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Hallengren et al., Lund, Sweden, studied the fracture incidence
up to 1993 in 333 patients who were treated for thyrotoxicosis between
1970-1974. For each patient two control patients without thyrotoxicosis
were selected. Comparing all types of fractures, in females there were
fewer fractures in patients than in controls, and the controls had their
fractures at an earlier age than the patients. There were no differences
between male patients and controls. (Comment: There is no doubt that thyrotoxicosis
induces osteoporosis. The results of this study either indicate that thyrotoxicosis
was generally detected at a very early stage without development of significant
osteoporosis and/or that patients were rather young, and still had strong
bones at the time thyrotoxicosis was detected and treated, because especially
the combination of old age and osteoporosis leads to an increased fracture
rate.)
Tielens et al., Rotterdam, The Netherlands, studied cardiovascular
status, using multi-gated equilibrium radionuclide ventriculography, in
11 patients with primary hypothyroidism at diagnosis and during substitution
when euthyroidism was reached and in 12 patients with hyperthyroidism at
diagnosis and at euthyroidism after treatment. The following results were
obtained; In hypothyroidism: impaired diastolic function, a decreased afterload
independent contractility and maintenance of cardiac output by a compensatory
increase in end-diastolic volume. In hyperthyroidism: a markedly increased
diastolic function, an augmented systolic cardiac performance and an increased
cardiac output due to an increased heart rate. All abnormalities disappeared
at the time of euthyroidism.
Verhoeven et al., Rotterdam, The Netherlands, studied the effects
of calcium channel blockers on T3 uptake in cardiac myocytes of neonatal
rats. They found that in the order of Nifedipine > Verapamil > Diltiazem
inhibition of both calcium entry and T3 transport in cardiac myocytes was
observed. It was concluded that the inhibition of thyroid hormone transport
into cardiac myocytes, effected by calcium channel blockers, may thus contribute
to the decrease in cardiac output being beneficial in angina pectoris.
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