This study demonstrates a surprisingly high prevalence of sporadic forms of medullary thyroid carcinoma in patients with nodular thyroid disease. Such forms of medullary thyroid carcinoma seem to be unrelated to iodine intake and may be pure or mixed with a follicular carcinoma. In these mixed thyroid carcinomas, only the neoplastic follicular pattern was seen on both cytological and histological examination. Routine measurements of serum calcitonin levels should therefore be considered an integral part of the diagnostic evaluation of thyroid nodules. Indeed, increasing the accuracy of diagnosis of medullary thyroid carcinoma encourages the surgeon to perform more radical treatment, thus achieving more frequent normalization of post-operative serum calcitonin levels.

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Cutaneous metastases from thyroid neoplasia are very rare. Most patients presenting with such a disease have also both internal metastases and a very enlarged thyroid gland. We reported here 2 patients presenting with differentiated thyroid microcarcinoma which was revealed by a solitary scalp lesion. The positive immunoperoxidase staining for thyroglobulin (TG) in the skin tumour cells asserted the diagnosis of metastatic thyroid carcinoma. The thyroid neoplastic micronodular formation was unrecognized by ultrasonography and it was only found at serial histological examination of the thyroid gland entirely removed during surgery. Histological procedure showed a solitary follicular microcarcinoma (diameter = 0.5 cm) in 1 patient, and two differentiated microcarcinoma, a follicular microcarcinoma (diameter = 0.4 cm) in a lobe and a follicular-papillary carcinoma (diameter = 0.5 cm) in the other lobe, in the second patient.

This study demonstrates that thyroid status can modulate thyroid autoimmunity expression, such as TSH-RAb and TPOAb, in patients with euthyroid or hypothyroid goitrous Hashimoto's thyroiditis. Similar results have been reported in patients with Graves' disease made euthyroid by the administration of thyroid hormone during antithyroid drug treatment.

We have studied clinical and endocrine parameters in a group (group A) of forth men referred to us because of persistent idiopathic gynaecomastia (of more than 18 months duration), before and during the administration of percutaneous dihydrotestosterone (DHT). The endocrine parameters (testosterone (T), 17 beta-oestradiol (E2), DHT, gonadotrophins (FSH and LH) and prolactin (PRL), were compared to those of control groups of 12 healthy men on DHT therapy (group B) and 10 on placebo (group C). Local administration of DHT was followed by the complete disappearance of gynaecomastia in 10 patients, partial regression in 19 and no change in 11 patients after 4 to 20 weeks of percutaneous DHT (125 mg twice daily). Before treatment the T + DHT/E2 ratio was significantly (P less than 0.001) lower in group A 244 +/- 21 (SEM) than in groups B and C (361 +/- 21) while T, DHT and E2 concentrations were all within the normal range. During DHT treatment plasma hormone levels were measured in 26 patients from group A: DHT levels increases significantly (day 0: 1.63 +/- 0.14 nmol/l; day 15: 12.8 +/- 1.6 nmol/l, P less than 0.001) while T and E2 levels fell significantly (T: day 0: 22.6 +/- 1.2 nmol/l; day 15: 11.0 +/- 1.5 nmol/l, P less than 0.001; E2: day 0: 110.5 +/- 7.12 pmol/l; day 15: 86.79 +/- 9.4 pmol/l, P less than 0.01). The T/E2 ratio decreased from 231 +/- 20 to 164 +/- 27 (P less than 0.05) while the T + DHT/E2 ratio increased significantly (P less than 0.02) to a normal mean value (day 15: 354 +/- 57).(ABSTRACT TRUNCATED AT 250 WORDS)

Gynaecomastia caused by Leydig cell tumours (LCT) in adult men may appear a long time before clinical evidence of testicular swelling. To evaluate the diagnostic criteria for LCT, hormonal status was studied in 14 cases and compared with results of a control group (CG) and 10 men with idiopathic gynaecomastia (IG). The mean plasma T level was significantly (P less than 0.005) lower in LCT (16.7 +/- 1.7 SEM nmol/l) than in CG (23.0 +/- 1.3 nmol/l). However, individual plasma T levels were in the normal range in 9/14 LCT. The mean plasma E2 level was significantly (P less than 0.001) higher in LCT (204.9 +/- 27.6 pmol/l) than in CG (87.9 +/- 7.7 pmol/l). However, individual plasma E2 levels were in the normal range in 5/14 LCT. In LCT, neither means of basal gonadotrophin levels nor the gonadotrophin responses to LHRH were different from CG. The mean of the plasma T responses to hCG did not differ between LTC, CG and IG. However the mean of E2 peak responses appeared significantly (P less than 0.005) higher in LCT (735.3 +/- 103.4 pmol/l) than in CG (420.5 +/- 40.4 pmol/l). The mean of the E2 peak responses was significantly (P less than 0.001) lower in IG (196.5 +/- 33.4 pmol/l) than in CG. Likewise the mean of plasma E2 levels, measured on day three following hCG administration, remained significantly (P less than 0.001) higher in LCT (662 +/- 94 pmol/l) than either in CG (228 +/- 14 pmol/l) or in IG (158 +/- 25 pmol/l). On day 3 following hCG administration, there was no overlap in individual plasma E2 levels between either LCT and CG or LCT and IG. In all LCT, plasma beta-hCG levels were in the normal range. A testicular echogram, performed in 12 LCT, confirmed the presence of a palpable tumour in 10 and revealed an occult tumour in two cases. We conclude that normal plasma beta-hCG levels, a prolonged plasma E2 response to hCG and testicular echogram appear to be the best criteria for early diagnosis of LCT responsible for gynaecomastia in adult men.

Serum insulin-like growth factor (IGF) and IGF-binding protein (IGF BP) levels were determined in 13 insulin-dependent diabetic patients (30-60 yr of age) during an episode of severe metabolic decompensation and the recovery phase. After separation by acidic gel filtration, the samples were assayed for IGF using a protein-binding assay (which measures mainly IGF I-related peptides) and for IGF BP by measuring the binding activity, in both assays using IGF I as tracer. The reference standard was a pool of normal adult serum with an assigned potency of 1 U IGF and 1 U IGF BP per ml. The mean IGF level in the uncontrolled state, 0.55 +/- 0.05 (SEM) U/ml, was about half that of normal subjects (1.03 +/- 0.03 U/ml, P less than 0.001). With treatment, IGF levels reached the normal range within 3 days. The pattern of changes in IGF BP levels was roughly similar, although the values in the uncontrolled state were less depressed (0.78 +/- 0.04 U/ml vs. 0.98 +/- 0.04 in normal subjects, P less than 0.01). Highly significant correlations (P less than 0.001) were found between IGF levels and the biological parameters reflecting control of the diabetes: glycosuria (r = -0.60), glycemia (r = -0.52), ketonemia (r = -0.65), and HCO3- (r = 0.58). Similar but less significant correlations were found for IGF BP. The mean GH level during the period of metabolic decompensation (9.0 +/- 1.5 ng/ml) was elevated compared to that after recovery (2.9 +/- 0.8 ng/ml) (P less than 0.025). There was a negative correlation between GH values and IGF levels (r = -0.67, P less than 0.001). The correlation with IGF BP was much less significant (r = -0.38, P less than 0.05). The results clearly reflect the role of insulin and nutritional factors in the control of IGF levels. They also support the notion that the biosynthesis of IGF and IGF BP is not regulated in the same way.

The aim of this study was to quantify modifications in the expression of skeletal myosin light chain (MLC) and myosin heavy chain (MHC) isoforms of five muscles, according to their fiber composition and function, following endurance training in rats. Rodents were assigned randomly to one of two groups: caged sedentary controls (C) or endurance-trained rats (T). In T rats, three out of the four fast and mixed muscles studied exhibited a significant increase in the expression of MLC1s, 1f and 2s and a significant decrease in MLC2f and 3f, the exception being the plantaris muscle. In two out of the four muscles we observed a significant increase in MHCI and IIa, the exception being both gastrocnemii, where the expression of MHCI did not change. In the soleus of T rats, the expression of MLC1s, 2f and 3f decreased significantly, while that of MLC2s increased significantly, compared with those of C rats. The expression of MHCIIa in T rats decreased significantly compared with that of C rats, while the expression of MHCI increased significantly. In all muscles studied, a significant slowing of myosin isoforms was observed after endurance training.