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Home , Acute pancreatitis, Pancreatic disease, Viral hepatitis

Postgraduate Medical Journal (1986) 62, 407-408 Postgrad Med J: first published as 10.1136/pgmj.62.727.407 on 1 May 1986. Downloaded from

Acute in A

A. Lopez Morante, C. Rodriguez de Lope, G. San Miguel and F. Pons Romero Unit 'Marques de Valdecilla' Medical Center, Faculty ofMedicine, Santander, Spain.

Summary: Hepatitis are an uncommon cause of . We present the case of a boy with acute pancreatitis complicating with satisfactory recovery. The finding of IgM- anti HAV implicates as the cause.

Introduction Several viral have been implicated as 2208 U/I (normal 20-40); alkaline phosphatase: aetiological factors of acute pancreatitis. The viruses 350 U/I (normal 38-85). The plasma electrolytes, most frequently thought to be responsible are , calcium, proteins and lipids were normal virus (Feldstein et al., 1974; Naficy et al., 1973), apart from an IgM of 515mg/dl (normal 35-56). (Capner et al., 1975; Ursing, 1973; surface (HBsAg) was negative; Tsui et al., 1972), Epstein-Barr virus (Wislocki, 1968), IgM antibodies to HAV were positive (RIA Abbot). and measles virus (Bunnel & Monif, 1972). An associa- The serum isoamylases were studied by electro- tion between viral hepatitis and acute pancreatitis has phoresis and there was a single peak caused by also been observed, although most of the patients P1. The 24-hour urinary amylase content was concerned had fulminating hepatitis and the causal 27,600 U and the amylase/creatinine clearance ratio agent has been identified in only a very few patients was 7.1% (normal < 5%). copyright. (Archod, 1968; Parbhoo et al., 1973; Wands et al., Plain films of showed distended small 1973). bowel loops with no fluid levels. Ultrasonographic We present here a patient with acute pancreatitis examination of the abdomen showed a layer of ascitic associated with acute hepatitis caused by hepatitis A fluid at the base ofthe lesser sac. The pancreatic region virus (HAV), who made a satisfactory recovery. could not be visualized because ofinterference by gas. Gall-bladder and were normal. Treatment was with fluid and electrolyte re-

Case report placement. Pain ceased after one day and intestinal http://pmj.bmj.com/ movement returned two days after. On discharge, AST A 12 year old boy with no previous medical history, was 170 U/1, ALT 483 U/1, bilirubin and amylase became ill 8 days before admission with tiredness, returned to normal values. Ten days after discharge general malaise and dark urine. He was admitted to the AST and ALT values were normal, and a new the Emergency Department because of severe epigas- ultrasonographic examination showed a normal pan- tric pain of abrupt onset accompanied by and creatic region and no ascitic fluid. . On admission, he was afebrile and jaun- diced. His abdomen was distended with general ten- on September 25, 2021 by guest. Protected derness on palpation and no bowel sounds were heard. Discussion The was enlarged 1 cm below the right margin. Laboratory investigations included: white The mechanism ofpancreatic damage by viruses is not count 12.8 x 109/l (81% polymorphs), haemoglobin known. The cytopathic effect may be direct or it may 16.3 g/dl, erythrocyte sedimentation rate 25 mm/h, be mediated through the patient's immune response. It serum amylase: 1200 U/dl (Somogyi) (normal < 180); has also been suggested that viral infections cause bilirubin: 7.3 mg/dl (normal 0.2-1.2) (conjugated oedema of Vater's ampulla and pancreatic ducts 3.3 mg/dl); aspartate aminotransferase (AST) 2100 U/l leading to pancreatitis as result of obstruction to the (normal 20-40); alanine aminotransferase (ALT) flow of pancreatic fluid (Tsui et al., 1972). When acute pancreatitis is associated with fulminat- Correspondence: F. Pons Romero, M.D., Residencia Piquio ing hepatitis, the virus may cause tissue damage 4 - 10 Dcha, Santander, Spain. directly, but there are several other factors which can Accepted: 22 October 1985 play an important role in the development of pan- C) The Fellowship of Postgraduate Medicine, 1986 408 CLINICAL REPORTS Postgrad Med J: first published as 10.1136/pgmj.62.727.407 on 1 May 1986. Downloaded from creatitis and these include acute , hypoten- core in the cytoplasm of pancreatic sion and drug induced disease. These factors were not acinar cells in patients infected with this virus. Pan- operative in our patient and so the pancreatic damage creatic lesions may be caused by immunological could only have been caused by HAV. mechanisms in a similar way to that in hepatocellular Shimoda et al. (1980) demonstrated the presence of .

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