Peri-operative SARS-CoV-2 infection increases postoperative mortality. The aim of this study was to determine the optimal duration of planned delay before surgery in patients who have had SARS-CoV-2 infection. This international, multicentre, prospective cohort study included patients undergoing elective or emergency surgery during October 2020. Surgical patients with pre-operative SARS-CoV-2 infection were compared with those without previous SARS-CoV-2 infection. The primary outcome measure was 30-day postoperative mortality. Logistic regression models were used to calculate adjusted 30-day mortality rates stratified by time from diagnosis of SARS-CoV-2 infection to surgery. Among 140,231 patients (116 countries), 3127 patients (2.2%) had a pre-operative SARS-CoV-2 diagnosis. Adjusted 30-day mortality in patients without SARS-CoV-2 infection was 1.5% (95%CI 1.4-1.5). In patients with a pre-operative SARS-CoV-2 diagnosis, mortality was increased in patients having surgery within 0-2 weeks, 3-4 weeks and 5-6 weeks of the diagnosis (odds ratio (95%CI) 4.1 (3.3-4.8), 3.9 (2.6-5.1) and 3.6 (2.0-5.2), respectively). Surgery performed ≥ 7 weeks after SARS-CoV-2 diagnosis was associated with a similar mortality risk to baseline (odds ratio (95%CI) 1.5 (0.9-2.1)). After a ≥ 7 week delay in undertaking surgery following SARS-CoV-2 infection, patients with ongoing symptoms had a higher mortality than patients whose symptoms had resolved or who had been asymptomatic (6.0% (95%CI 3.2-8.7) vs. 2.4% (95%CI 1.4-3.4) vs. 1.3% (95%CI 0.6-2.0), respectively). Where possible, surgery should be delayed for at least 7 weeks following SARS-CoV-2 infection. Patients with ongoing symptoms ≥ 7 weeks from diagnosis may benefit from further delay.

Our study suggests that thyroid volume and function may vary in obese women in association with body weight and fat mass; > 10% weight loss may affect thyroid volume and function, which however, is clinically insignificant.

Although skin tags are associated with diabetes mellitus, insulin resistance, hypertension, obesity, atherogenic lipid profile, no data in the literature show that the presence of skin tags is associated with serum high-sensitive C-reactive protein, uric acid, free fatty acid and leptin level. The purpose of this study was to evaluate the frequency of hypertension, dyslipidemia, insulin resistance and obesity in patients with skin tags and to compare patients with skin tags and normal healthy subjects for insulin resistance, serum lipids, insulin, glucose, leptin, high-sensitive C-reactive protein, free fatty acid levels. We evaluated 113 patients with skin tags and 31 healthy subjects. The two groups were compared with respect to BMI, lipid profile, blood pressure, insulin resistance, serum lipids, insulin, glucose, leptin, high-sensitive C-reactive protein, free fatty acid and homeostatic model assessment of insulin resistance (HOMA-IR). Total 53.9 and 33.6% of patients with skin tags were overweight and obese, respectively. The frequency of hypertension 30.1%, dyslipidemia 59.3% and insulin resistance 21.2% were detected. HOMA-IR (P < 0.001) and serum glucose (P < 0.001), insulin (P = 0.002), high-sensitive C-reactive protein (P = 0.001), uric acid (P = 0.001), free fatty acid (P = 0.002), HbA1c (P < 0.001), total cholesterol (P = 0.018), LDL-cholesterol (P = 0.023), and triglyceride levels (P = 0.001) were higher in patients with skin tags than control group. Overweight and/or obesity, dyslipidemia, hypertension, insulin resistance and elevated high-sensitive C-reactive protein are seen in patients with skin tags. Skin tags may be a marker of increased risk of atherosclerosis and cardiovascular disease.

Our data suggest that obesity, hypertension, dyslipidemia, and metabolic syndrome in T2DM were associated with increased plasma leptin levels. We conclude that plasma leptin levels may not be strongly associated with microangiopathy and macroangiopathy in T2DM individuals.

Obesity is a chronic metabolic disorder associated with cardiovascular disease and atherosclerosis. Platelet activation and aggregation are central processes in the pathophysiology of cardiovascular disease. Mean platelet volume (MPV), a determinant of platelet activation, is a newly emerging risk marker for atherothrombosis. Our objective was to evaluate the effect of weight loss on the MPV in obese patients. We selected 30 obese women patients and 30 non-obese healthy women subjects. All obese patients took the same content and caloric diet treatment for 3 months. Body mass index (BMI), metabolic parameters and MPV were measured at baseline and after 3 months diet treatment. Before diet treatment, obese group had significantly higher MPV levels than in the non-obese control group (8.18 +/- 1.09 fl vs. 8.01 +/- 0.95 fl, p = 0.004). MPV showed positive correlations with BMI level in the obese group (r = 0.43, p = 0.017). BMI significantly decreased after diet treatment (36.2 +/- 3.2 kg/m(2) vs. 34.7 +/- 3.6 kg/m(2), p < 0.001), in the obese group. MPV significantly decreased after diet treatment in the obese group (8.18 +/- 1.09 fl vs. 8.08 +/- 1.02 fl, p = 0.013). There was a positive correlation between weight loss and reduction in MPV (r = 0.41, p = 0.024). In addition to its well-known positive effects on cardiovascular disease risk, weight loss may also possess significant anti-platelet activation properties that can contribute its antiatherogenic effects in obese patients.