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pubmed:abstractText |
A 35-year-old woman experienced tetanic symptoms when treated with chorionic gonadotrophins or estrogenic oral contraceptives. Persistent hypocalcemia was found, with hyperphosphatemia, normal renal function and low normal plasma parathyroid hormone (PTH), all consistent with idiopathic hypoparathyroidism. During EDTA infusion, no PTH response was measured with a predominantly anti-NH2-terminal antiserum, but a normal response was found with a predominantly anti-COOH-terminal antiserum. This supposes secretion of an immunologically abnormal and biologically ineffective PTH. Oral administration of ethinyl estradiol caused an impressive hypocalcemia with tetanic symptoms. Estrogens might, therefore, inhibit bone resorption by a specific action on bone, and not by antagonizing the action of PTH.
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pubmed:otherAbstract |
PIP: Though tetany is not among the reported side effects of oral contraceptive usage, specifically of the use of estrogen, a case study is reported which links the development of tetany to administration of estrogen-containing oral contraceptives. The case was a 35-year-old woman, who presented with muscular cramps and hypocalcemia of unknown origen. 4 years earlier, shortly after taking an oral contraceptive preparation, she had experienced the same symptoms; now, she was reacting apparently to treatment with chorionic gonadotropins for mild obesity. Clinically, she evinced persistent hypocalcemia, hyperphosphatemia, normal renal function, and low plasma parathyroid hormone (PTH); such characteristics are consistent with hypoparathyroidism. With the former, no PTH response was measured, whereas with the latter antiserum, normal response of PTH was found; hence, it was concluded that the patient's PTH was immunologically abnormal and biologically ineffective. These data support the hypothesis that estrogens have a PTH-independent effect on bone; i.e., oral administration of estogens (in this case ethinylestradiol) caused hypocalcemia with tetanic symptoms resulting from estrogenic inhibition of bone resorption by specific action on the bone, not by antagonizing PTH action in vivo.
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