Related Experiment Videos
Non-functional C-cell adenoma in aged horses
H Ueki1, Y Kowatari, T Oyamada
1Department of Veterinary Pathology, Faculty of Veterinary Medicine and Animal Sciences, Kitasato University, 35-1 Higashi-23-bancho, Towada, Aomori 034-8628, Japan.
Journal of Comparative Pathology
|July 28, 2004
Summary
Most equine thyroid tumors in older horses are C-cell adenomas, not follicular tumors. These parafollicular cell-derived tumors are likely non-functional, avoiding calcitonin-related diseases.
Area of Science:
- Veterinary Pathology
- Equine Neoplasia
- Endocrinology
Background:
- Equine thyroid tumors are common in older horses, often presumed to originate from follicular epithelial cells.
- Limited immunohistochemical data exists for characterizing these equine thyroid neoplasms.
- Previous assumptions about tumor origin lack detailed investigation.
Purpose of the Study:
- To investigate the origin of equine thyroid tumors, specifically testing the hypothesis that they are parafollicular cell (C cell)-derived adenomas.
- To evaluate the pathogenesis and functional status of these equine thyroid tumors.
- To provide immunohistochemical characterization of equine thyroid lesions.
Main Methods:
- Histological, immunohistochemical, and ultrastructural examination of thyroid glands from 38 horses (aged 10-29 years).
- Evaluation of nodular tumor masses identified in the thyroids of horses.
- Immunohistochemical staining for calcitonin, neuron-specific enolase, and thyroglobulin.
Main Results:
- Nodular lesions were found in 31.6% of horses >10 years and 75.0% of horses >20 years.
- Tumor cells were positive for calcitonin and neuron-specific enolase, but negative for thyroglobulin.
- Ultrastructural analysis revealed minimal secretion granules in tumor cells.
Conclusions:
- The nodular thyroid lesions in older horses are identified as C-cell adenomas, not follicular adenomas.
- These equine C-cell adenomas are suspected to be non-functional.
- The tumors are unlikely to cause diseases related to calcitonin hypersecretion.