Hormones and Calcium Metabolism 



231 





reabsorption of phosphate. They attributed this to depression of the anterior pituitary 

 and thought it might explain the hypophosphataemic action of the oestrogens previ- 

 ously reported by Reifenstein and Albright (1947). An alternative explanation 

 would be, however, that 



the parathyroid glands were f/^^g phofomefry Aufo ono/yzer 



stimulated by the stilboestrol (3 Cases) (2SCases) 



which in turn suggest that 

 stilboestrol may lower the 

 plasma calcium. If this were 

 one of the actions of the 

 oestrogenic hormones it 



would also explain their '% /n\- '. ' ' " . '. t=2.Sp<0.0l 



effect upon urinary calcium 

 and possibly on urinary ci- 

 trate, which rises with para- 

 thyroid activity (Horwith 

 et ai, 1961). We have tested 

 this hypothesis by the ad- 

 ministration of ethinyl oest- 

 radiol to postmenopausal 

 women and our preliminary 

 data do in fact suggest that 

 this compound depresses 

 plasma calcium (Fig. 5). 



To sum up the effects of the gonadal hormones on bone and calcium metabolism, 

 it seems fair to say that the actions of androgenic and anabolic compounds in this 

 held are quite uncertain, though their effect upon nitrogen balance is well established. 

 The oestrogenic hormones, on the other hand, have little effect on nitrogen metabo- 

 lism but appear to reduce urinary calcium, raise urinary citrate, inhibit bone re- 

 sorption and depress plasma calcium. The overall effect is an improvement in calcium 

 balance but it is not clear whether this effect is achieved by inhibiting bone resorption 

 or whether bone resorption is inhibited as a result of the improvement in calcium 

 balance. The reverse effects of oestrogens on urinary calcium and citrate are of course 

 reminiscent of a metabolic alkalosis (Dedmon and Wrong, 1962) but there is no 

 convincing evidence that oestrogens have an effect on acid-base balance. 



@ ^ 



(g) 



Af^/Tf d/r/hff 



before 



during 



Fig. 5. 50 observations of plasma calcium before and 67 during the 

 administration of ethinyl oestradiol 0.1 nig. daily to 26 patients 



Corticosteroid hormones 



Compression fractures and "soft bones" were a feature of the original cases of 

 hyperadrenocorticism described by Cushing in 1932. Albright et al. (1941) intui- 

 tively attributed this syndrome to an overproduction of the adrenal cortical "sugar" 

 hormone, a prediction which was subsequently confirmed when the hormone was 

 indentified as Cortisol. It was also Albright (1942 — 1943) who recognised the bone 

 disease as osteoporosis and who attributed it as well to the antianabolic action of the 

 "S" hormone the existence of which he had himself been the first to postulate. In 

 accordance with this concept, he proposed that the osteoporosis of Cushing's syn- 

 drome was due to decreased formation of protein bone matrix, and this hypothesis 

 has remained popular for many years. 



