Evidence for intestinal malabsorption of iodine in protein-calorie malnutrition

Abstract

Iodine studies were performed in 24 Senegalese patients, 2 years of age, who were suffering from typical protein-calorie malnutrition (PCM); 12 were investigated orally and 12 intravenously with sodium iodide-131. The two protein-depleted groups may be considered comparable in respect to their nutritional status and thyroid function. By comparison with two thyrotoxic and six euthyroidal children, the significantly prolonged half-life of radioiodine in the upper bowel and the significantly higher amount of radioactivity found in the feces point to iodine malabsorption. Both the gastric and duodenal mucosa appear to play a prominent role in this malfunction. Iodine malabsorption seems to be partly related to morphological changes of the intestinal wall induced by protein and calorie deprivation. However, the level of thyroid activity, estimated by the maximal radioiodine uptake (RAIU_max), appears to be the determining factor in iodine regulation, as a high correlation is found between RAIU_max and ¹³¹I T_½ (r= –0.93) and between RAIU_max and fecal RAI (r = –0.90). These findings lead to the conclusion that metabolic studies, in which iodine is given orally to PCM patients may be disproved by an appreciable fecal loss. In situations in which iodine intake is limited, iodine deficiency may occur with time as a result of iodine malabsorption. Preliminary appraisal suggests that the improvement of the functional abnormality is extremely low and does not run parallel with nutritional rehabilitation. Under these circumstances, iodine malabsorption appears to be a long-term consequence of protein and calorie deficiency, and also might be regarded as a contributory factor for endemic goiter epidemiology.