1990
CORRESPONDENCE
no clinical symptoms. This can also be observed in the vast majority of patients treated with endoscopic sphincterotomy or surgical anastomosis of the common bile duct with the duodenum or jejunum, who sometimes have chronic aerobilia without clinical symptoms.4.5 Along this line, the sphincter of Oddi hypomotility described could be characterized as a functional incompetence of the sphincter. As in patients with a structural incompetence of the sphincter of Oddi, in patients treated with EPT, no typical clinical symptoms should be caused by the aerobilia. HANS-DIETERALLESCHER,M.D. Department ofInternal Medicine II Technical University ofMunich Isamningerstraje 22 8000 Munich, Germany 1. Staritz M. Pharmacology
2.
3. 4.
5.
of the sphincter of Oddi. Endoscopy 1988;20:171-174. Fox-Threlkeld JET, Manaka H, Manaka Y, Cipris S, Daniel EE. Stimulation of circular muscle motility of the isolated perfused canine ileum: relationship to VIP output. Peptides, 1991; 12:1039-1045. Kyosola K. Structure and innervation of the choledocho-duodenal junction. Ann Chir Gynecol 1976;65(Suppl 192):1-136. Burmeister W, Wurbs D, Hagenmtiller F, Classen M. Langzeituntersuchungen nach endoskopischer Papillotomie (EPT). Z Gastroenterol 1989;18:527-532. Whistanley PA, Ellis WR, Hamilton I, Lintott DJ, Axon ATR. Medium term complications of endoscopic biliary sphincterotomy. Gut 1980;26:730-735,
Determinants of Portal Hypertensive Gastropathy Reconsidered Dear Sir: We have read with interest the paper by Sarin et al.,’ who analyzed the factors influencing the development of portal hypertensive gastropathy (PGP) in patients with portal hypertension due to cirrhosis, noncirrhotic portal fibrosis (NCPF), and extrahepatic portal vein obstruction (EPVO). The development of PGP is significantly influenced by sclerotherapy, severity of liver disease, and etiology of portal hypertension. However, we have a few objections to these conclusions. The authors conclude that sclerotherapy led to an increased incidence of PGP. However, in the absence of data regarding the progression of Child’s status in patients with cirrhosis over the follow-up period of 23.2 + 3.4 months (range, l-52 months), such a conclusion underestimates the contribution of severity of liver disease in the development of PGP in patients with cirrhosis. While classifying the patients into different Child’s grades, the authors have included NCPF and EHPVO patients in Child’s group A despite their own observation that the incidence of PGP differs in different etiologlcal groups of portal hypertension. This led to their conclusion that only 13% of patients with Child’s A disease had PGP compared with 87% of patients with Child’s C disease. If NCPF and EHPVO patients are excluded, 6 of 11 patients (45%) with Child’s A disease had PGP, a proportion much higher than what has been reported. The etiology rather than the degree of portal hypertension as reflected by intravariceal pressure measurement has been stressed as one of the important determinants of development of PGP. Controversy exists whether intravariceal pressure truly reflects portal pressure.* Even in the study quoted by the authors,3 there was no correlation between intravariceal pressure and wedged hepatic and intrahepatic pressures in patients with NCPF. To our knowledge, no data are available in patients with EHPVO. Moreover, intravariceal pressure was measured only in 37 patients with portal hypertension of different etiology, and to
GASTROENTEROLOGY Vol. 103,No. 6
extrapolate these data to all patients with portal hypertension may not be appropriate. Thus, there is insufficient evidence to conclude that the differences in prevalence of PGP in different etiologic groups of portal hypertension is not due to different degrees of portal pressure. ANANYA DAS, M.D. UDAY CH. GHOSHAL, M.D.,D.N.B.E. Department of Gastroenterology Sanjay Gandhi Post Graduate Institute of Medical Sciences Lucknow, India Sarin SK, Sreenivas D, Lohoti D, Saraya A. Factors influencing development of portal hypertensive gastropathy in patients with portal hypertension. Gastroenterology 1992;102:994-999. Bosch J, Bordas JM, Rigau J, et al. Noninvasive measurement of pressure of oesophageal varices using an endoscopic gauge: comparison with measurement by variceal puncture in patients undergoing endoscopic sclerotherapy. Hepatology 1986;6:667. Sarin SK, Sethi KK, Nanda R. Measurement and correlation of wedged hepatic, intrahepatic, intrasplenic and intravariceal pressures in patients with cirrhosis of liver and non-cirrhotic portal fibrosis. Gut 1987;28:260-266.
Reply. We appreciate the interest in our work shown by Drs. Das and Ghoshal. The strength of our study lies in the inclusion of patients with cirrhosis, NCPF, and EHPVO. It has been shown by several workers, including us, that unlike in cirrhosis, liver disease is nonprogressive in NCPF and EHPVO.‘,’ We do not deny the role of severity of liver disease in causing PGP. However, by including patients with NCPF and EHPVO, we are able to exclude the influence of severity of liver disease and study the role of other factors that could affect the development of PGP. The Child’s status of patients with NCPF and EHPVO is unlikely to alter during the follow-up period. Although none of these patients had PGP before sclerotherapy, after sclerotherapy several patients with NCPF (8.7%) and EHPVO (16.7%)developed PGP. This observation clearly shows that sclerotherapy strongly influences the development of PGP. In Table 2 in our paper, we have clearly given the presclerotherapy and postsclerotherapy prevalence of PGP in patients with cirrhosis, NCPF, and EHPVO without clubbing them together into Child’s grades. Nevertheless, it is perfectly justified to include patients with NCPF and EHPVO along with those with Child’s A cirrhosis because liver functions are preserved or minimally impaired in all three groups’s3 The calculations performed by Drs. Das and Ghoshal do not appear to be correct. It is clearly shown in our Table 2 that only 3 of the 11 patients (27%)with cirrhosis (and not 6 of the 11, as calculated by these workers) had postsclerotherapy PGP. The prevalence figure of 45% calculated by them is therefore wrong. We do not agree with Drs. Das and Ghoshal that there is insufficient evidence to conclude that differences in the prevalence of PGP are not due to the etiology of portal hypertension. One of the important observation of our study was that while the intravariteal pressure (IVP) is comparable between the three study groups, the prevalence of PGP is much higher in patients with cirrhosis. It has been shown by several investigators, including our group, that intravariceal pressure closely correlates with postsinusoidal wedged hepatic venous pressure (WHVP), which in turn reliably reflects the portal pressure in patients with alcoholic cirrhosis4-’ In patients with presinusoidal (EHPVO) and presinusoidal and perisinusoidal portal hypertension (NCPF), WHVP, and intrahepatic pressure are bound to be lower than the portal pressure. In fact, we have shown the existence of two hemodynamic gradients (intrasplenic to intrahepatic and intrahepatic to WHVP) in pa-
CORRESPONDENCE
no clinical symptoms. This can also be observed in the vast majority of patients treated with endoscopic sphincterotomy or surgical anastomosis of the common bile duct with the duodenum or jejunum, who sometimes have chronic aerobilia without clinical symptoms.4.5 Along this line, the sphincter of Oddi hypomotility described could be characterized as a functional incompetence of the sphincter. As in patients with a structural incompetence of the sphincter of Oddi, in patients treated with EPT, no typical clinical symptoms should be caused by the aerobilia. HANS-DIETERALLESCHER,M.D. Department ofInternal Medicine II Technical University ofMunich Isamningerstraje 22 8000 Munich, Germany 1. Staritz M. Pharmacology
2.
3. 4.
5.
of the sphincter of Oddi. Endoscopy 1988;20:171-174. Fox-Threlkeld JET, Manaka H, Manaka Y, Cipris S, Daniel EE. Stimulation of circular muscle motility of the isolated perfused canine ileum: relationship to VIP output. Peptides, 1991; 12:1039-1045. Kyosola K. Structure and innervation of the choledocho-duodenal junction. Ann Chir Gynecol 1976;65(Suppl 192):1-136. Burmeister W, Wurbs D, Hagenmtiller F, Classen M. Langzeituntersuchungen nach endoskopischer Papillotomie (EPT). Z Gastroenterol 1989;18:527-532. Whistanley PA, Ellis WR, Hamilton I, Lintott DJ, Axon ATR. Medium term complications of endoscopic biliary sphincterotomy. Gut 1980;26:730-735,
Determinants of Portal Hypertensive Gastropathy Reconsidered Dear Sir: We have read with interest the paper by Sarin et al.,’ who analyzed the factors influencing the development of portal hypertensive gastropathy (PGP) in patients with portal hypertension due to cirrhosis, noncirrhotic portal fibrosis (NCPF), and extrahepatic portal vein obstruction (EPVO). The development of PGP is significantly influenced by sclerotherapy, severity of liver disease, and etiology of portal hypertension. However, we have a few objections to these conclusions. The authors conclude that sclerotherapy led to an increased incidence of PGP. However, in the absence of data regarding the progression of Child’s status in patients with cirrhosis over the follow-up period of 23.2 + 3.4 months (range, l-52 months), such a conclusion underestimates the contribution of severity of liver disease in the development of PGP in patients with cirrhosis. While classifying the patients into different Child’s grades, the authors have included NCPF and EHPVO patients in Child’s group A despite their own observation that the incidence of PGP differs in different etiologlcal groups of portal hypertension. This led to their conclusion that only 13% of patients with Child’s A disease had PGP compared with 87% of patients with Child’s C disease. If NCPF and EHPVO patients are excluded, 6 of 11 patients (45%) with Child’s A disease had PGP, a proportion much higher than what has been reported. The etiology rather than the degree of portal hypertension as reflected by intravariceal pressure measurement has been stressed as one of the important determinants of development of PGP. Controversy exists whether intravariceal pressure truly reflects portal pressure.* Even in the study quoted by the authors,3 there was no correlation between intravariceal pressure and wedged hepatic and intrahepatic pressures in patients with NCPF. To our knowledge, no data are available in patients with EHPVO. Moreover, intravariceal pressure was measured only in 37 patients with portal hypertension of different etiology, and to
GASTROENTEROLOGY Vol. 103,No. 6
extrapolate these data to all patients with portal hypertension may not be appropriate. Thus, there is insufficient evidence to conclude that the differences in prevalence of PGP in different etiologic groups of portal hypertension is not due to different degrees of portal pressure. ANANYA DAS, M.D. UDAY CH. GHOSHAL, M.D.,D.N.B.E. Department of Gastroenterology Sanjay Gandhi Post Graduate Institute of Medical Sciences Lucknow, India Sarin SK, Sreenivas D, Lohoti D, Saraya A. Factors influencing development of portal hypertensive gastropathy in patients with portal hypertension. Gastroenterology 1992;102:994-999. Bosch J, Bordas JM, Rigau J, et al. Noninvasive measurement of pressure of oesophageal varices using an endoscopic gauge: comparison with measurement by variceal puncture in patients undergoing endoscopic sclerotherapy. Hepatology 1986;6:667. Sarin SK, Sethi KK, Nanda R. Measurement and correlation of wedged hepatic, intrahepatic, intrasplenic and intravariceal pressures in patients with cirrhosis of liver and non-cirrhotic portal fibrosis. Gut 1987;28:260-266.
Reply. We appreciate the interest in our work shown by Drs. Das and Ghoshal. The strength of our study lies in the inclusion of patients with cirrhosis, NCPF, and EHPVO. It has been shown by several workers, including us, that unlike in cirrhosis, liver disease is nonprogressive in NCPF and EHPVO.‘,’ We do not deny the role of severity of liver disease in causing PGP. However, by including patients with NCPF and EHPVO, we are able to exclude the influence of severity of liver disease and study the role of other factors that could affect the development of PGP. The Child’s status of patients with NCPF and EHPVO is unlikely to alter during the follow-up period. Although none of these patients had PGP before sclerotherapy, after sclerotherapy several patients with NCPF (8.7%) and EHPVO (16.7%)developed PGP. This observation clearly shows that sclerotherapy strongly influences the development of PGP. In Table 2 in our paper, we have clearly given the presclerotherapy and postsclerotherapy prevalence of PGP in patients with cirrhosis, NCPF, and EHPVO without clubbing them together into Child’s grades. Nevertheless, it is perfectly justified to include patients with NCPF and EHPVO along with those with Child’s A cirrhosis because liver functions are preserved or minimally impaired in all three groups’s3 The calculations performed by Drs. Das and Ghoshal do not appear to be correct. It is clearly shown in our Table 2 that only 3 of the 11 patients (27%)with cirrhosis (and not 6 of the 11, as calculated by these workers) had postsclerotherapy PGP. The prevalence figure of 45% calculated by them is therefore wrong. We do not agree with Drs. Das and Ghoshal that there is insufficient evidence to conclude that differences in the prevalence of PGP are not due to the etiology of portal hypertension. One of the important observation of our study was that while the intravariteal pressure (IVP) is comparable between the three study groups, the prevalence of PGP is much higher in patients with cirrhosis. It has been shown by several investigators, including our group, that intravariceal pressure closely correlates with postsinusoidal wedged hepatic venous pressure (WHVP), which in turn reliably reflects the portal pressure in patients with alcoholic cirrhosis4-’ In patients with presinusoidal (EHPVO) and presinusoidal and perisinusoidal portal hypertension (NCPF), WHVP, and intrahepatic pressure are bound to be lower than the portal pressure. In fact, we have shown the existence of two hemodynamic gradients (intrasplenic to intrahepatic and intrahepatic to WHVP) in pa-
