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BACKGROUND & AIMS: Q6Although coronavirus disease 2019 (COVID-19) is characterized by fever and respiratory symptoms, some patients have no or mild symptoms. Severe acute respiratory syndromecoronavirus (SARS-CoV-2) has been detected in feces of patients. We investigated gastrointestinal symptoms and shedding of virus into feces of patients with asymptomatic or mild COVID-19. METHODS:We collected data from 46 patients (median age, 26 y; 46% men) with asymptomatic or mild COVID-19 (without fever and pneumonia) and prolonged respiratory shedding of SARS-CoV-2, quarantined from April 4, 2020, through April 24, 2020, in Korea. Respiratory specimens included upper respiratory specimens (nasopharyngeal and oropharyngeal swabs) and lower respiratory specimens (sputum), and were collected twice per week. The median interval between COVID-19 diagnosis to the start of fecal sample collection was 37 days (range, 29-41 d); 213 stool specimens were collected from 46 patients. We used real-time reverse-transcription polymerase chain reaction to detect SARS-CoV-2 in the respiratory and fecal specimens. RESULTS:Gastrointestinal manifestations were observed in 16 of the 46 patients (35%); diarrhea was the most common (15%), followed by abdominal pain (11%), dyspepsia (11%), and nausea (2%).Virus RNA was detected in feces from 2 patients without gastrointestinal symptoms (4%). Mean cycle threshold values from the time of quarantine to the time of fecal collection tended to be lower in patients with virus detected in fecal samples than in patients without virus in fecal samples (29.91 vs 33.67 in the first week, 29.47 vs 35.71 in the fifth week, respectively). Shedding of virus into feces persisted until day 50 after diagnosis; fecal samples began to test negative before or at approximately the time that respiratory specimens also began to test negative. CONCLUSIONS:In an analysis of fecal and respiratory specimens from patients with COVID-19 in quarantine in Korea, we found that the gastrointestinal tract could be a route of transmission of SARS-CoV-2 even in patients with asymptomatic or mild disease, with no gastrointestinal symptoms. The viral load of the respiratory specimens appears be related to shedding of the virus into feces in this group of patients.

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Several recent prospective studies have reported that obesity is associated with an increased risk for chronic kidney disease (CKD), but it is unknown whether weight gain increases the risk for CKD if one remains within the "normal" category of body mass index (BMI). We prospectively followed a cohort of 8792 healthy men who had no known risk factors for CKD and participated in a comprehensive health evaluation program at a large worksite. During 35,927 person-years of follow-up, 427 new incident cases of CKD (estimated GFR Ͻ64 ml/min per 1.73 m 2 ) developed. Cox proportional hazards modeling revealed that in both the normal-weight and overweight groups, a U-shaped association between weight change categories and development of CKD was observed after adjustment for age, baseline GFR, baseline BMI, HDL, fasting blood glucose, uric acid, and exercise habits. The lowest risk for CKD was observed among those whose weight changed Ϫ0.25 to Ͻ0.25 kg/yr (P Ͻ 0.001 for quadratic term). Weight change as a time-dependent variable was significantly related to CKD incidence. These relationships remained significant even after further adjustment for Homeostasis Model Assessment of Insulin Resistance, high-sensitivity C-reactive protein, systolic BP, diastolic BP, metabolic syndrome, incident hypertension, or incident diabetes. In summary, increases in body weight are independently associated with an increased risk for CKD, even when the BMI remains within the normal range.

POLYCYSTIC OVARY SYNDROME (PCOS) is one of the most common endocrinological problems in women. In addition to chronic oligo-anovulation, the main features of the PCOS include elevated levels of circulating androgens and/or clinical hyperandrogenism, polycystic ovary morphology, altered gonadotropin secretion, insulin resistance and/or compensatory hyperinsulinemia often associated with obesity [1]. Women affected by PCOS also show a higher risk of type 2 diabetes, dyslipidemia, hypertension and cardiovascular diseases [2][3][4].Differences of the association of anti-Müllerian hormone with clinical or biochemical characteristics between women with and without polycystic ovary syndrome Abstract. The aim of the present study was to compare the associations of anti-Müllerian hormone (AMH) with clinical or biochemical characteristics between women with and without polycystic ovary syndrome (PCOS). We also explored the optimal cutoff point of AMH to diagnose PCOS. A cross-sectional study was performed in 87 women diagnosed with PCOS and 53 healthy control subjects. Body mass index (BMI), indices of insulin resistance, metabolic syndrome-related variables, reproductive hormones and serum AMH were measured in all subjects. We conducted receiver operating characteristic (ROC) curve analysis to determine the cutoff of AMH for diagnosis of PCOS. Serum AMH levels were significantly (p <0.001) higher in women with PCOS after adjustment for age and BMI. AMH levels were not significantly related with obesity, indices of insulin resistance, and metabolic syndrome-related variables in both PCOS and control groups. In the control group, AMH levels showed positive correlations with total testosterone (p <0.001), free testosterone (p=0.024), and adiponectin (p=0.002), and showed negative correlations with age (p=0.010) and estradiol (E2) (p=0.012). However, only total (p=0.044) and free testosterone (p=0.012) levels showed significant positive correlations with serum AMH level in PCOS group. ROC curve analysis showed a cutoff point for AMH of 7.82 ng/mL (sensitivity 75.9%, specificity 86.8%) for diagnosis of PCOS. Differences of the association of AMH with clinical or biochemical characteristics between women with PCOS and control groups were observed. This might contribute to the pathogenesis of PCOS, although further investigation is necessary to elucidate the detailed mechanism.

Background: Decreased glomerular filtration rate (GFR) can increase the risk of bleeding tendency and hemorrhagic stroke. However, the relationship between the levels of GFR and hemorrhagic transformation (HT) after acute ischemic stroke is largely unknown. The aim of this study was to assess whether GFR level is associated with HT in acute ischemic stroke. Methods: We reviewed 770 consecutive patients with acute ischemic stroke within 7 days from September 2007 to February 2012 in a prospective stroke registry database. We calculated the patient’s GFR using the Cockcroft-Gault equation, and divided them into 3 groups: ≥60, 30–59 and <30 ml/min/1.73 m². HTs were identified by follow-up computed tomography (CT) or magnetic resonance imaging, and were defined as (1) any degree of high density within the area of low attenuation of vascular territory on noncontrast brain CT, or (2) low-signal intensity area in gradient echo within high-signal intensity meaning acute infarct on diffusion-weighted imaging. Multivariable logistic regression analyses were used to estimate the risk of GFR for HT. Stratification analyses were done according to the presence of HT high risk factors: atrial fibrillation (AF), thrombolysis and large size infarction. Additional logistic regression model for symptomatic HTs was established with the same variables. Results: HTs were noted in 131 patients (17.0%) and symptomatic HTs in 63 patients (8.2%). In univariate analysis, HTs were more frequent in patients with AF (51.9 vs. 16.7%, p < 0.001) and large-size infarction (42.0 vs. 5.3%, p < 0.001). The risk of HT was associated with decreased GFR among 3 subgroups classified according to the value of estimated GFR: 49/394 (12.4%) in the GFR ≥60 group, 66/312 (21.2%) in the 30≤ GFR <59 group and 16/64 (25.0%) in the GFR <30 group (p = 0.002). We found a significant association between the GFR <30 group and HTs in acute ischemic stroke (OR 2.90; 95% CI 1.26–6.68, p = 0.012) after adjusting for other risk factors. Moreover, the incidence of HTs was higher in the subgroups without thrombolysis (OR 3.49; 95% CI 1.44–8.46) and without AF (OR 3.44; 95% CI 1.10–10.76). Decreased GFR also had a tendency of increasing symptomatic HTs (OR 2.39; 95% CI 0.72–7.94, p = 0.154). Conclusions: Low levels of GFR are associated with a high risk of HT after acute ischemic stroke. Further studies are needed to elucidate whether HT in the patients with renal insufficiency are related to a worse outcome after acute ischemic stroke.

DPO-based multiplex PCR can be used as a practical method for the detection of H. pylori infection and the determination of clarithromycin susceptibility in addition to phenotypic antimicrobial susceptibility tests.