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Biomedical subjects

S O Kovacs

Publications and source records attributed to S O Kovacs.

7 recordsLinked to original sources
PubMed1998

Vitiligo.

The destruction of melanocytes is the cause of depigmented maculae that clinically represent the disease vitiligo. Although the cause is unknown, various theories such as the autoimmune, autocytotoxic, and neural hypotheses have been proposed. Extensive research has provided numerous answers regarding the pathogenesis, histopathologic evidence, and treatment of vitiligo. This discussion of vitiligo summarizes the varied clinical presentations of the disease, theories attempting to explain the mechanism of melanocyte destruction, histopathologic findings, and different treatment modalities currently available.

Adrenal Cortex Hormones↗
PubMed1998

Dermatomyositis.

Dermatomyositis is a rare inflammatory myopathy with characteristic skin manifestations and muscular weakness. The disease can be categorized as adult idiopathic, juvenile, or amyopathic dermatomyositis as well as that associated with a connective tissue disease or a malignancy. Immunologic factors are most likely involved in the pathogenesis of the disease; however, genetic and environmental issues may also play important roles. Treatment with immunosuppressive agents has proved successful in the majority of patients, although significant morbidity still occurs.

Autoantibodies↗
PubMed1996

Mechanisms of hepatocyte growth factor stimulation of keratinocyte metalloproteinase production.

Matrix metalloproteinases participate in normal physiologic processes; however, their overproduction has been associated with connective tissue destruction in a variety of pathological states. Migrating basal keratinocytes transiently express collagenase-1 during normal cutaneous reepithelialization. However, the overexpression of both collagenase-1 and stromelysin-1 has been associated with the pathogenesis of chronic nonhealing ulcers. Aberrant expression of metalloproteinases in inflammation is mediated, at least in part, by soluble factors. Since hepatocyte growth factor/scatter factor (HGF/SF) has been reported to promote keratinocyte migration and proliferation, key events in wound repair, and since HGF/SF is produced by dermal fibroblasts and its c-Met receptor is expressed by basal keratinocytes in wounded skin, we have studied the effects of HGF/SF upon keratinocyte metalloproteinase expression. We have found that HGF/SF can stimulate keratinocyte collagenase-1 and stromelysin-1 production in a dose-dependent and matrix-dependent manner. Expression of 92-kDa gelatinase was not affected by HGF/SF. We determined that HGF/SF regulation of collagenase-1 expression is transcriptionally mediated and requires tyrosine kinase and protein kinase C activaties. HGF/NK1, a naturally occurring, truncated form of HGF/SF, also stimulates collagenase-1 production, but much less efficiently than does the parent molecule. However, HGF/NK2, another HGF/SF splice variant, as well as heparin, potently inhibit HGF/SF-induced collagenase-1 synthesis. These results indicate that HGF/SF and its naturally occurring splice variants have diverse biological effects on keratinocytes and suggest an additional mechanism whereby HGF/SF may regulate keratinocyte function during wound repair.

Adult↗
PubMed1995

Superficial fungal infections. Getting rid of lesions that don't want to go away.

Systematic analysis of possible dermatophyte and candidal skin infections leads to an accurate diagnosis and prompt treatment with a specific regimen. The first steps are thorough skin examination and evaluation with a potassium hydroxide preparation. Tinea corporis, tinea cruris, tinea pedis, cutaneous candidiasis, and tinea versicolor can be treated with many topical antifungal agents, whereas tinea capitis requires oral griseofulvin therapy. Frequently used topical medications for tinea and candidal infections include clotrimazole (Lotrimin, Mycelex), econazole nitrate (Spectazole), ketoconazole (Nizoral), miconazole nitrate (Monistat-Derm, Micatin), oxiconazole nitrate (Oxistat), and ciclopirox olamine (Loprox). Topical selenium sulfide lotion can also be used for tinea versicolor, which is often a recalcitrant problem.

Candidiasis, Cutaneous↗
PubMed1993

Cell-matrix interactions modulate interstitial collagenase expression by human keratinocytes actively involved in wound healing.

We reported that interstitial collagenase is produced by keratinocytes at the edge of ulcers in pyogenic granuloma, and in this report, we assessed if production of this metalloproteinase is a common feature of the epidermal response in a variety of wounds. In all samples of chronic ulcers, regardless of etiology, and in incision wounds, collagenase mRNA, localized by in situ hybridization, was prominently expressed by basal keratinocytes bordering the sites of active re-epithelialization indicating that collagenolytic activity is a characteristic response of the epidermis to wounding. No expression of mRNAs for 72- and 92-kD gelatinases or matrilysin was seen in keratinocytes, and no signal for any metalloproteinase was detected in normal epidermis. Immunostaining for type IV collagen showed that collagenase-positive keratinocytes were not in contact with an intact basement membrane and, unlike normal keratinocytes, expressed alpha 5 beta 1 receptors. These observations suggest that cell-matrix interactions influence collagenase expression by epidermal cells. Indeed, as determined by ELISA, primary cultures of human keratinocytes grown on basement membrane proteins (Matrigel; Collaborative Research Inc., Bedford, MA) did not express significant levels of collagenase, whereas cells grown on type I collagen produced markedly increased levels. These results suggest that migrating keratinocytes actively involved in re-epithelialization acquire a collagenolytic phenotype upon contact with the dermal matrix.

Basement Membrane↗