Search PubMed⌕ Search

Biomedical subjects

G Plewig

Publications and source records attributed to G Plewig.

At least 217 records · Page 12Linked to original sources

[Kaposi's sarcoma after kidney transplantation].

A Kaposi's sarcoma of the skin with nodular and follicular lesions but no visceral involvement developed in a 44-year-old man nine months after transplantation of an haplo-identical kidney (a relative as donor). He was on an immunosuppressive regimen of daily 10 mg methylprednisolone and 2.5 mg/kg cyclosporin A. No HIV antibodies were demonstrated. After reduction of the dosage to 4 mg methylprednisolone and 1 mg/kg cyclosporin A no further growth of the skin lesions was observed, while transplant function was maintained. The lesions regressed after radiation of two areas in the right lower leg with 48 Gy. Ten months later the sarcoma again progressed and required further radiotherapy, which arrested growth, while there was no change in transplant function.

Adult↗

Pathogenesis and classification of solar urticaria: a new concept.

Although its exact mechanism remains unknown, evidence supports the immunologic nature of solar urticaria. On the basis of experimental findings in the literature and our own observations, a new concept of the pathogenesis and classification of solar urticaria is presented. We propose two types of solar urticaria: type I, IgE-mediated hypersensitivity to specific photoallergens, which are generated only in patients with solar urticaria, and type II, induction of IgE-mediated hypersensitivity to a nonspecific photoallergen, which is generated both in patients with solar urticaria and in normal persons.

Humans↗

Is the origin of atopy linked to deficient conversion of omega-6-fatty acids to prostaglandin E1?

Our hypothesis on the origin of atopy links alterations in omega-6-fatty acid metabolism in atopic persons (i.e., reduced formation of delta-6-desaturase products) to deficient T cell differentiation and function. We suggest that a relative deficiency in dihomo-gamma-linolenic acid-derived prostaglandin E1 is the major etiologic factor for diminished T cell maturation postpartum. Its precursors, gamma-linolenic acid and dihomo-gamma-linolenic acid, are physiologically provided in colostrum and mature breast milk of healthy mothers. Depressed cell-mediated immunity and uncontrolled B-cell response with increased IgE synthesis are explained as prostaglandin E1-dependent defects of T cell differentiation caused by insufficient supply of prostaglandin E1 precursors during early infancy. Thus, in our opinion atopy is a metabolic disorder and the associated immunologic disturbances are epiphenomena.

Adjuvants, Immunologic↗

Localized cicatricial pemphigoid (Brunsting-Perry): electron microscopic study.

Electron microscopic findings are presented in a patient with localized cicatricial pemphigoid (Brunsting-Perry). These findings revealed subepidermal separation below the basal lamina. The basal lamina and anchoring fibrils were well preserved and attached to the intact epidermis to form the roof of the blister. These findings support the concept that localized cicatricial pemphigoid, cicatricial pemphigoid, and disseminated cicatricial pemphigoid are closely related diseases and may explain the occurrence of scar formation in localized cicatricial pemphigoid. A review of 42 cases reported in the world literature is included, with emphasis on clinical, histologic, and immunofluorescence microscopic findings.

Aged↗

[Localized syringoma of the vulva].

A 26-year-old woman developed papular lesions symmetrically located on both labia majora during several years duration. Histopathological examination showed typical features of syringomas. In the literature, only 15 patients have been previously described.

Adenoma↗

Microanalytical screening of all major stratum corneum lipids by sequential high-performance thin-layer chromatography.

For rapid and sensitive screening of lipid biochemical abnormalities of scaling skin disorders a sequential, one-dimensional high-performance thin-layer chromatographic method (HPTLC) has been developed. All major human stratum corneum lipid classes, i.e., cholesterol sulfate, glucosylceramides, six major ceramide fractions, free sterols, free fatty acids, triglycerides, sterol esters, squalene, and n-alkanes, are separated and quantitated after a stepwise development of a single silica gel 60 HPTLC-plate using three consecutive solvent systems. Reproducible results have been obtained by degradative charring as well as fluorescence detection. By fluorescence detection the method is particularly suitable for the determination of minor amounts of cholesterol sulfate and other sterols.

Chromatography, High Pressure Liquid↗

Autosomal dominant lamellar ichthyosis exhibits an abnormal scale lipid pattern.

Autosomal dominant lamellar ichthyosis (ADLI) is a recently recognized genetic skin disorder. Clinically and histologically, it cannot be distinguished with certainty from the more frequent autosomal recessive lamellar ichthyosis (ARLI), which in itself may still be heterogeneous. By ultrastructural examination of ADLI a prominent transforming zone between the stratum granulosum and stratum corneum and lipid inclusions in the stratum corneum have been observed. Using sequential high-performance thin-layer chromatography, we studied the plantar scale lipid pattern of two patients, mother and daughter, affected with ADLI. We found a distinctive alteration in the relative composition of the scale lipid pattern characterized by excessive amounts of free fatty acids, triglycerides, elevated n-alkanes, reduced free sterols and decreased total ceramides. This scale lipid profile clearly differs from that of the erythrodermic and non-erythematous variants of ARLI and confirms that this disorder is a distinct entity of the heterogeneous group of lamellar ichthyoses.

Alkanes↗

[A new concept of the etiopathogenesis and prevention of atopic dermatitis].

The hypothesis proposed for the pathogenesis of atopy links the well-known alterations in cell-mediated and humoral immunity, the disturbances of mediator metabolism and the increased disposition of atopic epidermis for inflammation to a common underlying deficiency in the production of prostaglandin E1. The PGE1 deficiency is explained as the result of reduced delta-6-desaturase activity in atopic patients. The development of depressed cell-mediated immunity is regarded as a PGE1-dependent T-cell-maturation defect of the newborn's immune system post partum. Our hypothesis offers a novel approach to the prevention of atopy by administration of gamma-linolenic acid to newborns with increased risk of atopy and to nursing atopic mothers. Furthermore, it provides an explanation for the beneficial therapeutic effects of dietary supplementation of gamma-linolenic acid in patients with atopic dermatitis.

Alprostadil↗

[New lipid biochemical aspects in the pathogenesis of a follicular keratinization disorder in acne vulgaris].

Follicular hyperkeratinization of the epithelium of the acroinfundibulum of sebaceous follicles is one of the primary events in the pathogenesis of acne vulgaris. Oral treatment with 13-cis-retinoic acid can reduce these hyperkeratoses. In order to determine whether follicular hyperkeratinization is related to disturbances of epidermal follicular lipids, we analyzed the lipids of initial comedones from 10 patients with nodulocystic acne before and after a 6th weeks oral therapy with 13-cis-retinoic acid (0.7 mg/kg body weight). The treatment with retinoid resulted in a significant increase of epidermal lipids (free sterols: +34%; ceramides: +19%, whereas the lipids of sebaceous origin decreased (glycerides: -36%). The mass ratio of free sterols to cholesterol sulfate increased by 86% compared to pre-treatment levels. These findings support the hypothesis that local follicular deficiencies of epidermal lipids due to increased sebum secretion might induce abnormal follicular keratinization.

Acne Vulgaris↗

[Basal cell nevus syndrome with squamous cell carcinoma of the larynx].

We report on a 54-year-old patient suffering from basal cell nevus syndrome. At the age of 51, squamous cell carcinoma of the larynx had been diagnosed. The frequent occurrence of various kinds of benign and malignant neoplasms in patients with basal cell nevus syndrome illustrates the close relationship between this syndrome and phacomatoses.

Basal Cell Nevus Syndrome↗

Influence of oral isotretinoin treatment on the composition of comedonal lipids. Implications for comedogenesis in acne vulgaris.

One of the primary events in the pathogenesis of acne vulgaris is abnormal follicular keratinization. Since oral isotretinoin therapy reduces follicular hyperkeratinization in acne, our study has been designed to determine whether epidermal lipid composition of the epithelium of sebaceous follicles is affected by isotretinoin treatment. Noninflamed early comedones obtained from ten patients with nodulocystic acne before and after the 6th week of isotretinoin therapy (mean daily dose 0.7 mg/kg b. wt.) were used as probes of the hyperkeratinizing follicular epithelium. Comedonal lipids were analyzed by high-performance thin-layer chromatography. Oral isotretinoin caused a decrease of the comedonal glyceride fraction by 36% (P less than 0.01), whereas free sterols and total ceramides increased by 34% (P less than 0.10) and 19%, respectively. The changes of comedonal lipids were associated with a significant elevation of the free sterols/cholesterol sulfate ratio of 86% from pretreatment levels (P less than 0.05). The isotretinoin-induced changes of the comedonal lipid composition in direction to a pattern of epidermal lipids of normal desquamating stratum corneum are discussed as a possible comedolytic mechanism of oral isotretinoin treatment.

Acne Vulgaris↗

Acitretin versus etretinate in psoriasis. Clinical and pharmacokinetic results of a German multicenter study.

175 patients with severe psoriasis of different types were treated with 10, 25, or 50 mg acitretin and compared with patients receiving 50 mg etretinate over a period of 8 weeks in a randomized, double-blind multicenter study in the Federal Republic of Germany. Plasma concentrations of etretinate and its metabolite acitretin were measured during therapy and also 3 weeks after cessation of treatment. After 4 weeks of treatment, a trend toward clinical improvement was shown in all groups with increasing dosage. Those groups receiving the lower acitretin doses (i.e., 10 and 25 mg/day) had more dropouts than the groups taking 50 mg acitretin or 50 mg etretinate. Complete remissions before the end of therapy occurred only among those receiving higher doses. Enlargement of psoriatic lesions, however, could be observed during treatment with both retinoids, despite improvement of other parameters, as measured by psoriasis area and severity index (PASI) and psoriasis severity index (PSI). After 8 weeks, a significant improvement was calculated by the PASI score and by a newly defined, corrected PASI score for all four dose regimens compared with baseline levels. A greater than 50% PSI score improvement was seen in 50% of patients treated with 10 mg acitretin, 40.5% with 25 mg acitretin, 53.8% with 50 mg acitretin, and 61.1% with 50 mg etretinate. No statistical differences were found among these groups at any time during the 8-week period. No new or unexpected side effects occurred during acitretin treatment. Moreover, cholesterol levels did not significantly change. Three weeks after cessation of drug administration, the plasma concentrations of acitretin were below the sensitivity level of the assay, whereas etretinate was still quantifiable. It is interesting that acitretin plasma concentrations during therapy with 50 mg acitretin were markedly lower (means = 18 ng/ml) than were acitretin levels during treatment with 50 mg etretinate (means = 36 ng/ml).

Acitretin↗

Solar urticaria induced by visible light and inhibited by UVA.

A 17-year-old male with solar urticaria is described. The action spectrum ranged from 400 to 520 nm. Wheals induced by visible light were inhibited by simultaneous or subsequent irradiation of the skin with UVA radiation. UVA irradiation prior to exposure to eliciting wavelengths revealed no inhibitory effect, nor was an inhibitory effect found by pre- or postirradiation of test sites with visible light longer than 530 nm. In vitro activation of the patient's serum by exposure to visible light induced wheal formation at the injection site. The wheal formed by in vitro-activated serum was suppressed only when the serum was exposed to UVA after, but not before irradiation with wavelengths of the action spectrum. This suggests that the inactivation of a photoallergen rather than of its precursor is the mechanism by which UVA exerts an inhibitory effect.

Adolescent↗

[Photoallergy to Neotri and cross reaction to tenoretic--detection by systemic photoprovocation].

A patient is presented who suffered for 3 years from increasing photosensitivity with chronic eczematous lesions in sun-exposed areas. He had taken one Neotri (triamterene, xipamide) tablet daily for 6 years. After discontinuation of the drug, phototesting and a photopatch test failed to reveal pathological reactions. Eczematous lesions, however, were induced in test areas upon systemic photochallenging with Neotri. One year later, after the antihypertensive medication had been changed from Adalat (nifedipine) to Teneretic (atenolol, chlortalidone) the eczematous photosensitive reaction recurred. Since both xipamide and chlortalidone have a chlorsulfamoyl-substituted aromatic ring in common, it seems that a photoallergic cross-reaction occurred.

Aged↗