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Biomedical subjects

C Betterle

Publications and source records attributed to C Betterle.

At least 109 records · Page 6Linked to original sources
PubMed1985

Demonstration and characterization of anti-human mitochondria autoantibodies in idiopathic hypoparathyroidism and in other conditions.

We studied 32 patients with idiopathic hypoparathyroidism (IHP), 19 patients with organ-specific autoimmune diseases (OSAD) without IHP, 50 normal controls and a known serum with anti-mitochondrial autoantibodies (AMA). Patients' sera were tested by the classical indirect immunofluorescent technique and by the indirect immunofluorescent complement fixation technique on unfixed cryostat sections of normal human parathyroid, pancreas, thyroid, stomach, kidney, and rat kidney. Five out of 32 patients with IHP, three out of 19 patients with OSAD without IHP and one out of 50 normal controls revealed a bright reactivity against oxyphil cells and a weak reactivity against chief cells of normal parathyroid. These sera also brightly reacted with mitochondria-rich cells and weakly with the remaining cells of only human tissues. The absorption of positive sera with human mitochondria completely abolished this positivity but the absorption with rat mitochondria failed to prevent this reaction. This reactivity was due to an anti-human mitochondrial autoantibody (AHMA) of IgG class. By non-competitive ELISA and Western blot we also demonstrated that every AHMA-positive serum mainly reacted against a human mitochondrial membrane-bound protein of approximate mol. wt. of 46 kd, while the AMA-positive serum reacted against different mitochondrial antigens. The present study shows that a specific parathyroid autoantibody was not detectable in patients with IHP.

Adolescent↗
PubMed1984

Clinical and subclinical organ-specific autoimmune manifestations in type 1 (insulin-dependent) diabetic patients and their first-degree relatives.

Studying 239 Type 1 (insulin-dependent) diabetic patients and 144 of their first-degree relatives, we found a significant prevalence of autoimmune manifestations in both groups, compared with sex- and age-matched control subjects (p less than 0.001). In particular, in diabetic patients we found a high frequency of autoimmune thyroid disease and idiopathic Addison's disease and also a significant prevalence of thyroid (p less than 0.001), parietal cell (p less than 0.05) and adrenal antibodies (p less than 0.05). In the relatives a high frequency of thyroid disease, thyroid, parietal cell and adrenal antibodies and a significant prevalence of islet cell antibodies (p less than 0.05) were detected. In both groups functional glandular tests and gastric biopsies performed on the basis of autoantibody positivity revealed 13 examples of subclinical hypothyroidism, two cases of reduced adrenocortical reserve and five of atrophic gastritis. Autoantibody screening in diabetic patients and their relatives permitted the early diagnosis of the underlying endocrine disorders.

Adolescent↗
PubMed1984

Anti-ribosomal ribonucleoprotein autoantibodies in systemic lupus erythematosus.

Sera from systemic lupus erythematosus (SLE) patients giving a fluorescent ribosomal pattern on tissue and cell preparations also showed precipitating autoantibodies against purified rat liver ribosomes. Ribosomal antigen is also present in rabbit thymus cellular extract (RTE), since the same sera gave precipitin lines against RTE in identity with ribosomes. Immunofluorescent staining was completely inhibited by serum absorption with ribosomes or with RTE. However ribosomal RNA and RNase or trypsin-treated ribosomes failed to react with these autoantibodies as demonstrated in immunoabsorption and immunodiffusion studies. These data suggest that these sera contain autoantibodies directed against some antigenic site composed of a portion of both RNA and ribosomal protein. Ribosomal autoantibodies were detectable at a low frequency in SLE patients characterized by an active disease and renal involvement.

Antigens↗
PubMed1984

Autoantibodies against Leydig cells in patients after spermatic cord torsion.

This study is aimed at searching for the presence of circulating antibodies against frozen sections of human testis, ovary and trophoblast in patients that had spermatic cord torsion. Sixty-eight sera samples were studied. Nine patients (13.2%) were positive for organ specific anti-testis autoantibodies. Six patients were positive for antibodies against Leydig cells: five were positive only with the indirect immunofluorescence technique of complement fixing (ITT/CF), the sixth patient was positive only with the indirect immunofluorescence technique (ITT). The other three patients were positive for antibodies against germ line cells: two patients were positive with both techniques, the third was positive only with indirect immunofluorescence technique. Eight of these patients were negative for antibodies against adrenal cortex while only one case was positive with indirect immunofluorescence technique both on adrenal cortex and Leydig cells. Human lyophilized testis absorbed the reactive antibodies against Leydig cells and germ line cells, while adrenal cortex and lyophilized testosterone were ineffective. This study shows the identification of a specific antibody against Leydig cells and germ line cells in patients after spermatic cord torsion.

Adolescent↗
PubMed1983

Complement-fixing adrenal autoantibodies as a marker for predicting onset of idiopathic Addison's disease.

In a prospective investigation of the role of adrenal autoantibodies (AA) in predicting the onset of idiopathic Addison's disease, 9 initially non-addisonian AA-positive autoimmune subjects were followed for 42 months. In 4 of these subjects Addison's disease developed within 1-31 months. A fifth had reduced adrenocortical reserve at the start and at the end of the investigation. An AA capable of fixing the membrane attack complex of complement [(C5-C9) F-AA] was detected before onset of the disease in the sera of the 4 patients in whom Addison's disease developed. (C5-C9) F-AA may be involved in the pathogenesis of idiopathic Addison's disease and may be regarded as a marker for individuals in whom idiopathic adrenal insufficiency is likely to develop.

Addison Disease↗
PubMed1983

Detection of immunoglobulins G and A on the cell membrane of hepatocytes from patients with alcoholic liver disease.

The presence of immunoglobulins (Ig) G, A, and M and of complement fractions (C3-C4) on the liver cell surface was investigated by direct immunofluorescence in 40 patients with alcoholic liver disease. IgG was detected on the liver cell membrane with a linear staining pattern in 29 patients. The percentage of IgG-positive hepatocytes correlated with transaminase activities, independently of the histological findings. IgA was demonstrable with a coarse granular staining pattern in 11 of the 14 cases with established cirrhosis. The finding of IgG bound to the hepatocyte surface in patients with alcohol-induced liver damage suggests that alcohol could be responsible for antigenic modifications of hepatocyte membrane with consequent triggering of a humoral immune response.

Adult↗
PubMed1982

Immunohistochemical identification of factor X-like antigen in the A cells of the normal human pancreas.

An indirect immunofluorescence technique using two rabbit anti-human factor X sera was used to investigate the presence of factor X in various human tissues. Of all tissues studied only the cytoplasm of some islet cells of the six human pancreases illustrated specific reactivity for factor X-like material. No reaction was seen in the exocrine pancreas. Cross-absorption studies with factor X-deficient plasma, glucagon or alpha-1-antitrypsin did not modify the pattern. On the contrary, cross-absorption with factor X Friuli or with normal plasma eliminated the positivity. No factor X-like material was seen in rat or guinea pig pancreas. The double-immunofluorescence technique demonstrated that the reactivity was localized only in the cytoplasm of the A cells.

Animals↗
PubMed1981

Lymphocyte subpopulations in insulin-dependent diabetics with and without serum islet-cell autoantibodies.

The lymphocyte subpopulations of 26 insulin-dependent diabetics were studied. Thirteen of them had persistent pancreatic islet-cell serum antibodies (ICA) (mean (+/- SD) duration of diabetes 11 +/- 8 years). The others were ICA-negative (mean duration of diabetes 10 +/- 8 years). The mean fasting blood glucose in the week before the lymphocyte count was 1..37 +/- 0.45 g/l (two specimens for every patient). As controls 19 healthy volunteers, sex and age matched, were investigated. The T-lymphocyte count was no different in diabetics compared to controls. B-cells were significantly raised (p less than 0.01) in the ICA-positive group, when tested with anti-human gammaglobulin sera (IgG + IgA + IgM), anti-human IgM, while no difference was observed between ICA-negative patients and normal subjects. IgA-bearing lymphocytes were equally raised in both diabetic groups (p less than 0.05). These data show an altered immunological balance in type IB (autoimmune) diabetes, characterized by an increased number of B-lymphocytes.

Adolescent↗
PubMed1979

Circulating antibodies in malignant melanoma patients.

Sera from 46 patients with malignant melanoma (MM) in different clinical stages and from 25 healthy blood donors were studied by an indirect conventional immunofluorescent technique (IIT) and by an immunofluorescent complement-fixation test (ICFT). No specific and reliable serological reactivity could be demonstrated against autologous and homologous MM and other nonmalignant pigmented tissues. An increased incidence of diffused antinuclear (ANA; 41%) and cytoplasmic epidermal cell autoantibodies (A-CYT; 71%) was observed in the patients by IIT. Statistical evaluation of the results gave significant values in the chi 2 test in patients for ANA (chi 2 = 5.2061; p less than 0.05) and for A-CYT (chi 2 = 8.9176; p less than 0.01) versus age-matched controls. Thyroid microsomal, gastric parietal cell, smooth muscle and mitochondria autoantibodies were, respectively, detected in 4.3, 4.3, 4.3 and 0% of patients' sera.

Antibodies, Neoplasm↗