The
n e w e ng l a n d j o u r na l
of
m e dic i n e
Acute Liver Failure To the Editor: In their review article, Bernal and Wendon (Dec. 26 issue)1 state that lactulose is potentially dangerous in the treatment of acute liver failure. Although its side-effect profile may make it unacceptable for patients in whom liver transplantation is being contemplated, in resourcepoor settings where liver transplantation is not feasible, one has to fall back on other treatments. Lactulose is a first-line treatment to minimize the production and absorption of ammonia from the gut and is a well-established treatment for hepatic encephalopathy.2 The American Association for the Study of Liver Diseases recommends its use in the early stages of encephalopathy.3 Although the data are limited and not uniformly positive, lactulose can be used to treat early stages of encephalopathy, and it may help prolong survival.4 Bimal K. Agrawal, M.D. Maharishi Markandeshwar Institute of Medical Sciences and Research Mullana, India [email protected]
Usha Agrawal, M.D. National Institute of Pathology New Delhi, India No potential conflict of interest relevant to this letter was reported. 1. Bernal W, Wendon J. Acute liver failure. N Engl J Med 2013;
369:2525-34. 2. Zafirova Z, O’Connor M. Hepatic encephalopathy: current management strategies and treatment, including management and monitoring of cerebral edema and intracranial hypertension in fulminant hepatic failure. Curr Opin Anaesthesiol 2010;23: 121-7. 3. Lee WM, Stravitz T, Larson AM. Introduction to the revised American Association for the Study of Liver Diseases position paper on acute liver failure 2011 (http://www.aasld.org/ practiceguidelines/Documents/AcuteLiverFailureUpdate2011.pdf). 4. Larson AM. Diagnosis and management of acute liver failure. Curr Opin Gastroenterol 2010;26:214-21. DOI: 10.1056/NEJMc1400974
make the diagnosis of this disorder difficult because of low serum globulin and IgG levels, the frequent absence of autoantibodies, and atypical histologic hallmarks (centrilobular necrosis or perivenulitis2 rather than interface hepatitis). A characteristic pattern of heterogeneous hepatic hypoattenuation on unenhanced computed tomography has been described recently3 in autoimmune acute liver failure, as compared with the diffuse hypoattenuation that is seen in viral acute liver failure. High-dose prednisolone is the firstline therapy,1 although the absence of improvement may be an indication for transplantation. In addition, complicated forms of malaria, typhoid, leptospirosis, rickettsial infection, dengue, and hepatic amoebiasis can cause jaundice with encephalopathy and mimic acute liver failure. However, specific antimicrobial agents improve survival to 75% without liver transplantation.4 Spiking fever, splenomegaly, mild elevations of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (
n e w e ng l a n d j o u r na l
of
m e dic i n e
Acute Liver Failure To the Editor: In their review article, Bernal and Wendon (Dec. 26 issue)1 state that lactulose is potentially dangerous in the treatment of acute liver failure. Although its side-effect profile may make it unacceptable for patients in whom liver transplantation is being contemplated, in resourcepoor settings where liver transplantation is not feasible, one has to fall back on other treatments. Lactulose is a first-line treatment to minimize the production and absorption of ammonia from the gut and is a well-established treatment for hepatic encephalopathy.2 The American Association for the Study of Liver Diseases recommends its use in the early stages of encephalopathy.3 Although the data are limited and not uniformly positive, lactulose can be used to treat early stages of encephalopathy, and it may help prolong survival.4 Bimal K. Agrawal, M.D. Maharishi Markandeshwar Institute of Medical Sciences and Research Mullana, India [email protected]
Usha Agrawal, M.D. National Institute of Pathology New Delhi, India No potential conflict of interest relevant to this letter was reported. 1. Bernal W, Wendon J. Acute liver failure. N Engl J Med 2013;
369:2525-34. 2. Zafirova Z, O’Connor M. Hepatic encephalopathy: current management strategies and treatment, including management and monitoring of cerebral edema and intracranial hypertension in fulminant hepatic failure. Curr Opin Anaesthesiol 2010;23: 121-7. 3. Lee WM, Stravitz T, Larson AM. Introduction to the revised American Association for the Study of Liver Diseases position paper on acute liver failure 2011 (http://www.aasld.org/ practiceguidelines/Documents/AcuteLiverFailureUpdate2011.pdf). 4. Larson AM. Diagnosis and management of acute liver failure. Curr Opin Gastroenterol 2010;26:214-21. DOI: 10.1056/NEJMc1400974
make the diagnosis of this disorder difficult because of low serum globulin and IgG levels, the frequent absence of autoantibodies, and atypical histologic hallmarks (centrilobular necrosis or perivenulitis2 rather than interface hepatitis). A characteristic pattern of heterogeneous hepatic hypoattenuation on unenhanced computed tomography has been described recently3 in autoimmune acute liver failure, as compared with the diffuse hypoattenuation that is seen in viral acute liver failure. High-dose prednisolone is the firstline therapy,1 although the absence of improvement may be an indication for transplantation. In addition, complicated forms of malaria, typhoid, leptospirosis, rickettsial infection, dengue, and hepatic amoebiasis can cause jaundice with encephalopathy and mimic acute liver failure. However, specific antimicrobial agents improve survival to 75% without liver transplantation.4 Spiking fever, splenomegaly, mild elevations of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (
