Thyroid hormone status was assessed in 132 children with congenital heart defects undergoing cardiac surgery (median age 3.1 y; range 2 d to 16.2 y). Plasma TSH, thyroxine (T4), free thyroxine (fT4), triiodothyronine (T3), reverse triiodothyronine (rT3), thyroglobulin (Tg), and urinary iodine excretion were measured before and every other day after cardiac surgery (d 1-21). After surgery we observed strikingly low plasma concentrations of TSH (0.4 mU/L; 0.2-1.3), T3 (0.6 nmol/L; 0.3-1.2), T4 (48.9 nmol/L; 12.9-82.4), IT4 (12.9 pmol/L; 5.1-19.3), and Tg (9.4 micrograms/L; 1.5-20.6), whereas rT3 plasma concentrations increased (0.13 pmol/L; 0.05-0.3; n = 40). The maximal post-operative changes of TSH and rT3 preceded changes of T3, T4, fT4, and Tg. Postoperative urinary iodine excretion increased significantly (n = 109). Thyroid hormone plasma concentrations were lowest after cardiopulmonary bypass operations and in patients treated with dopamine. In patients with postoperative T3 plasma concentrations less than 0.6 nmol/L (n =52) the period of mechanical ventilation and intensive care treatment was significantly prolonged. Furthermore, the cumulative doses of inotropic and vasoactive catecholamines and furosemide were significantly higher in this patient group. Our results demonstrate transient secondary hypothyroidism in children after cardiac surgery that may contribute to postoperative cardiac and respiratory dysfunction and may delay recovery. Possible benefits of thyroid hormone replacement therapy need to be thoroughly examined.

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A nonradioactive method for the detection of insulin-like growth factor-binding proteins (IGFBPs) was developed utilizing human recombinant insulin-like growth factor-I (IGF-I) biotinylated with N-hydroxysuccinimido-biotin. Human plasma samples were separated by 15% SDS polyacrylamide gel electrophoresis, and proteins were transferred to nitrocellulose by Western blotting. The nitrocellulose sheets were incubated overnight with IGF-I-biotin at 4°C. The next day streptavidin-peroxidase was added for 1 h, and IGFBPs were visualized by an enhanced chemiluminescence system. Five characteristic bands with molecular weights of 41 and 39 (IGFBP-3), 34 (IGFBP-2), 30 (IGFBP-1) and 24 kD (IGFBP-4) were detected. Binding was specific for IGFs, since unlabeled IGF-I inhibited IGF-I-biotin binding. IGFBP ligand blots with biotinylated IGF-I and ¹²⁵I-IGF-I yielded comparable results. The suitability of the new assay for clinical purposes was demonstrated by several clinical examples. In summary, a rapid, reliable, nonradioactive assay for qualitative analysis of IGFBPs has been developed.

Intracellular glycolytic regulating enzyme activities, pyruvate kinase (PK) and phosphofructokinase (PFK), adenylate kinase (AK), energy charge (Ech), free amino acids (ICAA), and protein synthesis (PS) were measured in polymorphonuclear leukocytes--used as a cell model--in 62 adults and 12 children with chronic renal failure, and 66 normal adults and 21 children as comparison controls. In normal subjects, children had significantly lower enzyme activities and cell amino acid levels but similar Ech and higher PS than adults. ICAA concentrations were significantly higher than plasma amino acid concentrations (PAA) in both groups, and the PAA were not correlated with, nor indicative of, the ICAA concentrations. The variance (R2) in PS could be largely accounted for by a combination ("set") of six ICAA, as determined by multivariate analysis. The sets differed in children vs adults, suggesting that different proteins were being synthesized. In the uremic patients, reduced PF, PFK, Ech, most ICAAs and PS were indicative of cellular malnutrition. For the uremic adults, the abnormalities in cell metabolism were modified by therapy--nondialyzed uremics being worst, CAPD patients best and approximately normal, and hemodialyzed intermediate. The uremic CAPD children had reduced, PK, PFK, AK, most ICAA, and PS. Ech was increased. Cellular malnutrition in children with chronic renal failure may contribute to their poor growth.