The discoloration usually disappears spontaneously over a period of several months after giving birth or stopping the oral contraceptives or hormone replacement therapy.

Treatments are often ineffective as it comes back with continued exposure to the sun. Assessment by a dermatologist will help guide treatment. This may include use of a Woods lamp to determine depth of the melasma pigment. Treatments to hasten the fading of the discolored patches include:

- Topical depigmenting agents, such as hydroquinone (HQ) either in over-the-counter (2%) or prescription (4%) strength. HQ is a chemical that inhibits tyrosinase, an enzyme involved in the production of melanin.

- Tretinoin, an acid that increases skin cell (keratinocyte) turnover. This treatment cannot be used during pregnancy.

- Azelaic acid (20%), thought to decrease the activity of melanocytes.

- Tranexamic acid by mouth has shown to provide rapid and sustained lightening in melasma by decreasing melanogenesis in epidermal melanocytes.

- Cysteamine hydrochloride (5%) over-the-counter. Mechanism of action seems to involve inhibition of melanin synthesis pathway

- Flutamide (1%)

- Chemical peels

- Microdermabrasion to dermabrasion (light to deep)

- Galvanic or ultrasound facials with a combination of a topical crème/gel. Either in an aesthetician's office or as a home massager unit.

- Laser but not IPL (IPL can make the melasma darker)

Evidence-based reviews found that the most effective therapy for melasma includes a combination on topical agents.

In all of these treatments the effects are gradual and a strict avoidance of sunlight is required. The use of broad-spectrum sunscreens with physical blockers, such as titanium dioxide and zinc dioxide is preferred over that with only chemical blockers. This is because UV-A, UV-B and visible lights are all capable of stimulating pigment production.

Patients should avoid other precipitants including hormonal triggers.

Cosmetic camouflage can also be used to hide melasma.

Improvement or stabilization of the condition has been reported with topical and intralesional corticosteroids, antibiotics, hydroxychloroquine, topical and oral immunomodulators, tacrolimus, and most recently, 5-alpha-reductase inhibitors. In one study, the use of anti-androgens (finasteride or dutasteride) was associated with improvement in 47% and stabilization in 53% of patients

Spider angiomas are asymptomatic and usually resolve spontaneously. This is common in the case of children, although they may take several years to disappear. If the spider angiomas are associated with pregnancy, they may resolve after childbirth. In women taking oral contraceptives, they may resolve after stopping these contraceptives. The spider angiomas associated with liver disease may resolve when liver function increases or when a liver transplant is performed.

For spider angiomas on the face, techniques such as electrodesiccation and laser treatment can be used to remove the lesion. There is a small risk of a scar, although the results are generally good. Spider angiomas can recur after treatment.

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.

Hydroquinone solution was often mixed in an oil-free moisturizer that acted like a skin bleach. However the use of hydroquinone for skin whitening has been banned in European countries due to health concerns. In 2006, the United States Food and Drug Administration revoked its approval of hydroquinone for over the counter preparations warning that it may cause cancer or have many other detrimental effects.

The use of hydroquinone skin-whitening products can be toxic, harmful or lethal for humans.

Modern treatments include topical creams that are marketed for the condition (e.g. L'Oreal, Olay, Skin Doctors etc.). Various ingredients have been researched, developed and included in these creams. For example, recently, chemical compounds called alpha hydroxy acids (AHAs) have been added as a beneficial ingredient to creams for dark circles. Specialist treatments including laser and intense pulsed light skin surgery can also be used.

Owing to the self-limiting nature of the disease, treatment is generally not required. In cases where lesions appear to be interfering with the optic nerve, methyl prednisone is prescribed.

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.

Reticular pigmented anomaly of the flexures (also known as "dark dot disease", and "Dowling–Degos' disease") is a fibrous anomaly of the flexures or bending parts of the axillae, neck and inframammary/sternal areas. It is an autosomal-dominant pigmentary disorder that may appear in adolescence or adulthood. This condition is due to mutations in structural/desmosomal proteins found within stratified squamous epithelium.

Dark dot disease is associated with "KRT5".

Currently, there is no direct treatment for AEN. Only treatment is for the underlying main diseases or conditions. Appropriate hydration is set. Antacids are also added for further recovery support. Common support drugs of antacids are either H receptor antagonists, and/or a proton pump inhibitor. Sucralfate was used as an option. Parenteral nutrition greatly increased chance of recovery. An esophagectomy can be issued if the disorder is severe enough.

Drugs like ketoconazole,

voriconazole, and itraconazole are generally employed in treating the infection. Actinomycetes usually respond well to medical treatment, but the eumycetes are generally resistant and may require surgical interventions including amputation.

Galli–Galli disease is a rare inherited condition that has close resemblance clinically to Dowling-Degos' disease, but is histologically distinct, characterized by skin lesions that are 1- to 2-mm slightly keratotic red to dark brown papules which are focally confluent in a reticulate pattern. The disease is also characterized by slowly progressive and disfiguring reticulate hyperpigmentation of the flexures, clinically and histopathologically diagnostic for Dowling-Degos disease but also associated with suprabasal, nondyskeratotic acantholysis.

No vaccine is available. Simple hygienic precautions like wearing shoes or sandals while working in fields, and washing hands and feet at regular intervals may help prevent the disease.

No treatment modality has been unequivocally demonstrated to reduce the complications of alkaptonuria. Main treatment attempts have focused on preventing ochronosis through the reduction of accumulating homogentisic acid. Such commonly recommended treatments include large doses of ascorbic acid (vitamin C) or dietary restriction of amino acids phenylalanine and tyrosine. However, vitamin C treatment has not shown to be effective, and protein restriction (which can be difficult to adhere to) has not shown to be effective in clinical studies.

Several recent studies have suggested that the herbicide nitisinone may be effective in the treatment of alkaptonuria. Nitisinone inhibits the enzyme, 4-hydroxyphenylpyruvate dioxygenase, responsible for converting tyrosine to homogentisic acid, thereby blocking the production and accumulation of HGA. Nitisinone has been used for some time at much higher doses in the treatment of type I tyrosinemia. Nitisinone treatment has been shown to cause a larger than 95% reduction in plasma and urinary HGA. The main drawback is accumulation of tyrosine, the long-term risks of which are unknown; there is a particular concern about damage to the cornea of the eye. Long-term use would require frequent monitoring for complications.

Currently, there is no treatment for the disease. However, ophthalmologists recommend wearing sunglasses and hats outdoors and blue-light blocking glasses when exposed to artificial light sources, such as screens and lights. Tobacco smoke and second-hand smoke should be avoided. Animal studies also show that high doses of vitamin A can be detrimental by building up more lipofuscin toxin. Dietary non-supplemental vitamin A intake may not further the disease progression.

Clinical trials are being conducted with promising early results. The trials may one day lead to treatments that might halt, and possibly even reverse, the effects of Stargardt disease using stem cell therapy, gene therapy, or pharmacotherapy.

The Argus retinal prosthesis, an electronic retinal implant, was successfully fitted to a 67-year-old woman in Italy at the Careggi Hospital in 2016. The patient had a very advanced stage of Stargardt’s disease, and a total absence of peripheral and central visual fields.

Fleischer rings are pigmented rings in the peripheral cornea, resulting from iron deposition in basal epithelial cells, in the form of hemosiderin. They are usually yellowish to dark-brown, and may be complete or broken.

They are named for Bruno Fleischer.

Fleischer rings are indicative of keratoconus, a degenerative corneal condition that causes the cornea to thin and change to a conic shape.

It is important to distinguish between treatment of the underlying inflammation (PIC) and the treatment of CNV.

2-pronged approach:

Treatment is not always necessary and observation may be appropriate for lesions if they are found in non-sight threatening areas (that is not centrally).

Active lesions of PIC can be treated with corticosteroids taken systemically (tablets) or regionally by injections around the eye (periorbital). It has been argued that treating lesions in this way may help minimise the development of CNV.

The treatment of CNV:

Early treatment is required for this complication. There are several possible treatment methods, but none of these treatments appears to be singly effective for the treatment of CNV.

1. Corticosteroids: systemic or intraocular

2. ‘Second line’ immunosuppressants: There is evidence that combined therapies of steroids and second line immunosuppressants may be important.

3. Surgical excision of the affected area in well selected cases.

4. Intravitreal anti-VEGF agents. Examples are bevacizumab (avastin) and ranibizumab. These relatively new drugs are injected into the eye.

5. Photodynamic therapy (PDT): A photosensitive drug is ‘activated’ by strong light. Consideration may be given to combined therapy of PDT and anti VEGF.

6. Laser photocoagulation: This is occasionally used unless the CNV is subfoveal (affecting the central or macular part of the vision). The laser treatment can damage the vision.

The use of the intravitreal anti VEGF agents namely bevacizumab and ranibizumab have been described recently. The current evidence supporting the use of anti-VEGF agents is based on retrospective case studies and could not be described as strong. However, further data from prospective controlled trials are needed before the therapeutic role of anti-VEGF therapy in the uveitis treatment regimen can be fully determined. The anti VEGF agents furthermore have not been shown to have an anti-inflammatory effect.

Thus, treatment of the underlying inflammatory disease should play a central role in the management of uveitic CNV. A two-pronged treatment that focuses on achieving control of inflammation through the use of corticosteroids and/or immunosuppressive agents, while treating

complications that arise despite adequate disease control with intravitreal anti-VEGF agents, may be useful.

Regular monitoring is essential to achieve a good outcome. This is because even if there is no active inflammation, there may still be occult CNV which requires treatment to avoid suffering vision loss.

A punctal plug may be inserted into the tear duct by an optometrist or ophthalmologist, decreasing the removal of natural tears from the affected eye.

The use of contact lenses may help prevent the abrasion during blinking lifting off the surface layer and uses thin lenses that are gas permeable to minimise reduced oxygenation. However they need to be used for between 8–26 weeks and such persistent use both incurs frequent follow-up visits and may increase the risk of infections.

Alternatively, under local anaesthetic, the corneal layer may be gently removed with a fine needle, cauterised (heat or laser) or 'spot welding' attempted (again with lasers). The procedures are not guaranteed to work, and in a minority may exacerbate the problem.

Anterior Stromal Puncture with a 20-25 gauge needle is an effective and simple treatment.

An option for minimally invasive and long-term effective therapy is laser phototherapeutic keratectomy. Laser PTK involves the surgical laser treatment of the cornea to selectively ablate cells on the surface layer of the cornea. It is thought that the natural regrowth of cells in the following days are better able to attach to the basement membrane to prevent recurrence of the condition. Laser PTK has been found to be most effective after epithelial debridement for the partial ablation of Bowman's lamella, which performed prior to PTK in the surgical procedure. This is meant to smoothen out the corneal area that the laser PTK will then treat. In some cases, small-spot PTK, which only treats certain areas of the cornea may also be an acceptable alternative.

Granulosis rubra nasi is a rare familial disease of children, occurring on the nose, cheeks, and chin, characterized by diffuse redness, persistent hyperhidrosis, and small dark red papules that disappear on diascopic pressure.

People with recalcitrant recurrent corneal erosions often show increased levels of matrix metalloproteinase (MMP) enzymes.

These enzymes dissolve the basement membrane and fibrils of the hemidesmosomes, which can lead to the separation of the epithelial layer. Treatment with oral tetracycline antibiotics (such as doxycycline or oxytetracycline) together with a topical corticosteroid (such as prednisolone), reduce MMP activity and may rapidly resolve and prevent further episodes in cases unresponsive to conventional therapies. Some have now proposed this as the first line therapy after lubricants have failed.

Some confusion exists between Fleischer rings and Kayser-Fleischer rings. Kayser-Fleischer rings are caused by copper deposits, and are indicative of Wilson's disease, whereas Fleischer rings are caused by iron deposits. One example of a medical condition that can present with Fleischer rings is Keratoconus.

Handling may be painful and stressful because of their poor body movement and how the bones have grown. Due to the stress, handling should be kept to a minimum.

The treatment of choice by dermatologists is a safe and inexpensive oral medication, griseofulvin, a secondary metabolite of the fungus "Penicillium griseofulvin". This compound is "fungistatic" (inhibiting the growth or reproduction of fungi) and works by affecting the microtubular system of fungi, interfering with the mitotic spindle and cytoplasmic microtubules. The recommended pediatric dosage is 10 mg/kg/day for 6–8 weeks, although this may be increased to 20 mg/kg/d for those infected by "T. tonsurans", or those who fail to respond to the initial 6 weeks of treatment. Unlike other fungal skin infections that may be treated with topical therapies like creams applied directly to the afflicted area, griseofulvin must be taken orally to be effective; this allows the drug to penetrate the hair shaft where the fungus lives. The effective therapy rate of this treatment is generally high, in the range of 88–100%.

Other oral antifungal treatments for tinea capitis also frequently reported in the literature include terbinafine, itraconazole, and fluconazole; these drugs have the advantage of shorter treatment durations than griseofulvin. However, concern has been raised about the possibility of rare side effects like liver toxicity or interactions with other drugs; furthermore, the newer drug treatments tend to be more expensive than griseofulvin.

On September 28, 2007, the U.S. Food and Drug Administration stated that Lamisil (Terbinafine hydrochloride, by Novartis AG) is a new treatment approved for use by children aged 4 years and older. The antifungal can be sprinkled on a child's food to treat the infection. Lamisil carries hepatotoxic risk, and can cause a metallic taste in the mouth.

A related condition, bisphosphonate-associated osteonecrosis of the jaw (BON), has been described as a side-effect of amino-bisphosphonates, a class of phosphorus-based drugs that inhibit bone resorption and are used widely for treating osteoporosis, bone disease in cancer and some other conditions.

BON, sometimes called "bis-phossy jaw",

is primarily associated with the use of intravenous bisphosphonates in the treatment of cancer. The percentage incidence of BON from this use is approximately 1000 times higher than the incidence of BON caused by the use of oral bisphosphonates.

Periorbital hyperpigmentation is characterized by dark circles around the eyes, which are common, often familial, and frequently found in individuals with dark pigmentation or Mediterranean ancestry. Atopic dermatitis patients may also exhibit periorbital pigmentation (allergic shiners) due to lower eyelid venous stasis, and treatment is ineffective.

Preventing exposure to the causative antigen leads to resolution of the condition. Tacrolimus or clobetasol propionate have also been used to treat plasma cell cheilitis.