Defective Thyroidal Iodine Concentration in Protein-Calorie Malnutrition*

Open Access
Publisher Website
Google Scholar
Abstract
Although protein-calorie malnutrition (PCM) is known to result in various abnormalities of thyroid function, the exact relationship between the two is not clearly understood. Therefore, the thyroid function of 10 men, 13–55 yr of age, with severe PCM was studied in a clinical research ward before and 3–4 months after protein-calorie repletion. Before repletion, all subjects had low serum T4 (mean ± sem, 5.1 ± 0.5 μg/dl) and T3 (74 ± 6 ng/dl) concentrations. Eight subjects were chemically euthyroid, and their free T4 (1.5 ± 0.1 ng/dl) and serum TSH (2.9 ± 1.4 μU/ml) values were normal. Two subjects were chemically hypothyroid, with low free T4 values and high serum TSH values. After repletion, the 8 euthyroid subjects had significant increases in serum T4 (P < 0.01) and T3 (P < 0.005), but TSH did not change. Serum T4 and T3 were still lower (P < 0.05–0.001) and TSH higher (P < 0.01) than in 28 normal men of comparable age coming from the same area. After repletion, values remained unchanged in the 2 hypothyroid subjects, except for moderate increases in serum T3 and slight decreases in TSH. In all PCM subjects, values of thyroidal exchangeable iodine (23.1 ± 7 vs. 42.9 ± 8 mg; P < 0.02), estimated thyroidal I per g wet wt (1.05 ± 0.3 vs. 1.99 ± 0.36 mg; P < 0.02), and thyroidal iodide clearance (13.8 ± 1.6 vs. 19.4 ± 1.3 ml/min; P < 0.002) were lower before repletion than after; the protein-bound 131I level (72 h; 0.27% vs. 0.08 dose/liter; P < 0.05) was higher, but thyroid hormone secretion rates (200 ± 49 vs. 153 ± 25 μg/day) were not significantly different. Thyroid iodide clearance was lower even though plasma inorganic iodine (6.3 ± vs. 12.5 ± 3 μg/liter; P < 0.05) and daily urinary iodine excretion (158 ± 43 vs. 395 ± 62 μg; P < 0.01) were lower before than after repletion. In 2 PCM euthyroid subjects, baseline thyroid 131I uptake was lower before than after repletion, and the magnitude of the increase after TSH (10 U, im) stimulation was greater when the malnourished state improved. TSH increased concentrations of serum T4 and T3 both before and after protein repletion. After repletion, one hypothyroid patient failed to respond to TSH; the other had a small increase in 131 I uptake but not in serum T4 or T3. The results indicate defective thyroid iodine concentration in human PCM, but adequate hormone secretion. This situation leads to depletion of thyroid iodine stores. This alteration, if extreme, might result in hypothyroidism. Adequate protein-calorie intake tends to reverse these abnormalities.