Effect of Sibutramine on Weight Management and Metabolic Control in Type 2 Diabetes

OBJECTIVE—The aim of this study was to provide a comprehensive meta-analysis of randomized controlled clinical studies on the effects of sibutramine on weight loss and glycemic control in obese subjects with type 2 diabetes. RESEARCH DESIGN AND METHODS—Controlled clinical trials assessing the effect sizes of sibutramine on weight loss effects on glycemia in obese subjects with type 2 diabetes were identified and reviewed using the Cochrane Library, Medline, EMBASE, and a manual search. RESULTS—Eight placebo-controlled, double-blind, randomized trials of sibutramine were included. After sibutramine treatment, the decrease in body weight and waist circumference was significantly greater than in the placebo group. Fasting blood glucose and HbA1c significantly decreased after sibutramine treatment. Treatment benefits were seen in plasma triglycerides and HDL, without significant variations in serum total and LDL cholesterol. No differences in systolic blood pressure between the sibutramine and the placebo groups were seen, while recording of diastolic blood pressure and heart rate showed that sibutramine produced a small increase relative to placebo. CONCLUSIONS—A pharmacological approach in a weight management program for patients with type 2 diabetes may be helpful in glycemic control and in the management of other risk factors. Sibutramine may help improve glucose control because it is conducive to weight loss. The reviewed data on the effect of sibutramine further enforce the recommendations that weight management may be the most important therapeutic task for most obese subjects with type 2 diabetes

IM -ORIGINAL Rational error in internal medicine

Abstract Epistemologists have selected two basic categories: that of errors committed in scientific research, when a researcher devises or accepts an unfounded hypothesis, and that of mistakes committed in the application of scientific knowledge whereby doctors rely on knowledge held to be true at the time in order to understand an individual patient's signs and symptoms. The paper will deal exclusively with the latter, that is to say the mistakes which physicians make while carrying out their day-to-day medical duties. The paper will deal with the mistakes committed in medicine trying also to offer a classification. It will take into account also examples of mistakes in Bayesian reasoning and mistakes of reasoning committed by clinicians regard inductive reasoning. Moreover, many other mistakes are due to fallacies of deductive logic, logic which they use on a day-to-day basis while examining patients in order to envisage the consequences of the various diagnostic or physiopathologic hypotheses. The existence of a different type of mistakes that are part of the psychology of thought will be also pointed out. We conclude that internists often make mistakes because, unknowingly, they fail to reason correctly. These mistakes can occur in two ways: either because he does not observe the laws of formal logic, or because his practical rationality does not match theoretical rationality and so his reasoning becomes influenced by the circumstances in which he finds himself

Rational error in internal medicine

Epistemologists have selected two basic categories: that of errors committed in scientific research, when a researcher devises or accepts an unfounded hypothesis, and that of mistakes committed in the application of scientific knowledge whereby doctors rely on knowledge held to be true at the time in order to understand an individual patient's signs and symptoms. The paper will deal exclusively with the latter, that is to say the mistakes which physicians make while carrying out their day-to-day medical duties. The paper will deal with the mistakes committed in medicine trying also to offer a classification. It will take into account also examples of mistakes in Bayesian reasoning and mistakes of reasoning committed by clinicians regard inductive reasoning. Moreover, many other mistakes are due to fallacies of deductive logic, logic which they use on a day-to-day basis while examining patients in order to envisage the consequences of the various diagnostic or physiopathologic hypotheses. The existence of a different type of mistakes that are part of the psychology of thought will be also pointed out. We conclude that internists often make mistakes because, unknowingly, they fail to reason correctly. These mistakes can occur in two ways: either because he does not observe the laws of formal logic, or because his practical rationality does not match theoretical rationality and so his reasoning becomes influenced by the circumstances in which he finds himself

Clinical and diagnostic aspects of encephalopathy associated with autoimmune thyroid disease (or Hashimoto's encephalopathy)

Encephalopathy associated with autoimmune thyroid disease, currently known as Hashimoto's encephalopathy, but also defined as corticosteroid-responsive encephalopathy associated with autoimmune thyroiditis, is a relatively rare condition observed in a small percentage of patients presenting with autoimmune thyroid disease. It consists of a subacute, relapsing-remitting, steroid-responsive encephalopathy characterised by protean neurologic and neuropsychiatric symptoms, diffuse electroencephalographic abnormalities and increased titres of antithyroid antibodies in serum and/or in cerebrospinal fluid. Most of the cases presenting this neurologic complication are affected by Hashimoto's thyroiditis or, less frequently, by other autoimmune thyroid diseases, chiefly Graves' disease. The pathogenesis of this encephalopathy is still unknown and largely debated, because of extremely varied clinical presentation, possibly referable to different aetiologic and pathophysiologic mechanisms, as confirmed by the two clinical cases we report in this paper. Autoimmune aetiology is, however, very likely in view of the well established favourable response to corticosteroid administration. Both vasculitis and autoimmunity directed against common brain-thyroid antigens represent the most probable aetiologic pathways. Clinical manifestations include consciousness changes, neurologic diffuse or focal signs, headache, and altered cognitive function. Although unspecific, cerebral oedema has also been described. Cerebrospinal fluid examination often discloses an inflammatory process, with a mild increase in protein content and occasionally in lymphocyte count. In this review, clinical criteria for the diagnosis of defined, probable, or possible encephalopathy associated with autoimmune thyroid disease are suggested. Corticosteroid therapy currently allows us to obtain rapid remission of disease symptoms, but adverse outcomes as well as spontaneous remissions have also been reported

A critical reflection on the definition of metabolic syndrome.

Regulation of adipocyte differentiation is an important process in the control of adipose tissue development. So far, adipogenesis has been investigated through the use of various experimental models. In this work, we used human mesenchymal stem cells (hMSCs) obtained from amniotic fluid (AF) as an alternative model more representative of what naturally happens in vivo. In our opinion, these hMSCs are still not influenced by differentiation stimuli and could act in a way more correspondent to the physiological process of adipogenesis, representing also an ethically acceptable alternative to totipotent human embryonic stem cells (ES). Adipocyte differentiation was monitorated following the expressions of key genes. We measured the expression levels of PPARgamma2, PPARgamma-C1alpha, UCP-1, adipsin, and leptin genes using quantitative real-time PCR. We tested our experimental model with two different media. Understanding in vivo adipogenesis mechanisms will shed light on the pathophysiology of many diseases