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We report 2 cases of giant-cell lesions of the maxilla in two female patients aged 42 and 22 years. The initial diagnosis was giant-cell tumor and giant-cell repair granuloma. The diagnosis of brown tumor was established at discovery of primary hyperparathyroidism. We emphasize the importance of searching for hyperparathyroidism in patients with a giant-cell lesion of the maxilla.
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A case-control study was conducted among residents of Rochester, Minn, to assess the influence of prior therapeutic radiation on the risk of primary hyperparathyroidism. Fifty-one cases of surgically proven primary hyperparathyroidism diagnosed from 1975 through 1983 were each matched by age and gender to two control subjects, with radiation exposure documented through preexisting medical records. The overall odds ratio for any prior therapeutic radiation therapy was 1.9 (95% confidence interval, 0.9 to 4.4) and it was 2.3 (95% confidence interval, 0.9 to 5.7) when limited to those with prior head and neck radiation. Among women, the figures were 2.9 (95% confidence interval, 1.1 to 7.5) for any prior therapeutic radiation and 3.4 (95% confidence interval, 1.2 to 10.2) for head and neck exposure. This study confirms the association between primary hyperparathyroidism and prior therapeutic radiation exposure, at least for women in this population.
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Plasma levels of calcitonin (CT) are highest in patients with medullary thyroid carcinoma (MTC). Plasma CT is also raised in some patients with carcinoma such as that of the breast, the lung or the pancreas, and in pheochromocytoma. It must be kept in mind, however, that plasma CT can be similarly raised in patients with renal failure, non-tumoral pulmonary disease or acute pancreatitis. In hypercalcemia patients with primary hyperparathyroidism the plasma CT is normal or only marginally elevated. It is speculated that the raised levels in pregnant and lactating women and in new-born infants prevent excessive bone destruction at times of greater physiological need for calcium. Larger molecular weight forms than monomeric CT (1--32) are circulating at least in plasma of patients with calcitonin-producing tumors and in renal insufficiency. The biological function of these larger molecular weight forms is not yet known. The discrepancies among the results of different laboratories can in part be explained by the immunoheterogeneity of the hormone and the different antigenic recognition sites of the antisera used. The measurement of plasma CT levels is nevertheless important for the diagnosis of MTC and may prove useful in some patients with malignant tumors unrelated to the C-cells of the thyroid gland. CT-radioimmunoassay may be improved by using antibodies specific to the different forms of circulating calcitonin.
Endocrine tumors commonly produce characteristic clinical signs, and laboratory tests lead to accurate diagnosis in a high percentage of cases. The successful management of these tumors usually requires complete surgical resection. A large number of preoperative localization procedures to facilitate the operative management of these tumors have been developed. This report reviews the recent contributions to this literature, with a particular emphasis on cost-effective use of these procedures.
Families in which both parents are heterozygotes for the same autosomal dominant neoplasia syndrome are extremely unusual. Recently, we had the unique opportunity to evaluate three symptomatic siblings from the union between two unrelated individuals affected by multiple endocrine neoplasia type 1 (MEN1). When the three siblings and their parents and relatives were genotyped for 12 markers tightly linked to the MEN1 locus, at 11q13, two of the siblings were found to be homozygotes, and one a heterozygote, for MEN1. With regard to the MEN1 syndrome, no phenotypic differences were observed between the two homozygotes and the heterozygotes. However, the two homozygotes showed unexplained infertility, which was not the case for any of the heterozygotes. Thus, MEN1 appears to be a disease with complete dominance, and the presence of two MEN1 alleles with mutations of the type that occur constitutionally may be insufficient for tumor development.