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Feline hyperthyroidism remains a major area of interest within the veterinary field given its high prevalence, affecting nearly 10% of geriatric cats, and that causal factors leading to this disease are not completely understood.1,2 Feline hyperthyroidism shares clinical and histopathological similarities with Toxic Multinodular Goitre in humans and therefore the discovery of driving cellular mechanisms behind the pathogenesis of this feline disease may bring translational insight into the pathogenesis of the later.3,4 Gonadotropin hormones such as LH are structurally related to other glycoproteins including TSH and cross-reactivity between these and their receptors has been demonstrated.5 It is hypothesized that increased concentrations of gonadotropins in neutered cats might be implicated in the pathogenesis of hyperthyroidism. This study aimed to determine the long-term effect of neutering on plasma LH concentrations in cats. Stored plasma samples from client-owned cats were used for measurement of LH and TSH concentrations. Clinical data, including age, sex, neutering age and medical history were reviewed. Two study populations were included in this study: (1) a geriatric cat population (≥ 9 years old): 18 entire and 18 neutered cats matched for age, sex and date of sample collection; (2) an adult cat population (2-8 years old): 45 neutered cats. LH concentrations were measured using a feline ELISA and TSH concentrations were measured by the Immulite canine TSH assay. Geriatric neutered cats have higher plasma LH concentrations (median, 0.25 ng/ml [25th percentile, 0.25; 75th percentile, 2.1]) than age matched entire cats (0.25 ng/ml [0.25, 0.25], P < 0 .001). Cats neutered between 6-9 months of age have higher LH concentrations than cats neutered before or after that period (P = 0.004). No correlation was found between plasma LH and TSH concentrations (P = 0.422). In conclusion, neutering causes significant long-term increase in LH concentrations in cats. Further research to determine whether this results in activation of the TSH receptor and ultimately in thyrocyte hyperplasia and/or hyperfunction is warranted. References: 1. Mooney CT. Pathogenesis of feline hyperthyroidism. J Feline Med Surg 2002;4:167-169. 2. Peterson M. Hyperthyroidism in cats: what’s causing this epidemic of thyroid disease and can we prevent it? J Feline Med Surg 2012;14:804-818. 3. Krohn K, Fuhrer D, Bayer Y, et al. Molecular pathogenesis of euthyroid and toxic multinodular goiter. Endocr Rev 2005;26:504-524. 4. Gunn-Moore D. Feline endocrinopathies. Vet Clin North Am Small Anim Pract 2005;35:171-210, vii. 5. Jiang X, Dias JA, He X. Structural biology of glycoprotein hormones and their receptors: insights to signaling. Mol Cell Endocrinol 2014;382:424-451. |
