The impact of the COVID-19 pandemic on acute appendicitis patients in a tertiary care center in Lebanon.

INTRODUCTION: With it becoming a global pandemic, the coronavirus disease of 2019 (COVID-19) imposed public health restraints that hampered patient's presentation to hospitals. In Lebanon, little is known about the presentation patterns of acute appendicitis (AA) patients among different population groups during the COVID-19. Therefore, this study aims to assess the effects of the COVID-19 pandemic on the rates of cases seen during the pandemic period, the adopted management strategies, and evaluate the patient outcomes compared to presentations from previous years. METHODS: This is a retrospective, observational cohort study with no interventional procedures. All patients presented to our tertiary health care center were diagnosed with AA between February 2019 and February 2021 comprised the study analysis. We divided our patients into the pre-pandemic period cohort March 1st, 2019, till February 29th, 2020, and the pandemic period cohort March 1st 2020 till March 1st 2021. RESULTS: We collected data retrospectively from 342 patients: 201 patients presented in the pre-pandemic period and 141 during the pandemic period. Male predominance was seen in both cohorts (51.7% and 58.9% respectively). A decrease in the number of AA cases was seen during the pandemic, however, the duration of symptoms before presentation was similar in both cohorts (p = 0.382) Additionally, the number of complicated appendicitis cases was not different between cohorts. The main imaging modality was CT in both groups with no statistically significant difference in the type of imaging between them (p = 0.398). Further, the predominant treatment modality remained surgery during the pandemic, with no difference between both periods (p = 0.200), and no statistically significant difference in the type of surgery performed as laparoscopic surgery remained the most common surgery type in the pandemic period (p = 0.43). Finally, no extra surgical and post-surgical complications were identified. CONCLUSION: In conclusion, our study is an example of how the COVID-19 pandemic did not significantly affect patients presenting for AA. Despite the COVID-19-related restrictions, Lebanese patients with worrying symptoms were presenting to the emergency department and the American University of Beirut Medical Center was providing them with the standards of care. Our study mirrors the Lebanese experience and gives an example of a population that focused more on their current symptoms than the fear of acquiring the COVID-19 virus. Further research is needed to assess whether this was the correct approach during these times.

Macrophage polarization and signaling in diabetic kidney disease: a catalyst for disease progression.

Diabetic kidney disease (DKD) is a serious complication of diabetes affecting millions of people worldwide. Macrophages, a critical immune cell type, are central players in the development and progression of DKD. In this comprehensive review, we delve into the intricate role of macrophages in DKD, examining how they can become polarized into proinflammatory M1 or anti-inflammatory M2 phenotypes. We explore the signaling pathways involved in macrophage recruitment and polarization in the kidneys, including the key cytokines and transcription factors that promote M1 and M2 polarization. In addition, we discuss the latest clinical studies investigating macrophages in DKD and explore the potential of hypoglycemic drugs for modulating macrophage polarization. By gaining a deeper understanding of the mechanisms that regulate macrophage polarization in DKD, we may identify novel therapeutic targets for this debilitating complication of diabetes. This review provides valuable insights into the complex interplay between macrophages and DKD, shedding light on the latest developments in this important area of research. This review aims to enhance understanding of the role that macrophages play in the pathogenesis of DKD.

SGLT2 Inhibitor-Dapagliflozin Attenuates Diabetes-Induced Renal Injury by Regulating Inflammation through a CYP4A/20-HETE Signaling Mechanism.

Diabetic kidney disease (DKD) is a serious complication of diabetes, affecting millions of people worldwide. Inflammation and oxidative stress are key contributors to the development and progression of DKD, making them potential targets for therapeutic interventions. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have emerged as a promising class of drugs, with evidence demonstrating that they can improve renal outcomes in people with diabetes. However, the exact mechanism by which SGLT2i exert their renoprotective effects is not yet fully understood. This study demonstrates that dapagliflozin treatment attenuates renal injury observed in type 2 diabetic mice. This is evidenced by the reduction in renal hypertrophy and proteinuria. Furthermore, dapagliflozin decreases tubulointerstitial fibrosis and glomerulosclerosis by mitigating the generation of reactive oxygen species and inflammation, which are activated through the production of CYP4A-induced 20-HETE. Our findings provide insights onto a novel mechanistic pathway by which SGLT2i exerts their renoprotective effects. Overall, and to our knowledge, the study provides critical insights into the pathophysiology of DKD and represents an important step towards improving outcomes for people with this devastating condition.

Influence of intermittent fasting on prediabetes-induced neuropathy: Insights on a novel mechanistic pathway.

Aims: Peripheral neuropathy (PN) is correlated with obesity and metabolic syndrome. Intermittent fasting (IF) has been described as the cornerstone in the management of obesity; however, its role in prediabetic complications is not well elucidated. Cytochromes P450 Monooxygenases (CYP450) are major sources of Reactive Oxygen Species (ROS) that orchestrate the onset and development of diabetic complications. One of the CYP-metabolites, Expoxyecosatetraenoic Acids (EETs), are considered to be negative regulators of ROS production. In this study, we elucidated the role of IF on ROS production and investigated its influence on prediabetes-induced PN. Methods: C57/BL6 control mice, prediabetic, prediabetic that underwent alternate day fasting with different diet composition, and prediabetic mice treated with EET-metabolizing sEH-inhibitor, AUDA. Body mass composition, metabolic, behavioral, and molecular tests were performed. Results: High-fat diet (HFD) led to an increase in NADPH-induced ROS production; that was due to an alteration in the epoxygenase pathway assessed by the decrease in CYP1a1/1a2 expression. IF reinstated the homeostatic levels of EETs in HFD-fed mice. Moreover, treatment with AUDA mimicked the beneficial effect observed with IF. Conclusion: IF and EETs bioavailability have a protective role in prediabetes-induced PN, suggesting a novel interventional strategy in the management of prediabetes and its associated complications.