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Elberling et al., Copenhagen, Denmark, assessed choline and myo-inositol
concentrations in the brain of 16 patients with newly diagnosed and untreated
Graves’ disease and in 19 age and sex matched healthy volunteers. These substances
were measured using echo time proton magnetic resonance spectroscopy
(MRS) for acquiring spectra. Subsequent metabolic quantification was done by spectral
evaluation by LCMODEL. Three regions of interest were chosen i.e. parieto-occipital
white matter, occipital grey matter and frontal grey matter. A decrease of
total choline was detected in all three areas and of myo-inositol in two but not
occipital grey matter. The authors state that these abnormalities have not been
described before but do not know so far the consequences for brain function. Bogazzi et al., Pisa and Varese, Italy, reported on the effect of lithium on serum thyroid hormone levels in patients who were treated for Graves’ disease. After a short course of MMI that was discontinued 5 days prior to RAI administration, patients were randomly assigned to: G1 (RAI); G2 (RAI plus lithium for 6 days starting on the day of RAI); G3 (RAI plus lithium for 19 days starting on the day of MMI withdrawal). The results were that after withdrawal of MMI both FT4 and FT3 increased in G1 and G2 but not in G3. In the 30 days after RAI, FT4 values increased only in G1 during a few days, while serum FT3 levels decreased in all three groups. Hyperthyroidism was cured in 8/12 G1, 11/12 G2 and 11/12 G3, but prompter in G2 and G3 as compared to G1. Although the patients of the three groups received the same dose of RAI, committed radiation to the thyroid was higher in G3 and G2 than in G1 (p<0.03). Comment: Administration of lithium thus prevents an increase of thyroid hormone levels after thionamide withdrawal and also of FT4 after RAI administration. It seems certainly worthwhile to consider adjuvant lithium treatment in patients for whom a temporary increase in thyroid hormone concentrations is potentially dangerous. Pirnat et al., Ljubljana, Slovenia, did a prospective clinical study on the effect of pretreatment with MMI in 106 patients with Graves’ disease (95 females, age 17–80 years). All patients were treated with 55 MBq of 131-I. In 30 patients methimazole treatment was discontinued 7 days before RAI, in 35 patients methimazole was administered until the day of RAI treatment and 41 patients did not receive pretreatment with methimazole at all. Euthyroidism or hypothyroidism after 6 months was considered as a successful result. Patients did not differ with regard to goiter volume (between 27.5 and 30.3 ml). The median absorbed dose was 130.3 Gy, 91.8 Gy, and 115.7 Gy respectively. Therapy failure (hyperthyroidism) was 6.7%, 40 %, and 7.3% respectively. From these results the authors conclude that methimazole, if given, should be discontinued before treatment with RAI as it decreases success rate of treatment. Comment: This finding confirms that of previous studies. In this report it was not reported if the three groups were comparable with regard to severity of hyperthyroidism. Alevizaki et al., Athens, Greece, compared serum T3, in T4 treated hypothyroid patients, with T3 in healthy controls with same TSH levels. In total 243, T4 substituted patients and 114 controls were studied. The mean T4 and FT4 levels were significantly higher in patients as compared to controls (9.84 ± 1.78 µg/dl and 17.95 ± 3.33 pmol/L vs. 9.06 ± 2.62 and 16.61 ± 4,61 respectively, p<0.05). T3 levels were significantly lower in patients (1.04 ± 0.2 ng/ml vs. 1.21 ± 0.26 respectively, p<0.001). Mean TSH levels did not differ between the two groups, 1.52 ± 1.0 µU/ml vs. 1.49 ± 0.98). Mean SHBG levels were significantly lower in patients vs. controls (44.26 ± 20.17 vs. 57.83 ± 40.76 nmol/L, p < 0.005). The authors conclude that T4 treated hypothyroid patients have lower T3 levels, lower T3/T4 ratio and a lower SHBG and suggest that co-administration of T3 should probably be recommended. Comment: Substitution of thyroid function with T4 results in abnormal serum ratios of T3/T4 and T4/TSH. Since in different tissues nuclear T3 depends to different extents on locally produced T3 from T4 and T3 extracted from the plasma, organs are probably not receiving optimal T3 supply for adequate T3 nuclear occupancy and thus initiation of biological activity when substituted with T4. The result of this study showing that despite a normal TSH, but a lower serum T3, SHBG levels are decreased is suggestive of tissue hypothyroidism in the liver. Thus it would be theoretically possible that in these patients, organs that are predominantly dependent for T3 nuclear occupancy on plasma T3, are in a hypothyroid state (because plasma T3 is low) and organs that are predominantly dependent on local T4 for nuclear T3 occupancy are in a thyrotoxic state because more than normal T4 enters the tissues, effected by an elevated plasma (free)T4. Normalization of this situation can indeed be achieved by co-administration of T3 as the authors suggest. |
