Biomedical subjects
Publications and source records attributed to A Kahan.
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Pregnancy in Rat induces, as in humans suffering from rheumatoid arthritis, a striking improvement of adjuvant arthritis. This improvement is not associated with an enhancement of corticosteronemia; it does not appear either in pseudo-pregnancy, or in experimental deciduoma. It could rather be related to an immune mechanism; an enhancement of T suppressor lymphocytes associated to a decrease of T helper lymphocyte activity in peripheral blood as suggested by a high response to ConA and low response PHA and PWM during arthritis plus pregnancy. The influence of hormonal factors on recirculation and/or activity of peripheral lymphocytes is not excluded.
A case of severe cardiac failure during generalized Yersinia enterocolitica infection, in a previously healthy woman is described. It was possible to demonstrate the important role of coronary hypoperfusion in the late stages of septic shock. When beta stimulant drugs became ineffective, IABP improved cardiac function.
Adjuvant arthritis can be induced by a single injection of Freund's complete adjuvant (FCA) in the highly susceptible Lewis (LEW) rat strain, but not the resistant Wistar A.G. (WAG) strain. This strain-dependent susceptibility to the disease is correlated with differences in T suppressor cells regulation. In WAG rats, indeed, the in vitro response in LEW alloantigens was highly inhibited 11 days after FCA injection, while LEW rats in vitro response to WAG alloantigens was slightly increased. Furthermore, spleen cells from WAG rats given FCA 4 days before exhibited T cell-mediated active suppression of WAG in vitro response to LEW alloantigens when they were co-cultured with WAG normal spleen cells. This suppression was abolished by removal of T cells on nylon wool column. A previous irradiation of these T cells also inhibited their suppressive effect, suggesting that FCA-induced suppression might be due to soluble suppressor factor(s). On the other hand T cells from FCA treated LEW rats did not produce any modification of LEW in vitro response to WAG alloantigens. This suggests that the severe arthritis induced in LEW rats could be correlated with a defect of their suppressor cells functions, while in WAG rats FCA activated suppressor T cells could control the disease.
In each of the 16 patients included in our first study [6 idiopathic Raynaud's phenomenon (I), 4 associated with systemic lupus erythematosus (SLE) and 6 with progressive systemic sclerosis (PSS)] digital vasospasm could be reproduced by immersion of both hands in cold water (4 degree C). Each patient received in a double-blind manner and random order on two consecutive days, the calcium-channel blocking agent nifedipine (20 mg) and placebo. Nifedipine protection against vasospasm provoked by cold water (4 degrees C) was considered good or excellent in 14 of the 16 patients (p less than 0.001 versus placebo). In the second study, 30 patients [12 I, 10 PSS, 5 SLE and 3 rheumatoid arthritis (RA)] received in a double blind manner and random order, on two consecutive weeks, nifedipine (20 mg 3 time daily) and placebo. The improvement with nifedipine (in percentage of the decrease of the number of vasospastic attacks) was 90.95 in the 1 group, 78.63 SLE and RA and 64.02 in PSS (p less than 0.01). An open study during 3 months has confirmed the effectiveness of nifedipine (10 mg 3 times daily). The improvement was 88.92 in the 1 group, 76.33 in SLE and RA and 59.16 in PSS, 7 out of 30 patients stopped the treatment because of side effects (headache, flush, nausea, oedema of the ankles). Thus nifedipine appears to be extremely useful in the treatment of Raynaud's phenomenon.
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This paper deals with mitochondria microcrystal deposition in some human inflammatory rheumatism and in experimental arthritis. Hydroxyapatite microcrystals were observed in Ankylosing Spondylitis (AS) and Reiter Syndrome (RS) but never in rheumatoid synovitis nor in chondrocalcinosis synovitis. In Rat and Rabbit experimental arthritis, they were always seen in mitochondria as in AS and RS and never in lysosomes. This fact suggests mitochondrial abnormalities in calcium metabolism, which may be a consequence of synovial inflammation in a susceptible host.
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NZB/NZW F1 hybrid mice treated for long periods with type beta interferon developed early symptoms of autoimmune disease. In these animals the level of anti-dsDNA antibody begins to increase at 4-6 months while untreated NZB/NZW mice do not display similar levels until 12 months. The concomitant administration of isoprinosine and interferon delays the early appearance of autoimmune disorders. In interferon-treated NZB/NZW mice the cytotoxic activity of natural killer lymphocytes is maintained at high levels until the age of 5 months. Nevertheless, the natural killer activity is even stronger and detected until at least 7 months in NZB/NZW mice receiving a single dose of interferon 16 hr prior to the test. Lymphoblastoid ascitic tumours appeared early (2-3 months) during interferon treatment in all groups of NZB/NZW mice. However, in the presence of isoprinosine only a few animals developed tumours. Thus, isoprinosine seems to protect NZB/NZW mice both from early autoimmune disorders due to interferon and from early tumour development.
Nuclear refringence test (NRT) was studied in two inbred strains of rats: Lewis (LEW) and Wistar AG (WAG), the first develops a severe arthritis while the later only slight inflammation. Before adjuvant injection, a good NRT to ConA, PHA and Isoprinosine was observed in LEW but a poor one in WAG. After adjuvant injection a striking difference appears between the two strains concerning ConA response: in LEW the response is significantly lower on day 14, while in WAG the initial poor response is not modified. These data suggest that in WAG the suppressor T lymphocytes are already activated in vivo and are no longer responsive in vitro. The responses to PHA and Isoprinosine are parallel in both strains, the NRT response diminishes on day 14 in LEW and on day 21 in WAG.
After a double-blind trial of 4 months, 40 patients with RA were treated with 100 mg Levamisole. Clinical results were good or excellent in 50%. The immunological status is not a valuable criterion for the selection of patients apt to respond to Levamisole. A good correlation was found between clinical improvement, reduction of ESR, percentage of immunoblasts, rheumatoid factor titre and the enhancement of lymphoblastic response to polyclonal mitogens. The treatment maintenance rate for efficacy was much lower for Levamisole than for D-penicillamine.
The authors have measured the effects of methoxy-2 ethanol and derivatives or analogs on adjuvant arthritis in Rat, and the activity of methoxy-2 ethanol on humoral responsiveness to antigenic stimuli in Rat. Only methoxy-2 ethanol,1,2-dimethoxyethane and 1-methoxy 2 ethoxy ethane out of 13 tested derivatives, have an inhibitory activity on adjuvant arthritis. Methoxy-2 ethanol induces a significant depression of antibody production after immune stimuli and a significant effect on rejection of the skin graft. Although these results are of interest, toxicity of methoxy-2 ethanol will be a limiting factor for therapeutic use.
Articular manifestations may be the onset of genetic alpha galactosidase deficiency (Fabry's disease). Ultrastructural study shows typical osmiophilic lamellar inclusions of trihexosylceramides in synoviocytes, capillaries and adipocytes. Furthermore microcrystals identical to those seen in Gaucher's disease and type II hyperlipoproteinemia were observed in mitochondria and free in cytoplasm. These data suggest a microcrystalline pathogenesis of these arthropathies, as in gout and chondrocalcinosis, and what we have generally called crystallopathic arthropathies.
For 13 years polyarthritis with specific synovial involvement was observed in a case of type II hyperlipoproteinemia. Microcrystals similar to those described in Gaucher's and Fabry's disease were seen in synovial cytoplasm and mitochondria. These data suggest a microcrystalline pathogenesis for type II hyperlipoproteinemia arthritis as in gout and chondrocalcinosis.