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Biomedical subjects

H Menninger

Publications and source records attributed to H Menninger.

At least 37 records · Page 2Linked to original sources
PubMed1991

A double blind randomized parallel trial of intramuscular methotrexate and gold sodium thiomalate in early erosive rheumatoid arthritis.

In a double blind study 57 patients with active erosive rheumatoid arthritis without malalignment or deformities (median disease duration 13 months) were randomly treated with 50 mg gold sodium thiomalate (GSTM) or 15 mg methotrexate (MTX) intramuscularly for 6 months. In the GSTM group, 5/28 patients had to be withdrawn because of side effects; in 2/28 the dose was reduced. In the MTX group, 2/29 were withdrawn, one was lost to followup. The number of swollen joints improved by over 6 in 18/26 (MTX) and in 15/21 (GSTM). Five clinical variables and the sedimentation rate improved significantly in both groups without significant intergroup differences. The radiographs of hands, wrists and forefeet (32 joints evaluated according to Larsen) showed a radiological progression in 11/26 (MTX) and in 8/20 patients (GSTM); however, the deterioration of the mean Larsen index was not significant. While there was no significant difference in effectivity, tolerability was better in the MTX group.

Adolescent↗
PubMed1990

Expression of activation antigens on T cells in rheumatoid arthritis patients.

The aim of our study was to identify differences in cell surface marker expression between T cells taken from the peripheral blood (PB) of healthy individuals and T cells recovered from inflamed joints of rheumatoid arthritis (RA) patients. Out of 118 monoclonal antibodies (MoAbs) directed against activation antigens on haematopoietic cells, 12 MoAbs recognizing nine distinct surface molecules were selected after a screening procedure to study the expression of the corresponding antigens on T cells from the PB, synovial fluid and synovial tissue of RA patients, and also on T cells from PB and spleens of controls. Using two-colour flow cytometry and immunohistology we found the molecules B-C5, CD39, CD40, CD45 R0, CD54, CD76 and potentially 1D11 to be substantially up-regulated on T cells from various body compartments in RA patients. We thus could determine that the cell surface of T cells in RA patients not only differs in MHC class II expression, but also in a number of other activation-associated cell surface molecules from T cells in healthy individuals.

Adult↗
PubMed1986

Oxygen radicals as effectors of cartilage destruction. Direct degradative effect on matrix components and indirect action via activation of latent collagenase from polymorphonuclear leukocytes.

Degradation of intact cartilaginous tissue (bovine nasal cartilage) by oxygen-derived free radicals (ODFR) generated enzymatically by xanthine oxidase and hypoxanthine was studied. The degree of tissue destruction was determined by measuring the indentation under a defined compression force as well as by the loss of uronic acid- and hydroxyproline-containing matrix components. Cartilage slices altered by prior elastase treatment were more susceptible to oxygen radical attack than were intact tissue specimens. Degradation of cartilage matrix by ODFR was strongly inhibited by superoxide dismutase or catalase. Coincubation of latent collagenase from polymorphonuclear leukocytes with the ODFR-generating system led to activation of collagenolytic activity, resulting in marked degradation of the bovine cartilage slices. In further studies, activated polymorphonuclear leukocyte-collagenase was shown to degrade intact human articular cartilage to a degree of mechanical insufficiency. Thus, our assay system serves as an in vitro model of tissue damage, which may be relevant to pathophysiologic states such as rheumatoid arthritis.

Animals↗
PubMed1983

[Long-term drug therapy in inflammatory rheumatic diseases using chronic polyarthritis as an example. 2. Basic principles of long-term drug therapy: choice of optimal therapeutic agents].

The article reviews the principles of the long-term drug therapy of rheumatoid arthritis. A nomogram is presented which allows selection of adequate antiphlogistic and long-term drugs according to activity and progression of the disease. Steroids, non-steroidal antiphlogistics, gold, D-penicillamine and azathioprine are described in the order of their application during treatment of a severe polyarticular flare-up. Some of the drug regimens are relevant also to diseases other than rheumatoid arthritis, but drug therapy reflects only a single aspect in the treatment of these diseases and has to be applied together with non-pharmacologic methods (surgery, physical therapy, functional therapy, psychology etc.).

Antimalarials↗
PubMed1982

[Proteolytic occurrences in the metabolism of cartilage and their modification by antirheumatics].

Rheumatic diseases are characterized by the progressive loss of articular cartilage. According to a well established hypothesis proteolytic enzymes take part in these events. The initial attack in an normal cartilage can be exerted by proteoglycanases originating from either chondrocytes or cells from outside the cartilage like neutrophilic granulocytes or macrophages. In rheumatoid arthritis these latter cells are found in immediate vicinity to cartilage and it is assumed that they release their enzymes directly into the cartilage. Lysosomal elastase from neutrophilic granulocytes is a key enzyme made responsible for the degradation of cartilage, since it is able to soften up this tissue and thereby to deprive it of its normal mechanical properties. Therefore the pharmacological inactivation of elastase bears a therapeutic potential for rheumatic joint disease. The ultimate value of enzyme inhibitory antirheumatic drugs needs, however, further investigation since also enzyme independent variables play an important role in maintaining normal function of cartilage.

Anti-Inflammatory Agents↗
PubMed1981

Lysosomal elastase: effect on mechanical and biochemical properties of normal cartilage, inhibition by polysulfonated glycosaminoglycan, and binding to chondrocytes.

Rheumatic joint destruction usually starts with the destabilisation of cartilage. Lysosomal elastase is a candidate effector of this process, since this enzyme is found at the site of cartilage erosion by rheumatoid synovial tissue. In order to prove this hypothesis we assessed the mechanical stability of cartilage during treatment by this enzyme in vitro. An indentation apparatus was used for this purpose and biochemical as well as microscopic techniques were used to supplement the results thus obtained. Our findings show that elastase irreversibly impairs the stability of cartilage by lysis of matrix proteoglycans without the help of additive enzymes. Collagen fragmentation played no significant role during elastase-induced destabilisation, while specific collagenase attacked the collagen network within the matrix only subsequent to the removal of proteoglycans. These findings suggest that elastase is a leading enzyme during proteolytic cartilage degradation. In addition polysulfonated glycosaminoglycan was found to reduce the mechanical effect of elastase on normal cartilage. It is therefore concluded that local inhibition of elastase promises therapeutic benefit during rheumatic cartilage degradation. Upon treatment of cartilage with elastase we observed this enzyme not only within the matrix under destruction but also bound to chondrocytes. These findings support the hypothesis that elastase plays a role on the matrix not only by direct degradation, but also by an indirect effect mediated through living chondrocytes.

Adolescent↗
PubMed1981

[Radiological changes in systemic lupus erythematosis (author's transl)].

In a study of 50 patients with systemic lupus erythematosis, radiologically demonstrable lung changes and pleural effusions were found in 50%. Changes in the peripheral skeleton, such as osteoporosis, erosions or mutilations, were seen in only two patients. Our radiological analysis has shown that systemic lupus erythematosis does not produce changes in the joints, but is responsible for abnormalities in the lungs, as well as for pericardial and pleural effusions.

Adult↗
PubMed1979

[Morphologic indication for the participation of neutrophil granulocytes in rheumatic cartilage destruction].

Cartilage destruction in rheumatoid arthritis may be mediated by enzymes of the synovial fluid and by cells of the proliferating pannus tissue. Neutrophilic granulocytes are usually said to affect the cartilage via the synovial fluid, and their local occurrence in the pannus-cartilage border is denied. However, a morphological study on pannus tissue and cartilage by use of histochemistry and immunfluorescence (leucocytes antielastase) exhibited an accumulation of neutrophilic granulocytes in the immediate vicinity of the cartilage in destruction. This result is in contrast to the observation of most investigators reporting studies of the pannus cartilage junction. Experimental datas of the effect of elastase moreover indicate that this enzyme is capable to penetrate into the cartilage and to degrade proteoglycans. Therefore the results show that the occurrence of neutrophilic granulocytes at the pannus-cartilage border is an important phenomenon for understanding the progressive cartilage destruction and that elastase may be at least one enzyme responsible for the degradation of the cartilage matrix.

Cartilage Diseases↗