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Biomedical subjects

B Melnik

Publications and source records attributed to B Melnik.

At least 19 recordsLinked to original sources
PubMed2002

[Malignant atrophic papulosis (Köhlmeier-Degos disease). Failure to respond to interferon alpha-2a, pentoxifylline and aspirin].

A 45 year old female patient presented with the cutaneous manifestations of malignant atrophic papulosis (Köhlmeier-Degos disease) for two years. The typical papules with central porcelain-white atrophy correspond histologically to wedge-shaped necrosis of the connective tissue due to thrombotic occlusion of small vessels in the corium. The pathogenesis of malignant atrophic papulosis and effective treatment modalities are unknown. A slow virus infection has been suggested by some authors. Therefore, we attempted an immune therapy with interferon alpha-2a over a period of 11 months, but failed to cause a significant effect on the appearance and progression of the skin lesions. Furthermore, we could not confirm the effectiveness of a recently reported treatment modality with pentoxifylline and aspirin administered to our patient over a period of 5 months.

Aspirin↗
PubMed2000

[Erysipelas carcinomatosum in tubular adenocarcinoma of the stomach].

Erysipelas carcinomatosum is an inflammatory infiltration of dermal lymphatic vessels by tumor cells of a metastatic adenocarcinoma mimicking common erysipelas. It is most often due to adenocarcinomas, especially breast cancer. A 51 year-old male patient developed erysipelas carcinomatosum on his right chest wall due to a tubular adenocarcinoma of the stomach.

Adenocarcinoma↗
PubMed1996

[The value of oil baths for adjuvant basic therapy of inflammatory dermatoses with dry, barrier-disrupted skin].

The therapeutic value of oil baths for the treatment of dry skin with disturbed barrier function in atopic eczema, atopic xerosis, dry aged skin, exsiccation eczematid and psoriasis vulgaris is presented with special regard to modern concepts of epidermal barrier function. The use of oil baths with emollients as an integral and indispensable constitutent of maintenance therapy in dry skin conditions, atopic eczema and inflammatory dermatoses is reviewed.

Baths↗
PubMed1992

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↗
PubMed1992

[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↗
PubMed1991

Are deficiencies of prostaglandin-E-mediated immunoregulation involved in increased IgE synthesis of atopic mononuclear cells in vitro?

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 prostaglandin E1 (PGE1) or PGE2. 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. Decreased levels of 6-desaturated PGE-precursor fatty acids in plasma, T lymphocytes, monocytes, adipose tissue and breast milk have been observed in atopic individuals. These insights might offer a novel approach to 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.

Cells, Cultured↗
PubMed1991

[Immune regulatory importance of prostaglandins E in atopy].

The concept proposed for the pathogenesis and prevention of atopy [Hautarzt (1989) 40:685-692] is refined by further insights into the immunoregulatory role of E-prostaglandins. It is demonstrated that in vitro IgE synthesis of peripheral blood mononuclear cell cultures of patients with atopic dermatitis is suppressed by the addition of PGE1 or PGE2. The enhanced IgE production in atopy is explained by insufficient PGE-mediated down-regulation of interleukin-4-induced IgE synthesis.

Dermatitis, Atopic↗
PubMed1991

Effects of ultraviolet A and B on the skin barrier: a functional, electron microscopic and lipid biochemical study.

To investigate the effects of ultraviolet A (UVA) and B (UVB) on the skin barrier, functional, electron microscopic and lipid biochemical studies were performed on normal and UV-irradiated skin of volunteers. Skin reactivity against primary irritants was evaluated using the alkali resistance test, the dimethylsulfoxide test and the sodium lauryl sulfate test. In all 3 irritation models, UVA- and UVB-irradiated areas were more resistant to damage than normal skin, indicating improvement of the barrier function after UV irradiation. In a second series of experiments, biopsies were taken and processed for electron microscopic evaluation of the stratum corneum. UVB significantly increased the horny cell layers; UVA did not alter the thickness of the stratum corneum. Finally, stratum corneum lipids were extracted in vivo and quantified after high-performance thin-layer chromatography. UVB and, to some extent, UVA exposure increased the amount of all stratum corneum lipids. This was also observed in all major ceramide subfractions.

Adolescent↗
PubMed1989

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↗
PubMed1989

[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↗
PubMed1988

[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↗
PubMed1988

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↗