The metabolism of [75Se]selenite in patients with short bowel syndrome

Patients on home parenteral nutrition (HPN) require significantly higher amounts of selenium compared with controls. The purpose of the present study was to investigate if selenium deficiency of patients with short bowel syndrome is caused by selenium malabsorption or by excessive intestinal or renal loss.

The metabolism of [75Se]selenite was investigated in eight selenium-depleted short bowel patients on HPN and in six control subjects. The isotope was given orally, and in a subsequent study as bolus injection or as 12-hour IV infusion.

The fractional intestinal absorption of selenium was significantly reduced in the patients (2% to 58%, median 20%) when compared with the reference group (79% to 91%, median 82%) (p < .001). Within the group of patients we found a positive significant correlation between fractional selenium absorption and the length of the remaining small intestine (r = 0.95, p < .05). After parenteral [75Se]selenite administration, the patients showed a significantly higher fecal loss and a significantly reduced urinary excretion of 75Se when compared with the controls. Bolus injection vs 12-hour infusion of [75Se]selenite did not affect the cumulative fecal or urinary 75Se excretion in the HPN patients.

Reduced intestinal selenium absorption is probably the most important cause of the selenium deficiency reported in patients with short bowel syndrome, but increased endogenous intestinal selenium loss and low selenium intake may also contribute. Despite the renal counterregulation, which results in a low urinary selenium excretion, HPN patients need a supply of selenium with their parenteral nutrition.