Adiponectin Levels Differentiate Metabolically Healthy vs Unhealthy Among Obese and Nonobese White Individuals.

CONTEXT: Adiponectin levels (ADPN) are lower in individuals with central obesity and cardiometabolic diseases. Conversely, studies have shown paradoxical hyperadiponectinemia (HA) in metabolically healthy obese (MHO) individuals of non-European descent. Moreover, individuals with higher sc to visceral adipose tissue (ie, higher peripheral adiposity) distribution have higher ADPNs. However, it is not known whether metabolically healthy individuals have predominantly peripheral adiposity along with higher ADPNs. OBJECTIVE: This study aimed to evaluate the association of ADPN and adiposity distribution with metabolic health in white individuals. DESIGN AND SETTING: This was a cross-sectional study of members of "Take Off Pounds Sensibly" weight loss club and their relatives. PARTICIPANTS: We recruited 2486 (72% women, 61% obese) individuals. They were defined as metabolically healthy by absence of hypertension, diabetes, and dyslipidemia; and they were further classified into metabolically healthy nonobese (MHNO), metabolically unhealthy nonobese (MUNO), metabolically healthy obese (MHO), and metabolically unhealthy obese (MUO). Waist-to-hip ratios (WHRs) were used as markers of adiposity distribution. Insulin resistance was measured using homeostasis model assessment. RESULTS: Among the four groups, MHNO had the lowest WHRs (higher peripheral adiposity) and highest ADPN, and MUO had highest WHRs (higher central adiposity) and lowest ADPN (P < .001). Among both nonobese and obese, metabolically healthy individuals had higher ADPN than metabolically unhealthy individuals (P < .05) after adjustment for age, sex, and body mass index. MHNO also had lower WHRs compared with MUNO (P < .01). Although WHRs were lower among MHO compared with MUO, the difference was not significant. In addition, nonobese and obese individuals with HA (defined using sex-specific cutoffs) had lower homeostasis model assessment and dyslipidemia compared with individuals without HA. CONCLUSIONS: Higher ADPN and lower WHRs (higher peripheral adiposity) are associated with better metabolic health in both nonobese and obese white individuals. These results suggest that ADPN and peripheral adiposity play a key role in determining the metabolic health independent of body mass index.

Vancomycin-induced immune thrombocytopenia.

BACKGROUND: Vancomycin has only rarely been implicated as a cause of thrombocytopenia, and there is only limited evidence that this complication is caused by immune mechanisms. We conducted a study to determine whether thrombocytopenia is caused by vancomycin-dependent antibodies in patients being treated with vancomycin. METHODS: We identified and characterized vancomycin-dependent, platelet-reactive antibodies in patients who had been referred for testing during a 5-year period because of a clinical suspicion of vancomycin-induced thrombocytopenia. We obtained clinical information about the patients from their referring physicians. RESULTS: Drug-dependent, platelet-reactive antibodies of the IgG class, the IgM class, or both were identified in 34 patients, and clinical follow-up information was obtained from 29 of these patients. The mean nadir platelet count in these patients was 13,600 per cubic millimeter, and severe bleeding occurred in 10 patients (34%). Platelet levels returned to baseline in all 26 surviving patients after vancomycin was stopped. In 15 patients, the drug was continued for 1 to 14 days while other possible causes of thrombocytopenia were investigated. Vancomycin-dependent antibodies were not found in 25 patients who had been given vancomycin and in whom thrombocytopenia did not develop. CONCLUSIONS: Severe bleeding can occur in patients with vancomycin-induced immune thrombocytopenia. The detection of vancomycin-dependent antiplatelet antibodies in patients receiving the antibiotic in whom thrombocytopenia develops, and the absence of antibodies in patients given the drug in whom platelet counts remain stable, indicate that these antibodies are the cause of the thrombocytopenia.