Article Text

Steatorrhoea and pancreatic disease in HIV infected patients
  2. M GÖKE,
  3. M P MANNS
  1. Department of Gastroenterology and Hepatology,
  2. Medical School Hannover,
  3. 30623 Hannover, Germany
  1. Dr J Ockenga (email: ocken{at}
  1. Service de Gastroentérologie et Nutrition,
  2. Hôpital Rothschild,
  3. 33 Boulevard de Picpus,
  4. 75012 Paris, France

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Editor,—The study by Carbonnelet al (Gut1997;41:805–10) on macronutrient intake and steatorrhoea in HIV infected patients tackles one important clinical feature of HIV infection. On admission to hospital up to 60% of patients with AIDS are underweight (>10% weight loss).1Even asymptomatic patients at an early stage of disease have changes in body composition as shown by a reduction in body cell mass, which is associated with an increased mortality and morbidity.2 HIV associated malnutrition has a multifactorial origin but as shown by Carbonnel et al and other authors steatorrhoea is a common problem in HIV infected patients, especially in those with opportunistic infections of the gastrointestinal tract.3 Inadequate energy intake is a major determinant of malnutrition in these patients, which is confirmed by the fact that enteral refeeding can improve their nutritional status.4

Unfortunately Carbonnel et al’s study missed one important aspect of steatorrhoea—next to decreased fat absorption, exocrine pancreatic insufficiency may also result in lipid malassimilation. Raised pancreatic serum enzyme concentrations are frequently seen in patients with AIDS and also to a lower extent in asymptomatic HIV infected patients, suggesting the presence of pancreatic inflammation.5 A recently published study reported that 54% of patients with suspected AIDS related cholangitis who underwent endoscopic retrograde cholangiopancreaticography (ERCP) had a pathological pancreaticography (I°, 26%; II°, 47%; III°, 27% classified according to the Cambridge classification).6 Pathological pancreatographies were associated with opportunistic infections (candida, cytomegalovirus, cryptosporidia, microsporidia, and mycobacteria) and a CD4 count of less than 60/mm2. In the study by Carbonnelet al 60% of the patients with diarrhoea were infected with cryptosporidia or microsporidia and the mean CD4 count was 16/mm3, therefore these patients have an increased risk of pancreatic involvement. To our knowledge no studies have been published on exocrine pancreatic function in HIV infected adult patients. In a small preliminary study in HIV infected children five of 17 patients had pancreatic dysfunction and three of five had significant steatorrhoea.7

Further investigations of lipid malabsorption and weight loss in HIV infected patients, especially in those with advanced disease and cryptosporidial or microsporidial infection, should include a diagnostic work up of the exocrine pancreas. This is important because these patients may benefit from pancreatic enzyme supplementation.



Editor,—We appreciate Ockengaet al’s comments on our study. Although we did not assess pancreatic function in our patients, we would like to discuss the hypothesis that exocrine pancreatic insufficiency may contribute to steatorrhoea in malnourished HIV infected patients. As pointed out by Ockenga and colleagues, HIV infected patients frequently have elevated pancreatic serum enzymes and this can be due to several causes.1-1 Furthermore, a recent study has shown that pancreatic abnormalities are frequently found on ERCP of HIV infected patients with cholangitis.1-2 However, these biochemical or morphological abnormalities do not necessarily imply that exocrine pancreatic insufficiency is present. Indeed, roughly 90% of the secretory capacity must be lost before fat malabsorption occurs.1-3 In addition, previous studies have shown that faecal fat concentration is higher in patients with pancreatic insufficiency than in those with gastrointestinal diseases.1-4 In the paper by Bo-Linn and colleagues, all patients with pancreatic steatorrhoea had faecal fat concentrations of more than 9.5%. In our study, the faecal fat concentration was significantly lower in HIV infected patients than in patients with small bowel disease or short bowel syndrome, suggesting higher intestinal secretion; a faecal fat concentration of more than 9.5% was found in only one of 79 patients. Intestinal involvement is sufficient to explain faecal weight and steatorrhoea in HIV infected patients. Yet, these data do not exclude that, in some patients, particularly the severely malnourished ones, some degree of exocrine pancreatic insufficiency may aggravate malabsorption.


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