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Biomedical subjects

G Plewig

Publications and source records attributed to G Plewig.

At least 19 recordsLinked to original sources

Pyoderma faciale. A review and report of 20 additional cases: is it rosacea?

BACKGROUND AND DESIGN: Pyoderma faciale was originally described by O'Leary and Kierland in 1940. It is characterized by the sudden onset of monstrous coalescent nodules and confluent draining sinuses confined to the face of young women in their early 20s. This report summarizes our results in 20 cases. The women were 15 to 46 years old (mean, 25 years). RESULTS: All women were flushers and blushers. Histopathologic examination revealed a dense perivascular and periadnexial infiltrate, including granulocytes, eosinophils with epithelioid granulomas, and septal and lobular panniculitis. No consistent laboratory abnormalities were found. After much therapeutic experimentation, we developed an effective treatment plan, based on a combination of oral isotretinoin and corticosteroids. CONCLUSION: We regard it as an extreme form of rosacea and suggest it be renamed rosacea fulminans in analogy with its counterpart, acne fulminans.

Adolescent

Migration of a human keratinocyte cell line (HACAT) to interstitial collagen type I is mediated by the alpha 2 beta 1-integrin receptor.

The migratory response of the human keratinocyte cell line HaCaT to collagen type I and the molecular mechanism underlying collagen-mediated migration have been analyzed. The migratory response of HaCaT cells to collagen type I consisted of a dose-dependent migration to insoluble step gradients of substratum-bound collagen (haptotaxis) and to gradients of soluble collagen (chemotaxis). Checkerboard analysis demonstrated a minor chemokinetic component. Denatured collagen type I was less chemoattractive than the native triple-helical form. Pre-treatment of cells with 25-250 micrograms/ml of synthetic peptides containing the fibronectin cell-recognition sequence RGD (Arg-Gly-Asp) resulted in a concentration-dependent inhibition of fibronectin-mediated chemotaxis, whereas chemotaxis to collagen was not affected. We then investigated the role of VLA/collagen-receptors for collagen type I-induced chemotaxis. Monoclonal antibody (MoAb) 5E8, which selectively blocks function of the alpha 2 subunit of the VLA-2/collagen receptor, dose-dependently inhibited the chemotactic response of HaCaT cells to collagen. This effect was specific for collagen-mediated chemotaxis because the chemotactic response to fibronectin remained unaffected. In contrast, a function blocking MoAb directed to the alpha 3 subunit of the coexpressed VLA-3 receptor, which is also capable of binding collagen, had no effect. However, function blocking MoAb directed to the beta 1-chain of integrins completely inhibited chemotaxis to collagen type I. Based on our results, we propose that the chemotactic migration of the human keratinocyte cell line (HaCaT) to collagen type I is specifically mediated by the RGD independent VLA-2/collagen receptor (alpha 2 beta 1) of the integrin family.

Amino Acid Sequence

Are disturbances of omega-6-fatty acid metabolism involved in the pathogenesis of atopic dermatitis?

Recent evidence indicates that the primary defect in atopic dermatitis (AD) might concern the maturation and differentiation of T cells which infiltrate the skin or are unable to control T cell infiltration of the skin. Unfortunately, there is no information on thymus hormones, T cell differentiation factors or cytokines during early T cell maturation in atopic infants. One of these factors at fault might involve a deficiency of essential long-chain omega-6-fatty acids and E-type prostaglandins which are important for thymic T cell maturation and thymus hormone action. Deficiencies of 6-desaturated omega-6-fatty acids have been observed in plasma phospholipids, epidermal and red cell phospholipids of patients with AD, in umbilical cord plasma lecithin of newborn infants with increased cord blood IgE levels, in cord blood T-cells of 'atopy-at-risk' newborn infants, in atopic monocytes, in adipose tissue lipids of patients with AD, in breast milk lipids of mothers with a history of AD, and in breast milk lipids of mothers of infants with AD. Reduced release of arachidonic acid has been measured in atopic monocytes and platelets. Diminished formation of prostaglandin E2 (PGE2) has been observed in atopic monocytes under stimulated and unstimulated conditions and in inflamed and non-inflamed atopic epidermis. PGE2 is able to suppress interleukin 4-induced IgE synthesis of human non-atopic mononuclear cells in vitro. We have demonstrated a suppressive effect of PGE1 and PGE2 on in vitro IgE synthesis of mononuclear blood cells of patients with AD and respiratory allergies.(ABSTRACT TRUNCATED AT 250 WORDS)

Dermatitis, Atopic

[Angioimmunoblastic lymphadenopathy with cutaneous manifestations in a 13-year-old girl].

We describe a 13-year-old girl with angioimmunoblastic lymphadenopathy. The patient's main symptom was a generalized pruritic maculopapular rash located mainly on the upper and lower limbs. In addition to the skin lesions, physical examination revealed enlarged cervical, axillary and inguinal lymph nodes. There were also hepatosplenomegaly and oedema of both hands. Blood examination showed elevated ESR, haemolytic anaemia, polyclonal hypergammaglobulinaemia and eosinophilia. Virus serology including HIV I and II and HTLV I was negative. Histopathological examination of a lesional skin biopsy showed superficial and deep dermal infiltrate extending into the subcutaneous tissue. The infiltrate consisted of lymphocytes, some with atypical nuclei, histiocytoid cells, and few eosinophils. There was also proliferation of dermal blood vessels. Examination of an enlarged cervical lymph node disclosed typical histopathological features of angioimmunoblastic lymphadenopathy and confirmed the diagnosis.

Administration, Topical

[Neurothekeoma. A light and electron microscopy, histochemical and immunohistochemical study].

We report a 37-year-old man with neurothekeoma that developed on the tip of the nose. Histopathological examination revealed a lobulated myxoid dermal tumour. The tumour cells were spindle-shaped or bizarre configuration. In the lower part of the dermis the lesion contained abundant cells simulating glomus tumour or melanocytic naevus. Staining with S-100 protein, epithelial membrane antigen (EMA), neuron-specific enolase (NSE) and desmin were negative. The matrix of the tumour was positive for Alcian blue and periodic acid-Schiff (PAS). Electron microscopic examination showed that the lesion was composed of dendritic cells separated by abundant glassy matrix and varying amounts of collagen fibres. Some of the cells looked like fibroblasts, and others like perineurial cells. The histogenesis of the tumour is discussed with particular attention to histochemical, immunohistochemical, light and electron microscopic findings.

Adult

Photosensitivity induced by quinidine sulfate: experimental reproduction of skin lesions.

A case of quinidine sulfate-induced photodermatitis is reported. The photosensitive reaction to quinidine sulfate was reproducible in the photopatch test and after oral intake plus ultraviolet A (UVA) irradiation. Eczematous dermatitis was provoked after intradermal injection of in vitro UVA-irradiated quinidine sulfate only in the presence of patient's serum. The clinical picture and histology suggest an allergic reaction. The photobinding of quinidine sulfate to a potential carrier protein in skin or serum seems to be of crucial importance for this type of photodermatitis. Quinidine sulfate is frequently used as an antiarrhythmic drug. Its potential as a photosensitizer should always be considered.

Aged

[Sulzberger-Garbe exudative discoid and lichenoid chronic dermatosis ("Oid-Oid disease")--reality or fiction?].

In 1937, Sulzberger and Garbe singled out an exudative discoid and lichenoid chronic dermatosis characterized by the combination of various symptoms which by themselves are not specific from the heterogeneous eczema group. The report of a 7-year-old girl is used as a basis to describe the characteristics of the disease and to present the authors' own interpretation. Clinically, there were discoid and lichenoid lesions with severe pruritus. Blood examination revealed eosinophilia. Histopathological examination of skin lesions showed psoriasiform, spongiotic, lichenoid dermatitis. A therapeutic regimen of oral corticosteroids led to complete regression of the skin changes. We feel that there are no clinical or histological findings to differentiate Sulzberger-Garbe disease definitely from extensive nummular eczema.

Biopsy

[Actinic prurigo].

Actinic prurigo is a rare idiopathic photodermatosis, which shares some features with atopic dermatitis, polymorphous light eruption, hydroa vacciniforme and persistent light reaction. It is, however, recognized as a distinct entity. Among American Indians a familial variant is observed. Characteristic features are a chronic course with sustained exacerbations, which are seasonal at first, but later perennial. The disorder may improve in adulthood. The typical clinical features are urticarial plaques a few hours after UV exposure, and a persistent eczematous, prurigo-like rash distributed over skin areas exposed to light but sometimes extending even into photoprotected areas. Therapy is extremely difficult and unrewarding. In the present paper the entity is defined and three typical cases are presented.

Adult

[The effect of UV-A and UV-B irradiation on the skin barrier. Skin physiologic, electron microscopy and lipid biochemistry studies].

In order to gain insight into the effects of UV-irradiation on the skin barrier, functional (skin reactivity), electron microscopic and lipid-biochemical studies were performed. In three different irritation models, both UV-A-irradiated and UV-B-irradiated areas proved to be more resistant to damage than normal skin, providing evidence for improvement of barrier function after UV irradiation. Electron microscopic evaluation showed that UV-B induced a significant increase in horny cell layers, whereas after UV-A no change was detected. However, both UV-B and UV-A exposure resulted in an increase in the amount of all stratum corneum lipids. This was also observed in all major ceramide subfractions, which are believed to be the essential lipid constituents for the epidermal barrier function. These findings may explain the known beneficial effects of phototherapy in dermatoses with impaired barrier function, i.e., atopic dermatitis.

Dose-Response Relationship, Radiation

[Dowling-Degos disease with exclusively genital manifestations].

We report on two women with pigmented lesions of the vulva. The histopathology (filiform downgrowth of pigmented epithelial strands two to four cells wide, extending from the interfollicular epidermis and from follicular infundibula; no increased numbers of melanocytes; horn pseudocysts) was specific for Dowling-Degos disease. One patient also had acne inversa, and the other patient had been treated surgically for a pilonidal sinus some years before. The spectrum of conditions that should be considered in the differential diagnosis of genital pigmented lesions is discussed. Vulvar melanosis, genital lentigo, malignant melanoma, acanthosis nigricans maligna and benigna and syndromes occurring concomitantly with pigmentation of the mucosa need to be excluded. The association of Dowling-Degos disease with acne inversa, which was recently described for the first time, is discussed.

Adult

Cytogenetic effects during extracorporeal photopheresis treatment of two patients with cutaneous T-cell lymphoma.

The effect of extracorporeal photopheresis (EP) on various cytogenetic parameters has been investigated. During EP the photoactivatable agent 8-methoxypsoralen (8-MOP) was administered orally. After 2 h a leukocyte-enriched blood fraction was collected by haemocentrifugation, irradiated with UVA extracorporeally, and reinfused to the patient. Two patients suffering from cutaneous T-cell lymphoma showed a marked clinical improvement in response to therapy. In order to investigate the cytogenetic effects and mutagenic risk of EP, the mitotic index (MI), the type and number of chromosomal aberrations and the rate of sister chromatid exchanges (SCE) were studied. Following EP treatment the patients' lymphocytes were cultured and stimulated with phytohaemagglutinin (PHA) for 48 or 72 h. The cultured lymphocytes showed a decreased MI after 48 h as an indicator of cytotoxic effects, but not after 72 h. In lymphocyte cultures not stimulated with PHA, the MI was decreased even after 72 h. The number of chromosomal aberrations and SCE were increased upon treatment, but only transiently, returning to basal levels between consecutive treatments. Our data provides no evidence for increased mutagenic risk as a consequence of effective EP treatment.

Administration, Oral

UVA irradiation induces collagenase in human dermal fibroblasts in vitro and in vivo.

We report the effect of UVA irradiation on collagen metabolism of fibroblasts, including both synthesis of the collagen degrading enzyme collagenase and de novo synthesis of type I collagen as the major structural component of the dermis. For this purpose confluent fibroblast monolayers were irradiated under standardized conditions (5, 15, 35, 60 J/cm2 using UVASUN 3000, Mutzhas, Munich, FRG, and UV source Sellas sunlight type 2.001, Sellas, Gevelsberg, FRG). Subsequently, total RNA was isolated and subjected to dot blot and northern blot analysis using oligolabelled cDNA clones for human type I collagen, collagenase and beta-actin. Collagen type I and beta-actin mRNA levels remained unaltered following irradiation, suggesting that the synthetic pathway of collagen metabolism at the pretranslational level is not affected by short-term UVA irradiation. However, collagenase mRNA was found to be dose-dependently induced in fibroblasts after irradiation, thus probably contributing to the actinic damage to the dermis. These in vitro data were confirmed in vivo using in situ hybridization on frozen sections of biopsy material obtained from UVA irradiated patients.

Cell Division

Photopatch testing: the 5-year experience of the German, Austrian, and Swiss Photopatch Test Group.

A cooperative photopatch test study was conducted by 45 dermatologic centers in Austria, Germany, and Switzerland. Results obtained from 1985 to 1990 are presented. A standard photopatch test tray of 32 substances was applied to the back of patients with suspected photosensivity. After applications for 24 hours, test sites were irradiated with 10 joules/cm2UVA. Unirradiated controls were included. Readings were performed immediately and 24, 48, and 72 hours after irradiation; responses were qualitatively graded on a 4-point scale. All data were stored and processed by a computer. With computer-assisted analysis of reaction patterns photoallergic reactions were identified and distinguished from phototoxic reactions. Data of 1129 patients were evaluated. Among a total of 2859 positive test reactions in 870 patients, 2041 in 778 patients were found to be photoinduced and 818 in 413 patients were contact reactions; 108 reactions in 83 patients were classified as photoallergic. Nonsteroidal anti-inflammatory drugs, disinfectants, sunscreens, phenothiazines, and fragrances caused most often photoallergic reactions. Many unspecific phototoxic reactions were induced by tiaprofenic acid, promethazine, carprofen, chlorpromazine, fenticolar, wood balsam of Peru, and perfumes. Despite the distinction between photoallergic and phototoxic responses, many test reactions lacked relevance for the patients' dermatoses.

Adolescent

Disturbances of essential fatty acid- and prostaglandin E-mediated immunoregulation in atopy.

Impaired suppressor T lymphocyte maturation and function in atopic individuals are explained by an insufficient transmission of prostaglandin E (PGE) signals during thymic lymphocyte differentiation as well as an impaired ability of the atopic immune system to activate suppressor T-cells by PGE-mediated feed back mechanisms. We demonstrate that spontaneous in vitro immunoglobulin E synthesis of atopic peripheral blood mononuclear cells could be suppressed by the addition of 10(-6) M to 10(-5) M PGE1 or PGE2. Decreased plasma and breast milk levels of PGE-precursor fatty acids and reduced numbers of PGE2-receptors on atopic lymphocytes have been observed in atopic individuals. These insights might offer a novel approach for the prevention of atopic disease by substitution of the atopic pregnant and nursing woman and her newborn infant with long chain omega-6-fatty acids.

Adult