adenocarcinoma in 90% of cases and a gastric in 60%. Acanthosis Nigricans often develops concurrently with the tumor, although it may predate the tumor (by up to 15 years) or follow it. In 25–50% of patients, Acanthosis Nigricans presents as oral lesions (mostly tongue and lips), which are seldom pigmented. Indistinguishable from the benign form, malignant Acanthosis Nigricans is usually not associated with obesity. Instead, its skin lesions are more extensive, more rapidly spreading, atypical in location (palms, soles, and mucosae), and often symptomatic. Regression and progression follow the course of the underlying tumor.
It comprises one fifth of all cases, usually due to an aggressive underlying neoplasm—a GI
adenocarcinoma in 90% of cases and a gastric in 60%. Acanthosis Nigricans often develops concurrently with the tumor, although it may predate the tumor (by up to 15 years) or follow it. In 25–50% of patients, Acanthosis Nigricans presents as oral lesions (mostly tongue and lips), which are seldom pigmented. Indistinguishable from the benign form, malignant Acanthosis Nigricans is usually not associated with obesity. Instead, its skin lesions are more extensive, more rapidly spreading, atypical in location (palms, soles, and mucosae), and often symptomatic. Regression and progression follow the course of the underlying tumor.
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The most common are factors that stimulate epidermal keratinocyte and dermal fibroblast proliferation. In
benign Acanthosis Nigricans, these may be either insulin or an insulinlike growth substance; in the malignant form, they are instead neoplastic products. Overall, Acanthosis Nigricans can occur with: Obesity and insulin resistance: Lesions are weight dependent and may completely regress with slimming. Congenital syndromes: Typical of young women with type A or type B syndromes. The type A is also referred to as HAIR-AN syndrome (HyperAndrogenemia, Insulin Resistance, and AN syndrome). It affects primarily young African- American women, with polycystic ovaries, high testosterone levels, and signs of virilization (hirsutism and clitoral hypertrophy). The type B syndrome occurs instead in women with uncontrolled diabetes, ovarian hyperandrogenism, or an autoimmune disease (such as systemic lupus erythematosus [SLE], scleroderma, Sjögren’s syndrome, or Hashimoto thyroiditis). Anti-insulin receptor antibodies are often present. Drug reaction: Due to nicotinic acid, insulin, pituitary extract, systemic corticosteroids, and diethylstilbestrol Internal malignancy A condition characterized by brown-to-black, poorly defined, velvety plaques that may occur anywhere,
although typically on the intertriginous areas of axilla and groin. The umbilicus is also a preferred site, as are the posterior and lateral folds of the neck, especially in children. In hyperandrogenic and obese females, the vulva is the most commonly involved area. Lesions are often associated with skin tags (acrochordons) and may even occur on mucous membranes—such as the oral cavity, esophagus, and nasal/laryngeal mucosa. Nipple areolas are another common target. As an inverse form, affecting not the trunk, but the face, extremities, and flexural regions. Cell-mediated
immunity plays a pathogenetic role, since lymphocyte function is impaired in Tinea Versicolor. As the name implies (versicolor means multicolor), the condition is characterized by numerous, well marginated, finely scaly, oval-to-round macules over the trunk and/or chest. These range in color from white
to red to brown, and can be pruritic. They eventually coalesce, forming irregular patches of discoloration. The diagnosis is usually confirmed by potassium hydroxide (KOH) examination of scales. This demonstrates both the cigar-butt mycelial hyphae and the round thick-walled spores, in a pattern often referred to as “spaghetti and meatballs,” or “bacon and eggs.” Note that TV is more noticeable during the summer, since lesions cannot tan, thus making the discrepancy with surrounding skin even more apparent. A common, benign, and superficial fungal infection, characterized by hypo/hyperpigmented macules,
patches, and thin plaques, widely covering chest and back. The cause is Malassezia furfur, part of the normal skin flora (present in 20% of infants and close to 100% of adults). In situations of predisposition (genetics, immunosuppression, malnutrition, Cushing’s disease, and warm/humid environments—hence its predilection for Western Samoa and relative rarity in Scandinavia), the saprophytic yeast undergoes conversion to the parasitic and mycelial form, thus infecting the stratum corneum of the epidermis and thereby causing clinical disease. TV is not contagious, but in predisposed individuals may chronically recur. It is most common in the first and second decades, when the sebaceous glands are more active. Conversely, it is rare before puberty or after age 65. At least 10% of patients have serologic or clinical evidence of autoimmune disorders, the most common
being thyroid diseases, especially hypothyroidism of the Hashimoto variety. Diabetes, Addison’s, pernicious anemia, alopecia areata, and uveitis (Vogt-Koyanagi syndrome) are also frequent. A careful history and appropriate screening are therefore necessary. Still, treatment of concomitant diseases does not influence the course of vitiligo. Clinically. In patients with fair skin, the lack of contrast between normal and diseased areas may make
the identification of lesions more difficult, so that a Wood’s lamp becomes necessary. A biopsy will demonstrate no melanocytes, but their presence does not exclude the diagnosis. Segmental vitiligo: Characterized by unilateral depigmented macules and patches in a dermatomal or
quasi-dermatomal distribution. It generally has a stable course. Focal vitiligo: One or more pale macules in an area that is single but not segmental Universal vitiligo: It results in total or nearly total body involvement. Unpredictable, but generally characterized by slow progression, which may be interrupted by periods of
stability. Spontaneous repigmentation also may occur, but generally is incomplete. |