Search PubMed⌕ Search

Biomedical subjects

C Boitard

Publications and source records attributed to C Boitard.

196 records · Page 11Linked to original sources
PubMed1981

[Inhibition of insulin secretion in vitro by serum of diabetic subjects in the presence of complement].

In order to explore complement-dependent humoral immunity in insulin-dependent diabetic patients, their serum was incubated with Mouse isolated pancreatic islets in the presence of complement, after which the response of these islets to glucose was estimated by measuring insulin secretion. Out of 13 sera from insulin-dependent diabetic patients, 5 caused a significant inhibition of the insulin response. Morphological observation of islets suggested that this inhibition was due to a cytotoxic effect of the sera. In the absence of complement, the same sera were not able to suppress insulin release. No beta-cell inhibition or morphological damage was detectable on islets incubated with sera from 13 healthy subjects and 4 non-insulin dependent diabetic patients, in the presence or in the absence of complement. Complement-dependent humoral immunity may play a role in the beta-cell injury of insulin-dependent diabetes.

Animals↗
PubMed1981

Lymphocytes from diabetics suppress insulin release in vitro.

The insulin response of isolated islet cells to glucose and theophylline in vitro was studied after incubation with lymphocytes. The test was employed to explore cell-mediated immunity in diabetics. A significant inhibition of insulin response to glucose and theophylline as compared to insulin release in a "basal" medium was found after incubation with blood lymphocytes from 21 out of 23 insulin-dependent diabetics (mean secretion index 18 +/- 18 versus 118 + 8 (SEM) % in control subjects). Most of the patients studied had associated autoimmune diseases: all of these displayed inhibition of insulin release. In six cases, the diabetes had a recent onset with no associated autoimmune disease: four of them displayed the same inhibition. No inhibition was found in the 26 control subjects and in seven non-insulin-dependent diabetics (mean secretion index 134 +/- 17 versus 145 +/- 23 (SEM) % in four control subjects). Lymphocytes inhibiting islet cell response were not cytotoxic against mouse fibroblasts. Twenty-two insulin-dependent diabetics showed islet cell antibodies to human and/or mouse pancreatic islets. However, an inhibition of insulin release was found with no detectable islet cell antibodies in one case, and the converse in two cases. Lymphocyte cytotoxicity to islet cells could play a role in the natural history of insulin-dependent diabetes.

Adolescent↗
PubMed1981

Complement-fixing Islet cell antibodies from some diabetic patients alter insulin release in vitro.

To explore humoral immunity in insulin-dependent diabetic (IDDM) patients, we studied insulin release from isolated mouse islets stimulated by glucose + theophylline after incubation with the sera of these patients and complement. Eleven of 21 IDDM sera suppressed the stimulated insulin release while the arginine-stimulated glucagon release remained unchanged. Morphologic evidence and the trypan-blue exclusion test suggested that the suppression of insulin release was due to a cytotoxic effect of the sera. No beta-cell inhibition of morphologic damage was detectable in the presence of sera from 30 healthy subjects, 8 non-insulin-dependent diabetic patients, and 5 nondiabetic patients with autoimmune diseases. Beta-cell inhibition by IDDM sera was not observed when complement was omitted. After serum fractionation, the cytotoxic potency of IDDM sera was located in the immunoglobulin G fraction. Using human islets, insulin release was suppressed by 3 of 6 IDDM sera. Complement-dependent cytotoxicity was found in 1 of 5 recent-onset IDDM patients and 11 of 16 IDDM patients with autoimmune phenomena. It was associated in all cases with the presence of islet cell antibodies as detected by immunofluorescence, and with the presence of circulating lymphocytes which suppressed insulin release in vitro. Complement-fixing antibodies may contribute to the selective beta-cell damage in IDDM.

Adolescent↗
PubMed1979

[Anaemia and microcytosis during thyrotoxicosis. Physiopathological discussion. 36 cases (author's transl)].

Study of 36 cases of thyrotoxicosis demonstrated the prevalence of anaemia (17 cases) and of microcytosis (26 cases). In patients with a microcytosis, serum iron was measured in 9, being found to be low in 5 of them, whilst amongst twelve 10 had anti-thyroid antibodies and anti-gastric antibodies. Atrophic gastritis was seen in the 5 patients who underwent endoscopy. Four biopsies revealed 3 cases of atrophic gastritis and one of simple gastritis. The types of anaemia seen and their mechanisms are discussed: microcytic anaemia related to disturbed iron metabolism or to its impaired intestinal absorption; normocytic anaemia; macrocytic anaemia possibly preceding pernicious anaemia. It would seem to be possible to distinguish two pathogenic categories: thyrotoxicosis reversible changes in iron metabolism, and atrophic gastritis associated with hyperthyroidis in an "auto-immune context" and which has led to the concept of "thyro-gastric" disease.

Adolescent↗
PubMedDate not supplied

[Auto-immune hypoglycemic syndrome induced by pyritinol].

The auto-immune hypoglycemic syndrome is characterized by the association of hypoglycemia (clinical and/or biological) and anti-insulin antibodies in patients who have never received exogenous insulin. Initially this syndrome was most often described in Japanese patients some of whom were treated with drugs containing a sulfydril group. We now recall the case of a female caucasian patient treated with Pyritinol for rhumatoid polyarthritis and who presented severe spontaneous hypoglycemia linked with the presence of anti-insulin antibodies in her serum. The level of her antibodies decreased abruptly on suspension of the drug. The recent and more developed characterization techniques of the different forms of circulating insulin and of their antibodies may help to differenciate an auto-immune hypoglycemia from hypoglycemia due to the secret auto-administration of bovine and porcine insuline, and permit us to suggest that an abnormality in the structure of the molecule of insulin might be a cause of this syndrome. However, the exact mechanism of hypoglycemia linked with the presence of anti-insulin auto-antibodies is not yet clear as is the predisposition of a drug with a sulfydril group to induce such an auto-immune phenomenon.

Aged↗
PubMedDate not supplied

Course of pancreatic beta cell destruction in prediabetic NOD mice: a histomorphometric evaluation.

The course of pancreatic beta cell destruction during the prediabetic period of autoimmune diabetic syndromes is not precisely known. We have analyzed the course of insulitis (n = 140) and the beta cell and lymphocytic volume densities by morphometric methods (n = 80) in NOD mice aged 6 to 45 weeks. In the absence of diabetes the mean beta cell density was only slightly reduced with age: 0.64 +/- 0.04% glandular tissue (mean SEM; n = 12) in 6 wk-old mice, 0.52 +/- 0.06% in 45 wk-old mice (n = 12; ns). However, a minority of pancreases were free of insulitis or showed isolated periinsulitis at the end of the 45-wk follow-up period. Invasive insulitis (i.e. mononuclear cells invading the islet area) was detected in 60-85% of mice from the 12th week on. In non overtly diabetic mice, beta cell density was reduced only when insulitis was invasive in more than 40% of islets: 0.30 +/- 0.03%, (n = 11) vs 0.59 +/- 0.04% (n = 34) in moderately invasive insulitis (p < 0.05). These mice had significant metabolic abnormalities. In diabetic mice, the beta cell density was markedly decreased: 0.02 +/- 0.01% (n = 7; p < 0.001). On the whole, a lymphocytic infiltrate affecting less than 50% of the islet volume was compatible with a normal beta cell density. Beyond this 50% lymphocytic infiltration threshold, beta cell density was tightly and negatively related to the lymphocytic volume density.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗