What clinical and diagnostic features differentiate hypersomatotropism from other causes of insulin resistance in cats?

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Hypersomatotropism (HST) is the number one cause of insulin resistance in cats, with hypercortisolism (HC) occupying a more distant second place — distinguishing between them, and ruling out management-related causes first, drives the diagnostic approach.1 Before attributing insulin resistance to an endocrinopathy, management-related causes must be excluded. These include short insulin duration of action, inappropriate injection technique, and inappropriate insulin storage.1 Only after these are addressed should endocrine screening proceed. The clinical presentation of HST overlaps substantially with other causes of insulin resistance, making biochemical screening essential. Only approximately 25% of HST cats display the classic acromegalic phenotype of prognathia inferior and broadening of the face and paws.2 Features that raise suspicion without being pathognomonic include marked polyphagia, stertor or snoring, and persistently uncontrolled diabetes mellitus despite escalating insulin doses.23 Insulin doses as high as 35 U q12h have been reported in acromegalic cats.10 Cats may lose weight initially but gain weight or maintain weight later in the disease course despite severe polyuria, polydipsia, and polyphagia.10 In contrast, HC in cats is more often associated with fragile skin and alopecia with dermatologic disease, features not typical of HST.10 HST affects 15–32% of diabetic cats depending on the population studied, with reported prevalences of 24.8% in the UK, 17.8% in the Netherlands and Switzerland, 14.9% in Argentina, and 18–32% across multiple cohorts.4569 HC is considerably rarer in cats.1 This prevalence difference alone justifies screening for HST before HC in any insulin-resistant diabetic cat. Serum insulin-like growth factor-1 (IGF-1) is the diagnostic test of choice for HST screening and is recommended at the time of diabetes diagnosis regardless of whether insulin resistance is present and regardless of whether acromegalic features are visible.1