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Short bowel syndrome is a condition marked by weight, fluid, and nutrient loss in the absence of adequate small intestine length. In adults this is usually the result of surgical intestinal resection for Crohn's disease, acute bowel infarction, radiation strictures, and adhesive obstruction. Patients with a residual small bowel length of 100 cm (normal 600 cm) or less usually require parenteral nutrition for survival. Prior to the discovery of total parenteral nutrition (TPN) in 1968 by Dudrick and colleagues, patients with short bowel often died as a result of fluid and nutritional deficiency.1 2 During the past three decades we have learned that parenteral nutrition can be given in the home environment (home parenteral nutrition (HPN)) with good results.3 However, there are complications associated with long term HPN which include catheter sepsis, liver injury, and bone disease. Daily administration of HPN also requires dedication and planning by patients with regard to sterile catheter technique and travel away from the usual home environment. HPN can be expensive if given over an extended period of time.
Fortunately for some patients, the remaining small intestine undergoes clinically significant structural and functional changes (intestinal adaptation) following surgical resection which may eliminate the need for lifelong TPN. The process of intestinal adaptation can be observed clinically by documentation of weight, fluid, and electrolyte stabilisation. Over a 3–12 month period following resection, patients usually declare their need for lifelong TPN.
Various medical and surgical treatments have been attempted over the past 20 years to increase the surface area of the residual small intestine with the aim of increasing fluid and nutrient absorption. Perhaps the most interesting was the published work of Byrneet al in 1995.4 5 These investigators treated eight patients with short bowel syndrome who had been dependent on TPN for many years, with human recombinant growth hormone, glutamine, and a high carbohydrate/low fat diet for three weeks. They reported a significant increase in total caloric, carbohydrate, protein, and fluid absorption. However, they found no change in fat absorption however. In a subsequent study using the same treatment, where the end point was discontinuation of TPN rather than nutrient or fluid absorption, they were able to wean 40% of their patients off TPN.5 Unfortunately, evaluating only this end point does not directly answer the question of whether the treatment was solely responsible for the positive effects observed as absorptive studies were not performed. It is possible that these patients were not truly “TPN dependent” and the same results could have been found with conventional treatment alone. These two studies have been criticised for not including a placebo arm and making this method of treatment commercial without more objective data.
In this issue of Gut a group of investigators from Copenhagen who have a great deal of experience in short bowel syndrome report their results in eight short bowel patients treated with growth hormone, glutamine, and their usual diet (see page199).6 Unlike the previous studies, this was a randomised placebo controlled trial. They did not find a significant increase in fluid or caloric absorption in those patients with and without colons compared with placebo. Their reasons for not choosing to use a high carbohydrate/low fat diet given their earlier results are not clear.7 The lack of positive findings compared with the study of Byrne et al may be a reflection of diet and not growth hormone and glutamine. The results of Szkudlareket al are consistent with the work from our institution using the same experimental design.8 However, we used a high carbohydrate/low fat diet throughout the study. Although we reported a transient increase in body weight in those treated compared with placebo, we later reported the body composition data in this same group of patients and found that extracellular fluid retention, most likely from growth hormone, was responsible for the effects observed.9 Similarly, Szkudlareket al reported side effects from extracellular fluid retention in all eight patients. One patient required surgery for severe carpal tunnel syndrome.
One observation consistent in this current study as well as in those of Byrne et al and Scolapioet al is that fat absorption was unchanged. I believe this is a good indication that treatment with growth hormone and glutamine has little if any clinical effect on small bowel absorption. Five years and two randomised controlled studies later, I believe the findings reported by Byrne et alare the result of meticulous dietary counselling and not necessarily those of growth hormone and glutamine.
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