Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1175175 (SARS)
 19,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The severe acute respiratory syndrome (SARS) epidemic started in November 2002 and spread worldwide. The pathological changes in several human organs of patients with SARS have been extensively described. However, to date, little has been reported about the effects of this infection on the thyroid gland. Femoral head necrosis and low serum triiodothyronine and thyroxine levels, commonly found in patients with SARS, raise the possibility of thyroid dysfunction. We have undertaken this study to evaluate for any potential injury to the thyroid gland caused by SARS on tissue samples obtained from 5 SARS autopsies. The terminal deoxynucleotidyl transferase-mediated dUPT nick end-labeling assay was performed to identify apoptotic cells. The follicular epithelium was found to be damaged with large numbers of cells exfoliated into the follicle. The terminal deoxynucleotidyl transferase-mediated dUPT nick end-labeling assay demonstrated many cells undergoing apoptosis. Follicular architecture was altered and showed distortion, dilatation, and collapse. No distinct calcitonin-positive cells were detectable in the SARS thyroids. In conclusion, both parafollicular and follicular cells were injured. This may provide an explanation both for low serum triiodothyronine and thyroxine levels and the osteonecrosis of the femoral head associated with patients with SARS. Apoptosis may play a role in the pathogenesis of SARS associated coronavirus infection in the thyroid gland.
 ...
PMID:Pathology of the thyroid in severe acute respiratory syndrome. 1699 69

SARS-CoV-2 shares nearly 80% of its' genomic sequence with SARS-CoV and MERS-CoV, both viruses known to cause respiratory symptoms and liver impairment. The emergence of pediatric cases of multisystem inflammatory syndrome related to the SARS-CoV-2 infection (PIM-TS) has raised concerns over the issue of hepatic damage and liver enzyme elevation in the critically ill pediatric population with COVID-19. Some retrospective cohorts and case series have shown various degrees of ALT/AST elevation in SARS-CoV-2 infections. A limited number of liver histopathological studies are available that show focal hepatic periportal necrosis. This liver damage was associated with higher levels of inflammatory markers, C-reactive protein (CRP), and pro-calcitonin. Proposed pathophysiological mechanisms include an uncontrolled exacerbated inflammatory response, drug-induced liver injury, direct viral infection and damage to cholangiocytes, hypoxic-ischemic lesions, and micro-thrombosis in the liver. Based on the physiopathological characteristics described, our group proposes a clinical protocol for the surveillance, evaluation, management, and follow-up of critically ill pediatric COVID-19 patients with liver damage.
 ...
PMID:COVID-19 and Liver Damage: Narrative Review and Proposed Clinical Protocol for Critically ill Pediatric Patients. 3320 67