dependent upon the severity of their case. Children with OHS often receive physical and occupational therapy. They may require a feeding tube to supplement nourishment if they are not growing enough. In an attempt to improve the neurological condition (seizures) copper histidine or copper chloride injections can be given early in the child’s life.

However, copper histidine injections have been shown ineffective in studies of copper metabolic-connective tissue disorders such as OHS.

Pityriasis lichenoides et varioliformis acuta is a disease of the immune system. It is the more severe version of pityriasis lichenoides chronica. The disease is characterized by rashes and small lesions on the skin. The disease is more common in males and usually occurs in young adulthood, although it has been seen in every age group and every race. It is possible for the disease to go into remission for short periods of time or forever.

Corticosteroids remain the main treatment modality for IOI. There is usually a dramatic response to this treatment and is often viewed as pathognomonic for this disease. Although response is usually quick, many agree that corticosteroids should be continued on a tapering basis to avoid breakthrough inflammation.

Although many respond to corticosteroid treatment alone, there are several cases in which adjuvant therapy is needed. While many alternatives are available, there is no particular well-established protocol to guide adjuvant therapy. Among the available options there is: surgery, alternative corticosteroid delivery, radiation therapy, non-steroidal anti-inflammatory drugs, cytotoxic agents (chlorambucil, cyclophosphamide), corticosteroid sparing immunosuppressants (methotrexate, cyclosporine, azathioprine), IV immune-globin, plasmapheresis, and biologic treatments (such as TNF-α inhibitors).

Lichen ruber moniliformis is a rare skin disease named for Fred Wise and Charles R. Rein.

It is one of several diseases also known as Kaposi's disease, based on its characterization in 1886 by Moritz Kaposi.

It is thought to be a rare variety of lichen planus.It is also known as "Morbus moniliformis lichenoides".

Onychauxis presents with thickened nails without deformity, and this simple thickening may be the result of trauma, acromegaly, Darier's disease, psoriasis, or pityriasis rubra pilaris, or, in some cases, hereditary.

The disease causes numerous whitish punctiform papules and brownish macules arranged in a necklace-like pattern.