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Yair Liel, MD
Beer-Sheva, Israel

Arch Intern Med. 1996;156(3):341.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

While the controversy over the issue of the risks and proper treatment of patients who are receiving levothyroxine replacement therapy continues,¹ the following case from my clinical practice serves to illustrate the extent of the physiological influence of thyroid hormones on bone metabolism.²

Report of a Case.

A 53-year-old postmenopausal women was referred for investigation of bone pain, a pathologic bone scan, loss of weight, and markedly elevated serum alkaline phosphatase activity. Her serum calcium level was normal at 2.40 (9.6 mg/dL), while her serum phosphate level was low (0.60 mmol/L [1.9 mg/dL]). The initial workup disclosed hyperthyroidism. Since the patient was a traditional Bedouin, we suspected that the markedly increased alkaline phosphatase activity (>10 times the upper limit of normal) and the low serum phosphate level, which are atypical of thyrotoxicosis, could be related to vitamin D—deficiency osteomalacia.³ As the patient became euthyroid, after antithyroid drug . . . [Full Text PDF of this Article]

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