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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.

Fifteen pediatric renal allografts recipients under azathioprine (AZA) 2–2.5 mg/kg/day and prednisone (PRED) (5.4 $pM 2.9 mg/m2/d) had their immunosuppression switched to AZA/cyclosporin (CSA) to evaluate benefits on linear growth. Before and after conversion, growth hormone (GH) nocturnal spontaneous secretion (GHss) and somatomedin C basal levels were measured. GH stimulation test (GHst) and SMc generation (SMcG) were also measured but only during the AZA/PRED period. GHst was normal in all children. GH levels increased from 2.6 $pM 2.5 to 20.9 $pM 7.9 ng/ml (p $lt 0.005) after hypoglycemia. The SMc levels, during SMcG, increased from 1.12 $pM 0.41 to 3.73 $pM 1.48 (p $lt 0.005), which is considered a normal response in our laboratory. GH nocturnal secretion inversely correlated to PRED dosage (r = 0.6, p $lt 0.02). GHss increased after PRED withdrawal in the 6 children on PRED 7.0 $pM 3.0 mg/m2/d. On the other hand, bSMc levels did not increase after conversion. After conversion, growth rate increased from 0.34 $pM 0.21 to 0.68 $pM 0.20 cm/month (p $lt 0.0004). The group showed a catch‐up growth from – 3.7 $pM 1.6 to – 2.7 $pM 1.7 standard deviation scores (p $lt 0.0001) after 1 year of follow‐up. Serum creatinine increased slightly from 0.9 $pM 0.2 to 1.0 $pM 0.4 mg/dl. AZA/CSA represents a good alternative for the pediatric recipient of a renal allograft since it is safe to both the child and the graft. This immunosuppressive regimen allows linear growth to occur.