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Colzani et
al., Pisa, Italy, analysed the mechanism of bradycardia during
acute hypothyroidism in 9 patients (mean age 49 years) who were
on T4 suppressive therapy after total thyroidectomy followed by
131I ablation. Patients were studied when hypothyroid (6 weeks
after withdrawal of T4 when mean TSH was 75 mU/l and during T4
suppressive therapy when mean TSH was 0.16 mU/l). Sixteen healthy
volunteers served as controls. Heart rate in patients during
hypothyroidism and T4 therapy was 70 ± 3/min and 79 ± 3/min
respectively (p <0.05) whereas this value was 76 ± 2/min in
controls. As during hypothyroidism norepinephrine levels were
increased vs controls, a decreased sensitivity to sympathetic
drive was apparently present. Furthermore, a concomitant decrease
in parasympathetic tone, as measured from autoregressive spectral
analysis of heart rate variability, was also found. During T4
treatment norepinephrine levels normalised but parasympathetic
tone remained low. The authors conclude that the bradycardia
associated with severe acute hypothyroidism is dependent on the
loss of a direct positive chronotropic effect of thyroid hormones
on the sinus node and not on a decreased sensitivity to
norepinephrine because this was counterbalanced by a biologically
equivalent decrease in parasympathetic drive.
Konings et al., Amsterdam, The Netherlands, measured the biological activity of plasma TSH in 10 children with Down’s syndrome and subclinical hypothyroidism (mean TSH 6.5 mU/l). Biological activity was measured in Chinese hamster ovary cells transfected with the recombinant human TSH receptor. They found exactly the same biological activity in this system as was obtained by standard TSH of the same concentration. Similar findings were obtained with plasma from patients with diabetes mellitus who were euthyroid and from controls. The authors conclude that the biological activity of plasma TSH in children with Down’s syndrome is essentially normal. (Comment: These results indicate that the primary defect of subclinical hypothyroidism is located in the thyroid gland and we know from the literature that thyroid autoantibodies are relatively frequently found in this syndrome.) |
