ABSTRACT
Background: Right ventricular (RV) dysfunction in acute COVID-19 was reported to be associated with poor prognosis. We studied the association between parameters of RV dysfunction and in-hospital mortality during the surges caused by different SARS-CoV-2 variants. Methods: In a retrospective single-center study, we enrolled 648 consecutive patients hospitalized with COVID-19 [66 (10 %) hospitalized during the alpha variant surge, 433 (67 %) during the delta variant surge, and 149 (23 %), during the omicron variant surge]. Patients were reported from a hospital with an underreported population of mostly African American and Hispanic patients. Patients were followed for a median of 11 days during which in-hospital death occurred in 155 (24 %) patients [Alpha wave: 25 (38 %), Delta Wave: 112 (26 %), Omicron wave: 18 (12 %), p < 0.001]. Results: RV dysfunction occurred in 210 patients (alpha: 32 %, 26 %, delta: 29 %, and omicron: 49 %, p < 0.001) and was associated with higher mortality across waves, however, independently predicted in-hospital mortality in the Alpha (HR = 5.1, 95 % CI: 2.06-12.5) and Delta surges (HR = 1.6, 95 % CI: 1.11-2.44), but not in the Omicron surge. When only patients with RV dysfunction were compared, the mortality risk was found to decrease significantly from the Alpha (HR = 13.6, 95 % CI: 3.31-56.3) to the delta (HR = 1.93, 95 % CI: 1.25-2.96) and to the Omicron waves (HR = 11, 95 % CI: 0.6-20.8). Conclusions: RV dysfunction continues to occur in all strains of the SARS-CoV-2 virus, however, the mortality risk decreased from wave to wave likely due to evolution of better therapeutics, increase rate of vaccination, or viral mutations resulting in decrease virulence.Registration number of clinical studies: BronxCare Hospital center institutional review board under the number 05 13 21 04.
ABSTRACT
Various factors can lead to thyroiditis, including any acute inflammatory process, especially viral illness. While coronavirus disease 2019 (COVID-19) has been linked to disorders of various systems, there is a lack of literature showing an association of coronavirus with the cause of Hashimoto's thyroiditis. Several possible mechanisms for this outcome have been proposed; chief among them is molecular mimicry. Here, we are reporting a case of Hashimoto's thyroiditis incited by COVID-19 in a 34-year-old obese female who presented with anxiety, behavioral changes, and repeated head movements. The patient had an elevated thyroid stimulating hormone (TSH) level, a low thyroxine (T4) level, and a positive anti-microsomal antibody screen. The patient also tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA. Ultrasound of the patient's neck showed an enlarged heterogeneous thyroid gland. Thyroid replacement therapy with intravenous levothyroxine was started with the subsequent oral transition. Concurrently, she received antibiotics, steroids, and low-molecular-weight heparin for COVID-19. The patient exhibited significant improvement in her mental status, with an eventual return to baseline. The results of the thyroid panel obtained at the outpatient follow-up were normal. Although there is a paucity of data to show COVID-19 as a cause of this painless thyroiditis, this case demonstrates such causality between these two.
ABSTRACT
Non-alcoholic fatty liver disease (NAFLD) has emerged as one of the lethal causes of chronic liver disease globally. NAFLD can ultimately progress to non-alcoholic steatohepatitis (NASH) given persistent cellular insult. The crux of the problem lies in fat accumulation in the liver, such as increased fatty acid substrates owing to consumption of a high-fat diet, altered gut physiology, and excess adipose tissue. Being the hepatic manifestation of metabolic syndrome, insulin resistance is also among one of the many stimuli. Therefore, drugs, such as glucagon-like peptide-1 receptor agonist (GLP-1 RA) can play a significant role in reducing inflammation, in addition to weight loss and dietary habits. In this review article, we have reviewed the role of exenatide, liraglutide, and semaglutide in the management of NASH. Two of the agents, exenatide and semaglutide, have a predominant role in reducing alanine aminotransferase (ALT) levels, therefore reducing inflammation and promoting weight loss. However, these agents have a lesser impact on the degree of fibrosis. Liraglutide, on the other hand, has been shown to significantly decrease the degree of fibrosis and has been found helpful in reversing mild degrees of steatosis. Therefore, these agents warrant attention to the new perspective that has been presented so that future guidelines may incorporate and streamline individualized therapy.
