Miscellaneous
	Two studies concerning Free T4 were reported. One from Wang et al., Loma Linda and San Juan Capistrano, CA, USA, who assessed the relationship between total T4 and free T4 in 232 healthy children, 425 patients with nonthyroidal illness and 199 healthy adults. It appeared that the correlation between serum total T4 and free T4 was very weak in the 3 groups and that measurement of total T4 in these subjects is futile to detect any differences in FT4 status. The other report by Dallas et al., San Francisco, CA, USA, evaluated if heparin-supplemented parenteral nutrition (HSPN) in pre-term infants can cause falsely elevated FT4 serum concentrations as measured by equilibrium dialysis. Studies were performed in 67 blood samples from 23 infants born at 32 weeks of gestation, 7/67 samples demonstrated significant increases in FT4 concentration as a result of heparin use. From their data the authors conclude that if the molar ratio triglycerides/albumin is = 3, reflecting increased lipolysis by heparin, FT4 concentrations should be interpreted with care. (Comment: it has been shown several times that the augmenting effect of heparin on FT4 is caused by in vitro activity of heparin in drawn blood. If, after blood is taken, any present heparin effect is neutralized, a false increase of FT4 does not occur.) Fazio et al., Naples, Italy, measured systemic vascular resistance (SVR) by M-mode echocardiography in 19 patients with overt hyperthyroidism, 41 with subclinical hyperthyroidism, 12 with overt hypothyroidism, and 28 with subclinical hypothyroidism. SVR was significantly reduced in patients with overt hypothyroidism and significantly increased in overt hypothyroidism. Subclinical thyroid disease did not show any significant change of SVR. An inverse correlation between FT3 and FT4 vs SVR was present (r = -0.53, p < 0.01). There were two reports concerning possible brain effects in hyperthyroidism. Nyström et al., Göteborg, Sweden, measured concentrations of glial fibrillary acidic protein and S-100 protein, being sensitive indicators of minimal brain injury, in cerebrospinal fluid of 12 subjects with untreated overt hyperthyroidism. These parameters, when elevated, demonstrate neuronal degeneration or astrogliosis. No abnormalities were found in these subjects suggesting absence of brain damage, at least on the basis of these parameters. Bhatara et al., Sioux Falls, SD, USA, measured choline/creatine ratios, using frontal lobe proton magnetic-resonance spectroscopy in 13 patients with hyperthyroid Graves' disease before and when euthyroid after antithyroid treatment. Ratios were significantly higher after treatment than before (p < 0.001) suggesting reversible reductions in the levels of choline-containing compounds in the prefrontal area during hyperthyroidism. This prefrontal cortex biochemical dysfunction may form an explanation for several neuropsychological deficits that have been documented in patients with untreated hyperthyroidism. Lamadé et al., Heidelberg, Germany, continuously measured laryngeal nerve activity during thyroid surgery by transtracheal stimulation and action potential recording. Fifty patients underwent thyroid surgery, 30/50 for primary thyroid operation and 20/50 for re-operation of whom 10 had previous neck dissections as well. A very sensitive response to mechanical irritation of the nerve could be demonstrated by a decreased signal amplitude and, avoiding this effect during surgery, nerve damage could be prevented. No permanent recurrent nerve palsies resulted in these patients. (Comment: This technique seems exciting and is of special value in patients with thyroid carcinoma.) Singh et al., Los Angelos, CA, USA, investigated if in 21, T4 substituted hypothyroid patients (10 females) co-administration of 1200 mg elemental calcium would affect absorption of L-thyroxine. As compared to T4 ingestion alone, co-administration of calcium resulted in a slight decrease of mean free T4 from 1.5 ± 24 to 1.37 ± 26 ng/dl (p = 0.007). TSH increased from 2.02 ± 1.3 to 3.37 ± 2.0 (p = 0.004), and T3 did not change. Apparently the effect of elemental calcium ( administered as calcium carbonate) on T4 absorption is significant but mild. Arata et al., Tokyo, Japan, measured bone mineral density (BMD) of lumbar spine, femoral neck, trochanter and Ward triangle using dual energy X-ray absorptiometry in 8 postmenopausal women with a past history of hyperthyroid Graves' disease. Measurements were performed when subjects were at least 3 years in the euthyroid state and 4-7 (mean 5) years later. BMD at the indicated locations did not differ from matched healthy controls at the two time points of measurement. (Comment: This study indicates that at least after 3 years of euthyroidism bone mineral density is normal and also that the subsequent rate of bone loss is not different from controls.) Mirmiran et al., Teheran, Iran, measured median urinary iodine excretion (MUI) in 30 clusters of 10 school children between 8 and 10 years from 26 provinces, and in 2720 subjects between 6 and 80 years, randomly selected in 3 large cities. All these subjects were living in an area using iodine prophylaxis set at an optimal MUI between 100-200 µg/l (40 ppm iodized salt). In school children MUI was 223 µg/l and 2.6, 3.3, and 9% of them having values below 20, 50, and 100 µg/l respectively. In the 2720 subjects UI was below 50, 100, 150 µg/l in 7, 16, and 31% of 258 women between 18 and 40 years, respectively. Thyroid function parameters were normal in all the tested subjects except in 3 cases with hyperthyroidism and 4 with hypothyroidism. The prevalence of circulating thyroid antibodies was 2.1%. The authors conclude that when optimal MUI is set between 100-200 µg/l, many children and women of childbearing age may be iodine deficient. Trülzsch et al., Leipzig, Germany, assessed the incidence of constitutively activating TSH receptor and Gs· mutations in 75 consecutive toxic thyroid nodules using a more sensitive method of denaturing gradient gel electrophoresis (DGGE) that can detect mutant alleles in a mixture of mutant and wild type alleles present in as little as 3% of the sample. Using this technique in 57% of nodules, 28 TSH receptor mutations and 2 Gs· mutations were identified. The authors suggest that the incidence of constitutively activating TSH receptor mutations in thyrotoxic nodules is about 60% and of Gs· mutations, 3%. (Comment: What is the cause of hyperfunction in the other 40% of nodules??)