RAREFYING DISEASE OF THE SKELETON 4''27 



sorption of calcium when the intake was raised to 2.0 gm per day. 

 Some patients with osteoporosis had p\ elonephritis and a "calcium 

 leak" that caused negative calcium balance (Nordin, 1962/;). Of 29 

 balance studies on 17 patients, 5/17 were in negative calcium bal- 

 ance, and 12 17 were in slightly positive calcium balance. Inas- 

 much as the calcium lost in sweat was not measured in balance 

 studies, it was assumed that all the patients were in negative calcium 

 balance. The contention was, first, that osteoporotics were not able 

 to reduce their urinary calcium on low calcium diets, but had the 

 ability to retain calcium on high calcium diet (Bhandarkar and 

 Nordin, 1962 ) ; second, that the cause of the disorder was prolonged 

 negative calcium balance in subjects with higher than normal cal- 

 cium requirement or inability to adapt to inadequate intake. Some 

 severe osteoporotics, however, were able to adapt to low calcium 

 intake. In any case, the condition was relieved by dietary supple- 

 ments of calcium, but x-ray was not sensitive enough to detect the 

 new bone that was presumed to have been added (Nordin, 1962c). 

 Bhandarkar et al. ( 1961 ) fed 7.5 ^tc of Ca^ ' or 5 /xc of Ca^'' to meas- 

 ure calcium absorption, and noted that the majority of patients with 

 osteoporosis absorbed calcium normallv. Kinetic studies were inter- 

 preted to show that the rate of bone accretion in osteoporotics was 

 also the same as normal (Nordin et ah, 1962/?). 



Fraser (1962) divided patients with osteoporosis into three 

 groups, Cushing's svndrome, at\'pical or idiopathic, and tvpical or 

 postmenopausal, and corroborated Nordin's contentions. However, 

 sex hormones were prescribed in addition to calcium supplements 

 for senile osteoporosis. Haas et al. ( 1962 ) measured retention of 

 an infusion of calcium in 36 osteoporotics and 12 normal subjects, 

 and concluded that the lowest levels occurred in Cushing's syn- 

 drome, castration, and idiopathic osteoporosis. 



In the past, some investigators have assumed that typical osteo- 

 porosis represents chronic low-grade hyperparathyroidism of bone. 

 The calcium deficiency hypothesis ultimately leads to such an as- 

 sumption for an explanation of the bone tissue deficit. Gordan et al. 

 (1962) rejected hyperparathyroidism secondary to malabsorption 

 of calcium as a cause of osteoporosis; patients with hyperparathy- 

 roidism had only 35 to 75 per cent tubular reabsorption of phos- 



