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Biomedical subjects

D Abeck

Publications and source records attributed to D Abeck.

At least 127 records · Page 7Linked to original sources
PubMed1995

Acanthosis nigricans: a marker for hyperinsulinemia.

A 12-year-old girl developed acanthosis nigricans due to increased levels of serum insulin. Hyperinsulinemia has been recognized as the underlying cause in most cases of acanthosis nigricans. In this paper we outline a typical clinical case with special regard to the proposed pathogenesis.

Acanthosis Nigricans↗
PubMed1995

Results of German multicenter study of antimicrobial susceptibilities of Trichophyton rubrum and Trichophyton mentagrophytes strains causing tinea unguium. German Collaborative Dermatophyte Drug Susceptibility Study Group.

Thirty-two strains of Trichophyton rubrum and 16 strains of Trichophyton mentagrophytes isolated from patients with tinea unguium in various parts of Germany were subjected to a microdilution test with six systemic or topical antimycotic agents. Apart from griseofulvin, there were no species-specific differences between the two species. Terbinafine was the most active antimycotic agent, with a MIC not exceeding 0.05 micrograms/ml.

Antifungal Agents↗
PubMed1995

Pityrosporum ovale extracts increase interleukin-4, interleukin-10 and IgE synthesis in patients with atopic eczema.

Evidence for a possible role of the lipophilic yeast Pityrosporum ovale in the pathophysiology of atopic eczema has been found both in laboratory and therapeutical studies. Positive type I prick test reactions to P. ovale correlate with the intensity of eczematous skin lesions in the head and neck regions of patients with atopic eczema. Furthermore, antifungal treatment has been shown to be helpful in atopic eczema. In the present study the effect of P. ovale on IgE synthesis and cytokine production (IL-2, IFN gamma, IL-4, IL-10) was investigated in patients with atopic eczema, in vitro. Eight patients with atopic eczema were studied; of these, 5 patients had specific IgE antibodies against P. ovale, as determined by fluoroimmunoassay (RAST). The control group consisted of 5 healthy non-atopic, P. ovale IgE-antibody-negative volunteers. Freshly isolated peripheral blood mononuclear cells (PBMC) were incubated in the presence of different antigen concentrations (0.01, 0.1, 1.0, 10 micrograms/l x 10(6) cells) of P. ovale. IgE contents in the cell culture supematants were significantly elevated in RAST(+) patients with atopic eczema (p < 0.05), compared with RAST(-) atopic eczema patients and healthy volunteers. Coincubation of P. ovale-stimulated PBMC with IL-4 (50 U/l/ 1 x 10(6) cells) resulted in a significantly higher IgE synthesis only in the RAST(+) atopic eczema patients. Additionally, incubation of PBMC from RAST(+) patients with atopic eczema led to an elevated synthesis of the TH2 related cytokines IL-4 and IL-10. Within the atopic eczema group, two subgroups differed markedly in their response to P. ovale antigen stimulation with a good correlation to the presence of specific IgE in serum and in vitro IL-4 and IL-10 production. The data support the assumption that P. ovale antigens might play a role in skin inflammation in at least a subgroup of patients with atopic eczema characterized by the presence of specific IgE antibodies to P. ovale.

Adult↗
PubMed1994

[Food-induced anaphylaxis in latex allergy].

Contact uticaria and anaphylactic reactions to latex-containing rubber products are being recognized with increasing frequency in all kinds of medical disciplines. Recently a number of reports have been published describing anaphylactic reactions to food items in patients with latex allergy. The cases of three patients who developed anaphylactic reactions to both latex and food items are presented, and the importance of the association of latex and cross-reactivity with food items is stressed. The food items that led to anaphylactic reactions were banana and avocado; banana, avocado and buckwheat; and banana, avocado and tomato. The cross-reactivity of latex to buckwheat and tomato has not been reported before.

Adult↗
PubMed1993

Beta-adrenergic receptors in psoriasis: evidence for down-regulation in lesional skin.

Lesional psoriatic skin displays reduced responsiveness to beta-adrenergic stimulating agents. To elucidate whether the receptor protein itself is responsible for this, lesional and non-lesional psoriatic skin was investigated ex vivo for maximal beta-adrenergic binding density (Bmax) and beta-adrenergic binding affinity (KD). Epidermal crude membrane homogenates (ECMH) were prepared from split-thickness skin biopsies and saturated with the lipophilic beta-adrenergic antagonist (-)-125I-iodocyanopindolol (ICYP) as radioligand. Specific binding was saturable and Scatchard transformation of the binding data revealed a homogeneous class of beta-adrenergic receptors in all nine experiments. The maximal beta-adrenergic binding density was significantly less in lesional than in non-lesional psoriatic skin (Bmax = 49.7 +/- 7.2 fmol/mg protein vs. 67.1 +/- 2.2 fmol/mg protein, n = 9, P < 0.05). The binding affinity was similar in lesional and in non-lesional skin (KD = 9.0 +/- 1.5 pmol/l vs. 8.0 +/- 0.9 pmol/l). These results could at least partially explain the reduced responsiveness of the beta-adrenergic system in lesional psoriatic skin seen after stimulation with beta-adrenergic agonists.

Adult↗
PubMed1993

Chronic urticaria due to nickel intake.

A case of chronic urticaria is presented. The case of the disease was traced back to nickel intake by food as judged from type I and IV sensitization to nickel, a positive oral challenge test and long-standing, complete healing under a nickel-restrictive diet.

Adult↗
PubMed1993

[Chronic mucocutaneous herpes simplex infection. Occurrence within the scope of liver-induced immunodeficiency].

Herpes simplex virus (HSV) infections causing severe disease are reported frequently in patients suffering from human immunodeficiency virus (HIV) infection. This disease pattern may also be seen in an immunocompromised disease state with other causes, however, as in the case presented in this paper. An 84-year-old woman had hepatic cirrhosis resulting from chronic hepatitis C virus infection. The woman developed ulcerative lesions in and around her mouth and in the genito-anal region, and these persisted for some months. Diagnosis of HSV infection was not obtained until after extensive laboratory investigations. Aciclovir infusion therapy started immediately afterwards led to dramatic improvement of the skin and mucous membrane changes. Complete clearing of lesions was not obtained, however, because the patient died as a result of the immunosuppression.

Acyclovir↗
PubMed1992

Binding of Haemophilus ducreyi to extracellular matrix proteins.

A collection of Haemophilus ducreyi isolates were screened for the ability to bind to fibrinogen, fibronectin, collagen, gelatin and laminin by a particle agglutination test using latex beads coated with the individual proteins. Thirteen of 21 isolates reacted with all five extracellular matrix proteins. Binding of organisms to protein-coated latex beads was inhibited by pretreatment of the bacteria with detergent, trypsin or boiling. Two isolates did not bind to collagen and gelatin with one of these not reacting with laminin either. Seven strains which failed to react with laminin did not express pili when examined by electron microscopy. This observation suggests a specific interaction with the pili of H. ducreyi.

Agglutination Tests↗
PubMed1992

Lack of immunoglobulin A1 protease production by Haemophilus ducreyi.

A collection of 20 strains of Haemophilus ducreyi including freshly isolated, low-passage and multi-passage reference strains was examined for immunoglobulin A1 protease production by SDS-PAGE and immunoblotting. None of the strains demonstrated IgA1 protease activity despite the fact that different culture media were used. By direct immunofluorescence testing, binding of IgA to Haemophilus ducreyi organisms could be demonstrated.

Blotting, Western↗
PubMed1992

Atopic eczema: role of microorganisms on the skin surface.

The pathophysiology of atopic eczema (AE) is still poorly understood. One possible concept favors IgE-mediated reactivity towards allergens that enter the skin from the outside or through the blood. Microorganisms of the cutaneous flora also might represent a stimulus for allergic skin reactions. Abnormal bacterial skin colonization is a characteristic feature of AE. Staphylococcus aureus (S. aureus) is the most common pathogen. Binding to host cells involves special receptors, such as fibronectin or laminin. Specific IgE antibodies to S. aureus can be detected in the blood. Whereas the clinical relevance of anti-staphylococcal antibodies is still controversial, specific IgE antibodies to Pityrosporum species as well as positive type I prick test reactions to these yeasts seem to correlate with the intensity of eczematous lesions in the head and neck regions of patients with AE. Both antimicrobial and antifungal treatment has been shown helpful in some cases of AE.

Dermatitis, Atopic↗