668
CORRESPONDENCE
CASTROENTEROLOGY
7. Gillen
8. 9.
10.
11. 12.
13.
P, Peel ALG. Failure to improve survival by improved diagnostic techniques in patients with malignant jaundice. Br J Surg 1986; 73:631-3. Sarr MG, Cameron JC. Surgical management of unresectable cancer of the pancreas. Surgery 1982;91:123-33. Leung JWC, Emery R, Cotton PB, Russell RCG, Vallon AG, Mason RR. Management of malignant obstructive jaundice at The Middlesex Hospital. Br J Surg 1983;75:84-6. Huibregtse K, Tytgat GNJ. Endoscopic placement of biliary prostheses. In: Salmon PR, ed. Gastrointestinal endoscopy. Advances in diagnosis and therapy. London: Chapman and Hall, 1984:219-31. Cotton PB. Endoscopic methods for relief of malignant obstructive jaundice. World J Surg 1984;8:854-61. Speer AG, Cotton PB, Dineen LP, Ahearn RP. Endoscopic biliary prosthesis in 102 poor risk patients with carcinoma of the pancreas. Gut 1986;27:A1278-9. Speer AG, Cotton PB, Hatfield ARW, et al. Randomized trial comparing endoscopic and percutaneous prostheses in poor risk patients with malignant obstructive jaundice. Gut 1985: 26:A1135.
Cirrhosis
in Graft-Versus-Host
Disease
Dear Sir: A. B. Knapp and colleagues recently described a patient with chronic graft-versus-host disease who subsequently developed cirrhosis (1). The patient was also noted to have esophageal varices. They claimed that similar cases have not been reported previously. We did report a patient with chronic graft-versus-host disease who developed micronodular cirrhosis 42 mo after an allogeneic bone marrow transplantation (2). Our patient also had stable indices of liver function tests and esophageal varices before he died of bacterial meningitis. Both cases demonstrate that liver involvement in chronic graft-versus-host disease may progress to cirrhosis with portal hypertension and esophageal varices. JONATHAN C. YALJ, M.D., F.R.C.P.(C) #309 zz Sir Winston St. Albert, Alberta Canada T8N 184
Churchill
Avenue
AXEL R. ZANDER, M.D.
Department of Bone Marrow Transplantation Pacific Presbyterian Medical Center P.O. Box 7999 San Francisco, California 94129 1. Knapp
AB, Crawford JM, Rappeport JM, Gollan JL. Cirrhosis as a consequence of graft-versus-host disease. Gastroenterology 1987;92:513-9. 2. Yau JC, Zander AR, Srigley JR, et al. Chronic graft-versus-host disease complicated by micronodular cirrhosis and esophageal varices. Transplantation 1986;41:129-30.
Treatment Rationale
of Biliary Ascariasis
and Its
Dear Sir: We read with interest the case report describing a patient with biliary ascariasis that was published in GASTROENTEROLOGY (1). In this paper the authors have recommended instillation of piperazine citrate directly into the biliary tract through a nasobiliary drainage catheter as a logical therapy for this disease.
Vol. 93. No. 3
We, however, felt that the administration of an anthelmintic agent into the biliary tree cannot be advocated as treatment for biliary ascariasis in view of the following facts: (a) The paralysis or death of a worm occurring spontaneously or caused by piperazine citrate inside the biliary tract is highly undesirable as a dead worm often fails to move out of the biliary tract into the duodenum. The trapped dead worm will become fragmented and act as a nidus for stone formation (2-5). Hence, even the anthelmintic agents with enterohepatic circulation will be hazardous in this disease. (b) We have shown that live roundworms, being agile and motile, in the majority of cases migrate out of the biliary tree into the intestines within a period of a few hours to 2 wk and are then amenable to anthelmintic therapy there (2). Hence, rational treatment for biliary ascariasis is to treat cholangitis by conservative means and effect the paralysis of worms in the intestines by oral administration of anthelmintic agents. from whence they will be expelled by effective peristaltic activity of the intestines. The treatment (mebendazole 100 mg b.i.d., Janssen Pharmaceutical Co., Piscataway, N.J.) may have to be continued for up to 2 wk while monitoring the spontaneous exit of worms from the bile ducts by ultrasonography. In an endemic zone, reinvasion of the biliary tree can be prevented by keeping the intestines free of worms by advising the patient to take effective anthelmintic treatment every 8 wk. Surgery is indicated only if (a] worms continue to persist inside the biliary tree for >l mo, as by that time they are likely to die and thus be unable to migrate out of the biliary tree, (b) the biliary tree contains dead worms, or (c) worms inside the biliary tract coexist with stones. SI IOWKAT AL1 ZARGAR MOHAMMAD
SULTAN KHUROO
Department of Gastroenterology Sher-i-Kashmir Institute of Medical Srinagar Kashmir India
Sciences
Kamath PS. Joseph DC, Chundran R, Rama Rao SR. Sri Prakash ML, D’Cruz AJ. Biliary ascariasis: ultrasonography, endoscopic retrograde cholangiopancreatography, and biliary drainage. Gastroenterology 1986;91:730-2. Khurro MS, Zargar SA. Biliary ascariasis: a common cause of biliary and pancreatic disease in an endemic area. Gastroenterology 1985;88:418-23. Teoh TB. A study of gallstones and included worms in recurrent pyogenic cholangitis. J Path01 Bacterial 1963;86:123-9. Cobo A, Hall RC, Torres E, Cue110 CJ. Intrahepatic calculi. Arch Surg 1964;89:936-41. Cool GC. Tropical gastroenterology. New York: Delhi Oxford University Press, 1980. Reply. The predominant effect of piperazine on Ascaris lumbricoides is to cause a flacid paralysis that facilitates expulsion of the worm. The affected worms are not killed: complete recovery is seen if worms are incubated in a drug-free medium and worms are usually alive when passed (1). Even though trapped, dead worms have been suggested to act as a nidus for stone formation (2); these anecdotal findings need to be evaluated with accepted biostatistical principles to give more precise correlations as they are seen in populations with a prevalence rate of Ascarasis of >75% (3). Worm debris in gallstones may only be indicative of concommitant biliary ascariasis rather than a causeeffect relationship. The treatment of choice for roundworm infestation is pyrantel pamoate (1,3). Mebendazole is a good alternative agent. Standard recommendations are administration of mebendazole for 3 days (1,3). A second course may be administered after 3 wk if there is no improvement.