Facial hyperpigmentation is usually a reflection of an increased amount of melanin either within the epidermis, the dermis, or both (mixed pattern). The increase in melanin content is due to an increased number of functioning melanocytes (melanocytosis), an increased amount of melanin production without a numerical alteration of melanocytes (melanosis), or both. Topical hypo/depigmenting agents are most effective in those disorders where the increased melanin pigment (secondary to melanocytosis or melanosis) is within the epidermis. In patients with melasma, one of the more common causes of facial hyperpigmentation, two major groups of hypo/depigmenting agents have been used: phenolic derivatives and nonphenolic compounds. Hydroquinone, a phenolic derivative, has been used most extensively. It is applied to areas of involvement, either alone or in combination with one or two of the following: tretinoin, salicylic acid, glycolic acid, or corticosteroid. Phenolic thioethers are a new class of phenolic derivatives, and they exhibit both cytocidal and cytostatic effects selectively on melanocytes. Nonphenolic depigmenting agents include azelaic acid and kojic acid. If the facial hyperpigmentation is not improved by first‐line topical therapies, chemical peels may be used in combination. The precise cause of melasma is not known, and multiple factors have been implicated. However, a genetic predisposition and exposure to ultraviolet (UV) light are very important factors. Avoidance of direct exposure to sunlight and application of broad‐spectrum sunscreens are required during and after the period of active treatment. In addition to melasma, other causes of facial hyperpigmentation include Riehl's melanosis, photocontact dermatitis, the sequelae of inflammatory diseases such as acne vulgaris and cutaneous lupus, and nevus of Ota.
Sulfur-containing tyrosine analogs such as 4-S-cysteaminylphenol (4-S-CAP) and its N-acetyl derivative, N-acetyl-4-S-CAP, are tyrosinase substrates and can cause selective cytotoxicity or cell death of melanocytes and melanoma cells. It is not clear, however, if the cytotoxicity derives from a cytostatic or cytocidal effect. The latter can also be either apoptotic or necrotic. This paper summarizes our attempt to clarify the nature of melanocytotoxicity and cell death by using a new derivative of 4-S-CAP, N-propionyl-4-S-CAP (NPr-CAP). The i.p. administration of NPr-CAP caused marked depigmentation of black hair follicles in C57 mice. At 12 h postadministration of NPr-CAP, follicular melanocytes showed histochemical and morphologic features indicative of apoptosis by TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining and electron microscopy. The agarose gel electrophoresis of DNA from drug-treated melan a2 cells, an immortal melanocyte line of C57 black mice, showed the nucleosomal DNA ladder pattern. NPr-CAP caused irreversible cytotoxicity in melan a2 and the effect was inhibited by a tyrosinase inhibitor, phenylthiocarbamide. The tyrosinase-mediated cytotoxicity of NPr-CAP was further confirmed by the decreased viability of COS 7 monkey-kidney cells, which expressed a level of high tyrosinase activity through transfection of human tyrosinase cDNA. NPr-CAP, however, also transiently inhibited the proliferation of melan c cells, a control tyrosinase-negative albino melanocyte line, and vector-transfected COS 7 cells. Thus, the major process of NPr-CAP-mediated melanocytotoxicity involves cytocidal apoptosis associated with active tyrosinase. In addition, there is transient, nontyrosinase-mediated cytostatic cytotoxicity.
We report a case of lymphomatoid papulosis (LyP) that occurred in a 44-year-old Japanese male patient. Reddish papules with a small number of pustules and nodules were observed on the extremities, chest and upper back. Most lesions were also associated with central necrosis, ulceration and crusting, and regressed spontaneously within 4 to 6 weeks. Histopathological examination revealed wedge-shaped dense cellular infiltrate in the dermis, which was mixed with large atypical lymphoid cells, small lymphocytes, eosinophils and neutrophils. These large atypical cells expressed CD30 on their cell membrane and cytoplasm. Rearrangement of the T-cell receptor (TcR) beta-chain gene was detected in the skin lesion. Lymphadenopathy with histopathologic change similar to the skin lesions, but without TcR gene rearrangement, was found at the left inguinal area. Systemic administration of methotrexate (7.5-15.0 mg/week) was found to be dramatically effective in resolution of skin lesions and prevention of their recurrence.
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