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B Vergès

Publications and source records attributed to B Vergès.

45 records · Page 3Linked to original sources
PubMed1996

[Food-dependent Cushing syndrome: a new entity of organic hypercorticism].

Diagnosis of Cushing's syndrome is quite difficult in endocrinology. Spontaneous Cushing's syndrome is usually divided into two subgroups, one which is dependent on corticotropin (ACTH) and another one which is not. In the first class are Cushing's disease, the ectopic corticotropin syndrome and the rare ectopic corticotropin-releasing hormone (CRH) syndrome; these ACTH-dependent Cushing's syndrome have usually diffusely enlarged adrenal glands. In the second class are cortisol producing unilateral adrenocortical adenomas or carcinomas, and the recent Cushing's syndrome with food dependent periodic hormonogenesis. This food dependent Cushing's syndrome is an ACTH-independent Cushing's syndrome with multinodular enlargement of both adrenal glands. Pathogenesis is an aberrant adrenal sensitivity to physiologic secretion of gastric inhibitory peptide (GIP). Ectopic expression of GIP receptors on adrenal cells involve pathologic food induced cortisol secretion. Food dependent Cushing's syndrome is a new cause of Cushing's syndrome. Food induced cortisol secretion may have to be explored in the ACTH-independent Cushing's syndrome.

Adrenocortical Hyperfunction↗
PubMed1994

In vivo metabolism of apolipoprotein A-IV in severe hypertriglyceridemia: a combined radiotracer and stable isotope kinetic study.

Apolipoprotein (apo) A-IV is an intestinally derived apolipoprotein that plays a potentially important role in lipoprotein metabolism and reverse cholesterol transport. However, the factors that regulate its plasma concentrations are not well understood. Plasma apoA-IV levels have been previously shown to correlate with fasting triglyceride (TG) levels in humans with TG levels less than 300 mg/dl (Lagrost et al. 1989. J. Lipid Res. 30: 701-710). In this study, we established that apoA-IV levels were significantly elevated (mean 29.3 mg/dl) in a group of 15 hypertriglyceridemic patients (TG > 300 mg/dl) compared with normolipidemic controls (mean 13.4 mg/dl). In order to investigate the relationship between hypertriglyceridemia and apoA-IV metabolism, we then studied the in vivo kinetics of apoA-IV in two healthy hypertriglyceridemic patients (mean TG = 1297 mg/dl) compared with normolipidemic control subjects. Combined studies using endogenous stable isotope labeling (with a primed constant infusion of deuterated L-leucine) and exogenous radiolabeling (with 125I) of apoA-IV were performed. Both stable isotope and radiotracer studies demonstrated substantially decreased apoA-IV fractional catabolic rates (FCR) in the hypertriglyceridemic patients (1.24 +/- 0.13 day-1) compared with controls (2.33 +/- 0.08 day-1). The apoA-IV production rate was not significantly different between the two groups. Gel filtration chromatography of plasma indicated an increased proportion of apoA-IV in the triglyceride-rich lipoproteins (TRL) of the hypertriglyceridemic patients compared with controls and delayed catabolism of this TRL-associated apoA-IV. The rate of apoA-IV catabolism from the lipid deficient fraction was not different between the hypertriglyceridemic patients and controls. In summary, plasma levels of apoA-IV are significantly elevated in hypertriglyceridemic patients due to delayed catabolism of apoA-IV as demonstrated by both endogenous stable isotope labeling and exogenous radiotracer techniques.

Apolipoproteins A↗
PubMed1993

Familial HDL deficiency due to marked hypercatabolism of normal apoA-I.

In this article, we describe a 46-year-old man with severe high-density lipoprotein (HDL) deficiency and his kindred. In the proband, HDL cholesterol and apolipoprotein (apo) A-I levels were 5 and 4.5 mg/dL, respectively. Xanthomata, xanthelasma, arcus corneae, and hepatosplenomegaly were not present. The proband had coronary artery disease, but it was impossible to state whether the HDL deficiency cosegregated with premature coronary artery disease in this kindred. Pedigree analysis was suggestive of a codominant familial disease. Polymerase chain reaction amplification of the apoA-I gene of the proband, followed by subcloning and sequencing, did not reveal any mutation in either the coding regions or intron-exon junctions. A kinetic study using deuterated leucine to endogenously label apoA-I was performed to elucidate the metabolic basis of the apoA-I deficiency. We demonstrated marked hypercatabolism of apoA-I in the proband, with a fractional catabolic rate more than 10 times faster than normal; the plasma residence time of apoA-I in the proband was only 0.38 day compared with 4.10 days in a control subject. The apoA-I production rate was also substantially decreased in the proband. The association of a normal apoA-I gene sequence with marked hypercatabolism of apoA-I is similar to that described in Tangier disease. However, except for the presence of mild, diffuse, corneal deposits, this patient had no evidence of the reticuloendothelial cholesterol deposition characteristic of Tangier disease. This study establishes that a form of severe hypoalphalipoproteinemia distinct from Tangier disease can be caused by marked hypercatabolism of a normal A-I apolipoprotein.

Apolipoprotein A-I↗
PubMed1992

[Substernal goiters. 218 operated cases].

The authors are presenting a retrospective study on 218 retrosternal goiters operated between 1968 and 1991. 33% of the goiters were incidentally discovered on a plain X-ray of the chest. Symptoms of compression were present in 50.5% of patients and hyperthyroidism in 16.5%. Respiratory manifestations were more frequent and more severe in patients aged 70 and more. Moreover 90% of those old patients were symptomatic. Goiters migrated anteriorly in 57.7% of cases, posteriorly in 33.9%, both anteriorly and posteriorly in 5.5%. Type of migration was unknown in 2.5%. 3.7% were malignant. 27 patients with respiratory symptoms received corticosteroids to reduce the airway compression. Among 52 patients with hyperthyroidism, 36 were given antithyroid drugs. Among them, some received corticosteroid drugs in order to reduce risks of mediastinal compression. A simple cervicotomy was adequate in 92.7% of case and was completed by sternotomy in 7.3%. The operation was iterative for relapsing or forgotten thoracic goiters in 24 cases. Morbidity was slight even for sternotomized patients. Mortality was noted in 2 cases (0.9%) one of them operated on for poorly-differentiated and suffocating carcinoma of the thyroid. We advise a straightforward surgical attitude as a result of the slight morbidity and mortality, even in sternotomized patients in order to avoid severe compressive complications of the airways.

Adult↗
PubMed1985

[Role of peri-operative treatment in the surgery of advanced valvular cardiopathies].

Between January 1981 and October 1982, 100 consecutive patients with valvular heart disease (49 p. 100 polyvalvular disease) underwent surgery. All had severe lesions; Class III or IV of the NYHA classification; cardiomegaly with an average cardio-thoracic ratio of 59 +/- 7.7 p. 100; a cardiac index of less than 2.5 1/min/m2 in 70 p. 100 of cases; pulmonary hypertension (mean PAP : 31.93 +/- 12.17 mmHg) in 89 p. 100 of cases. Half the patients were in atrial fibrillation and all had been on chronic digitalo-diuretic therapy before surgery. Thirty of the 41 patients given preoperative venous vasodilator therapy had significant reductions of their cardiothoracic ratios (63 +/- 1.5 p. 100 vs 59.1 +/- 1.6 p. 100, p less than 0.001). Conservative surgical procedures were possible in 58 cases of mitral valvuloplasty and 5 aortic valvuloplasties. Correction of functional tricuspid regurgitation (34 p. 100) was systematic. Tricuspid regurgitation masked by salt and water depletion was detected by digital palpation after clamping the pulmonary artery. In 8 cases the aortic ring had to be enlarged. The low hospital mortality (6 p. 100) and the lack of postoperative complications (assisted ventilation for less than 24 hours in 92 p. 100 of cases) compare favourably with other reported series.

Adolescent↗
PubMedDate not supplied

[Anomalies of lipid metabolism in diabetes mellitus].

Atheroma is by far the most common cause of mortality in diabetic patients (66 to 75% of deaths). Several physiopathological mechanisms are suspected to account for the greater frequency and severity of atheroma in diabetes. Among these, lipid abnormalities hold first rank and include not only quantitative but also qualitative abnormalities of lipoproteins altering their kinetics and bindings to membrane receptors. The main quantitative abnormalities are an increase of triglycerides and very low density lipoproteins (VLDL) and a fall in high density lipoproteins (HDL) and their HDL2 subfraction. Qualitative abnormalities include non-enzymatic glucosylation of apoproteins, changes in lipoprotein size and increase in their triglyceride content, and excessive oxidation of low density lipoproteins (LDL). Both quantitative and qualitative abnormalities of lipoproteins are present in non-insulin-dependent diabetes, whereas only qualitative abnormalities are observed, as a rule, in treated insulin-dependent diabetes. The physiopathology of lipid metabolism disorders is complex, possibly multifactorial and still imperfectly known. However, such factors as modification of insulin status, hyperglycaemia and obesity frequently associated with diabetes, are thought to be involved.

Diabetes Mellitus↗
PubMedDate not supplied

[Association of Basedow's disease and autoimmune thrombopenic purpura. No effect of hyperthyroidism on antiplatelet autoimmunity].

The association between Graves' disease and autoimmune thrombocytopenic purpura is rare and yet more frequent than would be expected from a mere coincidence. The existence of an immunological disorder common to Graves' disease and autoimmune thrombocytopenic purpura and/or a direct responsibility of hyperthyroidism in the genesis of immunological disturbances resulting in autoimmune thrombocytopenic purpura are hypotheses put forward to try and explain why these two pathologies are associated. We report two cases in which the antiplatelet autoimmunity developed independently of the thyroid functional disorder, making it unlikely that hyperthyroidism played a direct role in the occurrence of the immunological disorders responsible for the autoimmune thrombocytopenic purpura. The physiopathology responsible for the Graves' disease-autoimmune thrombocytopenic purpura association remains imperfectly known. The existence of an immunological pathogenetic mechanism underlying both diseases seems to be likely; it probably acts through an antigenic determinant that is common to thyroid cells and platelets.

Adult↗
PubMedDate not supplied

Muscle metabolism assessed by phosphorus-31 nuclear magnetic resonance spectroscopy after myocardial infarction in rehabilitated patients: a 1-year follow-up.

BACKGROUND: The most common effect of postmyocardial infarction (post MI) rehabilitation is an increase of peak maximal oxygen consumption correlated with changes in calf muscle metabolism, but there are few data on follow-up after rehabilitation on skeletal muscle and maximal oxygen consumption. The purpose of this study was to investigate the respective modifications in skeletal muscle metabolism and peak oxygen consumption (VO2) occurring during a supervised rehabilitation program and 1 year after MI in patients free of heart failure. METHODS: Fifteen outpatients were studied prospectively after the acute phase of the MI, at the end of the rehabilitation program (2 months after the MI), and 1 year after. The rehabilitation comprised 20 sessions with three sessions per week. The program consisted of exercise training with bicycle, arm ergometer, and treadmill. The program also included respiratory exercises, psychological support, and counseling for secondary prevention of cardiovascular diseases. At each visit, a stress test on a bicycle ergometer was performed and the peak VO2 was measured. Phosphorus magnetic resonance spectroscopy of the gastrocnemius muscle was performed at rest and during a plantar flexion-type exercise against an adjustable load. Data were analyzed using analysis of variance and post-hoc test when appropriate. RESULTS: The mechanical power output measured during the bicycle exercise increased from 111 +/- 28 watts at the post MI test to 136 +/- 40 watts after rehabilitation (post rehab) and decreased to 125 +/- 36 watts at 1 year. The peak VO2 increased significantly (P < 0.05) from 22 +/- 7 ml/kg-1/min-1 (post MI) to 27 +/- 9 ml/kg-1/min-1 (post rehab), and decreased significantly to 24 +/- 8 ml/kg-1/min-1 (1 year). The mechanical power output measured in the magnet during the stress test increased from 2.22 +/- 0.13 watts (post MI) to 2.85 +/- 1.24 (post rehab), and stabilized at 2.78 +/- 1.10 watts at 1 year. At the highest workload attained in the three successive tests, the phosphocreatine/(phosphocreatine + inorganic phosphate) ratio rose significantly (P < 0.05) from 0.46 +/- 0.13 (post MI) to 0.51 +/- 0.13 (post rehab) and remained at 0.51 +/- 0.13 at 1 year. CONCLUSION: The improvement of the peak VO2 after training post MI is not maintained 1 year later. This decline is not accompanied by muscular metabolic abnormalities. This suggests that the muscle metabolism after MI remains normal, and that the long-term decrease of the peak VO2 reflects a global deconditioning that should be avoided by maintaining a long-term phase III rehabilitation program.

Adult↗