Abstract

Introduction: Alcoholic hepatitis (AH) is a common cause of hospital admissions and is associated with a high mortality rate. AH occurs frequently in patients with heavy alcohol use. Alcohol use disorder (AUD) commonly presents with comorbid psychiatric disorders such as bipolar disorder. Bipolar disorder patients are also known to be at an increased risk for chronic liver diseases. Bipolar 1 disorder (B1D) is often considered the most severe presentation among different types of bipolar disorder. This study assesses the clinical outcomes of patients admitted for AH with concomitant B1D.Methods: Adult patients with AH were identified within the 2014 National Inpatient Sample (NIS) database. International Classification of Diseases, Ninth Edition Revision, Clinical Modification (ICD-9 CM) codes were used to select for all of the diagnoses for this study. AH patients were subdivided into those with and without B1D. The outcomes of interest were sepsis, hepatic encephalopathy, acute respiratory failure, acute kidney injury, ischemic stroke, hepatic failure, coagulopathy, and inpatient mortality. A multivariate logistic regression analysis was performed to explore whether B1D is an independent predictor for the outcomes.Results: Among 4,453 patients with AH identified, 166 patients also had B1D. AH patients with comorbid B1D were seen to be younger (42.9 years old vs. 46.2 years old, p < 0.05) and more commonly female (55.4% vs. 36.5%, p < 0.05). The B1D subgroup of AH patients were found to less likely develop acute hepatic failure (adjusted odds ratio (aOR) 0.13, 95% confidence interval (CI): 0.02-0.97, p < 0.05). The adjusted odds ratios for the remaining outcomes were not statistically significant.Conclusions: Our study indicates that B1D may be an independent protective factor against acute hepatic failure in patients hospitalized with AH. This finding can be explained by frequent laboratory monitoring and psychiatric assessments performed by psychiatrists treating B1D patients, as well as the impact B1D has on cortisol release induced by hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis.

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