Diltiazem for tardive dyskinesia.
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Biomedical subjects
Publications and source records attributed to C R Charles.
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The necrobiotic disease granuloma annulare was studied with the electron microscope in an effort to develop a theory for the mechanism of development of necrobiotic connective tissue. That mechanism must provide for the disappearance of nuclei, the tinctorial change in collagen, and the retention of connective tissue outlines characteristic of necrobiosis. Our observations suggest that necrosis of histiocytes and fibroblasts with release of lysosomal enzymes is an important early event in the development of necrobiosis. Increased quantities of extracellular hyaluronic acid are also present in the earliest recognizable lesions. The combination of lysosomal enzymes and abundant hyaluronic acid in the interstitium results in swelling of collagen. Necrotic cellular debris is deposited about many collagen fibrils. This material seems to protect collagen from further destruction and may account for the preservation of connective tissue outlines observed at the light microscopic level. Some collagen fibrils not protected by cellular debris appear to be disrupted into constituent filaments. Crossbanded filamentous aggregates that resemble fibrous long spaced collagen were also observed and may represent an abnormal reassembly of disrupted collagen.
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Examination of specimens from lesions of hyperpigmented tinea versicolor and from unaffected skin disclosed that the lesions showed increased stratum corneum turnover (8.2 +/- 0.6 vs 14.8 +/- 0.4 days, respectively), slight to moderate routine histological changes, such as acanthosis and perivascular inflammation, and dramatic electron microscopical changes (larger, singly distributed melanosomes vs small, packaged melanosomes, respectively). Brown hyperpigmentation in tinea versicolor appears to arise from an increase in melanosome size and a change in their epidermal distribution pattern.