Purpose Diagnostic value of point-of-care lung ultrasound (POCUS) in detection of coronavirus disease (COVID-19) in an emergency setting is currently unclear. In this study, we aimed to compare diagnostic performance, in terms of sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and accuracy, of POCUS lung, chest CT, and RT-PCR for clinically suspected COVID-19 infections in patients submitting to the emergency room (ER). Material and methods This retrospective study enrolled 93 patients with a suspected COVID-19 infection, admitted to the ER between March 28th and April 20th, 2020. Test subjects showed one or more symptoms of an acute respiratory infection, for which consequent COVID-19 testing was achieved using POCUS lung, chest CT, and RT-PCR. CT images were analyzed by 2 radiologists blinded to RT-PCR results. POCUS lung was performed by three emergency medical doctors, and reports were analyzed by the researcher, blinded to clinical information, US imaging, CT, and RT-PCR test results. Results Compared with RT-PCR, POCUS lung demonstrated outstanding sensitivity and NPV (93.3% and 94.1% respectively) while showing poor values for specificity, PPV, and accuracy (21.3%, 19.2%, and 33.3% respectively). In contrast, similar inquiries using chest CT as index test, excellent sensitivity, specificity, NPV, and accuracy (80.0%, 86.7%, 95.6%, and 85.6%, respectively) were reported, beside a moderate value for PPV (54.5%). Conclusion POCUS may provide early ER triage with a useful, rapid, low-threshold, and safe screening tool in evaluating possible COVID-19 infections. Due to limited specificity, suggestive POCUS lung findings should be confirmed with RT-PCR or chest CT.

No abstract

No abstract

No abstract

Background and Aims Sex steroid levels have been reported to be decreased in male patients with chronic kidney disease (CKD), parallel to the severity of the kidney dysfunction. These studies, at large, used immuno-assays, a method that is inferior to gold standard chromatography measurements and, in addition, failed to give insights into the underlying pathophysiology as they lacked data on gonadotropin levels. The aim of this study was to comprehensively map the gonadal status in male CKD patients not yet on dialysis and age- and BMI-matched controls, using gold standard techniques. Method We performed a case-control study in 120 male CKD patients (age 65.0 y, BMI 26.8 kg/m2), matched (1:1) with non-CKD controls for age and BMI. We divided CKD patients into 3 categories based on KDIGO classification: CKD 1–2 (n = 24), CKD 3 (n = 42) and CKD 4–5 (n = 54). We measured total testosterone (T) and estradiol (E2) using liquid chromatography tandem mass-spectrometry. Sex hormone binding globulin (SHBG), prolactin, luteinizing hormone (LH) and follicle stimulating hormone (FSH) were measured on the Roche Cobas 8000 platform. Free T levels were calculated via Vermeulen formula. Inhibin B (a readout for testicular Sertoli cell function) was measured by ELISA. Results CKD patients showed lower total T (426.0 ng/dL [297.5-516.5] vs. 541.0 ng/dL [452.0-647.8]; p<0.0001) and free T levels (7.4 ng/dL ±3.2 vs. 9.4 ng/dL +/-2.2; p<0.0001) as compared to non-CKD counterparts. SHBG and E2 levels, conversely, were comparable in cases and controls. Inhibin B levels were lower in CKD patients as well (112.7 pg/mL [38.1-189.0] vs. 181.1 [122.2-236.4]; p<0.0001). LH and FSH levels were higher in CKD patients (9.1 IU/L [5.4-16.2] vs. 5.4 IU/L [3.6-8.1]; p<0.0001 and 7.8 IU/L [5.0-20.2] vs. 5.6 IU/L [4.0-9.7]; p<0.0001 respectively). Consequently, the T/LH ratio and inhibin B/FSH ratio, respectively reflecting Leydig and Sertoli cell function, were markedly depressed in CKD (1.8 nmol/IU [0.7-3.0] vs. 4.0 nmol/IU [2.4-5.2]; p<0.0001 and 14.4 ng/IU [1.2-33.6] vs. 32.2 ng/IU [32.2 [16.3-56.7]; p<0.0001). In the CKD cohort, regression analysis identified eGFR and age as independent determinants of T/LH ratio (R2 0.29). According to the T/LH ratio a male CKD patient of 45y old has a testicular age of an 81y old control. Conclusion Male patients with CKD not yet on dialysis show low total and free T levels, confirming CKD as a risk factor for male hypogonadism. The low T/LH and inhibin B/FSH ratio point to testicular failure as the underlying pathophysiological mechanism.