228 



B. E. C. NORDIN 



In view of the histological changes in the bone and the tendency to hyper- 

 calcaemia in thyrotoxicosis, one has to consider the activity of the parathyroid 

 glands. Some cases have in fact been reported of simultaneous hyperthyroidism and 



Fig. 1. Relation between plasma protein bound iodine and urinar 



calcium creatinine ratio in 38 thyrotoxic patients before and afte 



radioactive iodine therapy 



Fig. 2. Phosphate excretion indices 

 tients with thyrotoxicosis 



hyperparathyroidism (Bortz et ai, 1961). Generally, however, parathyroid activity 

 is probably reduced in hyperthyroidism. This at least is the implication of the low 

 phosphate clearances and subnormal response to phosphate loading reported by 

 Harden et al. (1964) (Fig. 2), and the high Tm phosphate reported by Parsons and 

 Anderson (1964). These changes are unlikely to be due to the thyroid hormone itself. 



To summarise, excessive secretion of thyroid hormone has the following effects on 

 calcium metabolism: 



It increases the rates of bone formation and resorption. 



It raises the plasma and urinary calcium. 



It diminishes parathyroid activity as measured by phosphate clearance. 



It reduces absorption of calcium, possibly by suppressing the parathyroids. 



These effects suggest that the action of the thyroid hormone on calcium meta- 

 bolism is qualitatively not unlike that of the parathyroid hormone. 



The gonadal hormones 



It was Albright et al. (1941) who first drew attention to the apparent relation 

 between osteoporosis and the menopause when they described 42 cases of osteoporosis 

 under the age of 65, 40 of whom were postmenopausal women. Before that time the 

 role of oestrogens in calcium and bone metabolism in birds and mice had been 

 appreciated (Gardner and Pfeiffer, 1938; Pfeiffer and Gardner, 1938) but the 

 extension of this to man had not been envisaged. 



