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Biomedical subjects

M F Kahn

Publications and source records attributed to M F Kahn.

At least 433 records · Page 24Linked to original sources
PubMedDate not supplied

Antilymphocyte antibodies in progressive systemic sclerosis.

Sera from 19 patients with scleroderma were tested for antilymphocyte antibodies (ALA) by indirect immunofluorescence assay. ALA were found in 47% of the cases when tested at 0 degrees, and in 27% at 25 degrees C. Anti-T cell specificity was shown after separation of B and T cells. The heterogeneity of the ALA detected was clear both among different patients and in serum from the same patient. A monoclonal antibody (UCHT1) inhibited ALA binding to T cells completely in one case, and partially in another three, implying that with these 4 sera, the lymphocyte receptors for ALA were either identical or very close to the UCHT1 receptor. This study defines another immunological abnormality in scleroderma: the presence of cold-reactive anti-T cell specific ALA. Their pathogenicity requires further investigation.

Antibodies↗
PubMedDate not supplied

Anti-RA 33 antinuclear autoantibody in rheumatoid arthritis and mixed connective tissue disease: comparison with antikeratin and antiperinuclear antibodies.

Besides rheumatoid factor (RF), antikeratin antibodies (AKA) and antiperinuclear factor (APN), anti-RA 33 antibody has been described as a highly specific antinuclear antibody for rheumatoid arthritis (RA). In this study RA 33 antibodies were detected using Western blotting with HeLa cell nuclear extract in a group of 94 RA patients and 259 controls. Anti-RA 33 was present in 35% of 94 RA patients, with a similar frequency in RF positive (32%) and RF-negative (45%) RA patients. RA-33 antibody was also present in 60% of a group of 30 patients with anti-U1 RNP positive mixed connective tissue disease. The specificity of anti-RA 33 for RA was 84.6%. Anti-RA 33 antibody was already present in sera from 23.5% of 18 patients with RA of less than one year's duration. Anti-RA 33 antibody was the only positive immunological marker in 3/20 cases of seronegative adult RA. No correlations were found between anti-RA 33 antibody and AKA or APF. Patients with erosive RA and patients whose ESR was > or = 50 mm after 1 hour were more likely to be anti-RA 33 positive (47.6% vs 24.4% and 42.8% vs 29.4%). These results suggest that anti-RA 33 antibody, in the absence of anti-U1-RNP antibodies, can be added to the list of the helpful serological markers for rheumatoid arthritis.

Adult↗
PubMedDate not supplied

[SAPHO syndrome].

The occurrence of musculoskeletal manifestations (including synovitis, chest wall arthroosteitis and multifocal osteomyelitis) in association with severe acne, palmoplantar pustulosis and perhaps with some presentations of psoriasis, have been described by many authors in the past 30 years. These different multifaceted descriptions have been designated by a variety of terms. More recently, a possible link between these conditions and spondarthritides has also been underlined by a slightly increased prevalence of HLA B27 and occasional occurrences of sacroiliitis, chronic inflammatory bowel disease and possibly psoriasis. An acronym, the SAPHO syndrome (which stands for Synovitis, Acne, Pustulosis Hyperostosis and Osteitis) is proposed for this group of diseases because of the similarity of musculoskeletal manifestations in patients with severe acne and pustulosis. The clinical, epidemiological, pathophysiological, immunogenetic and diagnostic aspects, as well as the management of this syndrome are reviewed.

Acne Vulgaris↗
PubMedDate not supplied

Neurological manifestations of systemic lupus erythematosus: role of antiphospholipid antibodies.

Antiphospholipid antibodies (APL) are associated with venous and arterial thrombosis in SLE patients. Various thrombotic and non-thrombotic neurological manifestations have been reported in SLE but whether or not they are related to the presence of APL antibodies remains uncertain. To assess the possible association between neurological involvement in SLE and APL antibodies, IgG anticardiolipin antibodies (IgG ACL) were looked for using an ELISA technique in 92 consecutive SLE patients seen over a one-year period. Other APL determinations included VDRL and lupus anticoagulant (LAC) testing using APTT and the diluted thromboplastin time. Twenty-four SLE patients presented with neurological manifestations (40 episodes): 15/24 (62.5%) were found positive for APL antibodies (11 VDRL, 8 LAC, 7 ACL antibodies) versus 22/68 patients (32%) without neurological symptoms (p < 0.01). APL antibodies antedated neurological symptoms in 13/16 cases. Neurological manifestations were subsequently divided into 3 groups: thrombotic (n = 14), psychosis and convulsions (n = 15), miscellaneous (n = 10). No correlation was found between APL antibodies and any of the 3 subgroups. Among patients with neurological SLE, APL antibodies were present in two with valvular heart disease, as well as in seven with a history of either deep vein thrombosis, livedo reticularis or miscarriage. Among 7 patients with thrombocytopenia and neurological symptoms, 6 had APL antibodies. These data suggest that APL syndrome is associated with neuro-ophthalmological manifestations of SLE regardless of whether or not the mechanism of neurological involvement is thrombotic. SLE patients with APL antibodies may be at risk for future neurological manifestations. However, it is still questionable that APL positivity has definite therapeutic consequences.

Adolescent↗
PubMedDate not supplied

Influence of the bacterial flora on collagen-induced arthritis in susceptible and resistant strains of rats.

Collagen-induced arthritis is an experimental model for rheumatoid arthritis which can be elicited in susceptible strains of rats by intradermal injection of native type II collagen. In order to investigate whether bacterial flora may alter the pathogenic response to type II collagen, we have immunized germ-free (GF) male rats from either highly resistant Fisher (F344) or highly susceptible Dark Agouti (DA) strains. The disease was markedly enhanced in GF DA as compared to conventional (CV) DA rats. The humoral response was also stronger in GF rats of both strains. Neither GF nor CV F344 developed arthritis, although GF F344 exhibited later inflammation of the tail. These data support a suppressive influence of bacterial flora on collagen-induced arthritis.

Analysis of Variance↗
PubMedDate not supplied

The history of rheumatoid factor.

The events that led to identification of rheumatoid factor are narrated, and the respective contributions of the researchers who worked to achieve this goal are clarified. Changes that have occurred over time in concepts concerning the clinical significance and pathophysiologic role of rheumatoid factor are briefly summarized.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Aggressive therapy for rheumatoid arthritis.

Although valuable progress has been made in the study of the etiopathogenesis of rheumatoid arthritis, available treatments have up to now been unable to control severe and resistant cases. Different approaches have been tried in order to stop the articular and/or systemic features of this disease. The present report reviews these attempts which, unfortunately, have thus far failed to provide fully satisfactory solutions.

Anti-Inflammatory Agents↗
PubMedDate not supplied

[Gougerot-Sjögren syndrome, connective tissue diseases and autoimmune pathology].

Each of the following conditions has a 4 to 6 percent frequency of association with the Gugerot-Sjögren syndrome: systemic lupus erythematous, scleroderma, autoimmune liver disease (simple biliary cirrhosis and chronic active hepatitis), and Hashimoto's thyroiditis. Association with a nodular periarteritis and a polymyositis is very much more unusual and should be discussed on account of the existence of myositis and the vascularity peculiar to the Gougerot-Sjögren syndrome. Very many true or supposedly autoimmune diseases have been reported in association with the Gougerot-Sjögren syndrome: mixed connectivity, atrophying polychondritis, Reynolds' syndrome (scleroderma plus simple biliary cirrhosis), thrombotic thrombocytopenic purpura, thyrotoxicosis of simple hypothyroidism, and total or partial lipodystrophy. The lacrymal and salivary condition is almost constant during systemic lupus erythematosus, scleroderma, simple biliary cirrhosis and mixed connectivity. From the point of view of autoimmune pathology, the Gougerot-Sjögren syndrome might constitute either an autonomous condition when found in isolation or represent the exocrine glandular expression of a dysimmunitary disease with which it is associated.

Autoimmune Diseases↗