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J C Homberg

Publications and source records attributed to J C Homberg.

At least 73 records · Page 4Linked to original sources
PubMed1983

[Anti-SS-B antibody : marker of Gougerot-Sjögren's connective tissue disease independent of the dry syndrome].

We studied the predictive value of anti-SS-B antibody on 48 patients having this antibody and no other antinuclear antibody. 25 patients had a typical Sjögren syndrome and the rest had no sicca syndrome but generally an unclassified disease. Between these two groups of patients we observed an identity of clinical and biological manifestations except for the sicca syndrome. We conclude that anti-SS-B antibody is not a marker for Sjögren syndrome, but is correlated with the presence of an autoimmune disorder inconstantly associated with the sicca syndrome. This auto-immune disorder has the clinical and biological features of systemic Sjögren syndrome but the sicca syndrome.

Adult↗
PubMed1983

[Antinuclear antibodies and lupus induced during treatment of arterial hypertension. Role of beta-blockers and alpha-methyldopa].

Comparison of hypertensive patients receiving no treatment with subjects of the same age reveals the presence of antinuclear antibodies in twice as many of the former as the latter. Various antihypertensive drugs increase this prevalence. They may induce iatrogenic lupus. Alpha-methyldopa: the frequency of antinuclear bodies is three times greater than in untreated hypertensive patients. However there are no reported cases of clinical symptomatology of induced lupus. Beta-blockers. Practolol, acebutolol, labetalol, atenolol, timolol, metoprolol, pindolol and oxprenolol are suspected of increasing antinuclear antibodies. These drugs may be weak inducers of iatrogenic lupus when compared with major drugs: procainamide, high doses of hydralazine and D-penicillamine.

Adrenergic beta-Antagonists↗
PubMed1983

Relevance of autoantigens to autoimmunity in African trypanosomiasis: study of DNA and thyroglobulin antibodies.

In order to investigate whether the autoantibody production in the course of African trypanosomiasis is the result of a generalized polyclonal activation or if it is a specific (antigen-dependent) phenomenon we looked for the presence of autoantibodies directed against autoantigens likely to be released (DNA) or unlikely to be released (thyroglobulin) into the circulation during human T. gambiense infection. Sera from 21 patients with African trypanosomiasis were screened for anti-native DNA or anti-denatured DNA antibodies by a Farr DNA binding radioimmunoassay. In addition, antibodies to native DNA were also assessed by indirect immunofluorescent assays using Crithidia luciliae or rat liver sections as substrates. Anti-thyroglobulin antibodies were studied by the passive hemagglutination technique. IgM levels and fluorescent anti-trypanosomal antibodies (FATA) were concomitantly evaluated. The denaturated DNA binding capacity was significantly higher in the sera from trypanosomiasis patients than in sera from healthy blood donors. These capacities were greater in patients with high IgM levels and high FATA titres. Anti-native DNA or anti-thyroglobulin antibodies were not detected. This preferential formation of anti-denatured DNA antibodies suggests a specific antigen-dependent) activation of autoreactive cells rather than a generalized polyclonal activation.

Adolescent↗
PubMed1983

[Iproniazid-induced hepatitis. The diagnostic value of a new antimitochondrial antibody anti-M6].

The authors report the observations of four patients with iproniazid hepatitis. Three of these patients died. An antimitochondrial antibody was found in the 4 patients at a high titer. This antibody differed from the antimitochondrial antibodies which have been described previously (anti-M1, anti-M5). This new antibody was called anti-M6. The evolution of the anti-M6 titer has been studied in the patient who survived. This titer progressively decreased; the antibody was no longer detectable 6 months after the withdrawal of iproniazid. Anti-M6 has not been found in other hepatic diseases. It was not detected in 15 patients receiving iproniazid without hepatitis or in 6 patients receiving isoniazid. Anti-M6 appears as a useful serologic marker for the diagnosis of iproniazid hepatitis.

Adult↗
PubMed1982

A new antimitochondria antibody (anti-M6) in iproniazid-induced hepatitis.

A new immunofluorescence pattern of non-organ- and non-species-specific antibody has been observed in occasional sera. Variations of the fluorescence were found in different species. Recognition of the new pattern was particularly characteristic in rat organs (liver: the hepatocytes showed intense roughly granular fluorescence evenly distributed in the cytoplasm; kidney: the bright fluorescence of the first portion of the proximal tubules contrasted with the negative aspect of the other portions of the tubules; stomach: only some cells probably corresponding to the APUD system were positive; pancreas: fluorescence was limited to the islets of Langherhans). The positivity in the ellipsoid region of the rods and cones of the eye and the absorption on different liver organelles showed that this aspect corresponded to the mitochondria. We propose to name this pattern 'antimitochondria antibody number 6' or 'anti-M6'. High titres of anti-M6 were found in four patients suffering from iproniazid-induced hepatitis. A decrease in the titre was obtained after stopping the treatment. The now exceptional use of iproniazid and the rare occurrence of anti-M6 suggest a link between these two phenomena.

Adult↗
PubMed1981

[Effect of rheumatoid factors on results for determination of antitoxoplasms IgM antibodies by immunofluorescence and agglutination technics (author's transl)].

Simultaneous presence of antitoxoplasm IgG antibodies and of rheumatoid factors gives rise to an IgM-type immunofluorescence reaction in 44 p. cent of cases. Three experiments showed that association of the two antibodies can give rise to false positives in the Remington test ; the mixture of the two antibodies renders the reaction positive in the majority of cases. On the other hand, after absorption of negative rheumatoid factors and separation of serum IgM and IgG, IgM fluorescence is no longer seen ; if they are again mixed, then a positive reaction will result. Interference of antitoxoplasm IgG antibodies and rheumatoid factors does not occur in direct toxoplasm agglutination tests. The presence of the rheumatoid factor is rare in the pregnant female. Nevertheless, it is necessary to test for rheumatoid factors using the latex test. If results are here positive, then serum should be absorbed on aggregated human IgG and the Remington test repeated. The probably rare simultaneous presence of antitoxoplasm IgG antibodies and of rheumatoid factors cannot be differentiated from these false positives without fractionation of the serum, separating IgM and IgG.

Agglutination Tests↗
PubMed1980

[Red cell autoimmunization in a "normal" population. 63 cases (author's transl)].

Anti-red auto-antibodies were found in 69 out of 892 000 blood donors aged between 20 and 60 years, 63 of whom were followed for up to five years. This would suggest an overall incidence of 1 in 13 000 members of a "normal" population. Uncontrolled methyl-dopa treatment could be incriminated in 25% of cases. Only 10% of autoimmune subjects had slight confirmed anaemia, but 72% had biological evidence of red cell destruction (i.e. hyper-reticulocytosis, elevated serum bilirubin levels and shortened red cell life span), which demonstrates the presence of subclinical autoimmune haemolytic disease in apparently normal people. The anti-red cell auto-antibodies were of the IgG type in 97% of the subjects and were associated with various anti-tissue antibodies in 41%, thus pointing to a multisystem autoimmune disorder. In most cases the abnormality persisted or spontaneously regressed during the observation period, but long-term follow-up is required to determine whether asymptomatic red cell autoimmunization is harmless or potentially dangerous.

Adult↗
PubMed1980

[Tienilic acid-induced hepatitis associated with liver/kidney microsomal antibody (author's transl)].

Six patients developed acute, subacute or chronic hepatitis after taking tielinic acid, a new diuretic used in the treatment of hypertension. Two died of acute liver failure. The condition was characterized by marked increase in serum transaminases, parenchymal necrosis and portal and/or lobular inflammatory fibrosis. In addition, the serum of all patients contained high titers of a liver/kidney microsomal antibody, which disappeared either after tienilic acid was discontinued or after prednisolone was introduced. The study shows that tienilic acid may be responsible for acute or chronic hepatitis and suggests that a liver/kidney microsomal antibody could be a sero-immunological marker of drug-induced liver disease.

Acute Disease↗
PubMed1980

[Congenital deficiency of factor XI: diagnosis and therapy in surgical patients (author's transl)].

Factor XI deficiency has to be diagnosed preoperatively since it may be symptomless until revealed by bleeding after surgical procedures. Replacement therapy prior to operation is advocated and its management defined; because the effects of plasma infusion on factor XI level are not constant and because of the wide variation in the half life of infused factor, it is strongly advised that regular measurement should be made when possible. Ovariectomy in a factor XI deficient patient was carried out with correct haemostasis.

Aged↗