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Biomedical subjects

B Canivet

Publications and source records attributed to B Canivet.

At least 19 recordsLinked to original sources
PubMed2002

[Clinical relevance of homocysteine monitoring in the diabetic patient].

Accelerated atherosclerosis is common in diabetes mellitus, although its extent is not always related to its strong association with classical cardiovascular risk factors. Diabetic patients, especially with type 2 diabetes, are prone to cardiovascular disease which is the leading cause of death in this population. Recent clinical studies among general population have shown that an even mild increase of homocysteinemia play an important role in the progression of atherosclerosis, either in coronary or peripheral arteries. An increasing amount of in vitro data is providing evidence that excess of homocysteine has a toxic effect on the arterial wall. This aminoacid thus appears to be not only a risk marker but also an emerging cardiovascular risk factor. The measurement of plasma homocysteine contributes to the identification, among the diabetic population, of patients at high cardio-vascular risk, with the aim of improving their global management. Moreover the addition of group B vitamins provides an easy and low-cost treatment to lower hyperhomocysteinemia.

Diabetes Complications↗
PubMed1999

Apparent activities of 21-hydroxylase, 17alpha-hydroxylase and 17,20-lyase are impaired in adrenal incidentalomas.

OBJECTIVE: An increased response of 17-hydroxyprogesterone to ACTH stimulation has been observed in adrenal incidentaloma and linked to an impairment of either 21-hydroxylase or of 11beta-hydroxylase activity. To analyse this question further, we investigated the steroidogenic pathways in a series of 17 adrenal incidentalomas. DESIGN AND PATIENTS: 17 patients (7 women, 10 men; mean age, 62 +/- 12 years) with non-histologically analyzed adrenal incidentalomas were prospectively evaluated. METHODS: The following variables were investigated: 24-h urinary methanephrines and free cortisol excretion; plasma levels of ACTH and dehydroepiandrosterone; overnight dexamethasone suppression test; 1-24 ACTH stimulation test with measurement of: cortisol, 11-deoxycortisol, 17-hydroxyprogesterone, aldosterone, 11-deoxycorticosterone, progesterone, 17-hydroxypregnenolone, Delta4-androstenedione, dehydroepiandrosterone and 21-deoxycortisol. RESULTS: Discordant features of subclinical hypercorticism were noted in one case. No patient had dehydroepiandrosterone sulfate levels in the normal range for his or her age. Peak 17-hydroxyprogesterone and peak 21-deoxycortisol disclosed impairment of 21-hydroxylase in 11 and 10 cases respectively. An increased 11-deoxycortisol/cortisol ratio identified reduced activity of 11beta-hydroxylase in 11 patients. Eight patients displayed features of mild 17,20-lyase impairment, which was related to 21-hydroxylase dysfunction. Whereas only 2 patients showed no enzyme modification, 9 displayed alterations of at least two pathways. CONCLUSION: In our hands, a combination of enzyme dysfunction was frequently observed. Shared biochemical mechanisms could explain combined 17,20-lyase and 21-hydroxylase alterations, whereas coexistence of 21-hydroxylase (particularly when based on peak 21-deoxycortisol) and 11beta-hydroxylase is more puzzling.

17-alpha-Hydroxypregnenolone↗
PubMed1999

Assessment of cardiac arrhythmic risk in diabetic patients using QT dispersion abnormalities.

The purpose of this study was to assess the abnormalities and prevalence of QT dispersion in 154 diabetic patients (DP) who underwent a standard 12-lead ECG. QT interval was measured from the beginning of the QRS complex until the T wave returned to baseline. Atrial fibrillation, pacemakers and the impossibility of measuring 6 QT intervals per ECG were reasons for exclusion from the study. Diabetic patients were compared with 104 sex- and age-matched controls (C): mean age 50.7 +/- 2.3 years (DP) vs 48.4 +/- 10.1 (C) (ns); diabetes duration: 11.6 +/- 7.9 years. Seventy-eight percent of DP were non-insulin-dependent. Mean QT duration was 0.383 +/- 0.031 s (DP) vs 0.381 +/- 0.026 (C) (ns); QT dispersion (difference between the longest and shortest QT interval measurement) 0.033 +/- 0.015 s (DP) vs 0.024 +/- 0.011 (C) (p < 0.001); and QT variability 3.003 +/- 1.23% (DP) vs 2.295 +/- 0.936 (C) (p < 0.001); with a standard deviation of 0.012 +/- 0.005 s (DP) vs 0.009 +/- 0.004 (C) (ns). QT dispersion indices (dispersion, variability) were significantly increased in DP, even for short diabetes duration. Future studies should focus on QT dispersion to assess the usefulness of such indices in detecting DP at high risk of sudden death and ventricular arrhythmias.

Arrhythmias, Cardiac↗
PubMed1997

[Macroprolactinemia, a variety of hyperprolactinemia. Apropos of 5 cases].

Macroprolactinemia, due to increased circulating levels of large molecular weight forms of prolactin, results in elevated level of immuno-reactive prolactin. The big variants have only weak biological activity; thus macroprolactinemia appears as a case of hyperprolactinemia without clinical significance as demonstrated by the five patients described. The diagnosis is based upon chromatography which separates the hormone and its variants. This disorder produces a pitfall in the diagnostic evaluation of hyperprolactinemia.

Adult↗
PubMed1994

Mycobacterium avium intracellulare suppurative thyroiditis in a patient with Hashimoto's thyroiditis.

A case of suppurative thyroiditis occurring in a 72-year-old woman is reported. The clinical history of this woman, treated by tianeptine for mild exogenous affective disorder and by conventional insulin therapy for long-standing insulin-dependent diabetes, was remarkable for the pseudotumoral signs which led to the simultaneous diagnosis of hypothyroidism due to Hashimoto's thyroiditis and of mycobacterium avium intracellulare suppurative thyroiditis. To our knowledge, this is the second reported case of mycobacterium avium intracellulare thyroiditis. This case is also exemplary, given its occurrence in the absence of severe immunodepression, setting apart the mild impact on the immune system of affective disorder and of long duration's insulin-dependent diabetes.

Aged↗
PubMed1992

[Insulin receptors: structure and physiology].

Insulin receptor is a transmembrane glycoprotein. It is synthetized, in endoplasmic reticulum, as a proreceptor which is processed (glycosylation, proteolytic cleavage) and transported to the cell surface. The receptor is a hetero-tetramer comprising 4 subunits: the two alpha-subunits are extracellular; they are held, through disulfide bonds, to the beta-subunits. These are located across the membrane; their intracellular domain possesses a tyrosine-kinase activity. Insulin receptor gene has been located on chromosome 19 and its nucleotide sequence is known. The first functional property of the receptor is to recognize the hormone. Specific and high affinity binding site is supported by the alpha subunit. Shortly after insulin binding, the tyrosine-kinase is activated, resulting in autophosphorylation and phosphorylation of various substrates. Current research focuses on these nature of there substrates which activate intracellular putative mediators of insulin action. Insulin-resistant states are associated with functional alteration of the receptor. But only a few cases are directly related to nucleotide mutations at the level of the gene resulting in structurally abnormal receptor.

Receptor, Insulin↗
PubMed1989

Autoimmune insulin syndrome.

Initially described in Japan, the autoimmune insulin syndrome is caused by the presence of anti-insulin antibodies in patients who have never received insulin. This syndrome accounts for spontaneous or reactive hypoglycaemia with very high levels of total immuno-reactive insulin. Discordance between the levels of immunoreactive insulin and C peptide indicate the possible presence of anti-insulin antibodies; this can avoid an incorrect diagnosis of insulinoma. These autoimmune hypoglycaemias often present a difficult diagnostic problem in distinguishing them from factitious hypoglycaemia. The course of the autoimmune insulin syndrome is usually favourable, with a spontaneous rapid diminution of the levels of anti-insulin antibodies. The reasons for the appearance of anti-insulin antibodies and the exact mechanisms of the hypoglycaemia remain uncertain. However, the frequent association of the autoimmune insulin syndrome with certain autoimmune diseases suggest a common immune dysfunction. Drugs containing a sulphydryl group have been implicated in the aetiology of this syndrome.

Autoimmune Diseases↗
PubMed1988

[Autoimmune hypoglycemia: the fault of pyritinol?].

Initially reported in Japan, autoimmune hypoglycemia is related to the presence of insulin-binding antibodies, even in patients who have never been treated with insulin. The authors report a case of spontaneous autoimmune hypoglycemia in a French woman receiving pyritinol. The difference between insulin and C peptide radioimmunoassay levels prompted a search for insulin antibodies. In vitro studies confirmed their presence and showed that they were immunoglobulins G with two binding sites without species specificity. The outcome of autoimmune hypoglycemia is usually favourable, with a rapid decrease of insulin antibodies but steroid therapy is needed when serious clinical manifestations are present. The differential diagnosis with factitious hypoglycemia may be difficult. The reasons for the appearance of the insulin antibodies and the exact mechanisms of hypoglycemia remain hypothetical. However, drugs with a sulfhydril group, such as pyritinol, could play a causative role in this syndrome.

Aged↗
PubMed1988

[Acanthosis nigricans, hyperandrogenism, insulin resistance and mixed hyperlipemia].

We report the case of a 22-year old woman who presented skin lesions of acanthosis nigricans, hirsutism and secondary amenorrhoea. She had high plasma levels of adrenal androgens and low plasma levels of sex steroid binding protein. Polycystic ovaries were discovered in the course of a laparotomy performed for paraovarian cyst. An oral glucose tolerance test revealed a state of hyperinsulinism with intolerance to carbohydrates, while the body mass index was normal. This insulin resistant state corresponded in vitro to a decrease in the number of erythrocyte insulin receptors without decrease in their affinity for insulin. Following paradoxical improvement during a full-term pregnancy, there was gradual deterioration of diabetes control requiring insulin therapy. This metabolic decompensation was accompanied by major hyperlipaemia followed by acute haemorrhagic pancreatitis. This case illustrates the course of a type A insulin resistance syndrome which was detected at an early stage in front of an hirsutism-acanthosis nigricans association. The underlying pathogenic mechanisms of these pathologies are discussed.

Acanthosis Nigricans↗