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Background Angiotensin-converting enzyme 2 (ACE2), the receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is highly expressed in the kidneys. Beyond serving as a crucial endogenous regulator of the renin–angiotensin system, ACE2 also possess a unique function to facilitate amino acid absorption. Our observational study sought to explore the relationship between urine ACE2 (uACE2) and renal outcomes in coronavirus disease 2019 (COVID-19). Methods In a cohort of 104 patients with COVID-19 without acute kidney injury (AKI), 43 patients with COVID-19-mediated AKI and 36 non-COVID-19 controls, we measured uACE2, urine tumour necrosis factor receptors I and II (uTNF-RI and uTNF-RII) and neutrophil gelatinase-associated lipocalin (uNGAL). We also assessed ACE2 staining in autopsy kidney samples and generated a propensity score–matched subgroup of patients to perform a targeted urine metabolomic study to describe the characteristic signature of COVID-19. Results uACE2 is increased in patients with COVID-19 and further increased in those that developed AKI. After adjusting uACE2 levels for age, sex and previous comorbidities, increased uACE2 was independently associated with a >3-fold higher risk of developing AKI [odds ratio 3.05 (95% confidence interval 1.23‒7.58), P  = .017]. Increased uACE2 corresponded to a tubular loss of ACE2 in kidney sections and strongly correlated with uTNF-RI and uTNF-RII. Urine quantitative metabolome analysis revealed an increased excretion of essential amino acids in patients with COVID-19, including leucine, isoleucine, tryptophan and phenylalanine. Additionally, a strong correlation was observed between urine amino acids and uACE2. Conclusions Elevated uACE2 is related to AKI in patients with COVID-19. The loss of tubular ACE2 during SARS-CoV-2 infection demonstrates a potential link between aminoaciduria and proximal tubular injury. [ABSTRACT FROM AUTHOR]

The molecular mechanisms that control innate immune cell trafficking during chronic infection and inflam-mation, such as in tuberculosis (TB), are incompletely understood. During active TB, myeloid cells infiltrate the lung [...]

Grade 1 or 2 liver toxicity during treatment with benznidazole is frequently reported, but rarely results in treatment discontinuation.[[4], [6]] DILI is acute, severe damage due to drugs. Chagas' disease (CD), a neglected tropical disease caused by I Trypanosoma cruzi i , endemic in Latin America and sporadic in many parts of the world, affects 6-7 million people.[1] Although the efficacy of drug treatment of late-stage CD remains uncertain,[2] it is expected to prevent severe cardiac, intestinal and/or neurological complications. [Extracted from the article]

Background: Descriptions of the pathological features of coronavirus disease-2019 (COVID-19) caused by the novel zoonotic pathogen severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) emanate from tissue biopsies, case reports, and small postmortem studies restricted to the lung and specific organs. Whole-body autopsy studies of COVID-19 patients have been sparse.Methods: To further define the pathology caused by SARS-CoV-2 across all body organs, we performed autopsies on 22 patients with COVID-19 (18 with comorbidities and 4 without comorbidities) who died at the National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS Hospital, Rome, Italy. Tissues from the lung, heart, liver, kidney, spleen, and bone marrow (but not the brain) were examined. Only lung tissues were subject to transmission electron microscopy.Results: COVID-19 caused multisystem pathology. Pulmonary and cardiovascular involvement were dominant pathological features. Extrapulmonary manifestations included hepatic, kidney, splenic, and bone marrow involvement, and microvascular injury and thrombosis were also detected. These findings were similar in patients with or without preexisting medical comorbidities.Conclusions: SARS-CoV-2 infection causes multisystem disease and significant pathology in most organs in patients with and without comorbidities. [ABSTRACT FROM AUTHOR]

Introduction: Hydrochlorothiazide and thiazide-like diuretics are considered first-line drugs for initial therapy in uncomplicated arterial hypertension. Acute cholecystitis is a well-known complication during treatment with thiazide, and these drugs are also reported to be followed by pronounced insulin resistance.Case Presentation: We describe a case of acute cholestatic hepatitis in a 68-year-old Caucasian man who was receiving olmesartan and hydrochlorothiazide for arterial hypertension. From the clinical and histologic findings, we diagnosed him as having hepatocellular-cholestatic injury and a disorder of glucose metabolism in the liver. To the best of our knowledge, no histopathologic description of hydrochlorothiazide hepatotoxicity has previously been documented in the literature.Conclusion: In the differential diagnosis of cholestatic hepatitis, clinicians should be aware of the possibility of liver damage in patients receiving hydrochlorothiazide therapy. [ABSTRACT FROM AUTHOR]

• HSV-2 is the most frequent cause of genital lesions. • A late diagnosis of HSV-2 infection may lead to a fatal condition. • Fulminant myocarditis can be a complication of HSV-2 primary infection. • Endomyocardial biopsy may help in the diagnosis of fulminant myocarditis. Herpes simplex virus type 2 (HSV-2) infection is the leading cause of genital lesions. Infrequently HSV-2 primary infection can spread and involve other tissue and organs, however in immunocompetent individuals extra-genital complications are rare findings. In this report we present a fatal case of fulminant myocarditis and terminal liver involvement, caused by HSV-2 infection, with a unique presentation. Diagnosis was made only post-mortem. [ABSTRACT FROM AUTHOR]

The Zika virus (ZIKV) genome, its negative-strand viral proteins, and virus-like particles were detected in placenta-derived mesenchymal cells (MSCs), indicating that ZIKV persists after virus clearance from maternal blood and can be rescued by in vitro cultivation. We report for the first time the presence of replication-competent ZIKV in MSCs from an asymptomatic woman who acquired infection during pregnancy. [ABSTRACT FROM AUTHOR]

The sinusoidal endothelial cells present in the liver (LSECs) are tipically characterized by the presence of pores (fenestrae). During some pathological conditions LSECs undergo "capillarization", a process characterized by loss of fenestrations and acquisition of a vascular phenotype. In chronic liver disease capillarization has been reported to precede the development of fibrosis. LSECs modification in the setting of HCV infection is currently poorly investigated. Considering that HCV accounts for important changes in hepatocytes and in view of the intimate connection between hepatocytes and LSECs, here we set out to study in great detail the LSECs modifications in individuals with HCV-dependent chronic hepatitis. Electron microscopy analysis, and evaluation of CD32, CD31 and caveolin-1 expression showed that in HCV infection LSECs display major morphological changes but maintain their phenotypical identity. Capillarization was observed only in cases at initial stages of fibrosis. Our findings showed that the severity of LSECs modifications appears to be correlated with hepatocytes damage and fibrosis stage providing novel insight in the pathogenesis of HCV-chronic hepatitis. [ABSTRACT FROM AUTHOR]

A 56-year-old woman presented to the emergency to be department with diarrhea, asthenia, cough, and dysgeusia. The patient had chronic obstructive pulmonary disease (COPD) and was found infected with coronavirus disease 2019 (COVID-19). On physical examination, a small basal cell carcinoma (BCC) lesion was identified on her scalp; however, following the administration of noninvasive ventilation, the appearance of both macroscopic and microscopic BCC worsened dramatically. Our findings point to positive pressure noninvasive ventilation used to treat COVID-19 associated with COPD as a possible causative agent for the progression of cutaneous BCC. ( SKINmed . 2022;20:463-465).