Pathology in Practice

Laura E. O'Sullivan Emergency Service, Compassion-First Pet Hospitals, Tinton Falls, NJ 07724.

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Marc Kent Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA 30602.

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Eric N. Glass Section of Neurology and Neurosurgery, Red Bank Veterinary Hospital, Compassion-First Pet Hospitals, Tinton Falls, NJ 07724.

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 MS, DVM
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Rachel B. Song Section of Neurology and Neurosurgery, Red Bank Veterinary Hospital, Compassion-First Pet Hospitals, Tinton Falls, NJ 07724.

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Joshua D. Warren Section of Neurology and Neurosurgery, Red Bank Veterinary Hospital, Compassion-First Pet Hospitals, Tinton Falls, NJ 07724.

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Alexander de Lahunta Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Andrew Miller Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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History

An 8-year-old 4.3-kg (9.4-lb) spayed female domestic shorthair cat was evaluated because of progressive behavioral changes of several months’ duration. The owner stated that the cat had been pacing in circles, clockwise and counterclockwise, and acting more aloof. Treatment initiated by a veterinary behaviorist initially consisted of administration of fluoxetine, which was then changed to administration of paroxetine. Despite treatment, the clinical signs became progressively worse. The cat had no prior medical history, and its vaccination status was current. The cat was kept indoors and was the only cat in the household. Given the progression of signs, the cat was referred for further evaluation.

Clinical and Gross Findings

At the referral evaluation, the physical examination findings were considered normal with the exception of a grade 2/6 heart murmur. On neurologic examination, the cat had dull mentation. The cat was constantly pacing with a normal gait and circled to the left and to the right. Postural reactions and spinal reflexes were normal in all limbs. There was an inconsistent menace response in the right eye. No other neurologic abnormalities were detected.

Three months earlier, a CBC and serum biochemical profile revealed lymphopenia (0.826 × 103 lymphocytes/μL; reference range, 0.85 × 103 to 5.85 × 103 lymphocytes/μL), monocytosis (1.652 × 103 monocytes/μL; reference range, 0.04 × 103 to 0.53 × 103 monocytes/μL), and hypochloremia (113 mmol/L; reference range, 114 to 126 mmol/L). A urine sample was obtained by means of cystocentesis for analysis, which revealed the presence of blood and struvite crystals and a urine specific gravity of 1.051. Serum total thyroxine concentration was within reference range.

Owing to concerns for the cat's poor quality of life, the owner declined diagnostic testing or empirical treatment and elected euthanasia by means of IV injection of a barbiturate solution. The owner allowed postmortem evaluation only of the brain. The brain was removed and preserved in neutral-buffered 10% formalin solution.

On gross examination of the brain, a 1.4 × 1.3 × 1.7-cm well-delineated dark tan soft mass was present on the ventral aspect of the brain located between the piriform lobes laterally, the optic chiasm rostrally, and the pons caudally in the location of the pituitary gland (Figure 1). The rostral aspect of the mass compressed and dorsally deviated the optic chiasm. On transverse section, the mass had expanded dorsally to compress the thalamus and hypothalamus and had caused dilation of the ventral aspect of the third ventricle. A thin rim of light tan tissue was present on the left lateral surface of the mass.

Figure 1
Figure 1

Photograph of a transverse section through the rostral aspect of the cerebrum at the level of the optic chiasm in an 8-year-old domestic shorthair cat that was examined because of abnormal mentation and circling. A large tan mass (asterisk) located in the area of the pituitary gland between the piriform lobes has deviated and compressed the optic chiasm (arrows). Bar = 5 mm.

Citation: Journal of the American Veterinary Medical Association 258, 8; 10.2460/javma.258.8.857

Histopathologic Findings

Microscopically, the mass was a well-demarcated, unencapsulated, densely cellular neoplasm composed of pseudorosettes, clusters, and packets of round to polygonal neoplastic cells that lacked a defined architecture (Figure 2). The neoplastic cells were uniform with abundant, pale amphophilic cytoplasm and distinct cell borders. The neoplastic cells each had a large, eccentrically positioned nucleus with vesicular chromatin and a single prominent nucleolus. Mitotic figures were rare. Invasion of the otherwise normal brain parenchyma was absent. On the periphery of the neoplasm, remnants of normal tissue from the adenohypophysis were present (Figure 3).

Figure 2
Figure 2

Photomicrographs of a section of the intracranial mass in the cat in Figure 1. The mass is densely cellular and composed of round to polygonal neoplastic cells without a defined architecture. Pseudorosettes (arrow) and packets of neoplastic cells that each have abundant, pale cytoplasm and a round to oval nucleus containing a single prominent nucleolus are present. H&E stain; bar = 20 μm. Inset—Rare mitotic figures (arrowhead) are observed. H&E stain; bar = 50 μm.

Citation: Journal of the American Veterinary Medical Association 258, 8; 10.2460/javma.258.8.857

Figure 3
Figure 3

Photomicrographs of another section of the intracranial mass. The transverse section illustrated in Figure 1 is shown (top left) with a rectangular outline that denotes the region where the section was obtained. At the dorsal aspect of the mass (asterisk), a thin rim of normal-appearing adenohypophyseal tissue (between arrows) was observed adjacent to the optic chiasm (arrowhead). H&E stain; bar = 500 μm. Inset—Higher-magnification view of the apparently normal pituitary tissue adjacent to the neoplasm (asterisk). H&E stain; bar = 50 μm.

Citation: Journal of the American Veterinary Medical Association 258, 8; 10.2460/javma.258.8.857

Morphologic Diagnosis and Case Summary

Morphologic diagnosis and case summary: pituitary adenoma (presumed nonfunctional chromophobe macroadenoma) in a cat.

Comments

For the cat of the present report, the antemortem anatomic diagnosis was consistent with a lesion involving the ascending reticular activating system (on the basis of the altered mentation) or the left prosencephalon (if the menace response deficit was an accurate finding). The differential diagnoses were neoplasia and infectious encephalitis. Because the right menace response was inconsistent, extracranial causes such as metabolic and toxic encephalopathies were also considered. The postmortem diagnosis was pituitary adenoma.

The pituitary gland has 2 parts, the adenohypophysis, which is composed of the pars distalis and pars intermedia, and the neurohypophysis, which is composed of nervous tissue within the infundibulum and neural lobe.1 The parenchyma of the pars distalis has 3 types of endocrine cells that have been classified on the basis of their staining characteristics, namely acidophils, basophils, and chromophobes.1 The primary hormones produced by acidophils are somatotropin and lactotropin.2 The primary hormones produced by basophils are thyrotropin and gonadotropin.2 As their name implies, chromophobe cells do not stain well; these cells primarily produce adrenocorticotrophin.2 In the case described in the present report, the gross and microscopic features of the mass were consistent with a pituitary macroadenoma, which was defined as a chromophobe variant.

In a study3 of 160 cats with intracranial neoplasia, pituitary neoplasms accounted for 8.8% of all neoplasms; this type of neoplasm was the second most common secondary intracranial neoplasm in affected cats. The 14 cats with pituitary neoplasms were primarily domestic shorthair cats with a median age of 10.1 years3; male cats outnumbered female cats, but the difference was not significant.3 Neurologic signs often reflected the anatomic location of the neoplasm and consisted of blindness and altered mentation.3 Nonspecific signs included lethargy, anorexia, weight loss, polydipsia, and polyuria.3 Of the 14 cats with pituitary neoplasms, 7 had diabetes mellitus and 3 had an alteration in the pituitary-adrenal axis.3

Cats with pituitary neoplasms often have concomitant endocrine dysfunction, and in some cats the neoplasm may be plurihormonal.4,5,6 Diabetes mellitus, which frequently is insulin resistant, is often a consequence of acromegaly (caused by excessive growth hormone secretion).7,8 Although there is currently no available assay for feline growth hormone, excessive growth hormone production may be inferred on the basis of an increase in serum insulinlike growth factor 1 concentration (IGF-1).9 In fact, acromegaly with a serum IGF-1 concentration > 1,000 ng/mL may be present in as many as 25% of cats with diabetes mellitus.10 Given the lack of historical data to suggest an endocrinopathy and the results of the serum biochemical profile and urinalysis, the pituitary neoplasm in the cat of the present report may have been endocrinologically inactive (ie, nonfunctional). Moreover, the cat lacked other endocrine phenotypic changes suggestive of acromegaly, such as a broad face, mandibular prognathia, enlarged paws, abdominal organomegaly, respiratory stridor, and marked weight gain.7,11 Altered facial features may go unrecognized by owners, but changes such as broadening of the head and thickened cranial bones and skin may be identifiable with CT or MRI.12,13 Likewise, cardiomyopathy may be present in an affected cat but unknown to the owner.14 Unfortunately, cross-sectional imaging of the head and echocardiography were not performed for the cat of the present report. Similarly, dermatologic abnormalities suggestive of hyperadrenocorticism, such as alopecia, footpad excoriations, or thin, fragile skin that tears easily with minor trauma, were notably absent.15 Without endocrinologic data, such as serum IGF-1 concentration or results of pituitary-adrenal axis testing, the functional status of the pituitary neoplasm in the cat of the present report remained speculative. The challenge of determining the functional status of a pituitary neoplasm can be compounded because diabetes mellitus may not be present in cats despite excessive serum IGF-1 concentrations and immunohistochemical expression of growth hormone by the pituitary neoplasm.16

The diagnosis of a pituitary neoplasm is achieved with cross-sectional imaging such as CT or MRI. With MRI, the mean length, width, and height of the pituitary gland in healthy cats is 0.54, 0.50, and 0.32 cm, respectively.17 Similar pituitary gland measurements are obtained with CT.18 Magnetic resonance imaging is preferred over CT, given the greater sensitivity of MRI for detection of pathological changes in the pituitary gland.19 Pituitary neoplasms that are larger than the normal size of the pituitary gland are considered macrotumors. On T2-weighted MRI images, a normal pituitary gland has a mixed intensity and strong, uniform contrast enhancement.17 However, pituitary neoplasms do not have a consistent pattern of signal intensity or degree of contrast enhancement on MRI images.20 Pituitary neoplasms may be hypo- to heterogeneously hyperintense on T2-weighted images and hypo- to isointense on T1-weighted images and may have irregular patterns of contrast enhancement ranging from ring to heterogenous enhancement.20,21

Treatment of cats with pituitary tumors includes palliative care or definitive interventions such as radiation therapy or hypophysectomy. Palliative care is directed at endocrine control and reversal of neurologic signs.19 With administration of corticosteroids, median survival time for cats with pituitary neoplasia is 52 days.3 Hypophysectomy may prolong survival time for affected cats; survival times ranging from 6 to 46 months for small numbers of cats have been reported.22,23 Although insulin requirements rapidly lessen after hypophysectomy, treated cats must be given supplements of other pituitary hormones during their lifetimes.22,23 Radiation therapy also prolongs survival time in cats with pituitary neoplasms. With conventional fractionated radiation therapy protocols, the median survival time in treated cats ranges from approximately 17 to 28 months.24,25,26,27 With stereotactic radiation therapy, median survival time is approximately 36 months.28 In cats with insulin resistance secondary to a functional pituitary neoplasm, radiation therapy results in a decrease in insulin requirements to maintain glycemic control in 55% to 95% of cats.24,25,26,27,28

Pituitary neoplasms may be more common in cats than previously considered.10 As highlighted by the cat of the present report, neurologic signs may be nonspecific and may simply involve abnormal mentation. Blindness may implicate a prosencephalic lesion or involvement of the optic nerve or chiasm. Conversely, clinical signs may solely relate to an endocrine dysfunction. Given the prevalence of pituitary neoplasms in diabetic cats, imaging of the pituitary gland should be considered in cats that are resistant to insulin treatment when an alternative explanation for that resistance is not identified.8 Likewise, postmortem gross and microscopic evaluation of the pituitary gland should be performed in cats with diabetes mellitus that undergo necropsy. Typical histologic findings include a well-demarcated mass that has replaced the normal pituitary tissue with pseudorosettes, nests, and cords of neoplastic pituitary epithelium. Cytoplasmic staining can vary depending on the cell of origin; however, immunohistochemical analysis in combination with endocrinologic testing is needed to further define the cell of origin. Data acquired by use of immunohistochemical staining for pituitary hormones may provide a greater understanding of the plurihormonal potential of pituitary neoplasms.

References

  • 1.

    Hullinger RL. The endocrine system. In: Evans HE, de Lahunta A, eds. Miller's anatomy of the dog. 4th ed. St Louis: Elsevier, 2013;406427.

    • Search Google Scholar
    • Export Citation
  • 2.

    Rosol TJ, Gröne A. Pituitary gland. In: Grant MM, ed. Jubb, Kennedy & Palmer's pathology of domestic animals. 6th ed. St Louis: Elsevier, 2016;276291.

    • Search Google Scholar
    • Export Citation
  • 3.

    Troxel MT, Vite CH, Van Winkle TJ, et al. Feline intracranial neoplasia: retrospective review of 160 cases (1985–2001). J Vet Intern Med 2003;17:850859.

    • Search Google Scholar
    • Export Citation
  • 4.

    Cross E, Moreland R, Wallack S. Feline pituitary-dependent hyperadrenocorticism and insulin resistance due to a plurihormonal adenoma. Top Companion Anim Med 2012;27:820.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Meij BP, van der Vlugt-Meijer RH, van den Ingh TS, et al. Somatotroph and corticotroph pituitary adenoma (double adenoma) in a cat with diabetes mellitus and hyperadrenocorticism. J Comp Pathol 2004;130:209215.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Sharman M, FitzGerald L, Kiupel M. Concurrent somatotroph and plurihormonal pituitary adenomas in a cat. J Feline Med Surg 2013;15:945952.

  • 7.

    Peterson ME, Taylor RS, Greco DS, et al. Acromegaly in 14 cats. J Vet Intern Med 1990;4:192201.

  • 8.

    Elliott DA, Feldman EC, Koblik PD, et al. Prevalence of pituitary tumors among diabetic cats with insulin resistance. J Am Vet Med Assoc 2000;216:17651768.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9.

    Niessen SJ, Petrie G, Gaudiano F, et al. Feline acromegaly: an underdiagnosed endocrinopathy? J Vet Intern Med 2007;21:899905.

  • 10.

    Niessen SJ, Forcada Y, Mantis P, et al. Studying cat (Felis catus) diabetes: beware of the acromegalic imposter. PLoS One 2015;10:e0127794.

  • 11.

    Lichtensteiger CA, Wortman JA, Eigenmann JE. Functional pituitary acidophil adenoma in a cat with diabetes mellitus and acromegalic features. Vet Pathol 1986;23:518521.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Lamb CR, Ciasca TC, Mantis P, et al. Computed tomographic signs of acromegaly in 68 diabetic cats with hypersomatotropism. J Feline Med Surg 2014;16:99108.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Fischetti AJ, Gisselman K, Peterson ME. CT and MRI evaluation of skull bones and soft tissues in six cats with presumed acromegaly versus 12 unaffected cats. Vet Radiol Ultrasound 2012;53:535539.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Borgeat K, Niessen SJM, Wilkie L, et al. Time spent with cats is never wasted: lessons learned from feline acromegalic cardiomyopathy, a naturally occurring animal model of the human disease. PLoS One 2018;13:e0194342.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Boland LA, Barrs VR. Peculiarities of feline hyperadrenocorticism: update on diagnosis and treatment. J Feline Med Surg 2017;19:933947.

  • 16.

    Fletcher JM, Scudder CJ, Kiupel M, et al. Hypersomatotropism in 3 cats without concurrent diabetes mellitus. J Vet Intern Med 2016;30:12161221.

  • 17.

    Wallack ST, Wisner ER, Feldman EC. Mensuration of the pituitary gland from magnetic resonance images in 17 cats. Vet Radiol Ultrasound 2003;44:278282.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18.

    Tyson R, Graham JP, Bermingham E, et al. Dynamic computed tomography of the normal feline hypophysis cerebri (Glandula pituitaria). Vet Radiol Ultrasound 2005;46:3338.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Niessen SJ, Church DB, Forcada Y. Hypersomatotropism, acromegaly, and hyperadrenocorticism and feline diabetes mellitus. Vet Clin North Am Small Anim Pract 2013;43:319350.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Posch B, Dobson J, Herrtage M. Magnetic resonance imaging findings in 15 acromegalic cats. Vet Radiol Ultrasound 2011;52:422427.

  • 21.

    Troxel MT, Vite CH, Massicotte C, et al. Magnetic resonance imaging features of feline intracranial neoplasia: retrospective analysis of 46 cats. J Vet Intern Med 2004;18:176189.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.

    Meij BP, Auriemma E, Grinwis G, et al. Successful treatment of acromegaly in a diabetic cat with transsphenoidal hypophysectomy. J Feline Med Surg 2010;12:406410.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Meij BP, Voorhout G, van den Ingh TS, et al. Transsphenoidal hypophysectomy for treatment of pituitary-dependent hyperadrenocorticism in 7 cats. Vet Surg 2001;30:7286.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24.

    Brearley MJ, Polton GA, Littler RM, et al. Coarse fractionated radiation therapy for pituitary tumours in cats: a retrospective study of 12 cases. Vet Comp Oncol 2006;4:209217.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Dunning MD, Lowrie CS, Bexfield NH, et al. Exogenous insulin treatment after hypofractionated radiotherapy in cats with diabetes mellitus and acromegaly. J Vet Intern Med 2009;23:243249.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Mayer MN, Greco DS, LaRue SM. Outcomes of pituitary tumor irradiation in cats. J Vet Intern Med 2006;20:11511154.

  • 27.

    Sellon RK, Fidel J, Houston R, et al. Linear-accelerator-based modified radiosurgical treatment of pituitary tumors in cats: 11 cases (1997–2008). J Vet Intern Med 2009;23:10381044.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Wormhoudt TL, Boss M-K, Lunn K, et al. Stereotactic radiation therapy for the treatment of functional pituitary adenomas associated with feline acromegaly. J Vet Intern Med 2018;32:13831391.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • Figure 1

    Photograph of a transverse section through the rostral aspect of the cerebrum at the level of the optic chiasm in an 8-year-old domestic shorthair cat that was examined because of abnormal mentation and circling. A large tan mass (asterisk) located in the area of the pituitary gland between the piriform lobes has deviated and compressed the optic chiasm (arrows). Bar = 5 mm.

  • Figure 2

    Photomicrographs of a section of the intracranial mass in the cat in Figure 1. The mass is densely cellular and composed of round to polygonal neoplastic cells without a defined architecture. Pseudorosettes (arrow) and packets of neoplastic cells that each have abundant, pale cytoplasm and a round to oval nucleus containing a single prominent nucleolus are present. H&E stain; bar = 20 μm. Inset—Rare mitotic figures (arrowhead) are observed. H&E stain; bar = 50 μm.

  • Figure 3

    Photomicrographs of another section of the intracranial mass. The transverse section illustrated in Figure 1 is shown (top left) with a rectangular outline that denotes the region where the section was obtained. At the dorsal aspect of the mass (asterisk), a thin rim of normal-appearing adenohypophyseal tissue (between arrows) was observed adjacent to the optic chiasm (arrowhead). H&E stain; bar = 500 μm. Inset—Higher-magnification view of the apparently normal pituitary tissue adjacent to the neoplasm (asterisk). H&E stain; bar = 50 μm.

  • 1.

    Hullinger RL. The endocrine system. In: Evans HE, de Lahunta A, eds. Miller's anatomy of the dog. 4th ed. St Louis: Elsevier, 2013;406427.

    • Search Google Scholar
    • Export Citation
  • 2.

    Rosol TJ, Gröne A. Pituitary gland. In: Grant MM, ed. Jubb, Kennedy & Palmer's pathology of domestic animals. 6th ed. St Louis: Elsevier, 2016;276291.

    • Search Google Scholar
    • Export Citation
  • 3.

    Troxel MT, Vite CH, Van Winkle TJ, et al. Feline intracranial neoplasia: retrospective review of 160 cases (1985–2001). J Vet Intern Med 2003;17:850859.

    • Search Google Scholar
    • Export Citation
  • 4.

    Cross E, Moreland R, Wallack S. Feline pituitary-dependent hyperadrenocorticism and insulin resistance due to a plurihormonal adenoma. Top Companion Anim Med 2012;27:820.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Meij BP, van der Vlugt-Meijer RH, van den Ingh TS, et al. Somatotroph and corticotroph pituitary adenoma (double adenoma) in a cat with diabetes mellitus and hyperadrenocorticism. J Comp Pathol 2004;130:209215.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Sharman M, FitzGerald L, Kiupel M. Concurrent somatotroph and plurihormonal pituitary adenomas in a cat. J Feline Med Surg 2013;15:945952.

  • 7.

    Peterson ME, Taylor RS, Greco DS, et al. Acromegaly in 14 cats. J Vet Intern Med 1990;4:192201.

  • 8.

    Elliott DA, Feldman EC, Koblik PD, et al. Prevalence of pituitary tumors among diabetic cats with insulin resistance. J Am Vet Med Assoc 2000;216:17651768.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9.

    Niessen SJ, Petrie G, Gaudiano F, et al. Feline acromegaly: an underdiagnosed endocrinopathy? J Vet Intern Med 2007;21:899905.

  • 10.

    Niessen SJ, Forcada Y, Mantis P, et al. Studying cat (Felis catus) diabetes: beware of the acromegalic imposter. PLoS One 2015;10:e0127794.

  • 11.

    Lichtensteiger CA, Wortman JA, Eigenmann JE. Functional pituitary acidophil adenoma in a cat with diabetes mellitus and acromegalic features. Vet Pathol 1986;23:518521.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Lamb CR, Ciasca TC, Mantis P, et al. Computed tomographic signs of acromegaly in 68 diabetic cats with hypersomatotropism. J Feline Med Surg 2014;16:99108.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Fischetti AJ, Gisselman K, Peterson ME. CT and MRI evaluation of skull bones and soft tissues in six cats with presumed acromegaly versus 12 unaffected cats. Vet Radiol Ultrasound 2012;53:535539.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Borgeat K, Niessen SJM, Wilkie L, et al. Time spent with cats is never wasted: lessons learned from feline acromegalic cardiomyopathy, a naturally occurring animal model of the human disease. PLoS One 2018;13:e0194342.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Boland LA, Barrs VR. Peculiarities of feline hyperadrenocorticism: update on diagnosis and treatment. J Feline Med Surg 2017;19:933947.

  • 16.

    Fletcher JM, Scudder CJ, Kiupel M, et al. Hypersomatotropism in 3 cats without concurrent diabetes mellitus. J Vet Intern Med 2016;30:12161221.

  • 17.

    Wallack ST, Wisner ER, Feldman EC. Mensuration of the pituitary gland from magnetic resonance images in 17 cats. Vet Radiol Ultrasound 2003;44:278282.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18.

    Tyson R, Graham JP, Bermingham E, et al. Dynamic computed tomography of the normal feline hypophysis cerebri (Glandula pituitaria). Vet Radiol Ultrasound 2005;46:3338.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Niessen SJ, Church DB, Forcada Y. Hypersomatotropism, acromegaly, and hyperadrenocorticism and feline diabetes mellitus. Vet Clin North Am Small Anim Pract 2013;43:319350.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Posch B, Dobson J, Herrtage M. Magnetic resonance imaging findings in 15 acromegalic cats. Vet Radiol Ultrasound 2011;52:422427.

  • 21.

    Troxel MT, Vite CH, Massicotte C, et al. Magnetic resonance imaging features of feline intracranial neoplasia: retrospective analysis of 46 cats. J Vet Intern Med 2004;18:176189.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.

    Meij BP, Auriemma E, Grinwis G, et al. Successful treatment of acromegaly in a diabetic cat with transsphenoidal hypophysectomy. J Feline Med Surg 2010;12:406410.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Meij BP, Voorhout G, van den Ingh TS, et al. Transsphenoidal hypophysectomy for treatment of pituitary-dependent hyperadrenocorticism in 7 cats. Vet Surg 2001;30:7286.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24.

    Brearley MJ, Polton GA, Littler RM, et al. Coarse fractionated radiation therapy for pituitary tumours in cats: a retrospective study of 12 cases. Vet Comp Oncol 2006;4:209217.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Dunning MD, Lowrie CS, Bexfield NH, et al. Exogenous insulin treatment after hypofractionated radiotherapy in cats with diabetes mellitus and acromegaly. J Vet Intern Med 2009;23:243249.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Mayer MN, Greco DS, LaRue SM. Outcomes of pituitary tumor irradiation in cats. J Vet Intern Med 2006;20:11511154.

  • 27.

    Sellon RK, Fidel J, Houston R, et al. Linear-accelerator-based modified radiosurgical treatment of pituitary tumors in cats: 11 cases (1997–2008). J Vet Intern Med 2009;23:10381044.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Wormhoudt TL, Boss M-K, Lunn K, et al. Stereotactic radiation therapy for the treatment of functional pituitary adenomas associated with feline acromegaly. J Vet Intern Med 2018;32:13831391.

    • Crossref
    • Search Google Scholar
    • Export Citation

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