Here we report a case of a 63-year-old male diagnosed with recurrent depressive disorder and current episode of severe depression with psychotic symptoms, developed hyponatremia soon after addition of olanzapine and increasing the dose of escitalopram. A possible causality association was established with olanzapine, and the possible etiological reasons of this clinically significant risk were discussed.
Background Early neurological deterioration (END) is a common occurrence in ischemic stroke and contributes significantly to poor outcomes. Although multiple factors that predict END have already been identified, the role of fibrinogen – a key component of the coagulation pathway, is controversial. Objective To assess the role of fibrinogen in predicting END and poor hospital outcome in patients with acute ischemic stroke. Design Single-centre prospective observational study. Methods 141 patients with acute ischemic stroke were analyzed in this prospective observational study from a single tertiary-care hospital in East India. END was defined as a worsening of ≥2 points on the National Institutes of Health Stroke Scale (NIHSS) within 7 days of admission. A score of 3-5 on the Modified Rankin Scale (mRS), a stroke recurrence event or death during hospital stay was considered poor hospital outcome. We performed univariate analysis using age, sex, body-mass index (BMI), hypertension, diabetes, NIHSS scores, stroke etiology, blood glucose and lipid parameters and plasma fibrinogen to develop a logistic regression model to establish the independent predictors of END and poor outcome. Results Age (Odds Ratio (OR) 1.034 [95% CI 1.001-1.069], P = .046), NIHSS score at admission (OR 1.152 [95% CI 1.070-1.240], P < .001) and fibrinogen (OR 1.011 [95%CI 1.006-1.015], P < .001) were independent predictors of END in patients with acute ischemic stroke. Factors independently associated with poor outcome were NIHSS score at admission (OR 1.257 [95% CI 1.150-1.357], P < .001), fasting plasma glucose (OR 1.007 [95% CI 1.001-1.013], P = .020), and fibrinogen [OR 1.004 [95% CI 1.000-1.007], P = .038). Conclusion The significant role of fibrinogen in determining neurological worsening and subsequent poor outcomes in patients with acute ischemic stroke may help in early prognostication and guided therapeutic interventions.
ObjectiveAlcoholic cardiomyopathy (ACM) is a leading cause of non-ischaemic dilated cardiomyopathy (DCM) in tribal and non-tribal population. However, no study has been done depicting the correlation between clinical profile and prognosis of ACM in tribal and non-tribal population. This study also defines the long-term outcome and prognostic markers of ACM.MethodsWe studied 290 patients with ACM who were evaluated in our institute between January 2013 and December 2016. The primary endpoint of the study was all-cause mortality. Statistical analysis was done by using Kaplan-Meier survival curves for the assessment of all-cause mortality and Cox regression for the assessment of risk factors.ResultsAfter a median follow-up period of 3.75 years (IQR: 3–4 years), 50 patients with ACM (37.3%) died among tribal population while 14 patients (9%) died among non-tribal population. Independent predictors of all-cause mortality in ACM identified by Cox regression were left ventricular ejection fraction (LVEF) (HR: 0.883; 95% CI 0.783 to 0.996; p=0.043), QRS duration (HR: 1.010; 95% CI 1.007 to 1.017; p=0.005) and Child-Turcotte-Pugh (CTP) Scoring (HR: 12.332; 95% CI 6.999 to 21.728; p<0.001) at admission. The Kaplan-Meier survival probability estimate was 95.1% at 1 year and all-cause mortality was found to be higher in patients with QRS>120 ms, LVEF ≤35%, CTP Grade B/C than patients with QRS≤120 ms, LVEF >35% and CTP Score A, respectively (log-rank χ²=55.088, p<0.001; log-rank χ²=32.953, p<0.001; log-rank χ²=139.764, p<0.001, respectively).ConclusionOur study indicated increased morbidity and mortality in tribal population. LVEF, QRS duration and CTP Scoring at the time of presentation were found to be the independent prognostic markers of patients with ACM.
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