Growth hormone, glutamine, and an optimal diet reduce parenteral nutrition in patients with short bowel syndrome: A prospective, randomized, placebo-controlled, double-blind clinical trial. Short bowel syndrome (SBS) is a malabsorptive disorder characterized by loss of intestinal length and consequent malnutrition. For those individuals who have less than one third of their small intestine remaining (<200 cm), parenteral nutrition (PN) is often necessary. This therapy carries a high morbidity, uses extensive healthcare resources, and diminishes the patient’s quality of life. A variety of growth factors and other substances are known to affect enterocyte function. Byrne and colleagues initiated a randomized trial in 41 PN-dependent patients with short bowel syndrome who were taking an optimal oral diet to determine whether PN requirements could be reduced through administration of growth hormone (GH) with or without glutamine (Gln). Following screening, patients were admitted to an in-house facility for 6 weeks. After 2 weeks of stabilization and dietary optimization, patients were randomized to one of 3 treatment arms (1:2:2 ratio): oral Gln (30 g/day) + GH placebo (control group, n = 9), Gln placebo + GH (0.1 mg/kg per day, n = 16), or Gln + GH (n = 16). Standard criteria based on clinical and laboratory measurements were followed to determine PN volume and content. After 4 weeks of treatment, patients were discharged and monitored; GH and GH placebo were discontinued, but the diet with Gln or Gln placebo was continued for 3 months. Patients receiving GH + Gln placebo + diet showed greater reductions in PN volume (5.9 ± 3.8 L/wk, mean ± SD), PN calories (4338 ± 1858 calories/wk), and PN infusions (3 ± 2 infusions/wk) than corresponding reductions in the Gln + diet group (3.8 ± 2.4 L/wk; 2633 ± 1341 calories/wk; 2 ± 1 infusions/wk, P < 0.05). Patients who received GH + Gln + diet showed the greatest reductions (7.7 ± 3.2 L/wk; 5751 ± 2082 calories/wk; 4 ± 1 infusions/wk, P < 0.001 versus Gln + diet). At the 3-month followup, only patients who had received GH + Gln + diet maintained significant reductions in PN (P < 0.005) compared with the Gln + diet. This study shows that treatment with GH + diet or GH + Gln + diet initially permitted significantly more weaning from PN than Gln + diet. Only subjects receiving GH + Gln + diet maintained this effect for at least 3 months. (Byrne T et al. Ann Surg 2005;242:655–661).

Short bowel syndrome following bariatric surgical procedures. McBride et al examined outcomes of patients with SBS following bariatric surgical procedures (BP) by retrospectively reviewing their SBS database and examining patient demographics, indications for resection, clinical course, and outcomes. Eleven of 265 patients had SBS following BP. Mean age was 31 years (range 23 to 45). All were female. Operative procedures included open gastric bypass (GB) (n = 6), laparoscopic GB (n = 2), jejunal-ileal bypass (JIB) (n = 1), revision of JIB (n = 1), and revision of open GB (n = 1). Five patients (45%) had internal hernia (IH). Two (18%) had bowel obstructions from adhesions that resulted in multiple resections. Two had mesenteric ischemia following revision of their BP. Two had mesenteric ischemia from a hypercoagulable state. Four SBS occurred in the initial 30-day postoperative period, 4 at 1 year, and 3 at greater than 10 years. Mean residual short bowel length was 54 cm (range 11.5 to 120 cm). All patients were on parenteral nutrition (PN) on presentation. Treatment included medical and surgical management. Currently 5 patients remain PN-dependent, 2 have died, and 4 are off PN after completing intestinal rehabilitation program/small bowel transplantation. The authors conclude that complications of GB can require massive small bowel resections leading to SBS. The risk does not diminish with time. Prevention of adhesions, closure of mesenteric defects, early diagnosis of internal hernias, and conservative resections for ischemia can reduce the risk. (McBride CL et al. Am J Surg. 2006 Dec;192(6):828-32).

Spectrum of gluten-sensitive enteropathy in first-degree relatives of patients with celiac disease: clinical relevance of lymphocytic enteritis. Lymphocytic enteritis (latent celiac disease) may produce symptoms of malabsorption. Esteve and coworkers evaluated the usefulness of human leucocyte antigen-DQ2 genotyping followed by duodenal biopsy for the detection of gluten-sensitive enteropathy in first-degree relatives of patients with celiac disease and to assess the clinical relevance of lymphocytic enteritis diagnosed with this screening strategy. First-degree relatives (n=221) of 82 DQ2+ patients with celiac disease were consecutively included. Duodenal biopsy (for histological examination and tissue transglutaminase antibody assay in culture supernatant) was carried out on all DQ2+ relatives. Clinical features, biochemical parameters and bone mineral density were recorded. Results showed that 130 relatives (58.8%) were DQ2+, showing the following histological stages: 64 Marsh 0; 32 Marsh I; 1 Marsh II; and 13 Marsh III. Forty-nine relatives showed gluten sensitive enteropathy, 46 with histological abnormalities and 3 with Marsh 0 but positive tissue transglutaminase antibody in culture supernatant. Only 17 of 221 relatives had positive serological markers. Differences in the diagnostic yield between the proposed strategy and serology were significant (22.2% v 7.2%, p<0.001). Relatives with Marsh I and Marsh II-III were more often symptomatic (56.3% and 53.8%, respectively) than relatives with normal mucosa (21.1%). Marsh I relatives had more severe abdominal pain, severe distension and anemia than those with Marsh 0. The prevalence of abnormal bone mineral density was similar in relatives with Marsh I (37%) and Marsh III (44.4%). Thus, the high number of symptomatic patients with lymphocytic enteritis (Marsh I) supports the need for a strategy based on human leucocyte antigen-DQ2 genotyping followed by duodenal biopsy in relatives of patients with celiac disease and modifies the current concept that villous atrophy is required to prescribe a gluten-free diet. (Esteve M et al. Gut. 2006 Dec;55(12):1739-45).