Adams and Davies (1986) described 4 XLH patients with spinal cord compression 3 had successful treatment with decompressive laminectomy. Moser and Fessel (1974) commented on the misdiagnosis of ankylosing spondylitis in adults. (1970) reported compression of the spinal cord or 'spinal stenosis,' and noted that treatment with vitamin D may be responsible. Patients with the X-linked disorder do not show muscle weakness, tetany, or hypocalcemia.Īdults, especially males, with XLH may develop progressive ankylosis of the spine and major joints, simulating ankylosing spondylitis ( 106300). In a study of patients with hypophosphatemia, Stickler (1969) concluded that hypophosphatemia was already present in the neonatal period, that alkaline phosphatase was elevated at 1 month of age, and that early treatment with high doses of vitamin D did not prevent growth failure. Affected persons, both males and females, showed a reduction in renal phosphate reabsorption per glomerular filtration rate (TmP/GFR) to about 50% of normal. There were no instances of male-to-male transmission of either bone disease or hypophosphatemia, and all daughters of hypophosphatemic males were themselves hypophosphatemic, suggesting X-linked dominant inheritance. The degree of depression of serum phosphate was the same in males and females, although the severity of bone disease was much less severe in females. (1958) observed hypophosphatemia in a large North Carolina family of English-Scottish extraction.
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