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Biomedical subjects

B Vergès

Publications and source records attributed to B Vergès.

At least 19 recordsLinked to original sources
PubMed2006

Inability of HDL from type 2 diabetic patients to counteract the inhibitory effect of oxidised LDL on endothelium-dependent vasorelaxation.

AIMS/HYPOTHESIS: In healthy normolipidaemic and normoglycaemic control subjects, HDL are able to reverse the inhibition of vasodilation that is induced by oxidised LDL. In type 2 diabetic patients, HDL are glycated and more triglyceride-rich than in control subjects. These alterations are likely to modify the capacity of HDL to reverse the inhibition of vasodilation induced by oxidised LDL. SUBJECTS AND METHODS: Using rabbit aorta rings, we compared the ability of HDL from 16 type 2 diabetic patients and 13 control subjects to suppress the inhibition of vasodilation that is induced by oxidised LDL. RESULTS: Oxidised LDL inhibited endothelium-dependent vasodilation (maximal relaxation [Emax] = 58.2+/-14.6 vs 99.3+/-5.2% for incubation without any lipoprotein, p < 0.0001). HDL from control subjects significantly reduced the inhibitory effect of oxidised LDL on vasodilatation (Emax = 77.6+/-12.9 vs 59.5+/-7.7%, p < 0.001), whereas HDL from type 2 diabetic patients had no effect (Emax = 52.4+/-20.4 vs 57.2+/-18.7%, NS). HDL triglyceride content was significantly higher in type 2 diabetic patients than in control subjects (5.3+/-2.2 vs 3.1+/-1.4%, p < 0.01) and was highly inversely correlated to Emax for oxidised LDL+HDL in type 2 diabetic patients (r = -0.71, p < 0.005). CONCLUSIONS/INTERPRETATION: In type 2 diabetes mellitus, the ability of HDL to counteract the inhibition of endothelium-dependent vasorelaxation induced by oxidised LDL is impaired and is inversely correlated with HDL triglyceride content. These findings suggest that HDL are less atheroprotective in type 2 diabetic patients than in control subjects.

Animals↗
PubMed2006

[Best of functional evaluation and cardiac rehabilitation in 2005].

The latest in cardiac rehabilitation has been impacted by: The East German PET publication which showed fewer ischaemic events and progression of the atheromatous disease in symptomatic and stable coronary patients who carry out regular physical exercise in comparison with patients who underwent angioplasty with stenting. Two meta-analyses updated the data showing the benefits of physical training: a 20% reduction in global mortality in coronary disease and 35% in cardiac failure. Two French studies reporting reassuring data for our daily practice: the serious complications of cardiac rehabilitation are exceptionally rare: the register for 2003 with data from 65 French centres, over 25,000 patients and 743,000 patient/exercise hours. Physical training two weeks after mitral valvuloplasty is not harmful for the valve repair and is beneficial in terms of exercise capacity for the patient. Epidemiological studies showing that women and elderly patients are, unfortunately, often excluded from programmes of cardiac rehabilitation.

Cardiovascular Diseases↗
PubMed2005

Long-term effects on lipids and lipoproteins of pioglitazone versus gliclazide addition to metformin and pioglitazone versus metformin addition to sulphonylurea in the treatment of type 2 diabetes.

AIMS/HYPOTHESIS: The aim of this study was to determine the long-term effects of pioglitazone add-on to metformin or sulphonylurea on plasma lipids and lipoproteins. MATERIALS AND METHODS: The effects of pioglitazone were studied in two clinical trials in patients with inadequately controlled type 2 diabetes (HbA1c > or =7.5 and < or =11%). In the first trial, patients currently receiving metformin were randomised to pioglitazone (15-45 mg/day, n=317) or gliclazide (80-320 mg/day, n=313) add-on therapy. In the second study, pioglitazone (15-45 mg/day, n=319) or metformin (850-2,550 mg/day, n=320) was added to sulphonylurea therapy. Patients were force-titrated to the maximum tolerated dose of add-on therapy, which was maintained to the 2-year endpoint. RESULTS: There were no statistically significant differences between the groups with respect to HbA1c reduction from baseline to week 104. Whether added to metformin or sulphonylurea, pioglitazone caused highly significant greater decreases in triglycerides and increases in HDL cholesterol from baseline to week 104 than treatments with gliclazide or metformin add-on therapies (p< or =0.001). The triglyceride reductions noted with pioglitazone were maintained over time, with decreases of 16-18% at 1 year and 17-23% at 2 years. In the pioglitazone groups, the improvement in HDL cholesterol at 1 year was maintained, with 21-22% augmentations at 2 years (p<0.001 between-group difference). Small but statistically significant greater reductions in LDL cholesterol were observed with gliclazide vs pioglitazone add-on to metformin and metformin vs pioglitazone add-on to sulphonylurea (p<0.001 for between-group difference). In the pioglitazone groups, mean LDL cholesterol at 2 years was similar to mean baseline LDL cholesterol. CONCLUSIONS/INTERPRETATION: After 2 years, highly significant decreases in triglycerides and increases in HDL cholesterol that were sustained over time or even improved were observed when pioglitazone was added to metformin or sulphonylurea therapy. These effects of pioglitazone on lipids may be potentially beneficial in reducing cardiovascular risk in type 2 diabetes.

Adult↗
PubMed2005

Normal metabolism of apolipoprotein B100-containing lipoproteins despite qualitative abnormalities in type 1 diabetic men.

AIMS/HYPOTHESIS: Type 1 diabetic subjects are at increased risk of cardiovascular disease and exhibit multiple qualitative abnormalities of apolipoprotein (apo) B100-containing lipoproteins. This stable isotope kinetic experiment was designed to study whether these abnormalities are associated with changes in the synthesis and fractional catabolic rates of VLDL-, IDL- and LDL-apoB100. METHODS: Using a bolus followed by a 16-h constant infusion of 13C-leucine, we performed a kinetic study in eight men with type 1 diabetes treated with a continuous subcutaneous insulin infusion administered by an external pump and in seven healthy men, in the fed state. RESULTS: The mean HbA1c level in the type 1 diabetic patients was 8.00+/-1.48%. Plasma triglyceride, and total, LDL and HDL cholesterol levels were similar in patients and control subjects. VLDL were less triglyceride rich in type 1 diabetic patients than in control subjects (VLDL triglyceride : apoB 6.91+/-0.81 vs 8.29+/-1.24 mmol/g, p=0.05). Conversely, the IDL and LDL of the type 1 diabetic patients contained relatively higher levels of triglycerides (IDL triglycerides : apoB 2.16+/-0.36 vs 1.57+/-0.30 mmol/g, p<0.01; LDL triglycerides : apoB 0.27+/-0.06 vs 0.16+/-0.04 mmol/g, p<0.05). The apoB100 pool size, production and fractional catabolic rates in the two groups of subjects were similar for all lipoprotein fractions. CONCLUSIONS/INTERPRETATION: Despite qualitative abnormalities, especially abnormalities of triglyceride content, the metabolism of apoB100-containing lipoproteins is not altered in type 1 diabetic men with fair glycaemic control with continuous subcutaneous insulin infusion. The high risk of atherosclerosis in these patients cannot be explained by kinetic abnormalities of apoB100-containing lipoproteins.

Adult↗
PubMed2005

New insight into the pathophysiology of lipid abnormalities in type 2 diabetes.

Lipid abnormalities in patients with type 2 diabetes are likely to play an important role in the development of atherogenesis. These lipid disorders include not only quantitative but also qualitative abnormalities of lipoproteins which are potentially atherogenic. The main quantitative abnormalities are increased triglyceride levels, related to an augmented hepatic production of VLDL and a reduction of both VLDL and IDL catabolism, and decreased HDL-Cholesterol levels due to an accelerated HDL catabolism. The main qualitative abnormalities include large VLDL particles (VLDL1), relatively rich in triglycerides, small dense LDL particles, increase in triglyceride content of LDL and HDL, glycation of apolipoproteins and increased susceptibility of LDL to oxidation. Moreover, although plasma LDL-cholesterol level is usually normal in type 2 diabetic patients, LDL particles show significant kinetic abnormalities, such as reduced turn-over, which is potentially harmful. The pathophysiology of lipid abnormalities in type 2 diabetes is not yet totally explained. However, insulin resistance and the "relative" insulin deficiency, observed in patients with type 2 diabetes, are likely to play a crucial role since insulin has an important function in the regulation of lipid metabolism. In addition, it is not excluded that adipocytokines, such as adiponectin, could play a role in the pathophysiology of lipid abnormalities in type 2 diabetes.

Atherosclerosis↗
PubMed2005

Diabetic dyslipidaemia: insights for optimizing patient management.

BACKGROUND: Lipid abnormalities in people with diabetes are likely to play an important role in the development of atherogenesis. These lipid disorders include potentially atherogenic quantitative (increased triglyceride levels and decreased high-density lipoprotein-cholesterol [HDL-C] levels) and qualitative abnormalities of lipoproteins (changes in lipoprotein size, increase in triglyceride content of low-density lipoprotein (LDL) and HDL, glycation of apoproteins and increased susceptibility of LDL to oxidation). Guidelines from the two main diabetes organizations, the International Diabetes Federation and the American Diabetes Association, recommend the aggressive management of diabetic dyslipidaemia to reduce the risk of cardiovascular disease (CVD). Statins are the first choice pharmacological therapy to address diabetic dyslipidaemia due to their effectiveness at lowering LDL-C levels in patients with diabetes. Fibrates (peroxisome proliferator-activated receptor [PPAR]alpha ligands) target another aspect of dyslipidaemia by lower ing triglycerides (to a greater extent than statins) and raising HDL-C levels, especially when baseline levels are low. The PPARgamma agonist, pioglitazone appears to affect lipid metabolism by decreasing plasma triglycerides, increasing HDL-C and decreasing the number of small, dense atherogenic LDL particles. SCOPE: This paper provides a review of the current literature (based on searches of MEDLINE and EMBASE from 1985 to 2005, inclusive) supporting the recommendations for the management of dyslipidaemia among patients with type 2 diabetes, including new strategies involving drug combinations that achieve good glycaemic and lipidaemic control that could potentially reduce the morbidity and mortality associated with type 2 diabetes.

Arteriosclerosis↗
PubMed2004

Clinical interest of PPARs ligands.

Cardiovascular disease is significantly increased in patients with metabolic syndrome and type 2 diabetes. Several factors such as chronic hyperglycemia, lipId abnormalities, endothelium dysfunction, inflammation, oxIdative stress, increased thrombosis and decreased fibrinolysis are likely to promote cardiovascular events in these patients. Because of positive effects on glucose homeostasis, lipId metabolism, proteins involved in all stages of atherogenesis, endothelium function, inflammation, thrombosis and fibrinolysis, PPARS alpha (fibrates) and PPARs gamma (glitazones) agonists are good candIdates to reduce cardiovascular disease, more precisely in subjects with metabolic syndrome or type 2 diabetes. PPARS alpha agonists (fibrates) are potent hypolipIdemic agents increasing plasma HDL-cholesterol and reducing free fatty acIds, triglycerIdes, LDL-cholesterol and the number of small dense LDL pArticles. Moreover, they reduce vascular inflammation and thrombosis, promote fibrinolysis and inhibit the production of the vasoconstrictor factor, endothelin-1, by the endothelium. They have been shown, in clinical trials, to reduce cardiovascular disease, more particularly in patients displaying lipId abnormalities typical of metabolic syndrome and type 2 diabetes (high triglycerIdes, low HDL-cholesterol). PPARS gamma agonists (glitazones) have not only beneficial effects on glucose homeostasis, by increasing insulin sensitivity and reducing blood glucose level but also on lipId metabolism by elevating plasma HDL-cholesterol, decreasing free fatty acIds and the number of small dense LDL pArticles, and for pioglitazone by reducing plasma triglycerIdes. Furthermore, they diminish vascular inflammation and vasoconstriction, inhibit monocyte chemotaxis, proliferation and migration of smooth muscle cells, in the vascular wall and decrease the production of adhesion molecules and metalloproteinases. PPARs gamma agonists (glitazones) have been shown to reduce the development of atherosclerotic lesions in rats. The potential clinical benefit of PPARs gamma agonists on the reduction of cardiovascular disease, in type 2 diabetic patients, will be specified by the ongoing intervention studies.

Animals↗
PubMed2004

Serum adiponectin and metabolic parameters in HIV-1-infected patients after substitution of nevirapine for protease inhibitors.

BACKGROUND: In the context of HIV infection and antiretroviral therapy, adiponectin concentrations have been shown to be related to lipodystrophy, metabolic alterations and HIV-protease inhibitor (PI) use. The replacement of PI by nevirapine has improved the lipid profile of patients under antiretroviral therapy. The aim of the present study was to examine whether adiponectin concentration or insulin sensitivity level correlate with the modifications of lipid parameters after the switch of PI by nevirapine. MATERIAL AND METHODS: The evolution of metabolic parameters before and after 6 months of substitution of nevirapine for protease inhibitors was evaluated in a cohort of 55 HIV-1 infected patients. Adiponectin concentration, insulin sensitivity, lipid profile, cholesterol ester transfer protein (CETP) mass concentration and triglyceride enrichment of HDL were determined before and after the replacement of PI by nevirapine. Insulin sensitivity was evaluated by the HOMA model assessment. RESULTS: Twenty-four weeks of treatment with nevirapine improved significantly the lipid profile with a significant reduction of apoB (from 0.98 to 0.92 g L(-1); P = 0.005) and triglyceride (from 2.02 to 1.66 mmol L(-1); P = 0.02). HDL cholesterol and apoA1 increased significantly (from 0.99 to 1.19 mmol L(-1); P = 0.001 and from 1.40 to 1.57 g L(-1); P < 0.001, respectively). The triglyceride enrichment of HDL significantly decreased after the replacement of PI by nevirapine (from 0.248 +/- 0.092 to 0.213 +/- 0.093; P = 0.003). At baseline, and after 24 weeks of nevirapine treatment, we observed significant correlations between adiponectin level and lipid parameters [(HDL-cholesterol (r = 0.66, P = 0.001 and r = 0.69, P = 0.001); triglycerides (r = -0.42, P = 0.002 and r = -0.57, P = 0.001), and triglyceride enrichment of HDL (r = -0.43, P = 0.005 and r = -0.53, P = 0.005)]. Twenty-four weeks of treatment with nevirapine did not significantly change adiponectin concentrations (from 984 to 1086 micro g L(-1), P = 0.22), CETP mass and insulin sensitivity. CONCLUSION: This study shows that even though a strong correlation was found between adiponectin and some metabolic parameters at baseline and after 24 weeks of treatment by nevirapine, the improvement of lipid profile observed after the replacement of PI by nevirapine was not in relation to the change of plasma adiponectin concentration. The significant decrease of triglyceride enrichment of HDL after the replacement of PI by nevirapine probably leads to a decreased catabolism of HDL lipoprotein, and consequently explains the increase of plasma HDL concentration observed in this study.

Adiponectin↗
PubMed2004

Effects of cardiac rehabilitation on exercise capacity in Type 2 diabetic patients with coronary artery disease.

AIM: To determine whether Type 2 diabetic patients with coronary disease can obtain, after cardiac rehabilitation, a similar benefit on exercise capacity to non-diabetic coronary individuals. RESEARCH DESIGN AND METHODS: Fifty-nine Type 2 diabetic patients and 36 age-matched non-diabetic patients were enrolled in a 2-month cardiac rehabilitation programme, after an acute coronary event. At the beginning and at the end of the cardiac rehabilitation programme, each subject underwent a cardiopulmonary exercise test to assess exercise capacity as measured by peak workload, duration of test, maximal heart rate, peak VO2 and anaerobic threshold. The two groups of patients were not different in age, sex ratio, type of coronary event or left ventricular ejection fraction. RESULTS: The baseline exercise capacity parameters were not different between diabetic and non-diabetic subjects. After cardiac rehabilitation, improvement of exercise capacity was significantly less in patients with diabetes compared with those without diabetes: peak workload (19% vs. 29%, P = 0.022), peak VO2 (13% vs. 30%, P = 0.002), anaerobic threshold (12% vs. 31%, P = 0.017). In the diabetic patients, a significant inverse relation between fasting blood glucose and change in peak VO2 was observed on both univariate (r = -0.40, P = 0.002) and multivariate (P = 0.001) analyses. CONCLUSIONS: The benefit of cardiac rehabilitation, after an acute ischaemic heart event, in exercise capacity is significantly lower in Type 2 diabetic patients. The response to cardiac rehabilitation in those with diabetes appears to be influenced by blood glucose levels.

Cholesterol↗
PubMed2004

[Do the pleiotropic effects of statins have a clinical significance?].

The effectiveness of statins in the treatment of hypercholesterolaemia and the reduction in cardiovascular risk have now been clearly demonstrated. While their beneficial effects on the reduction of atherosclerosis and its clinical manifestations occur mainly due to the reduction in LDL-cholesterol, some pleiotropic actions which are independent of LDL-cholesterol have frequently been put forward in recent years. In effect, an improvement in endothelial function (increased vasodilatation in particular), an in vitro reduction in smooth muscle cell proliferation, a reduction in thrombosis, promotion of fibrinolysis and positive effects on atheromatous plaque stabilisation have been observed. Elsewhere, some anti-oxidant and anti-inflammatory properties have been attributed to statins. However, many of the described 'pleiotropic' effects are not due to the direct action of statins, but occur with the reduction in LDL-cholesterol. Furthermore, certain in vitro effects only occur at much higher than therapeutic doses. These considerations have therefore caused doubt about the clinical significance of the statins' pleiotropic effects. Finally, analysis of the results of human clinical trials on statins have proved that their effectiveness relies on the reduction in LDL-cholesterol and that the pleiotropic effects do not actually have a clinical implication.

Anti-Inflammatory Agents↗
PubMed2002

High-density lipoprotein apolipoprotein A-I kinetics in obese insulin resistant patients. An in vivo stable isotope study.

AIMS/HYPOTHESIS: Mechanisms responsible for the decreased high-density lipoprotein (HDL) cholesterol level associated with insulin resistance in obese patients are not clearly understood. To determine the influence of insulin resistance at an early stage on HDL metabolism, we performed a stable isotope kinetic study of apolipoprotein (apo) A-I, in five obese insulin resistant women with normal fasting triglycerides and without impaired glucose tolerance, and in five age-matched control women. METHODS: Each subject received a 16 h constant infusion of L-[1-(13)C]leucine at 0.7 mg/kg/h following a primed bolus of 0.7 mg/kg. RESULTS: ApoA-I fractional catabolic rate (FCR) was significantly increased in insulin-resistant women compared to controls (0.316+/-0.056 vs 0.210+/-0.040 per day, P<0.01), indicating a significant 50% increase of apoA-I catabolism, leading to an important reduction of plasma apoA-I residence time (3.25+/-0.59 vs 4.92+/-1.11, P<0.01). ApoA-I production rate tended to be higher in insulin resistant women than in controls (364+/-77 vs 258+/-60 mg/l/day, P=0.13), but the difference was not statistically significant. ApoA-I FCR was correlated with triglycerides during the fed state (r=0.69; P=0.026) and HDL triglycerides-esterified cholesterol ratio (r=0.73; P=0.016), suggesting that alteration of apoA-I metabolism in insulin resistance may be partly related to HDL enrichment in triglycerides. CONCLUSIONS: Our kinetic study shows that patients, at an early stage of insulin resistance (without impaired glucose tolerance nor fasting hypertriglyceridaemia), already have a significant alteration of apoA-I metabolism (increased apoA-I catabolism), which is consistent with the increased risk of atherosclerosis in this population.

Adult↗
PubMed2002

The impact of prandial glucose regulation in practice.

Post-prandial hyperglycaemia, which occurs early in the development of impaired glucose tolerance and Type 2 diabetes mellitus (T2DM), has been receiving increased attention recently. Post-prandial hyperglycaemia is likely to promote or aggravate fasting hyperglycaemia and contributes entirely to HbA1c elevation, which is associated with microvascular and macrovascular complications in people with T2DM. Moreover, post-prandial hyperglycaemia is coupled with coagulation activation and may be associated with an increased risk of cardiovascular disease in people with or without diabetes. For these reasons, reduction of post-prandial hyperglycaemia is an important target in patients with impaired glucose tolerance or T2DM. Several treatments have therefore been developed to reduce post-prandial hyperglycaemia; of these, repaglinide, a prandial glucose regulator taken orally before each meal, is now available. Drugs that reduce post-prandial hyperglycaemia significantly also decrease HbA1c (up to 2% with repaglinide) and fasting glucose concentrations (up to 3.9 mmol/l with repaglinide), with consequent decreases in coagulation activation and, in some studies, post-prandial lipidaemia. In clinical trials in patients with T2DM, repaglinide significantly reduced 2-hr post-prandial glucose concentrations and significantly reduced the risk of hypoglycaemia, compared with sulphonylureas, especially when participants missed or postponed a meal. Treatment with the prandial glucose regulator repaglinide allows patients with T2DM to have a more flexible lifestyle, which is likely to improve their quality of life and compliance.

Blood Glucose↗
PubMed2001

[Blood lipid abnormalities during treatment with protease inhibitors].

HYPERLIPIDEMIA: HIV-1 protease-inhibitors therapy is associated with increased levels of triglycerides, LDL-cholesterol and Lp(a). But the understanding of hyperlipidaemia occurring in patients treated with HIV-1 protease-inhibitors is not easy since HIV infection itself is associated with lipid abnormalities and since HIV-1 protease-inhibitors therapy is also responsible for the development of a lipodystrophy syndrome (insulin resistance) which may influence lipid metabolism. However, many data indicate that HIV-1 protease-inhibitors therapy itself modifies significantly lipid metabolism. UNDERLYING MECHANISMS: The mechanisms involved in HIV-1 protease-inhibitors induced hyperlipidaemia are still unclear. HIV-1 protease-inhibitors could bind to LRP (Low density lipoprotein receptor Related Protein), impairing hepatic chylomicron-remnants and VLDL uptake. They could interact with the retinoid X receptor (RXR), which functions as a heterodimer with PPAR (Peroxisome Proliferator Activator Receptor). HIV-1 protease-inhibitors could also modify lipoprotein metabolism through cytokines.

HIV Infections↗
PubMed2001

[Hypercalcemia in the elderly].

UNLABELLED: A COMMON FINDING: Hypercalcemia is not rare among elderly patients. Hyperparathyroidism and neoplasia are the most frequent causes of hypercalcemia in old patients. Symptoms due to hypercalcemia are usually non specific in old subjects, leading to consider easily this diagnosis and to measure plasma calcium level. DIAGNOSIS: Biological diagnosis of hypercalcemia is not always obvious in old patients because of frequently decreased plasma albumin levels leading to lower plasma total calcium level. Thus, it is always necessary to calculate plasma total calcium level corrected by albumin in order not to underestimate hypercalcemia in elderly subjects. PROGNOSIS: The short-term risk of hypercalcemia is acute hypercalcemia, which may be lifethreatening. The long-term risk of hypercalcemia is renal failure. TREATMENT: When hypercalcemia is due to primary hyperparthyroidism, the treatment of choice is surgery. However, for old patients with high surgical risk surgery with local anesthesia or ultrasonically guided percutaneous ethanol injection into parathyroid adenoma can be proposed.

Age Factors↗
PubMed2001

Hyperparathyroidism in multiple endocrine neoplasia type I: surgical trends and results of a 256-patient series from Groupe D'etude des Néoplasies Endocriniennes Multiples Study Group.

The French and Belgian GENEM study group's multiple endocrine neoplasia type I (MEN-I) database was used to evaluate trends in clinical presentation, surgical treatment of primary hyperparathyroidism (pHPT) (n = 245), and prognostic factors for hypercalcemia correction among 256 MEN-I cases. The patients were retrieved through the GENEM network from various Belgian and French institutions with the help of genetics laboratories. Among the 245 pHPT patients (96%), 42% were men. The mean age at the time of diagnosis was 39.5 +/- 13.3 years. Trends were studied for three periods: before 1986, from 1986 to 1990, and thereafter. After 1990 MEN-I patients were more often diagnosed with isolated pHPT (8%, 11%, 28%, for the three periods, respectively; p = 0.002); it was seen more often in screened patients (31%, 28%, 53%; p = 0.001), more often among those in already known MEN-I families (64%, 45%, 72%; p = 0.005), and among those with lower preoperative calcemia (2.93, 2.87, 2.79 mmol/L; p = 0.001). The age at pHPT diagnosis remained constant throughout the study. The percentage of cervical explorations dropped during the entire study (87%, 87%, 53%; p < 0.0001). After 1985 the percentage of subtotal parathyroidectomies increased (25%, 59%, 51%; p = 0.0004). Pathology disclosed more hyperplasias (59%, 85%, 74%; p = 0.008). Postoperative hypercalcemia decreased (47%, 15%, 19%; p < 0.0001); and postoperative hypocalcemia increased nonsignificantly (5%, 15%, 15%; p = 0.1). Subtotal parathyroidectomy [odds ratio (OR) 13], no MEN-I family background (OR 3), and the most recent study period (> 1985) (OR 3) were significant predictive factors of hypercalcemia correction according to the multivariate analysis. This is the first multicentric study on the management of MEN-I-related pHPT. Immediate postoperative hHPT cure increased, but only 80% of the operated patients were cured after 1990. Fifteen percent were hypocalcemic. Because MEN-I-related hHPT cure remains difficult to achieve, we advocate that subtotal parathyroidectomies be performed in specialized centers.

Adult↗
PubMed2001

[Statins and diabetic hyperlipidemia].

Type 2 diabetic patients show frequent lipid abnormalities characterized by increased triglyceride and decreased HDL-cholesterol levels, but also by qualitative and metabolic abnormalities of all lipoproteins (VLDL, IDL, LDL et HDL). Treatment of diabetic hyperlipidemia is important in order to reduce the incidence of cardiovascular events, which is high in type 2 diabetes. Treatment with statins is recommended when hypercholesterolemia is associated with diabetes. But the efficacy of statins in the treatment of the typical diabetic hyperlipidemia (hypertriglycerideùmia, decreased HDL-cholesterol) remains to be demonstrated, since their effects on triglycerides and HDL-cholesterol is moderate. However, the new statins (cerivastatine, atorvastatine), which are more powerful to reduce hypertriglyceridemia could be useful for the treatment of diabetic hyperlipidemia. But, only on going clinical trials with statins in diabetic patients will be able to precise their possible efficacy on the prevention of cardiovascular disease.

Cholesterol, HDL↗
PubMed2001

[Insulin sensitiviy and lipids].

Insulin plays a central role in regulation of lipid metabolism, with different sites of action. In the adipose tissue, insulin inhibits lipolysis via an inhibition of the lipase, leading to reduce the flux of free fatty acids into the circulation. Insulin inhibits the VLDL production by the liver. Insulin is a potent activator of the lipoprotein lipase, promoting the catabolism of triglyceride-rich lipoproteins (Chylomicrons, VLDL). insulin promotes the clearance of LDL. Indeed, insulin stimulates apoB/E receptor (LDL-receptor) activity and enhances LDL degradation via the LDL-receptor pathway. Insulin also plays an important role in HDL metabolism since it activates LCAT activity, it reduces PLTP activity and modulates the hepatic triglyceride lipase activity. Because of the key role of insulin in lipid metabolism, we can easily understand that all diseases with impaired insulin action, such as insulin resistance or diabetes mellitus, will be characterized by important lipid abnormalities, which are important factors responsible for the increased cardiovascular risk in the patients.

Adipose Tissue↗