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Biomedical subjects

M Moisy

Publications and source records attributed to M Moisy.

At least 19 recordsLinked to original sources
PubMed1981

Quantitation of C2 by rocket immunoelectrophoresis in 120 pathological sera.

A potent monospecific anti-C2 was used for quantitation of serum C2 by rocket immunoelectrophoresis (RIE). This ready procedure was compared to the one-step hemolytic titration utilizing C2-deficient human serum. RIE detected 4 nanograms C2 in 5 microliters samples. Using highly purified C2 as a reference, C2 concentration in pooled normal human sera was estimated around 50 micrograms/ml by both test systems. The reliability of RIE was assessed when immunochemical and hemolytic determinations were comparatively performed in 120 pathological sera. The correlation coefficient was significant (r = 0.69) and only 8 sera were found outside the expected range, exhibiting an abnormally high C2 protein. They were obtained from 6 patients with cryoglobulinemia associated connective tissue disease and 2 with acute glomerulonephritis. These occasional findings suggested the possibility of an activation of C2 hemolytic activity without simultaneous loss of C2 protein. In 16 sera of individuals with familial C2 deficiency (r = 0.83) and 29 sera of patients with angioneurotic edema (r = 0.72), RIE provided an extremely simple and reliable alternative to the time consuming hemolytic titration of C2.

Animals↗
PubMed1980

[Evaluation of C3d in primitive chronic glomerular nephritis (author's transl)].

Plasma levels of C3d, which is liberated by enzymatic cleavage of C3, are determined in 97 patients with primitive chronic glomerular nephritis. This level is indicative of an abnormally high consumption of C3. In all cases where C3 is low, C3d is found at abnormally high levels. When the level of C3 is normal, C3d may, however, be elevated: a more subtle interpretation of the pathologic significance of C3 in immune disease is thus possible.

Complement C3↗
PubMed1979

[Measurements of serum C3d in primitive chronic glomerular nephropathies (author's transl)].

Measurement of serum C3 does not provide precise informations concerning an eventual consumption of this complement component during an immunological process. An increased synthetic rate may compensate an accelerated catabolism. The study of breakdown products of C3, such as C3d is a more sensitive approach of the role of complement in some immunological disorders. Therefore C3d was measured in the serum of patients with chronic non systemic glomerular diseases. High values of serum C3d were found in all cases of hypocomplementemic glomerulonephritis. Circulating C3d was also increased to a lower extent, in patients with normocomplementemic nephritis such as minimal change disease, mesangial nephritis with IgA deposits and membraneoproliferative (type I) glomerulonephritis. The data suggested the involvement of complement in a number of glomerulonephritis. Participation of complement in immunological disorders particularly in chronic non systemic glomerulonephritis could require a reevaluation when functional tests are performed in addition to static measurements.

Complement C3↗
PubMed1979

Hereditary C2 deficiency associated with non-systemic glomerulonephritis.

A patient with non-systemic idiopathic glomerulonephritis was found to have a complete deficiency of C2, the second component of complement. The clinical course, histological findings and serological abnormalities are reported in detail. The renal disease was a mild glomerulonephritis with mesangial and subendothelial immune deposits comprising IgG, IgM and C3, increased mesangial matrix without significant cell proliferation. An immunogenetic analysis of the patient's family was carried out. It was demonstrated that the homozygous C2 deficiency was associated with heterozygotism for HLA-A, B and D. Only one of the C2 deficient genes was associated with the expected HLA-A10, B18 haplotype and the propositus was HLA-D2 negative. This report confirms the fact that non-systemic glomerulonephritis should be included in the variety of immunological disorders associated with a complement deficient state. However, C2 deficiency does not seem to be related specifically to a given histological variety of glomerulonephritis.

Adult↗
PubMed1978

[Treatment of hereditary angioneurotic edema with androgens].

Hereditary angioedema (HANE) is a rare, life-threatening disease due to the deficiency of C1 inhibitor (C1 Inh). Androgen therapy has been recently shown to be effective for prophylaxis of Hane attacks. Since life-long androgen therapy may be hazardous, this study was designed to define the minimal doses required for effectiveness. Ten patients from six different families were treated during cumulative 73 months by danazol and/for methandrostenolone. One tablet/day of either drug was the minimal requirement to prevent any attack in all patients. When 3 tablets/day were given, complement abnormalities were simultaneously rapidly reversed. When 1 tablet/day was given the biological effect was barely detectable, except for C2. Serum C2 levels may, therefore, represent the best criteria of androgen therapy effectiveness. Thus, an excellent clinical result can be obtained with much lower doses of androgens than previously stated. This result seemed important with respect to the serious dose-dependent risk of androgens.

Adult↗
PubMed1978

The second component of complement (C2) as an index of hereditary angioneurotic edema.

Measurements of C2 hemolytic activity were performed in the sera of 13 patients with Hereditary Angioneurotic Edema. Prior to treatment, C2 values correlated with the severity of the disease in each patient. During androgen therapy with Danazol, C2 measurements reflected the clinical benefit of the drug more accurately than C4 levels, thus explaining the effectiveness of low drug doses. This study also suggests that breakdown products of C2 may play an essential role in the pathogenesis of the edema.

Angioedema↗
PubMed1976

[Action of pyridinol carbamate on hetero-immune Masugi nephritis in the rat (author's transl)].

Pyridinol-carbamate (P.C.) is a new substance with various properties including an anti-inflammatory (anti-kinin) and an antiplatelet aggregation activity. Since a coagulation process has been demonstrated in Masugi nephritis in Rats, we investigated the effect of P.C. in this experimental model. P.C. (150 mg/kg/day) was given orally from day 1 to day 28. It prevented partially the G.N.: proteinuria was significantly lower than in nephritic untreated animals with a reduction of seromucoid blood levels and B.U.N. Histological examination revealed that glomerular injury was limited in treated animals specially with regards to G.B.M. alterations and deposits.

Animals↗
PubMed1975

Biochemical criteria for the evaluation of drug efficiency on adjuvant arthritis and nephrotoxic serum nephritis in the rat: studies with phenylbutazone, L-Asparaginase, colchicine, lysine acetylsalicylate, and pyridinol carbamate.

The levels of serum orosomucoid, haptoglobin, and seromucoid were evaluated as possible quantitative criteria for the estimation of drug efficiency in adjuvant arthritis and nephrotoxic serum nephritis. In adjuvant arthritis, haptoglobin, seromucoid, and chiefly orosomucoid serum levels were generally very sensitive to anti-inflammatory agents such as phenylbutazone and pyridinol carbamate, and to immunosuppressive agents such as L-asparaginase. There was a significant correlation between the serum levels of these glycoproteins and the arthritis scores. In nephrotoxic serum nephritis, seromucoid levels were correlated with the proteinuria of the autologous phase and were found to be a good complementary criterion for the analysis of the efficiency of pyridinol carbamate, colchicine, iysine acetylsalicylate, and L-asparaginase.

Animals↗
PubMed1975

[ Products of fibrin degradation in the urine during experimental and human glomerulonephritis].

Intravascular coagulation localized in glomeruli is of pathologic importance in human and experimental GN. The measure of fibrinogen related antigen (FRA) in serum and urine after concentration (Merskey's technique) was used to detect and estimate this phenomenon. In Rabbit Masugi GN, FRA were detected in urine 5 to 20 mg/24 h, in close correlation with the amount of proteinuria, the intesity of histological changes and the presence of fibrin deposits in glomeruli. In human GN, urine FRA were detected in many cases (0,5-10 mg/24 h) in correlation with the histological type of lesions (FRA + in primary or secondary proliferative GN) and with the evolutivity of disease (FRA + in cases with rapidly progressive kidney function deficiency). Urine FRA are also in correlation with intraglomerular fibrin deposits : this suggests that urine FRA originate from lysis of fibrin deposited within glomeruli. So urine FRA appears to be an indicator of type and severity of GN and probably of therapeutic measures, indicating anticoagulant and/or antithrombic therapy : the variations of urine FRA during treatment is of value to assess the effects of these drugs and to establish the prognosis of the disease.

Animals↗