Thyroid Hyperplasia

Although thyroid neoplasms have been commonly reported in fish, most of these thyroid masses were probably goitres rather than neoplasms (Harshbarger, 1984; Hoover, 1984b; Leatherland, 1994). Thyroid hyperplasia occurs most often in captive fish or in wild fish from certain geographical areas such as the Great Lakes. Prevalence of these lesions can be high, up to 93.5% in Lake Erie coho salmon (Oncorhynchus kisutch), and the lesions can occur seasonally (Leatherland and Sonstegard, 1980). Causes of goitre in fish are not always evident but can include endocrine stimulation of the thyroid, problems with iodine metabolism, or direct stimulation of the thyroid (Leatherland, 1994). Exposure to goitrogens can reduce or eliminate thyroxine (T4) synthesis or release from the thyroid; without the normal negative feedback of T4 on the pituitary, thyrotropin secretion rates increase. The higher concentration of circulating thyrotropin stimulates the thyroid, resulting in hyperplasia and depletion of colloid reserve.

Invasiveness and apparent metastasis are common features of hyperplastic thyroid tissue in fish. The thyroid in many teleosts is a diffuse organ located in the hypobranchial area near the ventral aorta and afferent branchial arteries, although some species such as the reef parrotfishes have a compact, circumscribed thyroid (Grau et al., 1986). The commonly observed invasiveness of goitre in fish is probably related to the unencapsulated and diffuse nature of the thyroid. Ectopic (extrapharyngeal) follicles are often in the spleen, kidney and other organs of fish without thyroid hyperplasia, especially when iodine is limiting (Baker, 1959); therefore, 'metastatic' or invasive lesions in fish with thyroid hyperplasia do not indicate that the lesion is neoplastic.

Although thyroid hyperplasia in fish is common, thyroid carcinomas seem to be rare. Experimental induction of thyroid neoplasms is complicated by the dual action of chemicals that are carcinogens and goitrogens. This increases the difficulty of diagnosing thyroid masses in fish exposed to a carcinogen, and

Fig. 3.3. A non-neoplastic inflammatory disease in mangrove rivulus; the aetiological agent is unknown. (a) Granulomatous exudate (G) causing distension of the peritoneal cavity. Bar = 500 mm. (b) Higher magnification of (a). Macrophages are the most prominent component of the exudate. Giant cells (arrow) are present. Bar = 25 mm.

Fig. 3.3. A non-neoplastic inflammatory disease in mangrove rivulus; the aetiological agent is unknown. (a) Granulomatous exudate (G) causing distension of the peritoneal cavity. Bar = 500 mm. (b) Higher magnification of (a). Macrophages are the most prominent component of the exudate. Giant cells (arrow) are present. Bar = 25 mm.

criteria in addition to histological appearance are probably necessary (Grizzle and Thiyagarajah, 1988). Iodine supplementation and transplantation experiments are two approaches for aiding in the distinction between thyroid hyperplasia and carcinoma. Both of these techniques were used in an experiment in which thyroid masses were apparent 2 months after 7-day-old mangrove rivulus, Rivulus marmoratus, were exposed for 2 hours to A-methyl-A'-nitro-A-nitrosoguanidine (MNNG) (Park et al., 1993). Throughout the experiment, 50 mg iodine per litre was added to the water to achieve a total iodine concentration of 150-200 mg l-1. While no thyroid lesions were found in controls, thyroid masses were present in almost all fish exposed to the highest dose of MNNG (25 mg l-1) for 4 months, and most lesions were diagnosed as papillary carcinomas. The thyroid carcinomas were successfully transplanted to the anterior chamber of the eye of other mangrove rivulus. Although transplant recipients were probably isogenic, transplanted control thyroid tissue degenerated.

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