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Received 30 Jub 1987; revised 25 Januaty 1988; accepted fm publication 24 February I988

TRAW.ACT~ON~ OF THE ROYAL SOCIETY OF TROPICAL. MEDICINE AND HYGIENE (1988) 82, 620

1 Short Report 1

lntrahepatic cholestasis after thiabendazole

R. N. Davidson W. R. C. Weir, G. L. Kaye2 and N. McIntyre2 Hospital for Tropical Diseases, Lon- ah, NW1 OPE, UK; Liver Unit, Royal Free Hospital, London, NW2, UK

Thiahendazole is widely used to treat parasitic infections and is available without prescription in the UK; we report a case of prolonged, severe, intrahepa- tic cholestasis following its use.

Case report A 17 year old English schoolboy had travelled in

Central Africa where he contracted asymptomatic Stmngyloides stercoralis infection. On 10 December 1986 he was prescribed thiabendazole l-5 g twice daily for 3 d. 10 d after finishing the course, he developed a dry mouth with swollen parotid and salivary glands suggestive of the sicca complex. Shortly after this, on 4 January 1987, he became jaundiced with dark urine and pale stools. The past medical history was unremarkable. He had taken Maloprim@ and proguanil but these drugs were discontinued in August 1986. Investigations revealed cholestatic jaundice with no ultrasound evidence of biliary obstruction. Serum markers of hepatitis A, hepatitis B, leptospirosis, cytomegalovirus, Epstein- Barr virus, and toxoplasmosis were negative. His jaundice deepened and his general health deteriorated with 10 kg weight loss. On 14 March 1987 his liver function tests showed serum bilirubin 408 qol/litre (402 conjugated), alkaline phosphatase 350 IU/litre,

alanine transferase 102 IU/litre and y-glutamyl trans- ferase 186 IU/litre.

Liver biopsy cobed intrahepatic cholestasis and, while aetiology was not proven, the appearances were fully compatible with idiosyncratic drug injury. The patient was followed up at regular intervals and, although his clinical jaundice resolved by July 1987, his liver function tests did not return to normal until December 1987 (12 months after ceasing thiahenda- zole) .

Comment Cholestatic jaundice induced by thiabendazole was

first reported by JOLATA & FRESTON (1974). The link with sicca complex was described in 2 members of a family in 1979 by FINK & MACKAY (1979) and REX et al. (1983). Cholestasis can be fatal, or prolonged up to 3 years (CARLOS MANIVEL et al., 1987), and an auto-immune pathogenesis has been suggested (STRICKER & SPOELSTRA, 1985). Our case of cholesta- tic jaundice due to thiabendazole adds to the 16 reported in the world literature.

References Carlos Manivel, J., Bloomer, J. R. & Snover, D. C. (1987).

Progressive bile duct injury after tbiabendazole adminis- tration. Gastroenterology, 93, 245-249.

Fink, A. I. & Mackay, C. J. (1979). Sicca complex and choangiostatic jaundice in two members of a family probably caused by tbiabendazole. Ophthalnwlog% 86, 1892-18%.

Jolata, R. & Freston, J. W. (1974). Severe intrabepatic choletasis due to tbiabendazole. American Jouwwl of Tropical Medicine and Hygkne, 23, 676-678.

Rex, D., Lumeng, L., Eble, J. & Rex, L. (1983). Intrabepatic cholestasis and review of the literature. Gaszroenterology, 85, 718-721.

Stricker, B. & Spoelstra, P. (1985). Drug Induced Hepatic Znjuty. Amsterdam, etc.: Elsevier.

Received 5 April 1988; accepted for publication 5 May 1988