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The Role of Hepatic Venous Pressure Gradient in Hepatitis C Virus Compensated Cirrhosis
2076
CORRESPONDENCE
Second, although the treatment implication of our results is that a decrease in abdominal circumference (presumably through weight loss) may decrease the risk of Barrett’s esophagus, this hypothesis is unproven. Unfortunately, vigorous antireflux treatments, including surgery, have not been proven to decrease the risk of Barrett’s esophagus, much less the risk of esophageal adenocarcinoma (the clinically significant endpoint), although they may result in improved health and well-being for other disorders (including GERD symptoms).3–5 We echo Dr Sugerman’s call for trials that evaluate the effects of weight loss, and its effects on GERD physiology, Barrett’s esophagus, and esophageal adenocarcinoma. Until then, maintenance of an ideal weight can certainly be recommended regardless for its other health benefits. DOUGLAS A. CORLEY Division of Research Kaiser Permanente Oakland, California 1. Corley DA, Kubo A, Levin TR, et al. Abdominal obesity and body mass index as risk factors for Barrett’s esophagus. Gastroenterology 2007;133:34 – 41. 2. Edelstein ZR, Farrow DC, Bronner MP, et al. Central adiposity and risk of Barrett’s esophagus. Gastroenterology 2007;133:403– 411. 3. Ortiz A, Martinez de Haro LF, Parrilla P, et al. Conservative treatment versus antireflux surgery in Barrett’s oesophagus: long-term results of a prospective study. Br J Surg 1996;83:274 –278. 4. Parrilla P, Martinez de Haro LF, Ortiz A, et al. Long-term results of a randomized prospective study comparing medical and surgical treatment of Barrett’s esophagus. Ann Surg 2003;237:291–298. 5. Spechler SJ, Lee E, Ahnen D, et al. Long-term outcome of medical and surgical therapies for gastroesophageal reflux disease: follow-up of a randomized controlled trial. JAMA 2001;285:2331–2338. doi:10.1053/j.gastro.2007.10.018
The Role of Hepatic Venous Pressure Gradient in Hepatitis C Virus Compensated Cirrhosis Dear Sir:
In a prospective cohort study of 213 patients with compensated cirrhosis and portal hypertension but no esophageal varices, Ripoll et al1 suggest baseline hepatic venous pressure gradient (HVPG) to be the most important predictor of clinical decompensation. Sixty-two patients clinically decompensated during follow-up, including 7 with hepato-
GASTROENTEROLOGY Vol. 133, No. 6
cellular carcinoma (HCC), and an additional 12 patients developed HCC without decompensating but subsequently required orthotopic liver transplantation. Overall, 19 of 74 (26%) patients with ⱖ1 liver-related event developed an HCC, whereas only 7 of 62 (11%) patients clinically decompensated in the presence of an HCC. In the latter group, it is not clear whether HCC was the cause of clinical decompensation. In Ripoll et al’s study, the overall rates of HCC development and clinical decompensation in the presence of HCC are surprisingly low (⬍10%). HCC in fact is known to be the first and most frequent complication in HCVcompensated cirrhotics; up to 35% of patients decompensate after development of HCC.2–5 The low rates of HCC in cirrhotics in the Ripoll et al study contrast with the high rates (63%) of transplanted patients for an HCC, which are much higher than those (7%–13%) reported by others.2,5 We acknowledge the clinical relevance of HVPG as a predictor of decompensation in cirrhotics, but would like to see the predictive value of HVPG also investigated in a patient series where HCC represents the first complication to develop and access to liver transplantation is limited. MAURO VIGANÒ ALESSIO AGHEMO MASSIMO IAVARONE Division of Gastroenterology IRCCS Fondazione Policlinico Ospedale Maggiore Mangiagalli e Regina Elena University of Milan Milan, Italy 1. Ripoll C, Groszmann RJ, Garcia-Tsao G, et al. Hepatic venous pressure gradient predicts clinical decompensation in patients with compensated cirrhosis. Gastroenterology 2007;133:481– 488. 2. Sangiovanni A, Prati GM, Fasani P, et al. The natural history of compensated cirrhosis due to hepatitis C virus: a 17-year cohort study of 214 patients. Hepatology 2006;43:1303–1310. 3. Benvegnù L, Gios M, Boccato S, et al. Natural history of compensated viral cirrhosis: a prospective study on the incidence and hierarchy of major complications. Gut 2004;53:744 –749. 4. Sangiovanni A, Del Ninno E, Fasani P, et al. Increased survival of cirrhotic patients with a hepatocellular carcinoma detected during surveillance. Gastroenterology 2004;126:1005–1014. 5. Viganò M, Aghemo A, Iavarone M, et al. Increased survival of patients with HCV related cirrhosis with long-term response to interferon therapy [abstract 598]. Hepatology 2005;42(Suppl 1):432A. doi:10.1053/j.gastro.2007.10.021
CORRESPONDENCE
Second, although the treatment implication of our results is that a decrease in abdominal circumference (presumably through weight loss) may decrease the risk of Barrett’s esophagus, this hypothesis is unproven. Unfortunately, vigorous antireflux treatments, including surgery, have not been proven to decrease the risk of Barrett’s esophagus, much less the risk of esophageal adenocarcinoma (the clinically significant endpoint), although they may result in improved health and well-being for other disorders (including GERD symptoms).3–5 We echo Dr Sugerman’s call for trials that evaluate the effects of weight loss, and its effects on GERD physiology, Barrett’s esophagus, and esophageal adenocarcinoma. Until then, maintenance of an ideal weight can certainly be recommended regardless for its other health benefits. DOUGLAS A. CORLEY Division of Research Kaiser Permanente Oakland, California 1. Corley DA, Kubo A, Levin TR, et al. Abdominal obesity and body mass index as risk factors for Barrett’s esophagus. Gastroenterology 2007;133:34 – 41. 2. Edelstein ZR, Farrow DC, Bronner MP, et al. Central adiposity and risk of Barrett’s esophagus. Gastroenterology 2007;133:403– 411. 3. Ortiz A, Martinez de Haro LF, Parrilla P, et al. Conservative treatment versus antireflux surgery in Barrett’s oesophagus: long-term results of a prospective study. Br J Surg 1996;83:274 –278. 4. Parrilla P, Martinez de Haro LF, Ortiz A, et al. Long-term results of a randomized prospective study comparing medical and surgical treatment of Barrett’s esophagus. Ann Surg 2003;237:291–298. 5. Spechler SJ, Lee E, Ahnen D, et al. Long-term outcome of medical and surgical therapies for gastroesophageal reflux disease: follow-up of a randomized controlled trial. JAMA 2001;285:2331–2338. doi:10.1053/j.gastro.2007.10.018
The Role of Hepatic Venous Pressure Gradient in Hepatitis C Virus Compensated Cirrhosis Dear Sir:
In a prospective cohort study of 213 patients with compensated cirrhosis and portal hypertension but no esophageal varices, Ripoll et al1 suggest baseline hepatic venous pressure gradient (HVPG) to be the most important predictor of clinical decompensation. Sixty-two patients clinically decompensated during follow-up, including 7 with hepato-
GASTROENTEROLOGY Vol. 133, No. 6
cellular carcinoma (HCC), and an additional 12 patients developed HCC without decompensating but subsequently required orthotopic liver transplantation. Overall, 19 of 74 (26%) patients with ⱖ1 liver-related event developed an HCC, whereas only 7 of 62 (11%) patients clinically decompensated in the presence of an HCC. In the latter group, it is not clear whether HCC was the cause of clinical decompensation. In Ripoll et al’s study, the overall rates of HCC development and clinical decompensation in the presence of HCC are surprisingly low (⬍10%). HCC in fact is known to be the first and most frequent complication in HCVcompensated cirrhotics; up to 35% of patients decompensate after development of HCC.2–5 The low rates of HCC in cirrhotics in the Ripoll et al study contrast with the high rates (63%) of transplanted patients for an HCC, which are much higher than those (7%–13%) reported by others.2,5 We acknowledge the clinical relevance of HVPG as a predictor of decompensation in cirrhotics, but would like to see the predictive value of HVPG also investigated in a patient series where HCC represents the first complication to develop and access to liver transplantation is limited. MAURO VIGANÒ ALESSIO AGHEMO MASSIMO IAVARONE Division of Gastroenterology IRCCS Fondazione Policlinico Ospedale Maggiore Mangiagalli e Regina Elena University of Milan Milan, Italy 1. Ripoll C, Groszmann RJ, Garcia-Tsao G, et al. Hepatic venous pressure gradient predicts clinical decompensation in patients with compensated cirrhosis. Gastroenterology 2007;133:481– 488. 2. Sangiovanni A, Prati GM, Fasani P, et al. The natural history of compensated cirrhosis due to hepatitis C virus: a 17-year cohort study of 214 patients. Hepatology 2006;43:1303–1310. 3. Benvegnù L, Gios M, Boccato S, et al. Natural history of compensated viral cirrhosis: a prospective study on the incidence and hierarchy of major complications. Gut 2004;53:744 –749. 4. Sangiovanni A, Del Ninno E, Fasani P, et al. Increased survival of cirrhotic patients with a hepatocellular carcinoma detected during surveillance. Gastroenterology 2004;126:1005–1014. 5. Viganò M, Aghemo A, Iavarone M, et al. Increased survival of patients with HCV related cirrhosis with long-term response to interferon therapy [abstract 598]. Hepatology 2005;42(Suppl 1):432A. doi:10.1053/j.gastro.2007.10.021