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Background. The diagnosis of medullary thyroid carcinoma (MTC) depends on the calcitonin immunohistochemistry. Familial MTC is associated with C-cell hyperplasia (CCH), whereas sporadic MTC is not. A specific and sensitive calcitonin immunohistochemistry is necessary for the diagnosis of MTC and CCH. Methods. An affinity-purified anti-calcitonin antiserum APxCT) was used for immunohistochemistry of the thyroids of 15 patients with MTC. The thyroids of five patients with familial MTC were studied in detail, with each gland sectioned in 48 areas. Results. Between three and ten independent MTC were found in each thyroid, and CCH was found in all five patients (24.2%, varying from 8.4-56.3% of the 48 areas from each thyroid). MTC and CCH were localized mainly in the middle third and in the central axis of the thyroid lobes. They often were found together in the same area (in a total of 21 areas for the five thyroids sectioned in 48 areas) but ten areas with MTC did not have CCH, and 37 areas with CCH did not have MTC. In ten thyroids partially studied, CCH was indicated in three patients thought to have sporadic MTC. In two thyroids, with follicular and papillary carcinoma, a higher density of C-cells was found around the tumors, but disease was not characterized as CCH. Conclusions. APxCT antiserum increased the immunohistochemical specificity and sensitivity. The distinction of the familial from the sporadic MTC requires a careful and extensive search of CCH. C-cells in high density may be found around follicular cell carcinomas, being a potential source of diagnostic error.

Pathology normally comes to the attention of the physician in the form of illness. Occasionally, however, pathological changes are identified at autopsy and reveal diseases for which there were no clinical symptoms. This may be especially true of pathology of the thyroid gland, which generally gets little attention at postmortem examination. To determine the incidence of thyroid pathology in patients who had no evidence of thyroid disease, 300 whole thyroids were obtained sequentially at autopsy; the only selection characteristic being no clinical evidence of thyroid disease. The patients ranged from 13 to 82 years of age; 75.8 percent were between their fourth and seventh decade. Males outnumbered females two to one in this sample. The glands were fixed in formalin and subjected to routine histological analysis. In 6.6 percent there was some sort of thyroid tumor evident. A total of seven malignancies were identified, representing 2.3 percent of the sample; five of these seven were seen in otherwise normal thyroid glands. Less than half (42.3 percent) of the thyroid glands were normal. Colloid goiter and thyroiditis were the most frequently observed conditions. Clearly, an apparently normal thyroid gland not only may have hidden pathology, but is indeed likely to have hidden pathology. (Consumer Summary produced by Reliance Medical Information, Inc.)

H-Y antigen, the proposed inducer of testicular organogenesis, was determined serologically in 3 patients with male pseudohermaphroditism due to Leydig cell hypoplasia, a pathological model with lack of Leydig cell differentiation but normal seminiferous tubule embryogenesis. One patient was the offspring of consanguineous parents and 2 siblings presented as women with a lack of breast development and primary amenorrhea. Gonads were palpable in the inguinal canal, except for the right intra-abdominal testis in 1 patient. Two patients had female external genitalia and 1 had partial labial fusion. Karyotypes were 46XY. Gonadotropin levels were elevated, and testosterone was low and failed to increase after stimulation with human chorionic gonadotropin. Testosterone precursors were not elevated. Testicular histology showed absence of mature Leydig cells but relatively preserved seminiferous tubules. Family history was consistent for autosomal recessive inheritance. H-Y antigen expression measured by an enzyme-linked immunosorbent assay was normal, indicating that lack of other inductive factors for Leydig cell differentiation are responsible for Leydig cell hypoplasia.