Feline acromegaly: an essential differential diagnosis for the difficult diabetic

Abstract

Practical relevance: Clinicians who deal with diabetic cats can have mixed experiences. Some patients are 'textbook cases', responding very well to insulin administration; others prove to be more challenging. Recent studies have shown a significant proportion of problem diabetic cats to have underlying acromegaly (hypersomatotropism). Recognising this syndrome in these cats will be key to successfully managing the concurrent diabetes.

Patient group: Just like the 'normal' (non-acromegalic) diabetic cat, the acromegalic diabetic cat tends to be a middle-aged to older male neutered domestic short hair. However, with increasing case experience, this signalment may change. Most patients are insulin resistant, although this may not be the initial presenting sign. No breed predispositions have been recognised to date.

Clinical challenges: There is no single diagnostic test for feline acromegaly - a confident diagnosis relies on a combination of clinical signs, feline growth hormone and insulin-like growth factor 1 levels, and intracranial imaging. Additionally, the ideal treatment protocol has yet to be established. Currently, radiotherapy is considered by many to be the best treatment; however, costs, the need for multiple anaesthetics, and the often delayed and unpredictable treatment response represent serious limitations of this modality. Previously, medical treatment has proven unsuccessful. Recent studies provide some evidence in favour of, and some against, the use of newer long-acting somatostatin analogue preparations in a proportion of acromegalic cats.

Evidence base: Two recent studies have revealed a relatively high prevalence of acromegaly among diabetic cats. One also specifically assessed the value of hormonal tests, computed tomography and magnetic resonance imaging during the diagnostic process.

Fig 1.

Production of GH and IGF-1 is normally finely regulated thanks to feedback mechanisms (left). In the case of a GH-producing pituitary adenoma (right), feedback mechanisms tend to fail to control GH and, in turn, IGF-1 production. GHRH = growth hormone releasing hormone, SS = somatostatin, GH = growth hormone, IGF-1 = insulin-like growth factor 1; + = stimulates, — = inhibits

Fig 2.

Intraoral view of a cat with confirmed acromegaly showing thickening of oropharyngeal tissues, in particular the soft palate. This is thought to underlie the inspiratory stridor that is encountered in these cats. Bar = 1 cm. Courtesy of Dr Julia Beatty

Fig 3.

Histopathology of the soft palate of the cat shown in Fig 2 reveals severe thickening, mostly due to hyperplasia of mucous (salivary) glands with irregular connective tissue between some acini and a wide zone of loose connective tissue beneath the oral mucosa. Courtesy of Dr Julia Beatty

Fig 4.

Two confirmed acromegalic cats with very different phenotypical appearances. (a) This cat looks like any other domestic short hair, whereas the cat pictured in (b) displays clear morphological facial changes induced by overexposure to GH and IGF-1

Fig 5.

Prognathia inferior (protrusion of the mandible) in an acromegalic cat. Note the increased distance between the upper and lower canine teeth

Fig 6.

Computed tomography should be aimed at visualising the pituitary fossa before and after contrast administration. (b) Transverse section of the brain of an acromegalic cat, showing a mass at the level of the pituitary fossa

Fig 7.

Depigmentation in an acromegalic cat as a result of radiotherapy treatment