LETTERS TO THE EDIT(
25O The authors gratefully thank the nursing staff of the Clinical Investigation Unit and of the Angiography Department.
Gilles A. Morali, Kenneth W. Sniderman, Kevin 1 Deitel, Sheldon Tobe, Helga Witt-Sullivan, Mal Simon, Jenny Heathcote and Laurence M. Blendis Departments of Medicine and Radiology. Toronto, Canada
References 1 Campbell P, Greig PD, Cranford J, Langer B, Silverman M, Blendis LM. A comparison of acute reversiblepre- and postsinusoidal portal hypertension on salt and water retention in the dog. Hepatology 1982; 2: 54-8. 2 UnikowskyB, Wexler MJ, Levy M. Dogs with experimentalcirrhosis
The Toronto HospiA
of the liver but without intrahepatic portal hypertension do n retain sodium or form ascites. J Clin Invest 1983; 72:1594-1604 3 Rector WG. Portal hypertension: a permissive factor only in 1 development of ascites and variceal bleeding. Liver 1986; 6: 2214 Bosch J, Arroyo V, Betriu A, et al. Hepatic hemodynamicsand 1 renin-angiotensine-aldosterone system in cirrhosis. Gastroenter ogy 1980; 78: 92-9.
HEPAT 01281
DNA ploidy in hepatocellular carcinoma Although DNA ploidy is generally an independent predictor of prognosis in various cancers; the prognosis of D N A diploid tumors being better than that of D N A aneuploid tumors, its value is controversial for hepatocellular carcinoma (HCC) as shown in the Leader by Dr. Feldmann in this issue (1). We have also compared clinicopathologic details between diploid and aneuploid HCCs after hepatic resection (2). D N A ploidy did not show any correlation with age, sex, alcohol abuse, hepatitis B virus, serum ct-fetoprotein level or underlying liver disease. Histopathologically, the incidence of H C C smaller than 2 cm in diameter tended to be higher in the diploid group, but no difference was seen for tumors larger than 5 cm. The grade of tumor differentiation also tended to be higher in this group of small HCC. The ploidy pattern did not influence the rate of capsule or daughter nodule formation, or venous invasion. There were no significant differences in survival rate or in the incidence and time of intrahepatic tumor recurrence between patients with diploid H C C and those with aneuploid tumor. The patients in our study were rather selected; recur-
rent HCCs were compared with their primary tume only in patients who had undergone a second hepal resection. With regard to synchronous HCCs, appare intrahepatic metastases were not included. We compar~ the ploidy pattern of two synchronous H C C nodul which were uncertain if they were of m o n o c e n t r i c multicentric origin. Such patient selection would ha made some difference in the disagreement rate of DN ploidy from that in the study by Kuo et al (3). Th, found different ploidy in 29% (4/14) of synchrono multiple H C C s and in one of 3 recurrent H C C s fro their primary tumors. They also observed a differe D N A distribution in 12% (2/17) of different parts of t] same H C C nodule. We have studied the ploidy patte: between nodules in the same nodule of HCC, and h a found no heterogeneity in 22 untreated HCCs of vario~ sizes. We, therefore believe at present that D N A ploic is a reliable method to determine the clonal origin HCC.
References
diploid and aneuploid hepatocellular carcinomas: a flow cytometl study. Br J Surg (in press). 3 Kuo S-H, Sheu J-C, Chen D-S, et al. DNA clonal heterogeneity hepatocellular carcinoma demonstrated by Feulgen-DNA analys Liver 1987; 7. 359-63.
1 Feldmann G. Liver ploidy. J Hepatol 1992; 16: 7-10. 2 Nagasue N, Yamanoi A, Takemoto Y, et al. Comparison between
Naofumi Nagasue Second Department of Surgery, Shimane Medical University, lzumo 6~ Japan
25O The authors gratefully thank the nursing staff of the Clinical Investigation Unit and of the Angiography Department.
Gilles A. Morali, Kenneth W. Sniderman, Kevin 1 Deitel, Sheldon Tobe, Helga Witt-Sullivan, Mal Simon, Jenny Heathcote and Laurence M. Blendis Departments of Medicine and Radiology. Toronto, Canada
References 1 Campbell P, Greig PD, Cranford J, Langer B, Silverman M, Blendis LM. A comparison of acute reversiblepre- and postsinusoidal portal hypertension on salt and water retention in the dog. Hepatology 1982; 2: 54-8. 2 UnikowskyB, Wexler MJ, Levy M. Dogs with experimentalcirrhosis
The Toronto HospiA
of the liver but without intrahepatic portal hypertension do n retain sodium or form ascites. J Clin Invest 1983; 72:1594-1604 3 Rector WG. Portal hypertension: a permissive factor only in 1 development of ascites and variceal bleeding. Liver 1986; 6: 2214 Bosch J, Arroyo V, Betriu A, et al. Hepatic hemodynamicsand 1 renin-angiotensine-aldosterone system in cirrhosis. Gastroenter ogy 1980; 78: 92-9.
HEPAT 01281
DNA ploidy in hepatocellular carcinoma Although DNA ploidy is generally an independent predictor of prognosis in various cancers; the prognosis of D N A diploid tumors being better than that of D N A aneuploid tumors, its value is controversial for hepatocellular carcinoma (HCC) as shown in the Leader by Dr. Feldmann in this issue (1). We have also compared clinicopathologic details between diploid and aneuploid HCCs after hepatic resection (2). D N A ploidy did not show any correlation with age, sex, alcohol abuse, hepatitis B virus, serum ct-fetoprotein level or underlying liver disease. Histopathologically, the incidence of H C C smaller than 2 cm in diameter tended to be higher in the diploid group, but no difference was seen for tumors larger than 5 cm. The grade of tumor differentiation also tended to be higher in this group of small HCC. The ploidy pattern did not influence the rate of capsule or daughter nodule formation, or venous invasion. There were no significant differences in survival rate or in the incidence and time of intrahepatic tumor recurrence between patients with diploid H C C and those with aneuploid tumor. The patients in our study were rather selected; recur-
rent HCCs were compared with their primary tume only in patients who had undergone a second hepal resection. With regard to synchronous HCCs, appare intrahepatic metastases were not included. We compar~ the ploidy pattern of two synchronous H C C nodul which were uncertain if they were of m o n o c e n t r i c multicentric origin. Such patient selection would ha made some difference in the disagreement rate of DN ploidy from that in the study by Kuo et al (3). Th, found different ploidy in 29% (4/14) of synchrono multiple H C C s and in one of 3 recurrent H C C s fro their primary tumors. They also observed a differe D N A distribution in 12% (2/17) of different parts of t] same H C C nodule. We have studied the ploidy patte: between nodules in the same nodule of HCC, and h a found no heterogeneity in 22 untreated HCCs of vario~ sizes. We, therefore believe at present that D N A ploic is a reliable method to determine the clonal origin HCC.
References
diploid and aneuploid hepatocellular carcinomas: a flow cytometl study. Br J Surg (in press). 3 Kuo S-H, Sheu J-C, Chen D-S, et al. DNA clonal heterogeneity hepatocellular carcinoma demonstrated by Feulgen-DNA analys Liver 1987; 7. 359-63.
1 Feldmann G. Liver ploidy. J Hepatol 1992; 16: 7-10. 2 Nagasue N, Yamanoi A, Takemoto Y, et al. Comparison between
Naofumi Nagasue Second Department of Surgery, Shimane Medical University, lzumo 6~ Japan
