ABSTRACT
BACKGROUND: New onset hyperglycemia is common in patients with severe coronavirus disease 2019 (COVID-19) infection. Cytokine storm due to COVID-19 infection is an essential etiology for new-onset hyperglycemia, but factors like direct severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced pancreatic ß-cell failure have also been postulated to play a role. AIM: We plan to investigate further the mechanisms underlying SARS-CoV-2 infection-induced hyperglycemia, particularly the rationale of the cytokine-induced hyperglycemia hypothesis, by evaluating the association between inflammatory markers and new onset hyperglycemia in non-diabetic patients with COVID-19 infection. METHODS: We conducted a retrospective case-control study on adults without diabetes mellitus hospitalized for COVID-19 infection. The serum levels of glucose and inflammatory markers at presentation before initiation of corticosteroid were collected. Hyperglycemia was defined as glucose levels ≥ 140 mg/dL. C-Reactive protein (CRP) ≥ 100 mg/L, ferritin ≥ 530 ng/mL, lactate dehydrogenase (LDH) ≥ 590 U/L, and D-dimer ≥ 0.5 mg/L were considered elevated. We used the χ 2 test for categorical variables and the Mann-Whitney U test for continuous variables and calculated the logistic regression for hyperglycemia. RESULTS: Of the 520 patients screened, 248 met the inclusion criteria. Baseline demographics were equally distributed between patients with hyperglycemia and those who were normoglycemic. Serum inflammatory markers in patients with or without new-onset hyperglycemia were elevated as follows: CRP (58.1% vs 65.6%, P = 0.29), ferritin (48.4% vs 34.9%, P = 0.14), D-dimer (37.1% vs 37.1%, P = 0.76) and LDH (19.4% vs 11.8%, P = 0.02). Logistic regression analysis showed LDH odds ratio (OR) = 1.623 (P = 0.256). We observed significantly higher mortality (24.2% vs 9.1%, P = 0.001; OR = 2.528, P = 0.024) and length of stay (8.89 vs 6.69, P = 0.026) in patients with hyperglycemia. CONCLUSION: Our study showed no association between CRP, ferritin, LDH, D-dimer levels, and new-onset hyperglycemia in non-diabetic patients with COVID-19 infection. It also shows an increased mortality risk and length of stay in patients with hyperglycemia. With new-onset hyperglycemia being closely associated with poor prognostic indices, it becomes pivotal to understand the underlying pathophysiological mechanisms behind the SARS-CoV-2 infection-induced hyperglycemia. We conclude that the stress hyperglycemia hypothesis is not the only mechanism of SARS-CoV-2 infection-induced hyperglycemia but rather a multicausal pathogenesis leading to hyperglycemia that requires further research and understanding. This would help us improve not only the clinical outcomes of COVID-19 disease and inpatient hyperglycemia management but also understand the long-term effects of SARS-CoV-2 infection and further management.
ABSTRACT
This study was conducted with the primary aim to distinguish patients with a true stroke versus a stroke mimic based on clinical features and imaging. We conducted a retrospective case-control study on 116 adult patients who received alteplase (tPA) to treat acute stroke at our hospital. We further analyzed 79 patients with a normal computed tomography angiography (CTA). Based on their magnetic resonance imaging (MRI) of the brain, they were divided into cases (stroke mimics) and controls (true strokes). Data were collected retrospectively by reviewing individual medical charts on the electronic medical record (EMR), including age, gender, history of stroke, seizure, hypertension, diabetes, atrial fibrillation, hyperlipidemia, presenting NIH Stroke Scale/Score, hemorrhagic conversion, history of migraine, history of depression, sidedness of symptoms and aphasia. Data were categorized to separate those who were later diagnosed to be stroke mimics by being-postictal, encephalopathic, in acute migraine, suffered post-stroke recrudescence (PSR) due to metabolic insult, or had conversion disorder when symptoms could not be attributed to any medical condition or mental illness. Of the 79 study subjects, 48 (60%) were stroke mimics. The mean age of the cohort was 68.67 years, and 46.8% of the study subjects were females. Based on the multivariate logistic regression analysis, factors associated with being a stroke mimic were older age, history of migraine, and a history of prior stroke. In conclusion, increased attention to history and clinical examination as the first step can aid in the proper diagnosis of strokes versus stroke mimics. Identifying stroke mimics early could help expedite hospital workup and prevent inadvertent investigations, reducing hospital occupancy during the ongoing COVID-19 pandemic. We could potentially avoid the administration of tPA to such patients, reducing both the cost and adverse effects of it. Every stroke can cause neurological deficits, but every deficit need not be a stroke.
ABSTRACT
BACKGROUND: Since December 2019, an outbreak of pneumonia caused by severe acute respiratory syndrome - coronavirus-2 (SARS-CoV-2) has led to a life-threatening ongoing pandemic worldwide. A retrospective study by Chow et al showed aspirin use was associated with decreased intensive care unit (ICU) admissions in hospitalized coronavirus disease 2019 (COVID-19) patients. Recently, the RECOVERY TRIAL showed no associated reductions in the 28-d mortality or the progression to mechanical ventilation of such patients. With these conflicting findings, our study was aimed at evaluating the impact of daily aspirin intake on the outcome of COVID-19 patients. AIM: To study was aimed at evaluating the impact of daily aspirin intake on the outcome of COVID-19 patients. METHODS: This retrospective cohort study was conducted on 125 COVID-19 positive patients. Subgroup analysis to evaluate the association of demographics and comorbidities was undertaken. The impact of chronic aspirin use was assessed on the survival outcomes, need for mechanical ventilation, and progression to ICU. Variables were evaluated using the chi-square test and multinomial logistic regression analysis. RESULTS: 125 patients were studied, 30.40% were on daily aspirin, and 69.60% were not. Cross-tabulation of the clinical parameters showed that hypertension (P = 0.004), hyperlipidemia (0.016), and diabetes mellitus (P = 0.022) were significantly associated with aspirin intake. Regression analysis for progression to the ICU, need for mechanical ventilation and survival outcomes against daily aspirin intake showed no statistical significance. CONCLUSION: Our study suggests that daily aspirin intake has no protective impact on COVID-19 illness-associated survival outcomes, mechanical ventilation, or progression to ICU level of care.
ABSTRACT
BACKGROUND: Our understanding of coronavirus disease 2019 (COVID-19) and its implications for patients with inflammatory bowel diseases (IBD) is rapidly evolving. We performed a systematic review and meta-analysis to investigate the epidemiology, clinical characteristics, and outcomes in IBD patients with COVID-19. METHODS: We searched PubMed, EMBASE, Cochrane Central, Clinicaltrials.gov, Web of Science, MedRxiv, and Google Scholar from inception through October 2020. We included studies with IBD patients and confirmed COVID-19. Data were collected on the prevalence, patient characteristics, pre-infection treatments for IBD, comorbidities, hospitalization, intensive care unit (ICU), admission, and death. RESULTS: Twenty-three studies with 51,643 IBD patients and 1449 with COVID-19 met our inclusion criteria. In 14 studies (n = 50,706) that included IBD patients with and without COVID-19, the prevalence of infection was 1.01% (95% confidence interval [CI], 0.92-1.10). Of IBD patients with COVID-19, 52.7% had Crohn's disease, 42.2% had ulcerative colitis, and 5.1% had indeterminate colitis. Nine studies (n = 687) reported outcomes according to IBD therapy received. Compared with patients on corticosteroids, those on antitumor necrosis factor (anti-TNF) therapy had a lower risk of hospitalization (risk ratio [RR], 0.24; 95% CI, 0.16-0.35; P < .01; I2 = 0%) and ICU admission (RR, 0.10; 95% CI, 0.03-0.37; P < .01) but not death (RR, 0.16; 95% CI, 0.02-1.71; P = .13; I2 = 39%). Compared with patients on mesalamine, those on antitumor necrosis factor therapy had a lower risk of hospitalizations (RR, 0.37; 95% CI, 0.25-0.54), ICU admissions (RR, 0.20; 95% CI, 0.07-0.58), and death (0.21; 95% CI, 0.04-1.00). Comparing patients on immunomodulators vs mesalamine or anti-TNF therapy, there was no difference in these outcomes. CONCLUSIONS: The prevalence of COVID-19 in IBD patients was low. Use of corticosteroids or mesalamine was significantly associated with worse outcomes, whereas use of anti-TNFs was associated with more favorable outcomes. Further investigation clarifying the mechanisms of these disparate observations could help identify risk and adverse outcome-mitigating strategies for patients with IBD.