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Indianapolis, IN, United States

Liangpunsakul S.,Indiana University | Liangpunsakul S.,Roudebush Veterans Administration Medicial Center | Liangpunsakul S.,Clarian Digestive Disease Center
Journal of Clinical Gastroenterology | Year: 2011

Background and aims: Alcoholic hepatitis (AH) is the most florid manifestation of alcoholic liver disease. In this study, we examined the clinical characteristics and risk factors associated with mortality in hospitalized AH patients in the United States using the 2007 Nationwide inpatient sample of the Healthcare Cost and Utilization Project. Methods: Patients who were hospitalized with the primary diagnosis of AH in the United States in 2007 were identified using International Classification of Diseases-9 code. We further characterized these subjects based on associated symptoms (such as ascites, hepatic encephalopathy, and coagulopathy), complications during hospitalization (such as sepsis, pneumonia, spontaneous bacterial peritonitis, and acute renal failure), and categories pertaining to hospital characteristics, such as teaching status. The predictors of mortality were calculated using logistic regression analyses. Results: There were 8,043,415 in-patient admissions, of which 56,809 (0.71%) were hospitalized with the primary diagnosis of AH. The mean age was 53.2 years, and 27% were female. The average length of stay was 6.5±7.7 days and 3,881 subjects (6.8%) died during hospitalization. Medicare and Medicaid were the main primary expected payer sources (51.8%) with the average total charges during hospital stay of $37,769. In the multivariate analyses, older age, presence of sepsis, spontaneous bacterial peritonitis, pneumonia, urinary tract infection, acute renal failure, hepatic encephalopathy, and coagulopathy were independently associated with in-patient mortality. Conclusions: In-hospital mortality rate for AH remains high, especially in those with infectious complications, hepatic encephalopathy, coagulopathy, and acute renal failure. Our analysis documented significant healthcare cost and utilization among hospitalized AH patients. © 2011 by Lippincott Williams and Wilkins.

Vuppalanchi R.,Indiana University | Vuppalanchi R.,Clarian Digestive Disease Center | Juluri R.,Indiana University | Ghabril M.,Clarian Digestive Disease Center | And 6 more authors.
Journal of Clinical Gastroenterology | Year: 2011

Goals and Background: Nearly 40% of cytochrome P450 3A (CYP3A) activity is located in the small intestine. An earlier study has shown that cirrhotics with transjugular intrahepatic portosystemic shunts (TIPS) have diminished intestinal CYP3A activity. We hypothesized that oral CYP3A substrates known to prolong QT interval may cause further prolongation of the QT interval in cirrhotic patients with TIPS. Study: A total of 23 patients (9 healthy controls, 6 cirrhotics without and 8 cirrhotics with TIPS) participated in a study that tested this hypothesis using erythromycin as the probe drug. Participants with cirrhosis with and without TIPS were matched for age, sex, race, BMI and etiology of liver disease. Serial electrocardiograms were obtained at baseline, after single dose of erythromycin 500 milligrams, and after 7 days of erythromycin (500 milligrams orally twice daily). QT intervals were measured in 3 consecutive beats in 3 leads and corrected QT intervals (QTc) were obtained using various correction formulae. The maximal QTc change (ΔQTc Max) after single and multiple dose administration was the primary outcome. Results: At baseline, the QTc intervals (mean±S.E) in cirrhotics with TIPS (418±6 msec) and cirrhosis (431±6 msec) were significantly higher compared with controls (388±9 msec, P=0.021). After a single dose of erythromycin, there was no significant difference among the 3 groups in ΔQTc Max (P=0.7). However, after a 7 day course, cirrhotics with TIPS developed significantly greater ΔQTc Max (179.5±67.8 msec) compared with cirrhotics (31.2±9.5 msec) and healthy controls (38.3±3.3 msec) (P=0.03). Conclusion: This study suggests that patients with TIPS are potentially at increased risk for abnormal QT prolongation when exposed to oral CYP 3A substrates with QT prolonging effect. © 2011 by Lippincott Williams & Wilkins.

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