Sumeet K. Asrani M.D.

Garg, S. K., S. Sarvepalli, D. Singh, I. Obaitan, T. Peeraphatdit, L. Jophlin, S. K. Asrani, V. H. Shah and M. D. Leise (2019). “Incidence and Risk Factors Associated With 30-Day Readmission for Alcoholic Hepatitis.” J Clin Gastroenterol Apr 3. [Epub ahead of print].

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BACKGROUND: Alcohol abuse and liver disease are associated with high rates of 30-day hospital readmission, but factors linking alcoholic hepatitis (AH) to readmission are not well understood. We aimed to determine the incidence rate of 30-day readmission for patients with AH and to evaluate potential predictors of readmission. METHODS: We used the Nationwide Readmissions Database to determine the 30-day readmission rate for recurrent AH between 2010 and 2014 and examined trends in readmissions during the study period. We also identified the 20 most frequent reasons for readmission. Multivariate survey logistic regression analysis was used to identify factors associated with 30-day readmission. RESULTS: Of the 61,750 index admissions for AH, 23.9% were readmitted within 30-days. The rate of readmission did not change significantly during the study period. AH, alcoholic cirrhosis, and hepatic encephalopathy were the most frequent reasons for readmission. In multivariate analysis female sex, leaving against medical advice, higher Charlson comorbidity index, ascites, and history of bariatric surgery were associated with earlier readmissions, whereas older age, payer type (private or self-pay/other), and discharge to skilled nursing-facility reduced this risk. CONCLUSIONS: The 30-day readmission rate in patients with AH was high and stable during the study period. Factors associated with readmission may be helpful for development of consensus-based expert guidelines, treatment algorithms, and policy changes to help decrease readmission in AH.

Agbim, U. and S. K. Asrani (2019). “Non-invasive assessment of liver fibrosis and prognosis: an update on serum and elastography markers.” Expert Rev Gastroenterol Hepatol 13(4): 361-374.

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INTRODUCTION: Non-invasive assessment of fibrosis is increasingly utilized in clinical practice to diagnose hepatic fibrosis. Non-invasive assessment of liver fibrosis relies on biologic and/or physical properties to assess tissue fibrosis. Serum markers estimate fibrosis by incorporating markers reflecting hepatic function (indirect markers) and/or markers measuring extracellular matrix degradation/fibrogenesis (direct markers). Radiology based techniques relay the mechanical properties and stiffness of a tissue, with increased stiffness associated with more advanced fibrosis. Areas covered: In this comprehensive review, the recent literature discussing serum markers and elastography-based techniques will be covered. These modalities are also explored in the setting of various liver diseases. Expert opinion: The etiology of liver disease and clinical context should be taken into consideration when non-invasive markers are incorporated in clinical practice. Non-invasive assessment of fibrosis has been most extensively utilized in hepatitis C, followed by hepatitis B and nonalcoholic fatty liver disease, but its role remains less developed in other etiologies of liver disease such as alcohol-associated liver disease and autoimmune liver disease. The role of non-invasive markers in predicting progression or regression of fibrosis, development of liver-related events and survival needs to be further explored.

Asrani, S. K., L. W. Jennings, J. F. Trotter, J. Levitsky, M. K. Nadim, W. R. Kim, S. A. Gonzalez, B. Fischbach, R. Bahirwani, M. Emmett and G. Klintmalm (2019). “A Model for Glomerular Filtration Rate Assessment in Liver Disease (GRAIL) in the Presence of Renal Dysfunction.” Hepatology 69(3): 1219-1230.

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Estimation of glomerular filtration rate (eGFR) in patients with liver disease is suboptimal in the presence of renal dysfunction. We developed a model for GFR assessment in liver disease (GRAIL) before and after liver transplantation (LT). GRAIL was derived using objective variables (creatinine, blood urea nitrogen, age, gender, race, and albumin) to estimate GFR based on timing of measurement relative to LT and degree of renal dysfunction (www.bswh.md/grail). The measured GFR (mGFR) by iothalamate clearance (n = 12,122, 1985-2015) at protocol time points before/after LT was used as reference. GRAIL was compared with the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) and Modification of Diet in Renal Disease (MDRD-4, MDRD-6) equations for mGFR < 30 mL/min/1.73 m(2) . Prediction of development of chronic kidney disease (mGFR < 20 mL/min/1.73 m(2) , initiation of chronic dialysis) and listing or receipt of kidney transplantation within 5 years was examined in internal cohort (n = 785) and external validation (n = 68,217, 2001-2015). GRAIL had less bias and was more accurate and precise as compared with CKD-EPI, MDRD-4, and MDRD-6 at time points before/after LT for low GFR. For mGFR < 30 mL/min/1.73 m(2) , the median difference (eGFR-mGFR) was GRAIL: 5.24 (9.65) mL/min/1.73 m(2) as compared with CKD-EPI: 8.70 (18.24) mL/min/1.73 m(2) , MDRD-4: 8.82 (17.38) mL/min/1.73 m(2) , and MDRD-6: 6.53 (14.42) mL/min/1.73 m(2) . Before LT, GRAIL correctly classified 75% as having mGFR < 30 mL/min/1.73 m(2) versus 36.1% (CKD-EPI), 36.1% (MDRD-4), and 52.8% (MDRD-6) (P < 0.01). An eGFR < 30 mL/min/1.73 m(2) by GRAIL predicted development of CKD (26.9% versus 4.6% CKD-EPI, 5.9% MDRD-4, and 10.5% MDRD-6) in center data and needing kidney after LT (48.3% versus 22.0% CKD-EPI versus 23.1% MDRD-4 versus 48.3% MDRD-6, P < 0.01) in national data within 5 years after LT. Conclusion: GRAIL may serve as an alternative model to estimate GFR among patients with liver disease before and after LT at low GFR.

Devarbhavi, H., S. K. Asrani and P. S. Kamath (2019). “Reply to: ‘Alcohol-associated liver disease, not hepatitis B, is the major cause of cirrhosis in Asia.’” J Hepatol Feb 19. [Epub ahead of print].

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We appreciate the comments by Singh et al. regarding our review article “Burden of liver diseases in the world”. The data presented in our paper was extracted from published sources particularly World Health Organization (WHO) publications and published literature. The causes of liver disease in Asia were generalized and we did not dwell specifically into causes of liver diseases in the populous countries of China and India. Singh et al. quote several studies on patients from tertiary care referral centers in India, published in regional journals. Using such studies to derive conclusions regarding national prevalence of disease may have methodological limitations. Further, the studies cited may have weaknesses as they addressed portal hypertension, thyroid dysfunction in cirrhosis, acute precipitants of acute-on-chronic liver failure and causes of decompensation in cirrhosis rather than specifically focusing on determining the etiology of disease.Further, Table 4 in our paper was in relation to the highest burden of age standardized death rates in various countries; they were not in relation to quantum of burden in overall population. In Table 1, herein, we report age standardized death rates from alcohol across the top 10 most populous countries in Asia. Although the data was extracted from a recent publication from WHO, the numbers in Table 1 are much smaller than the numbers quoted in Table 4 of our original publication. Indeed, population attributable fractions for cirrhosis stratified by causes of liver disease such as hepatitis, B, C and alcohol, still demonstrate hepatitis B as the major cause in all regions of Asia including India which is a part of South Asia. A recent multi-centre study from India with the specific aim of determining the aetiology of chronic liver diseases among new patients seen in an inpatient setting (n = 13,014) concluded that HBV was the most common cause of chronic liver disease (33.3%), followed by HCV (21.6%), alcohol (17.3%), and non-alcoholic fatty liver disease (12.8%). When stratified by presence of cirrhosis (n = 4,413), alcohol was the most common cause (34.3%); a significant limitation of this data was that more than 99% of patients with cirrhosis were decompensated and may not accurately reflect the burden of cirrhosis. Further there was significant regional heterogeneity within different regions of India; viral hepatitis B and C being more common in northern and eastern regions compared to southern regions where alcohol was more common. With increasing global coverage of universal vaccination against hepatitis B in India and the easy availability and affordability of direct-acting antivirals including provision for free treatments for hepatitis C in certain groups and regions, the burden of liver disease from B and C is expected to decrease in the future. Liver disease from alcohol is likely to increase in India in the absence of government policies aimed at reducing alcohol consumption. (Full text of correspondence.)

Asrani, S. K. and J. Hasse (2019). “Reply: Bariatric Surgery and Liver Transplantation.” Liver Transpl 25(3): 516.

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We appreciate the interest by Yildiz in our work that looked at the association between bariatric surgery and outcomes among patients evaluated for liver transplantation. We share the sentiment that some of the outcomes noted in the study may be related to malabsorptive rather than restrictive weight reduction surgery. As reflected in the results, rates of delisting or death were high for gastric bypass versus non–gastric bypass patients (44% versus 16.7%; P = 0.04). However, rates of moderate or severe malnutrition were similar between the groups (68% versus 57%; P = 0.5). Hence, in this analysis of historical data, it is hard to assess whether it is the surgery itself or a consequence of malnutrition regardless of surgery type that is driving the effect. In an independent population–based cohort, we are currently evaluating the impact of bariatric surgery on the natural history of compensated and decompensated cirrhosis. To our knowledge, there are no longitudinal prospective data collected looking at longterm outcomes (beyond 1‐2 years) starting from the time of surgery. Such efforts are needed to assess the absolute impact of the surgery type on outcomes in patients with or without recognized liver disease. Portal vein thrombosis remains an important complication of bariatric surgery. Reliable data on portal vein thrombosis among all patients with bariatric surgery evaluated for transplantation were not available. However, among those who underwent liver transplantation, only 1 patient had portal vein thrombosis. (Full text of this letter.)