Is it necessary to stop glucagon-like peptide-1 receptor agonists prior to endoscopic procedure? A retrospective study.

BACKGROUND: Glucagon-like peptide-1 receptor agonists (GLP-1 RA) are effective in diabetes and obesity, reducing hyperglycemia by increasing insulin release and delaying gastric emptying. However, they can cause gastroparesis, raising concerns about aspiration during procedures. Recent guidelines advise discontinuing GLP-1 RA before surgery to reduce the risk of pulmonary aspiration. AIM: To evaluate the effect of GLP-1 RAs on gastric residual contents during endoscopic procedures. METHODS: A retrospective chart review at BronxCare Health System, New York, from January 2019 to October 2023, assessed gastric residue and aspiration in GLP-1 RA patients undergoing endoscopic procedures. Two groups were compared based on dietary status before the procedure. Data included demographics, symptoms of gastroparesis, opiate use, hemoglobin A1c, GLP-1 agonist indication, endoscopic details, and aspiration occurrence. IBM SPSS was used for analysis, calculating means, standard deviations, and applying Pearson's chi-square and t-tests for associations, with P < 0.05 as being significant. RESULTS: During the study, 306 patients were included, with 41.2% on a clear liquid/low residue diet and 58.8% on a regular diet before endoscopy. Most patients (63.1%) were male, with a mean age of 60 ± 12 years. The majority (85.6%) were on GLP-1 RAs for diabetes, and 10.1% reported digestive symptoms before endoscopy. Among those on a clear liquid diet, 1.5% had residual food at endoscopy compared to 10% on a regular diet, which was statistically significant (P = 0.03). Out of 31 patients with digestive symptoms, 13% had residual food, all from the regular diet group (P = 0.130). No complications were reported during or after the procedures. CONCLUSION: The study reflects a significant rise in GLP-1 RA use for diabetes and obesity. A 24-hour liquid diet seems safe for endoscopic procedures without aspiration. Patients with upper gastrointestinal symptoms might have a higher residual food risk, though not statistically significant. Further research is needed to assess risks based on diabetes duration, gastroparesis, and GLP-1 RA dosing, aiming to minimize interruptions in therapy during procedures.

Association between right ventricular dysfunction and in-hospital mortality in surges of SARS-CoV-2 infection attributed to the Alpha, Delta, and Omicron variants.

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.

Hashimoto's Thyroiditis Encephalopathy Induced by COVID-19 Infection.

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.

Role of Glucagon-Like Peptide-1 Receptor Agonists in the Management of Non-Alcoholic Steatohepatitis: A Clinical Review Article.

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.