TL;DR: Chronic Cd exposure causes preneoplastic changes and functional differentiation of parafollicular cells of the thyroid gland, the first celltype being present in the area of diffuse hyperplasia, and the other C cell type being the constituent of microadenomas secreting CGRP exclusively.
Abstract: Summary Purpose: The objective of our study was to make morphological and functional analysis of thyroid C cells in rats chronically exposed to cadmium (Cd). Methods: The study was carried out on female albino Wistar rats (n=22, age=35-37 days, body mass 120-140 g), divided in control (n=11) and experimental group (n=11). The rats of the experimental group were treated with 15 mg/kg Cd dissolved (as CdCl2) in drinking water. The animals were sacrifi ced 3 months later. The thyroid glands were removed and macroscopic, histological and immunocytochemical examinations were done. Monoclonal antibodies for chromogranin A (Chr A), neuron specifi c enolase (NSE), calcitonin (CT), somatostatin (SST) and calcitonin gene related peptide (CGRP) were used for immunocytochemical examinations. Results: No pathological changes were found in parafollicular cells of the animals of the control group. All the animals of the experimental group showed bilateral diffuse C cell hyperplasia, mostly in the middle and upper thirds of the lobes. Strong immunoreactivity was present to all tested polypeptides (Chr A, CT, NSE, CGRP and SST). In 5 (45%) of the animals of the experimental group, C cell microadenomas were exclusively made of CGRP-secreting cells. Conclusion: Chronic Cd exposure causes preneoplastic changes and functional differentiation of parafollicular cells of the thyroid gland, the fi rst cell type being present in the area of diffuse hyperplasia, and the other C cell type being the constituent of microadenomas secreting CGRP exclusively. The results of this study indicate that chronic Cd exposure disturbs the structure and function of C cells of the thyroid gland.
TL;DR: It is concluded that the decrease in C-cell count in primary hyperparathyroidism patients with chronic hypercalcemia is due to consumption of calcitonin in the C cell.
Abstract: This study was conducted in order to establish whether C cells, which are responsible for secretion of calcitonin within the thyroid gland, change either in volume or morphology under conditions of chronic hypercalcemia in primary hyperparathyroidism. Out of 106 primary hyperparathyroid patients undergoing surgery, in 11 cases the thyroids were excised and examined for changes in the C cell. As a control group we used thyroids removed in another 14 cases undergoing thyroidectomy or laryngectomy. Calcitonin in the C cell was observed by optical microscope after immuno staining using the indirect peroxidase-labeled antibody technique. C cells are not evenly distributed within the thyroid. However, there is excellent positive correlation (p less than 0.001) between the C-cell index, which is the average of two tissue samples excised from the area at the border between the upper 1/3 and middle 1/3 of the thyroid lobe (the area where most C cells are found), and the total number of C cells. The C-cell index can thus be used as an indicator of the total number of C cells in the thyroid. The number of C cells decreased (p less than 0.01) as the level of calcium in serum increased. In patients with primary hyperparathyroidism, this decrease in C cells was significantly greater (p less than 0.025) than in the controls. Focal C cell hyperplasia and diffuse C cell hyperplasia were present in both the control group and primary hyperparathyroid group, but there was no significant difference between the two groups as to the frequency of occurrence. For both these conditions the rate of occurrence was considered within normal ranges for C cell morphology. We concluded that the decrease in C-cell count in primary hyperparathyroidism patients with chronic hypercalcemia is due to consumption of calcitonin in the C cell.