Hypersomatotropism in 3 Cats without Concurrent Diabetes Mellitus

A 16-year-old, 6.8 kg, castrated male Domestic Short-haired cat was presented to Louisiana State University Veterinary Teaching Hospital with a 3-day history of progressive ataxia, tetraparesis, and altered mentation. The owner did not report having observed evidence of polyuria or polydipsia. The cat had been diagnosed with hypertrophic cardiomyopathy (HCM) 4 years earlier and was receiving atenolol, benazepril, and aspirin. Dull mentation, patchy truncal alopecia, and a grade III of VI systolic heart murmur were noted during the physical examination. The neurologic examination revealed ambulatory tetraparesis that was more severe in the pelvic limbs, plantigrade stance, proprioceptive deficits in all limbs, and positional vertical nystagmus. The CBC, biochemistry profile, and abdominal ultrasound were unremarkable. The blood glucose concentration measured with the chemistry analyzer was 130 mg/dL (7.2 mmol/L). Subsequent blood glucose measurements (n = 6) using a glucometer validated for use in cats ranged from 122 mg/dL (6.7 mmol/L) to 159 mg/dL (8.7 mmol/L) during the 5-day period the cat was hospitalized. These blood glucose concentrations combined with a normal serum fructosamine concentration (228 lmol/L, RI 192–288) ruled out overt diabetes mellitus (DM). Two-dimensional echocardiogram revealed severe asymmetric septal hypertrophy (8.7 mm in diastole). The left atrium was normal in size and all valves appeared normal. Continuous wave Doppler through the left ventricular outflow tract revealed dynamic outflow tract obstruction. Color Doppler demonstrated marked turbulence in the left ventricular outflow tract and a narrow eccentric jet of mitral regurgitation associated with systolic anterior motion of the mitral valve. Magnetic resonance imaging (MRI) images of the head were obtained in multiple planes prior to and following contrast administration at a dose of 0.1 mmol/kg. In the region of the pituitary gland, there was a T2 hyperintense, T1 hypointense nodule having marked uniform contrast enhancement (Fig 1). This nodule had moderate extension dorsal to the sella turcica and was increased in size compared to a normal pituitary gland: length (0.63 cm), width (0.83 cm), and height (0.85 cm). On T2* weighted (gradient recalled echo) images, some regions of reduced signal and small signal voids were present within the pituitary gland, mostly on the left side, consistent with magnetic susceptibility likely due to regions of hemorrhage within the nodule. Additionally, there was moderate dilation of the entire ventricular system with most severe ventricular enlargement occurring in the fourth ventricle, which caused dorsal elevation and compression of the cerebellum. Findings were most consistent with a pituitary macroadenoma, hydrocephalus, and hydrosyringomyelia. The degree of pituitary enlargement and severity of 4th ventricular dilation did not support obstruction due to the pituitary mass. A cystic accumulation of cerebrospinal fluid (CSF) within the 4th ventricle or obstructive hydrocephalus due to an additional lesion not visible on the MRI could not be ruled out. A clinical diagnosis of hypersomatotropism was supported by the presence of a pituitary mass and a total From the Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70810 (Fletcher, Pipe-Martin, Granger); Department of Clinical Science and Services, The Royal Veterinary College, University of London, North Mymms, AL9 7TA, Herts, UK(Scudder, Kenny, Mantis, Fenn, Niessen); Department of Pathobiology and Diagnostic Investigation, Diagnostic Center for Population and Animal Health, Michigan State University, Lansing, MI 48910 (Kiupel); Department of Pathology and Pathogen Biology, The Royal Veterinary College, University of London, North Mymms, AL9 7TA, Herts, UK(Smith); Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70810(Blair). Corresponding author: J.M. Fletcher, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70810; e-mail: jmfletcher@lsu.edu Submitted March 31, 2016; Revised May 12, 2016; Accepted May 16, 2016. Copyright © 2016 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. DOI: 10.1111/jvim.14360 Abbreviations: