Patients with COVID-19 who require ICU admission might have the cytokine storm. It is a state of out-of-control release of a variety of inflammatory cytokines. The molecular mechanism of the cytokine storm has not been explored extensively yet. The attachment of SARS-CoV-2 spike glycoprotein with angiotensin-converting enzyme 2 (ACE2), as its cellular receptor, triggers complex molecular events that leads to hyperinflammation. Four molecular axes that may be involved in SARS-CoV-2 driven inflammatory cytokine overproduction are addressed in this work. The virus-mediated down-regulation of ACE2 causes a burst of inflammatory cytokine release through dysregulation of the renin-angiotensin-aldosterone system (ACE/angiotensin II/AT1R axis), attenuation of Mas receptor (ACE2/MasR axis), increased activation of [des-Arg9]-bradykinin (ACE2/bradykinin B1R/DABK axis), and activation of the complement system including C5a and C5b-9 components. The molecular clarification of these axes will elucidate an array of therapeutic strategies to confront the cytokine storm in order to prevent and treat COVID-19 associated acute respiratory distress syndrome.
Since the first emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also known as novel coronavirus (2019-nCoV), in Wuhan, China, in December 2019 (Tan et al., 2020), the virus has spread rapidly worldwide and, therefore, has been officially declared a pandemic outbreak with more than 10 million confirmed cases and 499,000 deaths according to the WHO report (Situation Report, 2020). Pneumonia with fever seems to be the most common presentation of SARS-CoV-2 infection (Guan et al., 2020; Wang, Hu et al., 2020). SARS-CoV-2 was also detected in specimens of faeces and a small percentage of blood and urine
Background. In this study, we report the epidemiology of COVID-19 among recipients of organ transplantation and evaluate associated factors with death. Methods. We screened 6969 patients who had organ transplantations in our center for COVID-19. Specific data on presentation, clinical course, treatment, and prognosis were acquired. Results. We found 85 patients (66 liver, 16 kidney, 2 kidney-pancreas, and 1 liver-kidney recipient) who acquired COVID-19. Most common symptoms included fever (48.2%), cough (41.2%), myalgia (41.2%), and fatigue (40%). Dyspnea developed in 33% of patients. Overall, one-third of patients had an oxygen saturation of below 90% on admission. Patients were hospitalized for a median (interquartile range) of 9 (5, 13.7) days and had a 33.9% intensive care unit admission rate. Overall, 17 patients (20%) died, which included 31.3% of patients with kidney transplantations and 18.2% of patients with liver transplantations. All 4 pediatric patients in our series died. In our univariate analysis among adults, rates of leukopenia (38.4% versus 13.2%; P = 0.04), low albumin levels (53.8% versus 10.2%; P = 0.001), and shorter duration between transplantation and COVID-19 (P = 0.02), were higher among patients who died. In our least absolute shrinkage and selection operator regression model, low albumin levels (OR, 4.48; 95% confidence interval, 1.16-17.27) were associated with higher risk of death. Conclusions. This is the largest single-center report on abdominal transplantations and COVID-19. Liver and kidney transplant recipients have an increased risk of mortality compared with the general population due to COVID-19. More specifically, pediatric patients and those with low albumin levels are at higher risks of death due COVID-19.
Background To explore the potential mechanisms of SARS-CoV-2 in targeting the prostate gland, leading to exacerbation of benign prostatic hyperplasia (BPH) symptoms and greater risks of BPH complications such as acute urinary retention. Methods A categorized and comprehensive search in the literature has been conducted by 10 April 2021 using international databases including PubMed, Embase, Web of Science, Scopus, and Cochrane Library in line with the PRISMA guidelines recommendations. PICO strategy was used to formulate the research question. The following terms were used: urology, COVID-19, coronavirus, BPH, inflammation, androgen receptors, LUTS, IPSS, PSA, and SARS-CoV-2 or a combination of them. Studies with irrelevant purposes and duplicates were excluded. The selected studies were performed on humans and published in English. Results The research revealed 89 articles. After title screening and considering exclusion criteria, 52 papers were included for the systematic review. BPH is a common condition affecting older men. SARS-CoV-2 infects the host cell by binding to angiotensin converting enzyme 2 (ACE2). A hyperactivated RAS system during infection with SARS-CoV-2 may lead to activation of pro-inflammatory pathways and increased cytokine release. Thus, this virus can lead to exacerbation of lower urinary tract symptoms (LUTS) and trigger inflammatory processes in the prostate gland. Since androgen receptors (AR) play an important role in the BPH pathophysiology and infection with SARS-CoV-2 may be androgen-mediated, BPH progression and its related symptoms can be a complication of COVID-19 through AR involvement and metabolic disturbances. Conclusions Based on the current findings, SARS-CoV-2 can possibly damage the prostate and worsen BPH and its related LUTS through ACE2 signaling, AR-related mechanisms, inflammation, and metabolic derangement. We encourage future studies to investigate the possible role of COVID-19 in the progression of BPH-related LUTS and examine the prostatic status in susceptible patients with relevant available questionnaires (e.g., IPSS) and serum biomarkers (e.g., PSA).
Background Methanol is widely used in industry; however, methanol poisoning is not common. In this regard, a number of outbreaks have been recently reported due to inappropriate processing of alcoholic beverages. Shiraz, a city located in the southern part of Iran, faced one of such outbreaks in 2020 during COVID-19 pandemic. There is no sufficient literature on the electrocardiographic findings in methanol toxicity. This study aimed to address this gap in the literature. Method A total of 356 cases with methanol toxicity referred to Shiraz University of Medical Science Tertiary Hospitals (Faghihi and Namazi) in March and April, 2020. The clinical findings of blindness and impaired level of consciousness, lab data such as arterial blood gas, electrolytes, and creatinine, and the most common findings from ECGs were collected. Results The most common ECG findings were J point elevation (68.8%), presence of U wave (59.2%), QTc prolongation (53.2% in males and 28.6% in females), and fragmented QRS (33.7%). An outstanding finding in this study was the presence of myocardial infarction in 5.3% of the cases. This finding, to the best of our knowledge, has only been reported in a few case reports. Brugada pattern (8.1%) and Osborn wave (3.7%) were the other interesting findings. In multivariate analysis, when confounding factors were adjusted, myocardial infarction, atrioventricular conduction disturbances, sinus tachycardia, and the prolonged QTC > 500 msecond were four independent factors correlated with methanol toxicity severity measured with arterial blood PH on arterial blood gas measurements, with odds ratios of 12.82, 4.46, 2.32 and 3.15 (P < 0.05 for all), respectively. Conclusion Electrocardiographic variations during methanol intoxication are remarkable and well-correlated with poisoning severity. Myocardial infarction was an egregious and yet a common concerning finding in this sample, which need to be ruled out in methanol toxicity.
Background: Uremic pruritus (UP) is a common, bothersome symptom in hemodialysis (HD) patients with end-stage renal disease. Immunohypothesis is currently favored as an explanation of the cause of UP. Fumaria parviflora L (FP) is a medicinal herb with several pharmacological properties, including prominent anti-inflammatory activity. Objectives: This study aimed to assess the efficacy of FP for reducing UP severity among HD patients. Methods: A total of 79 HD patients with pruritus were randomly assigned to receive either FP or a placebo for eight weeks. The visual analogue scale (VAS), the Duo score for calculating pruritus score, serum interferon-γ (IFN-γ) level, interleukin-4 (IL-4), and high-sensitivity C-reactive protein were measured in the patients before and after treatment. Results: At the end of the treatment phase, the pruritus score decreased in both groups (P < 0.001); however, the mean reduction
Members of Coronaviridae family have been the source of respiratory illnesses. The outbreak of SARS-CoV-2 that produced a severe lung disease in afflicted patients in China and other countries was the reason for the incredible attention paid toward this viral infection. It is known that SARS-CoV-2 is dependent on TMPRSS2 activity for entrance and subsequent infection of the host cells and TMPRSS2 is a host cell molecule that is important for the spread of viruses such as coronaviruses. Different factors can increase the risk of prostate cancer, including older age, a family history of the disease. Androgen receptor (AR) initiates a transcriptional cascade which plays a serious role in both normal and malignant prostate tissues. TMPRSS2 protein is highly expressed in prostate secretory epithelial cells, and its expression is dependent on androgen signals. One of the molecular signs of prostate cancer is TMPRSS2-ERG gene fusion. In TMPRSS2-ERG-positive prostate cancers different patterns of changed gene expression can be detected. The possible molecular relation between fusion positive prostate cancer patients and the increased risk of lethal respiratory viral infections especially SARS-CoV-2 can candidate TMPRSS2 as an attractive drug target. The studies show that some molecules such as nicotinamide, PARP1, ETS and IL-1R can be studied deeper in order to control SARS-CoV-2 infection especially in prostate cancer patients. This review attempts to investigate the possible relation between the gene expression pattern that is produced through TMPRSS2-ERG fusion positive prostate cancer and the possible influence of these fluctuations on the pathogenesis and development of viral infections such as SARS-CoV-2.
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