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Comments regarding "Subclinical hyperthyroidism in cats: a spontaneous model of subclinical toxic nodular goiter in humans?"
Ferguson DC, Hoenig M, Kaptein EM, et al. Thyroid, 2008. 18(12): p. 1339-40; author reply 41. We would like to comment on some of the points made by Wakeling et al. in their manuscript entitled ‘‘Subclinical Hyperthyroidism in Cats: A Spontaneous Model of Subclinical Toxic Nodular Goiter in Humans?’’ (1). The authors state: ‘‘The purpose of this study was to determine whether a relationship exists between TSH concentration and thyroid histopathology in biochemically euthyroid cats (as assessed by T4 [serum total T4 concentration] thereby providing further evidence for the existence of subclinical hyperthyroidism in cats.’’ We certainly support the idea that the histopathological changes associated with spontaneous feline hyperthyroidism provide a model of toxic nodular goiter (Plummer’s disease), and have contributed to the literature in this regard (2–4). Undoubtedly, there is a prodromal period for this disease associated with clinically and biochemically undetectable hyperthyroidism. However, the authors of this manuscript have chosen a ‘‘healthy’’ population dominated by cats with chronic renal disease which we propose confounds the interpretation of their data. The concern rises from the observation in human patients with chronic kidney disease, both before as well as following kidney transplantation, that there is an increased frequency of goiter and thyroid adenomas (as well as hypothyroidism, probably due to increased serum iodine levels). In one study (5) of patients with chronic renal disease, the incidence of abnormal thyroid structures (nodules |