Retrospective analysis of anti-inflammatory therapies during the first wave of COVID-19 at a community hospital.

BACKGROUND: Our understanding of the severe acute respiratory syndrome coronavirus 2 has evolved since the first reported cases in December 2019, and a greater emphasis has been placed on the hyper-inflammatory response in severely ill patients. The purpose of this study was to determine risk factors for mortality and the impact of anti-inflammatory therapies on survival. AIM: To determine the impact of various therapies on outcomes in severe coronavirus disease 2019 patients with a focus on anti-inflammatory and immune-modulating agents. METHODS: A retrospective analysis was conducted on 261 patients admitted or transferred to the intensive care unit in two community hospitals between March 12, 2020 and June 17, 2020. Totally 167 patients received glucocorticoid (GC) therapy. Seventy-three patients received GC alone, 94 received GC and tocilizumab, 28 received tocilizumab monotherapy, and 66 received no anti-inflammatory therapy. RESULTS: Patient survival was associated with GC use, either alone or with tocilizumab, and decreased vasopressor requirements. Delayed administration of GC was found to decrease the survival benefit of GC therapy. No difference in survival was found with varying anticoagulant doses, convalescent plasma, tocilizumab monotherapy; prone ventilation, hydroxychloroquine, azithromycin, or intravenous ascorbic acid use. CONCLUSION: This analysis demonstrated the survival benefit associated with anti-inflammatory therapy of GC, with or without tocilizumab, with the combination providing the most benefit. More studies are needed to assess the optimal timing of anti-inflammatory therapy initiation.

Factors associated with increased mortality in hospitalized COVID-19 patients.

BACKGROUND: The rapid spread of the coronavirus disease 2019 (COVID-19) epidemic has significantly impacted global health. So far, the evidence regarding the risk factors that predict the outcomes of COVID-19 patients is limited. In this study, we identified several risk factors that are associated with increased mortality in COVID-19 patients. METHODS: We performed a retrospective review of electronic medical records of the patients admitted with an initial diagnosis of COVID-19. We extracted several patient variables (including demographics, lab results, and pre-existing conditions) and examined for their association with increased mortality. RESULTS: Of the 487 people included in the study, 340 survived and 147 expired. Significant differences existed in demographics and underlying comorbidities between the two groups. A higher proportion of patients were age 65 and older (87.76% vs 53.24%, p < 0.001), and were predominantly male (63.27% vs 52.94%, p = 0.0351). Multivariate analysis showed five variables to be the predictors for mortality: age ≥65 [OR = 3.87, 95% CI (2.01, 7.46), p < 0.001], initial presentation with dyspnea [OR = 1.71, 95% CI (1.03, 2.82), p = 0.037], history of cardiomyopathy [OR = 3.33, 95% CI (1.07, 10.41), p < 0.038], positive initial chest imaging findings [OR = 2.24, CI (1.26, 3.97), p = 0.006], and acute kidney injury (AKI) [OR = 3.33 CI (2.10, 5.28), P < 0.001]. CONCLUSION: Identifying COVID-19 patients with these characteristics may help guide the management and improve mortality.

Renal effects of high-dose celecoxib in elderly men with stage D2 prostate carcinoma.

AIM: To prospectively study the clinical renal effects of daily high-dose celecoxib, a COX-2 inhibitor, in a cohort of elderly sick men (mean age 74.5 years) with advanced prostate cancer. MATERIAL AND METHOD: 44 men with advanced hormoneresistant prostate cancer participated in oncologic Phase II trials. All received celecoxib 400 mg bid for a median 6 months. Monthly laboratory measurement and blood pressure were monitored, and all cases of acute kidney injury (creatinine > 50% above baseline) and hyperkalemia (potassium > 5.5 mmol/l) were evaluated. Mean chemistries, BP, and estimated GFR (e-GFR) during treatment were compared to 6-month periods before and after treatment. RESULTS: There was no change in e-GFR (pre, 78.1 ± 22 ml/min; during treatment, 76 ± 19 ml/min). Serum K rose (4.25 ± 0.4 mmol/l to 4.39 ± 0.3 mmol/l, p = 0.03), and bicarbonate fell (28.16 ± 0.2 to 26.18 ± 0.2 mmol/l, p < 0.01) with treatment. 15% of patients developed AKI, close to the incidence of AKI episodes in the pre- (9%) and post-treatment periods (13%). AKI was mild, short-lived, and reversible, except in a terminal patient who withdrew. All AKI occurred in states of renal hypoperfusion, and were not related to celecoxib alone. Hyperkalemia developed in 9% of patients. No patient developed new-onset proteinuria. CONCLUSION: High-dose celecoxib for 6 months was relatively well tolerated. e-GFR remained stable and there were minor electrolyte alterations. Although the AKI incidence was much higher than other studies, it was not much higher than in the pre- and post-treatment periods (high "background noise"). All AKI occurred in states of renal hypoperfusion, not unexpected for prostaglandin inhibitors.