Abstract
Askanazy 1 found a parathyroid adenoma in a case of ostitis fibrosa and he suggested a cause and effect relationship between the parathyroid tumor and the bone disease. After his finding, many other instances of parathyroid enlargement were reported in association with ostitis fibrosa deformans, ostitis fibrosa cystica, osteomalacia and rickets. Parathyroid enlargement has also been noted in rats suffering from experimental rickets. The consensus until recently was that the parathyroid enlargement observed in association with these bone diseases was of a secondary nature, and appeared as a result of a compensatory hypertrophy due to the bone deficiency.
Mandl, 2 and after him others, removed parathyroid adenomas in cases of ostitis fibrosa cystica and reported rapid clinical improvement of their patients, with cessation of the negative mineral balance.
We felt that, if the extirpation of a parathyroid adenoma resulted in the clinical improvement of a case of ostitis fibrosa cystica, injections of parathyroid extract might produce similar or analogous bone lesions, if parathyroid hypersecretion was at the basis of the disease.
Attempts have been made to produce experimental ostitis fibrosa by dietary deficiencies and by injury to the bone marrow 3 , 4 with negative results.
Dogs treated with parathyroid extract develop very extensive bone resorption, in both the cortex and the medulla, but fibrous repair is difficult to elicit. It is suggestive that in the dog doses large enough to raise serum calcium to very high levels and to produce a recognizable overdosage complex, sometimes leading to death, are not sufficient to cause lesions severe enough to elicit the response of fibrous repair. In the guinea pig, however, doses which, while high in terms of parathormone units, produce very much smaller effects on serum calcium and few, if any, of the overdosage effects, will cause bone lesions with fibrous repair.
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