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Pityriasis (tinea) versicolor is a superficial infection of the stratum corneum caused by the yeast Malassezia furfur (synonyms, Pityrosporum ovale, P. orbiculare). It is found worldwide with a higher prevalence in tropical climates. Young adults ages 15 to 35 are the most commonly affected age group, which is likely due to the higher lipid content of their skin. M. furfur is a saprophytic, lipophilic organism, considered a part of normal skin flora. Humidity, warm climates, family history of pityriasis versicolor, oily skin, Cushing's syndrome, hyperhidrosis, immunosuppression, and malnutrition predispose to clinical infection.
Papulosquamous, follicular, and inverse patterns of pityriasis versicolor have been described. Papulosquamous lesions are the most common presentation and present initially as a reddish macule, which evolves into either a hypopigmented or a hyperpigmented superficial scaly plaque.
Treatment of pityriasis versicolor is difficult. Recurrence rates run as high as 60% to 80% within 2 years after treatment. Patients should be advised that the goal of treatment is to control rather than abolish the offending organism. The scalp frequently serves as a reservoir for spores of the organism.
Cafe au lait macules are well-circumscribed, 0.2- to 10-cm, uniform, well-circumscribed, brown macules with irregular margins. They are scattered on the trunk and extremities and favor sun-protected areas. The lesions appear at birth or soon afterwards and tend to resolve with age.
Neurofibromatosis-1 is a neurocutaneous syndrome affecting multiple organ systems. This autosomal dominant disorder involves chromosome number 17 and affects up to 1 in 3000 people. The length of the gene predisposes it to a high frequency of new mutations, resulting in a 50% rate.
Neurofibromatosis-2, an autosomal dominant disorder involving chromosome number 22, affects several thousand patients in the United States. It is associated with the presence of bilateral acoustic neuromas.
The characteristic lesion seen in Albright's syndrome is a large tan-to-brown macule located on the forehead, nuchal area, sacrum, or buttocks. The irregular margins give it a coast of Maine appearance. The lesions tend to remain unilateral and do not cross the midline. Polyostotic fibrous dysplasia.
Melasma is a common, acquired hypermelanosis that primarily affects sun-exposed areas in women. It appears as irregular, light brown-to-gray macules on the cheeks, forehead, upper lip, nose, and chin. This disease is most apparent in Latinos, blacks, and Asians, but all races can be affected.
Epidermal hypermelanosis in patients with melasma appears tan-to-brown on physical examination, and the macules are accentuated by a Wood's lamp. Dermal melanosis appears blue-gray.
Sunscreen, hydroquinone, and time are the triad found to be most effective in controlling epidermal melasma. Hydroquinone is a hydroxyphenolic compound that inhibits the conversion of dopa to melanin by inhibiting the tyrosinase enzyme. It is available as 2% to 4% creams and gels and a 3% solution. Side effects include allergic and irritant contact dermatitis, nail discoloration, depigmentation of surrounding normal skin, and postinflammatory hyperpigmentation. The dopa reaction of melanocytes.
Acanthosis nigricans is a mucocutaneous disorder that appears more commonly in Latinos (5.5%) and blacks (13.3%) than in whites (1%). It appears as hyperpigmented, hyperkeratotic plaques with a velvety texture. This usually symmetric eruption affects the axillae, neck, groin, and breast folds.
Malignant acanthosis nigricans is a cutaneous disorder that is a marker of an underlying malignancy. It is imperative to consider an underlying malignancy when a patient presents with sudden, generalized acanthosis nigricans, especially if mucosal papillomas or tylosis (keratoderma of palms and soles) or
Treatment of acanthosis nigricans is guided by its cause. Weight loss and treatment of underlying disorders can lead to a reversal of skin disease. Topical retinoic acid, oral isotretinoin, topical corticosteroids, topical keratolytics, ketoconazole, and
In 1949, Becker first described a "concurrent melanosis and hypertrichosis in distribution of nevus unius lateris" in two young men after severe sun exposure. Becker's melanosis (nevus) is a unilateral hyperpigmented, hypertrichotic patch usually located on the upper back, chest, or shoulder. It occurs
The lesion starts as a hyperpigmented macule or patch that enlarges and increases in color with age. These typically solitary lesions are not infiltrated and are irregular, even geographic in their outline. A year or two after the melanotic presentation, hair begins to appear within the lesion. The observed hair is darker and thicker than hair in surrounding normal skin. Acneiform lesions are occasionally seen within
Associated abnormalities of soft tissue and bony structures may be seen with Becker's melanosis, particularly in females. The ratio of males to females in those affected with developmental anomalies is 2:5. A 12-year-old girl with Becker's melanosis was reported to have associated ipsilateral foot
The hyperpigmentation and hypertrichosis of Becker's melanosis usually persists for life. The pigment can decrease in intensity with time, but the appearance of the hair remains constant. Bleaching agents
Medications are a common cause of cutaneous pigmentation. A careful history is essential in making this correlation. Pigmentation resolves to some degree after discontinuation of the offending drug but may
Oral cavity staining has been reported to occur after minocycline ingestion as well as staining of the teeth in prepubertal children. One study found 12 out of 78 patients had blue-to-black pigmentation of their incisor and premolar teeth, gingiva, and alveolar bone after 2 months of therapy, which is probably
A fixed drug eruption is a localized cutaneous response to an ingested drug or chemical and is characterized by solitary, or sometimes multiple, lesions that appear within 8 hours after exposure by a
Common | Less Common |
---|---|
Minocycline | Barbiturates |
Zidovudine | Phenacetin |
Bleomycin | Salicylates |
Busulfan | Sulfonamides |
Chlorpromazine | Quinacrine |
Oral contraceptive pills | Amodiaquine |
Hydantoins | Chloroquine |
Hydrochlorothiazide | |
Amiodarone | |
Tetracycline |
Zidovudine, a commonly used antiretroviral agent, is a common cause of drug-induced hyperpigmentation. Progressive pigmentation of all 10 fingernails and later all 10 toenails in two patients after a dose of 200 mg every 4 hours for 2 to 6 weeks has been reported. The pigmentation can be
Bleomycin, a chemotherapeutic antibiotic commonly used for the treatment of carcinomas and lymphomas, achieves a high concentration in the skin. Cutaneous changes observed in a series of eight
Busulfan (Myleran), an alkylating agent commonly used for chronic myelogenous leukemia, may cause diffuse brown pigmentation of the face, forearms, chest, and abdomen in up to 10% of patients. It has
Postinflammatory hyperpigmentation is an acquired increase in cutaneous melanin occurring after inflammation, whereas postinflammatory hypopigmentation is an acquired partial to total loss of melanin. The shape of the cutaneous lesions corresponds to the site of the original inflammatory process. The lesions can be diffuse or localized depending on the initiating incident. Causes of postinflammatory
Vitiligo is a cutaneous disorder of unknown cause that destroys melanocytes in the skin, mucous membranes, eyes, and hair bulbs. It affects 1% to 2% of the world's population and at least 1 to 2 million individuals in the United States alone. There is no sexual predilection, and although all races are affected, it is more noticeable in patients with darker complexions. The peak onset of disease is between 10 and 30 years of age, and in half of the cases the disease manifests within the first two
Ocular pigmentary abnormalities (hypopigmented or hyperpigmented choroid and retinal pigmented epithelium, uveitis) have been reported in 40% of patients with vitiligo. Decreased acuity, poor night vision, and photophobia are seen in about 5% of patients. In a study of 35 patients with a matched
Diagnosis depends on a good history and physical examination. It is important to establish the course of the disease to determine the aggressiveness of subsequent treatment. Asking about precipitating factors,
The goal of treatment is to restore pigmentation and thus improve the appearance of affected patients. The reserve melanocytes needed for repigmentation migrate from surrounding normal skin and hair follicles. Oral and topical psoralen photochemotherapy (PUVA), heliotherapy (trisoralen and sunlight), topical corticosteroids, and cosmetic camouflage have been used. Of these, PUVA has the highest efficacy rate but may take several months of thrice weekly treatments to show substantial improvement. Newer therapies include dermabrasion and topical 5-fluorouracil, khellin and UVA light, and
Pityriasis alba (pityriasis streptogenes, pityriasis corporis, pityriasis faciei) occurs in all races but is more apparent on darker skin in the summertime, when the affected areas fail to tan. This is primarily an
Pityriasis alba is an eczematous dermatosis with hypomelanosis secondary to postinflammatory changes and the UV screening properties of the hyperkeratotic and parakeratotic epidermis. Drying agents such
Clinical presentation and history are usually sufficient for diagnosis. Pityriasis alba lacks the complete depigmentation and distinct margins present in vitiligo. It is also important to rule out dermatophytic infections with scrapings and microscopic examination. Usually the lesions clear with puberty and
Ash leaf macules can be found in tuberous sclerosis, a neurocutaneous syndrome affecting multiple organs. This disorder, affecting about 3 to 10 individuals per 100,000, is autosomal dominant with high
The lance ovate hypopigmented macule (ash leaf macule) is the characteristic lesion of tuberous sclerosis. It was first described by Fitzpatrick et al in 1968, who coined the term lance ovate to
At times, it may be difficult to distinguish ash leaf macules from macules of vitiligo. Vitiligo lesions, however, tend to be depigmented, symmetric, and progressive. The ash leaf macules are not depigmented but hypopigmented, with functional melanocytes remaining in the affected areas that are