Eur J Pediatr (2003) 162: 872–874 DOI 10.1007/s00431-003-1315-7
O R I GI N A L P A P E R
Stephanie Van Biervliet Æ Kathleen De Waele Myriam Van Winckel Æ Eddy Robberecht
Transient exocrine pancreatic insufficiency as a possible complication of an enterovirus infection
Received: 29 May 2003 / Revised: 18 August 2003 / Accepted: 19 August 2003 / Published online: 26 September 2003 Springer-Verlag 2003
Abstract Exocrine pancreatic insufficiency is an exceptional problem in children, mostly associated with diseases like cystic fibrosis, Shwachman-Diamond syndrome or chronic pancreatitis, as is the case in idiopathic fibrosing pancreatitis. Many viral infections are known to cause acute pancreatitis. Most of them, however, are transient with no remaining damage. The differential diagnosis of persisting diarrhoea after gastrointestinal infection does not routinely include a search for exocrine pancreatic insufficiency. Conclusion: This is the first description of a child with a transient but severe exocrine pancreatic insufficiency probably induced by an ordinary enterovirus infection. Keywords Enterovirus infection Æ Exocrine pancreatic insufficiency Abbreviations cPDR cumulative percentage absorption Æ FE-1 faecal elastase 1 Æ MTG mixed triglyceride Æ PERT pancreatic exocrine replacement therapy Æ SPI secondary pancreatic insufficiency
Introduction Exocrine pancreatic insufficiency is an exceptional problem in children, mostly associated with diseases such as cystic fibrosis, Shwachman-Diamond syndrome or chronic pancreatitis, as is the case in idiopathic fibrosing pancreatitis [4]. Different indirect tests can be used to prove pancreatic insufficiency [5]; however, the S. Van Biervliet (&) Æ K. De Waele Æ M. Van Winckel E. Robberecht Department of Paediatric Gastroenterology and Nutrition, University Hospital Ghent, De Pintelaan 185, 9000 Gent, Belgium E-mail:
[email protected] Tel.: +32-92-403966 Fax: +32-92-403875
differential diagnosis of persistant diarrhoea after a gastrointestinal infection does not routinely include a search for exocrine pancreatic insufficiency. Even if an acute pancreatitis is caused by a viral infection, most are transient with no remaining damage. This case demonstrates a severe but transient exocrine pancreatic insufficiency after a mild viral pancreatitis.
Case report A 9-year-old white boy with no previous history developed fever, abdominal pain, diarrhoea and vomiting. He was admitted for administration of intravenous fluids. The blood chemistries showed a slight increase in amylase 116 U/l (1.33· upper limit of normal), lipase 129 U/l (2.86· upper limit of normal) (Fig. 1), transaminases (SGOT 171 U/l (4· upper limit of normal), SGPT 343 U/l (8.5· upper limit of normal), alkaline phosphatase 2,046 U/l (2· upper limit of normal) and c-glutamyltransferase 193 U/l (5.5· upper limit of normal). Electrolytes and blood counts were normal. Albumin was 4.43 g/dl and total protein 7.14 g/dl. The abdominal ultrasound scan showed an oedematous pancreas. There was a spontaneous resolution of the fever, abdominal pain and vomiting as well as the blood results within 5 days. The diarrhoea persisted. One month after this incident he was referred to our hospital because of persistant diarrhoea with a frequency of four times a day. The boy had a voracious appetite, had lost 8% of his weight and complained about yellow diarrhoea. He had no abdominal discomfort. There were no other abnormal clinical findings. Family history was negative. He had not taken any drugs or alcohol. At this first consultation, blood was drawn and stool examinations were requested. Stool cultures and a search for parasites were negative. Additional investigations showed normal serum amylase, lipase, liver enzymes and fat-soluble vitamin levels (A, E, D). The anti-gliadin IgA and IgG as well as anti-endomysium antibodies were negative. Total serum protein level was 7 g/dl and albumin was 4.43 g/dl. The total IgG, IgA, IgM and IgE were normal. The stool collection revealed a steatorrhoea of 20 g/day in a stool volume of 195 g; this represents an absorption coefficient of 82%. Faecal elastase 1 (FE-1) was 200 lg/g stool) and the pH of the stools was always above 6. The aetiological search for this important fat loss was continued 2 weeks later with additional pancreatic function tests, radiological investigations as well as sweat tests. The sweat test was repeatedly normal and genetic analysis did not show any of the current 33 mutations for cystic fibrosis. Immunoreactive trypsin was
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Fig. 1 Time evolution of weight (kg), stool frequency (stools/day) and laboratory data on lipase (· upper normal value), SGOT (· upper normal value), stool fat content and results of the C13-MTG breath test performed with or without PERT
