BackgroundIt is well known that some viral infections may affect male fertility. Coronavirus disease (COVID-19) can lead to multiorgan damage through the angiotensin-converting enzyme-2 receptor, abundant in testicular tissue. However, little information is available regarding the shedding of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) in semen and its impact on spermatogenesis and fertility potential. We planned to investigate the presence of SARS-CoV-2 in the semen of COVID-19 males and to study the effect of COVID-19 on semen quality and sperm DNA fragmentation index. Material and methodThirty COVID-19 male patients aged 19-45 registered to AIIMS Patna hospital participated in the survey between October 2020 and April 2021. We conducted a real-time reverse transcriptase test on all the semen samples. Detailed semen analysis, including the sperm DNA Fragmentation Index, was done at first sampling that is during COVID-19. After 74 days of the first sampling, we obtained the second sampling and repeated all the above tests. ResultsAll semen samples collected in the first and second sampling tested with real-time reverse transcriptionpolymerase chain reaction (RT-PCR) were negative for SARS-CoV-2. In the first sampling, semen volume, vitality, total motility, sperm concentration, total sperm count, % normal morphology, % cytoplasmic droplet, and fructose were significantly lower. In contrast, semen agglutination, % head defect, DNA Fragmentation Index, liquefaction time, semen viscosity, and leukocytes were increased. These findings were reversed at the second sampling but not to the optimum level. All these findings were statistically significant (p < 0.05 for all). Thus, COVID-19 negatively affects semen parameters, including sperm DNA fragmentation index. ConclusionAlthough we could not find SARS-CoV-2 in the semen, the semen quality remained poor until the second sampling. Assisted reproductive technology (ART) clinics and sperm banking facilities should consider assessing the semen of COVID-19 males and exclude men with a positive history of SARS-CoV-2 until their semen quality returns to normal.

BackgroundAnxiety and stress in COVID-19 lead to continual pro-inflammatory cytokine activity resulting in excessive inflammation. Levels of different bio indices of COVID-19 may predict clinical outcomes and the severity of COVID-19 disease and may correlate with anxiety and stress levels. ObjectivesTo measure the level of anxiety in COVID-19 patients using the coronavirus anxiety scale (CAS) as an assessment of psychological stress. To measure the levels of blood biomarkers and biochemical and hematological markers of inflammation in COVID-19. To record and measure the indices of short-term HRV in COVID-19 patients to assess their physiological and psychological stress levels. To determine the relationship between anxiety scores, levels of laboratory indices (blood biomarkers), and HRV parameters across mild, moderate and severe cases of COVID-19. Material and methodA total of 300 COVID-19 patients aged between 18 and 55 years were included. A questionnaire-based CAS was used to assess anxiety levels. Short-term HRV was recorded to measure stress. Blood biomarkers: Biochemical and hemato-cytological markers of inflammation were measured. Statistical analyses were performed using the SPSS software version 20.0. ResultsAnxiety and stress increased with the severity of COVID-19. A positive correlation was detected between anxiety and serum ferritin, IL-6, MCV, and MCH levels, and a negative correlation between the corona anxiety score and RBC count. The increase in the severity of COVID-19 showed elevated levels of WBC count, neutrophil%, platelet count, neutrophil/lymphocyte ratio, serum ferritin, D-dimer, C-reactive protein, procalcitonin, interleukin-6, and lactate dehydrogenase, and decreased lymphocyte and monocyte percentages. The increase in the severity of COVID-19 decreased lymphocyte, monocyte, and eosinophil counts. ConclusionThe Corona Anxiety Scale and heart rate variability can be used as complementary tools to index COVID-19related anxiety and stress. An association exists between immune dysregulation and heart rate variability, which can be used to predict the inflammatory response and prognosis of COVID-19.

Itagi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

IntroductionThe clinical course of non-alcoholic fatty liver disease (NAFLD) in its long term may follow a benign course or have an adverse outcome leading to hepatocellular carcinoma (HCC) or end-stage liver disease requiring liver transplantation. Such patients represent only a small proportion of all NAFLD cases, making case finding a real challenge. AimsThis study was planned to test the efficacy of simple laboratory parameters for their ability to screen advanced cases of NAFLD who need early attention to extricate them from the cumbersome outcome.

Background and Aim: It is necessary to find out whether fasting blood samples are must for lipid profile determination. Aim of this study to find out is there any difference between fasting and non-fasting lipid profile in young healthy adults. Methods: This study was done on 100 MBBS students of medical college. Lipid profile was done in these healthy young adults for fasting and postprandial statuses. Results: The lipid profile parameters were compared in both the groups of fasting and postprandial statuses. In fasting group, the mean total cholesterol level was 192.1 mg/dl and mean postprandial total cholesterol level was 194.98 mg/dl (P = 0.0407). The mean fasting serum triglyceride level was 121.16 mg/dl and mean postprandial serum triglyceride level was 126.18 mg/dl (P = 0.0001). The mean fasting high density lipoprotein (HDL) level was 45.08 mg/dl and mean postprandial HDL was 43.84 mg/dl (P = 0.0656). The mean fasting serum VLDL level was 24.23 mg/dl and mean postprandial VLDL level was 25.24 mg/dl (P = 0.0001). The mean fasting LDL was 122.8 mg/dl and mean postprandial LDL was 125.9 mg/dl (P = 0.0416). Conclusion: Finally, from this study we found that there is no significant clinical difference between fasting and non-fasting levels of total cholesterol, HDL, LDL, VLDL and TG. Thus, for estimation of lipid profile we can use the blood samples at any time or irrespective of mealtime.