Recent Progress in Osteomalacia and Rickets

Evaluation of Factors Determining the Tissue-Level Haversian Bone Formation Rate in Man

“…In this regard, numerous studies of human biopsy material have shown with reasonable certainty that all major bones reflect, both meaningfully and accurately, the effects of generalized bone disease; any differences between different bones and sampling sites involve degree rather than kind, and continue to follow the intersubject patterns previously mentioned. [7][8][9]12,15,17,22,23,2728,[31][32][33][34][35][36][37][38][39][40][41] …”

Axial osteomalacia

“…One patient followed up for 5 years is still well without treatment (Arnstein et al, 1967) and the symptoms and radiological findings of our patient have not changed for 18 years.…”

“…With the exception of a slightly raised plasma alkaline phosphatase in one subject, plasma calcium, phosphate and alkaline phosphatase values were normal in all patients; 24-hr urinary calcium estimations were also normal. Only two other examples of this syndrome have been reported (Arnstein, Frame & Frost, 1967).…”

Primary Hypophosphatemic Rickets in an Elderly Woman

“…The diagnosis of rickets in this pa¬ tient is supported by (1) the clinical progression of the condition starting with hip pain and Milkman-type in¬ complete fractures and culminating in complete pathologic fractures, (2) the biochemical findings of a low se¬ rum phosphorus, a normal serum cal¬ cium, and an elevated alkaline phos¬ phate level, (3) an accelerated rate of radiocalcium turnover out of keeping with the age of the patient, (4) poor calcium absorption despite large doses of ergocalciferol, and (5) a favorable response to therapy with large doses of ergocalciferol and phosphate and calcium supplements. The failure to confirm the diagnosis by iliac crest bone biopsy was proba¬ bly due to the unavailability of a technique for studying undecalcified samples of bone since decalcified specimens may sometimes fail to dis¬ close an increased amount of unmineralized osteoid tissue.1·2·6 Investiga¬ tion indicated a diagnosis of primary hypophosphatemic rickets since hypophosphatemia and phosphaturia were present in the absence of nondiabetic glycosuria, aminoaciduria, or a defect in urinary acidification.…”

“…1 Other conditions which commonly cause rickets are chronic renal glomerular insufficiency and renal tubular disorders such as renal tubular acidosis and the Fanconi syndrome.2 On rare occasions, rickets may complicate hypoparathyroidism, hyperthyroidism, ureterosigmoidostomy, the prolonged ingestion of magnesiumaluminum gel antacids, and hypophosphatasia. 2,3 Primary hypophosphatemic rickets (phosphate diabetes) unrelated to the conditions enumerated above may be either familial or sporadic.2 The familial variety is transmitted by sex-linked or autosomal inheritance and usually begins in infancy or childhood, whereas the sporadic variety may occur at any age. The biochemical characteristics of the two varieties of hypophosphatemic rickets are similar, and defective renal tubu¬ lar reabsorption of phosphorus can be demonstrated uniformly.…”