Clear cell acanthoma: not of sweat gland origin.
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Biomedical subjects
Publications and source records attributed to N S Penneys.
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Factor VIII-related antigen (VIIIR-Ag), a marker for endothelial cells, was used to explore the histogenesis of Kaposi's sarcoma. Formaldehyde-fixed, paraffin-embedded routine histologic sections from 37 cases of Kaposi's sarcoma and from 16 other spindle-cell tumors of the skin were stained for the presence of VIIIR-Ag, using an immunoperoxidase technique. Positive reactions were noted in all cases of Kaposi's sarcoma regardless of their histologic variations. Although the intensity of reaction was greater in cells that lined vascular channels and blood-filled clefts, many intertwining spindle cells contained VIIIR-Ag in their cytoplasm as well. Since VIIIR-Ag is elaborated only by endothelial cells and megakaryocytes, positive immunologic reaction for this factor in the cells of Kaposi's sarcoma strongly supports an endothelial derivation.
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A 52-year-old woman with rheumatoid arthritis experienced painless spontaneous hemorrhage, tearing, and necrosis of the skin on the lower laternal aspect of both legs. Thereapy with systemic prednisone had been used to suppress active synovitis for almost four years and was associated with moon facies, hirsutism, truncal obesity, thinning of the skin, extensive purpura on the extremities, and other manifestations of hypercortisolism. There was no evidence of rheumatoid vasculitis, trauma, or blood dyscrasia. The leg lesions may represent an exaggerated type of steroid-induced purpura resulting in localized areas of gangrenous skin.
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Components of the culture medium employed in phytohemagglutinin (PHA)-induced lymphocyte blastogenesis were tested individually to determine their effects on the conversion of PGE2 into PGF2 alpha by the enzyme, PGE2 9-ketoreductase. PHA at concentrations up to 10 microgram/ml completely inhibited the activity of PGE2 9-ketoreductase. Heat inactivated fetal bovine serum (FBS) stimulated a greater than two-fold increase in the conversion of PGE2 into PGF2 alpha. Although the mechanism of lymphocyte activation by the lectin, PHA, remains obscure, our data suggests that in vitro exposure of lymphocytes to the tissue culture medium as well as mitogens could result in intracellular alterations in prostaglandin metabolism.
Microsomal preparations from petrolatum-treated wound skin contained significantly less arachidonic acid-dependent oxidative capacity when compared to activities in untreated wounded skin (t = 6.06, P < 0.001). Microsomes from both untreated and petrolatum-treated wounded skin produced similar quantities of PGE2 and PGF2 alpha; however, microsomal lipoxygenase activity in petrolatum-treated wounded skin was depressed when compared to that in untreated wounded skin. Microsomal preparations from normal pig skin treated with petrolatum oxidized arachidonic acid at a similar rate to those from untreated control skin. Increasing quantities of petrolatum progressively inhibited the synthesis of PGE2 and PGF2 alpha by fetal calf skin microsomes in vitro as determined by both the oxidation of arachidonic acid and the quantification of radioactive product. Topical application of banal compounds that contain lipid substances may therefore alter the cutaneous inflammatory response by local suppression of pathways that generate hydroxy-fatty acids, substances that are known to be chemotactic and pro-inflammatory.
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Limitation of the inflammatory cascade has been demonstrated in man by an inhibitor(s) of the prostaglandin system and by inhibitor(s) for chemotaxis of leukocytes. Other factors may exist in vivo that inhibit other inflammatory sequences. In this report, homogenates from human skin interfered with 2 standard assays of lymphocyte function, mitogen-induced transformation and cytotoxicity while homogenates of human placenta did not. Differential centrifugation studies located inhibitory factor(s) primarily in the nuclear fractions. Therefore, reversible transitory depressions of the cell-mediated immune response that are observed concomitantly with chronic dermatoses may reflect release of inhibitory material dermatitic skin in vivo.
Four patients with systemic lupus erythematosus (SLE) had a vesicobullous eruption that histologically resembled dermatitis herpetiformis. Immunofluorescence microscopy patterns in the skin studied in three patients, however, were characteristic of SLE. Treatment of the underlying collagen-vascular disease improved the eruption, while recurrence coincided with exacerbation of the systemic disease. This distinctive lesion is an important parameter of SLE activity.
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An autosomal dominant genodermatosis that is characterized by painful callosities develops over pressure points. Histologically, these lesions are similar to epidermal nevi.
Inhibition of the activity of sheep vesicular gland prostaglandin synthetase (a rare limiting enzyme in the biosynthesis of prostaglandins) was demonstrated in the presence of homogenates prepared from skin lesions characterized histologically by epidermal disruption. These inhibitory effects were not observed in homogenates of skin lesions characterized by a lack of epidermal disruption.
The evolving vesicular patch test reaction served as a human model for immunologically induced epidermal damage. We observed that inhibitory factor(s) were detectable in the homogenates only after epidermal disruption had appeared. Maximum inhibition correlated with acute changes seen histologically in the evolving patch test reaction. During resolution of the patch test reaction, the presence of inhibitory factor(s) in the skin homogenates became undetectable. A white ring similar to the Woronoff ring described after ultraviolet light and coal tar therapy of psoriatic plaques was reproduced surrounding the vesicular patch test reaction, suggesting that the inhibitory substance(s) detected following epidermal trauma of various types (physical, immunologic, inflammatory, etc.) functioned in vivo in a similar fashion. Our results suggest that Woronoff's ring is a nonspecific phenomenon that can be formed following various types of trauma to the skin rather than a specific occurrence associated only with the treatment of psoriatic plaques.
The biosynthesis of PGE2 and PGF2alpha was measured in intact peritoneal exudate preparations obtained from C. parvum-treated and control C3H mice. Although both the control and stimulated preparations biosynthesized PGF2alpha and PGE2 from [1-14C] arachidonic acid, the stimulated preparations generated more of both prostaglandins than did nonstimulated preparations, probably as a result of increased synthesis within macrophages. Increased transformation of PGE2 into PGF2alpha by PGE2 9-ketoreductase was noted in stimulated preparations when compared to that in control cells. The data suggest that stimulated macrophages are capable of generating increased quantities of PGF2alpha and therefore might function as one source of this substance in resolving inflammatory reactions.
Using a sensitive new assay, we have measured the cholesteryl ester and cholesterol contents of stratum corneum from callus, normal skin, psoriatic lesions (plantar and nonplantar), and lamellar ichthyotic lesions (plantar and nonplantar). Cholesteryl ester content of normal stratum corneum was significantly higher than that of callus, suggesting that callus was not a suitable control tissue for further biochemical studies involving sterol content of stratum corneum. Both psoriatic and lamellar ichthyotic scale have increased levels of free cholesterol and decreased levels of esterified cholesterol when compared to appropriate controls.