Thyroid hyperplasia in elasmobranchs:
Can it be a window to goiter in humans?

Gerald L. Crow
Waikiki Aquarium, University of Hawaii

Wednesday, April 28, 1999
3:00 p.m.—Pacific Forum

Thyroid hyperplasia (goiter) is a common clinical finding in both elasmobranchs and human beings throughout the world. If left untreated, the thyroid gland can expand to almost 300 times its normal size. Management of thyroid hyperplasia has typically been centered on iodide or hormone replacement—as an additive in water, an injection, or an oral supplement.

The thyroid gland produces hormones (T4, T3) which help to regulate physiology. The hormone T4 (thyroxine) is converted extrathyroidally to T3 (triiodothyronine). Goitered elasmobranchs are hypothyroid and exhibit reduced concentrations of these hormones.

A review of captive elasmobranch thyroid hyperplasia cases from the Registry of Tumors in Lower Animals reveals an interesting dichotomy. Cases of diffuse hyperplastic goiter were found to have mostly small follicles with little to no colloid—a condition that could be expected in iodine deficiency goiter. However, five additional cases were characterized by an enlargement of follicles, filled with colloid. When left untreated in humans, colloid goiters often progress to multinodular colloid goiters, and there is reason to believe that this is also the case in elasmobranchs. Since colloid goiters are more likely to occur in the presence of goitrogenic agent(s), water chemistry studies are needed for the diagnosis of thyroid hyperplasia in elasmobranchs

In elasmobranch necropsy cases there is a striking similarity to goiter in humans. Detailed studies are now underway to determine the timeline and morphological changes that occur during goiter development. The findings may aid in our understanding of goiters in humans.

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