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Need for early thrombolysis in Budd-Chiari syndrome
CORRESPONDENCE
April 1988
difference was observed between the sucralfate healers and nonhealers in any of these methods, indicating that the observation that cigarette smoking affected cimetidine healing was unlikely to be a spurious finding. Furthermore, we adopted the conservative two-tailed approach for the p-value determination, instead of the one-sided approach, which was in fact justifiable in view of the known cigarette association with cimetidine and the known cigarette nonassociation with sucralfate, and which would have increased the p-value even further. We did not put up any strong claim for the association of alcohol and ulcer healing because only 3.5% of our patients used alcohol habitually whereas 30% of them used cigarettes for at least 5 yr. Based on these observations, we then went on, as we indicated in our paper, to compare the cimetidine and sucralfate healing with respect to both smoking and nonsmoking. We made two observations: (a) that there was a significant difference [p < 0.01) between the healing rates of smokers and nonsmokers in the cimetidine group but nil in the sucralfate group, and (b) that in smokers, but not in nonsmokers, cimetidine healing was significantly less (p < 0.05) than sucralfate healing. It was based on this multitude of observations on 283 patients [a number which was prospectively designed to allow meaningful analysis of healing factors), and not on the last observation as Dr. Shapowal et al. thought we did, that we conclude that smoking adversely affects duodenal ulcer healing by cimetidine but not so by sucralfate. We were careful not to make any claim that sucralfate healed smokers significantly better than cimetidine. as Dr. Shapowal et al. seemed to think we did. We fully agree that there is now a strong need to prestratify patients into smokers and nonsmokers for comparative studies between acid-reducing agents and cytoprotective agents in order to closely examine the fundamental difference of these two groups of agents with respect to cigarette smoking. S.K. LAM, M.D.
Deportment of Medicine University of Hong Kong Queen Mary Hospital Hong Kong 1.
Lam SK, Hui WM, Lau WY, et al. Sucralfate overcomes adverse effect of cigarette smoking on duodenal ulcer healing and prolongs subsequent remission. Gastroenterology 1987;92: 1193-201. 2. Lam SK. Prostaglandins for duodenal ulcer and gastric ulcer. J Gastroenterol Hepatol 1986;1:471-81. 3. Lam SK. The stomach. In: Gitnick G, ed. Current gastroenterology. Chicago: Year Book Medical Publishers, 1986:33-62.
Need for Early Thrombolysis Budd-Chiari Syndrome
in
Dear Sir: In the discussion of a recent article, Valla et al. (1) emphasized the need for noninvasive procedures that do not preclude the use of thrombolytic agents in Budd-Chiari syndrome. We observed a recent case that confirms this opinion. A 34-yr-old woman started taking oral contraceptives after her seventh pregnancy in January 1987. In July 1987 she had ascites. jaundice, and abdominal pain. Prominent esophageal varices were seen on upper endoscopy. In August 1987 she developed unilateral edema of the right inferior limb. Ultrasonography and computed tomography scan showed a large heterogeneous liver with a prominent Spiegel lobe and a partial thrombosis of the inferior vena cava. Thrombolytic therapy was begun with a dose
1109
of 250,000 U of streptokinase in bolus and 150,000 U/h in continuous infusion. Forty-eight hours later, streptokinase was discontinued and lys-plasminogen (100 pkat/2 h) was administered. Streptokinase was then used again at a dose of 160,000 U/h in continuous infusion during 48 h. Heparin sodium infusion was used concurrently. Jaundice, ascites. and esophageal varices disappeared within 1 wk. No predisposition factors except recent pregnancy and use of oral contraceptives were found. In this case, diagnosis was affirmed by noninvasive procedures (i.e., ultrasonography and computed tomography] that are correlated with invasive methods (2,3). These noninvasive methods allowed us to use streptokinase, which acts as a plasminogen activator. During thrombolysis, especially when liver insufficiency is present, a fall in pjasminogen level involving a decrease in streptokinase activity occurs (4). An increase in fibrinogen level and of euglobulin lysis time leads us to infuse lys-plasminogen (Substrene; lab. Choay, Paris, France]. To our knowledge this is the first case of Budd-Chiari syndrome treated with streptokinase and lys-pjasminogen. Several patients with Budd-Chiari syndrome have been treated with streptokinase alone (5); however, reports of follow-up examinations have been limited. Sholar and Bell (6) reported a follow-up of 2 yr for a patient and 5 yr for another one treated with fibrinolysis with a disparition of portal hypertension. Early thrombolysis may be an alternative to surgery in acute BuddChiari syndrome.
J.M. GUERIN P. MEYER Intensive Care Unit Hhpital LariboisiBre 2 Rue Amhroise Pare 75010 Paris, France 1. Valla D, Dhumeaux D, Babany G, et al. Hepatic vein thrombosis in paroxysmal nocturnal hemoglobinuria. Gastroenterology 1987;93:569-75. 2. Baert AL, Fevery J, Marchal G, et al. Early diagnosis of BuddChiari syndrome by computed tomography and ultrasonography: report of five cases. Gastroenterology 1983;84:587-95. 3. Gupta S, Barter S, Phillips GWL, Gibson RN, Hodgson HJF. Comparison of ultrasonography, computed tomography and ggmTc liver scan in diagnosis of Budd-Chiari syndrome. Gut 1987;28:242-7. 4. Sharma GVRK, Cella G, Parisi AF, Sasahara AA. Drug therapy: thrombolytic therapy. N Engl J Med 1982;306:1268-76. 5. Mitchell MC, Boitnott JK, Kaufman S, Camerpn JL, Maddrey WC. Budd-Chiari syndrome: etiology, diagnosis and management. Medicine 1982;61:199-218. 6. Sholar PW, Bell WR. Thrombolytic therapy for inferior vena cava thrombosis in paroxysmal nocturnal hemoglobinuria. Ann Intern Med 1985;103:539-41.
Chylous Ascites and Esophageal Sclerotherapy Dear Sir: The article by Knauer and Fogel reporting their cases of pericarditis complicating esophageal sclerotherapy piqued my interest (1). I have had the recent experience of discovering chyloqs ascites in a 62-yr-old man. His ascites was first evaluated 18 mo earlier and was found to be the typical transudate seen in cirrhosis. Cirrhosis was confirmed with a liver biopsy. Six months later, he bled from esophageal varices, and a course of sclerotherapy was begun.
Over
a 3-mo
period,
the varices
were
obliterated
using
a
April 1988
difference was observed between the sucralfate healers and nonhealers in any of these methods, indicating that the observation that cigarette smoking affected cimetidine healing was unlikely to be a spurious finding. Furthermore, we adopted the conservative two-tailed approach for the p-value determination, instead of the one-sided approach, which was in fact justifiable in view of the known cigarette association with cimetidine and the known cigarette nonassociation with sucralfate, and which would have increased the p-value even further. We did not put up any strong claim for the association of alcohol and ulcer healing because only 3.5% of our patients used alcohol habitually whereas 30% of them used cigarettes for at least 5 yr. Based on these observations, we then went on, as we indicated in our paper, to compare the cimetidine and sucralfate healing with respect to both smoking and nonsmoking. We made two observations: (a) that there was a significant difference [p < 0.01) between the healing rates of smokers and nonsmokers in the cimetidine group but nil in the sucralfate group, and (b) that in smokers, but not in nonsmokers, cimetidine healing was significantly less (p < 0.05) than sucralfate healing. It was based on this multitude of observations on 283 patients [a number which was prospectively designed to allow meaningful analysis of healing factors), and not on the last observation as Dr. Shapowal et al. thought we did, that we conclude that smoking adversely affects duodenal ulcer healing by cimetidine but not so by sucralfate. We were careful not to make any claim that sucralfate healed smokers significantly better than cimetidine. as Dr. Shapowal et al. seemed to think we did. We fully agree that there is now a strong need to prestratify patients into smokers and nonsmokers for comparative studies between acid-reducing agents and cytoprotective agents in order to closely examine the fundamental difference of these two groups of agents with respect to cigarette smoking. S.K. LAM, M.D.
Deportment of Medicine University of Hong Kong Queen Mary Hospital Hong Kong 1.
Lam SK, Hui WM, Lau WY, et al. Sucralfate overcomes adverse effect of cigarette smoking on duodenal ulcer healing and prolongs subsequent remission. Gastroenterology 1987;92: 1193-201. 2. Lam SK. Prostaglandins for duodenal ulcer and gastric ulcer. J Gastroenterol Hepatol 1986;1:471-81. 3. Lam SK. The stomach. In: Gitnick G, ed. Current gastroenterology. Chicago: Year Book Medical Publishers, 1986:33-62.
Need for Early Thrombolysis Budd-Chiari Syndrome
in
Dear Sir: In the discussion of a recent article, Valla et al. (1) emphasized the need for noninvasive procedures that do not preclude the use of thrombolytic agents in Budd-Chiari syndrome. We observed a recent case that confirms this opinion. A 34-yr-old woman started taking oral contraceptives after her seventh pregnancy in January 1987. In July 1987 she had ascites. jaundice, and abdominal pain. Prominent esophageal varices were seen on upper endoscopy. In August 1987 she developed unilateral edema of the right inferior limb. Ultrasonography and computed tomography scan showed a large heterogeneous liver with a prominent Spiegel lobe and a partial thrombosis of the inferior vena cava. Thrombolytic therapy was begun with a dose
1109
of 250,000 U of streptokinase in bolus and 150,000 U/h in continuous infusion. Forty-eight hours later, streptokinase was discontinued and lys-plasminogen (100 pkat/2 h) was administered. Streptokinase was then used again at a dose of 160,000 U/h in continuous infusion during 48 h. Heparin sodium infusion was used concurrently. Jaundice, ascites. and esophageal varices disappeared within 1 wk. No predisposition factors except recent pregnancy and use of oral contraceptives were found. In this case, diagnosis was affirmed by noninvasive procedures (i.e., ultrasonography and computed tomography] that are correlated with invasive methods (2,3). These noninvasive methods allowed us to use streptokinase, which acts as a plasminogen activator. During thrombolysis, especially when liver insufficiency is present, a fall in pjasminogen level involving a decrease in streptokinase activity occurs (4). An increase in fibrinogen level and of euglobulin lysis time leads us to infuse lys-plasminogen (Substrene; lab. Choay, Paris, France]. To our knowledge this is the first case of Budd-Chiari syndrome treated with streptokinase and lys-pjasminogen. Several patients with Budd-Chiari syndrome have been treated with streptokinase alone (5); however, reports of follow-up examinations have been limited. Sholar and Bell (6) reported a follow-up of 2 yr for a patient and 5 yr for another one treated with fibrinolysis with a disparition of portal hypertension. Early thrombolysis may be an alternative to surgery in acute BuddChiari syndrome.
J.M. GUERIN P. MEYER Intensive Care Unit Hhpital LariboisiBre 2 Rue Amhroise Pare 75010 Paris, France 1. Valla D, Dhumeaux D, Babany G, et al. Hepatic vein thrombosis in paroxysmal nocturnal hemoglobinuria. Gastroenterology 1987;93:569-75. 2. Baert AL, Fevery J, Marchal G, et al. Early diagnosis of BuddChiari syndrome by computed tomography and ultrasonography: report of five cases. Gastroenterology 1983;84:587-95. 3. Gupta S, Barter S, Phillips GWL, Gibson RN, Hodgson HJF. Comparison of ultrasonography, computed tomography and ggmTc liver scan in diagnosis of Budd-Chiari syndrome. Gut 1987;28:242-7. 4. Sharma GVRK, Cella G, Parisi AF, Sasahara AA. Drug therapy: thrombolytic therapy. N Engl J Med 1982;306:1268-76. 5. Mitchell MC, Boitnott JK, Kaufman S, Camerpn JL, Maddrey WC. Budd-Chiari syndrome: etiology, diagnosis and management. Medicine 1982;61:199-218. 6. Sholar PW, Bell WR. Thrombolytic therapy for inferior vena cava thrombosis in paroxysmal nocturnal hemoglobinuria. Ann Intern Med 1985;103:539-41.
Chylous Ascites and Esophageal Sclerotherapy Dear Sir: The article by Knauer and Fogel reporting their cases of pericarditis complicating esophageal sclerotherapy piqued my interest (1). I have had the recent experience of discovering chyloqs ascites in a 62-yr-old man. His ascites was first evaluated 18 mo earlier and was found to be the typical transudate seen in cirrhosis. Cirrhosis was confirmed with a liver biopsy. Six months later, he bled from esophageal varices, and a course of sclerotherapy was begun.
Over
a 3-mo
period,
the varices
were
obliterated
using
a