Soluble triggering receptor expressed on myeloid cells-1 in acute respiratory infections.

Levels of the soluble form of the triggering receptor expressed on myeloid cells (sTREM)-1 are elevated in severe sepsis. However, it is not known whether sTREM-1 measurements can distinguish milder bacterial infections from noninfectious inflammation. The present authors studied whether serum sTREM-1 levels differ in community-acquired pneumonia, exacerbations of chronic obstructive pulmonary disease (COPD), asthma and controls, and whether sTREM-1 may be used as a surrogate marker for the need for antibiotics. Serum sTREM-1 levels in 150 patients with pneumonia, COPD and asthma exacerbations and 62 healthy controls were measured. Serum sTREM-1 levels were significantly elevated in pneumonia (median 295.2 ng x mL(-1)), COPD (280.3 ng x mL(-1)) and asthma exacerbations (184.0 ng x mL(-1)) compared with controls (83.1 ng x mL(-1)). Levels were higher in pneumonia and Anthonisen type 1 COPD exacerbations than in type 2 and 3 COPD and asthma exacerbations. The area under the receiver operating characteristics curve for sTREM-1 as a surrogate marker for the need for antibiotics was 0.77. Serum levels of the soluble form of the triggering receptor expressed on myeloid cells-1 were elevated predominantly in pneumonia and Anthonisen type 1 COPD exacerbations versus type 2 and 3 chronic obstructive pulmonary disease exacerbations, asthma and controls. Serum levels of the soluble form of the triggering receptor expressed on myeloid cells-1 has moderate but insufficient accuracy as a surrogate marker for the need for antibiotics in lower respiratory tract infections.     

Laparoscopic adjustable gastric banding for patients with body mass index of ≤35 kg/m

BACKGROUND: Many mild-to-moderately obese individuals (body mass index [BMI] 30-35 kg/m(2)) have serious diseases related to their obesity. Nonoperative therapy is ineffective in the long term, yet surgery has never been made widely available to this population. METHODS: Between 1996 and 2004, 93 patients with a BMI of 30-35 kg/m(2) underwent laparoscopic adjustable gastric banding with the LAP-BAND. All patients were referred by their primary physician, entered into a comprehensive bariatric surgery program at one Australian center, and operated on by one surgeon. Data on all patients were collected prospectively and entered into an electronic registry. The study parameters included preoperative age, gender, BMI, presence of co-morbidities, percentage of excess weight loss, and resolution of co-morbidities. RESULTS: The mean age was 44.6 years (range 16-76), mean weight was 98 kg, and the mean BMI was 32.7 kg/m(2) (range 30-34). Of the 93 patients, 42 (45%) had co-morbidities, including asthma, diabetes, hypertension, and sleep apnea. The proportion of patients in follow-up was 79%, 85%, and 89% at 1, 2, and 3 years, respectively. The mean weight was reduced to 71 kg at 1 year, 72 kg at 2 years, and 72 kg at 3 years. The mean BMI was reduced to 27.2 +/- 2.2, 27.3 +/- 3.1, and 27.6 +/- 3.7 kg/m(2), respectively, and the mean percentage of excess weight loss was 57.9% +/- 24.5%, 57.6 +/- 29.3%, and 53.8% +/- 32.8% at 1, 2, and 3 years, respectively. At 3 years, the BMI was 18-24 kg/m(2) in 34%, 25-29 kg/m(2) in 51%, and 30-35 kg/m(2) in 10%. At 3 years, the percentage of excess weight loss was <25% in 10%, 25-50% in 24%, 50-75% in 51%, and >75% in 10%. The co-morbidities improved or completely resolved in most patients. No mortality occurred. CONCLUSION: We are very encouraged by this series of low BMI patients treated with the LAP-BAND. Their weight loss has been good, the complications have been minimal, and the co-morbidities have partially or wholly resolved. With additional study, it is reasonable to expect the weight guidelines for bariatric surgery to be altered to include patients with a BMI of 30-35 kg/m(2).     

Analysis of insulin signaling pathways through comparative genomics. Mapping mechanisms for insulin resistance in type 2 (non-insulin-dependent) diabetes mellitus.

The precise molecular cause of insulin resistance has not yet been elucidated. Resistance to the normal action of insulin contributes to the pathogenesis of a number of common human disorders, including type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetes mellitus, hypertension, and the Metabolic Syndrome X, thus constituting a major public health problem. A disease program aimed at combating this disorder should focus on the identification of targets for therapeutic intervention which may overcome insulin resistance and hence the associated metabolic consequences characteristic of the Metabolic Syndrome. Although the primary defect in the pathogenesis of type 2 diabetes is unknown, genetic and environmental factors are likely to contribute to the manifestation of this progressive metabolic disorder, which is usually not clinically apparent until mid-life. Defects at the level of glucose uptake/phosphorylation characterize insulin resistance in skeletal muscle of type 2 diabetic patients. Identification of putative components of the insulin receptor-signaling pathway may offer insights into mechanisms involved in insulin resistance. Enhanced flux of free fatty acids due to impaired lipid metabolism may contribute to impaired insulin secretion and peripheral insulin resistance. Genes regulating lipolysis are prime candidates for susceptibility towards the metabolic syndrome. Here we describe pathways constituting complex interactions that control glucose homeostasis. We will be considering (1) regulation of glucose uptake by the insulin receptor signaling pathway, and (2) control of adipogenesis and insulin sensitivity by the sterol response element binding protein (SREBP) pathway.     

Cost-effectiveness analysis of screening for abdominal aortic aneurysms based on five year results from a randomised hospital based mass screening trial.

BACKGROUND: The aim of this study was to estimate the cost effectiveness of screening for abdominal aortic aneurysm (AAA). MATERIAL AND METHODS: All 12,639 men born in the years 1921-1933 (aged 64-73) living in Viborg County, Denmark, were randomly allocated either to receive an invitation to abdominal ultrasound scanning for AAA or to be controls. Costs for screening and surveillance were assessed prospectively. Diagnosis Related Group (DRG) costs from 1999 were used concerning admissions with uncomplicated and complicated operations. Admissions for AAA surgery were retrospectively classified according to complications in patient records. RESULTS: Mean follow-up time was 52 months. 76.6% of invited men attended screening, and 191 (4.0%) had an AAA. As previously reported, the cumulative 5-year AAA-specific mortality in the invited group was significantly reduced by 67% compared to the control group (P = 0.003). The costs were estimated to be Euro 11.23 per scan. The costs per life-year saved were Euro 9057 (Euro 5872-20,063) after 5 years, and were expected to decrease to Euro 2708 (Euro 1758-6031) after 10 years and to Euro 1825 (Euro 1185-4063) after 15 years. CONCLUSION: Screening of 64-73 years old males in Denmark seems cost effective.     

Prediction and Detection of Secondary Hemorrhages after Thrombolytic Therapy in Ischemic Stroke

Abstract It is well established that thrombolytic therapy increases the risk of secondary intracerebral hemorrhage in ischemic stroke patients. However, the term “intracerebral hemorrhage” (ICH) covers a wide spectrum from tiny spots of blood to massive space-occupying hematoma. We will review the etiology and clinical consequences of secondary hemorrhage after thrombolysis in ischemic stroke patients and discuss the ability of magnetic resonance imaging (MRI) to predict this phenomenon. MRI is a highly sensitive tool for detection of hemorrhagic transformation after ischemic stroke. The definitions of a so-called symptomatic hemorrhage after ischemic infarction differ considerably and will also be described. Attributing a causal relationship of a clinical deterioration to a secondary hemorrhage is not easy and should be only addressed when it exceeds at least 30% of the infarct volume. In other patients, secondary hemorrhage might be regarded as side effect of reperfusion within the region with the most severe perfusion deficit. Cerebral microbleeds (CMBs) are a frequent finding in patients with leukoaraiosis and appear to be a general marker of various types of bleeding- prone small vessel disease and a predictor of recurrent vascular events. Current data do not support the hypothesis that the detection of CMBs is a useful diagnostic criterion for the exclusion of patients with CMBs from thrombolytic therapy. However, an increased risk for the rare patients with numerous CMBs can not be ruled out.