Diagnostic imaging findings and endocrine test results in dogs with pituitary-dependent hyperadrenocorticism that did or did not have neurologic abnormalities: 157 cases (1989–2005)

Farica D. Wood Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Rachel E. Pollard Departments of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Megan R. Uerling Departments of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Edward C. Feldman Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Abstract

Objective—To compare imaging findings in dogs with pituitary-dependent hyperadrenocorticism (PDH) that did or did not have neurologic abnormalities.

Design—Retrospective case series.

Animals—157 dogs with PDH that did (n = 73) or did not (84) have neurologic abnormalities.

Procedures—Medical records were reviewed for the presence and nature of clinical signs of CNS disease, and computed tomographic and magnetic resonance images were reviewed for evidence of a pituitary tumor.

Results—60 of the 84 (71%) dogs without neurologic abnormalities and 48 of the 73 (66%) dogs with neurologic abnormalities had a detectable pituitary tumor. However, 17 of the 84 (20%) dogs without neurologic abnormalities had a pituitary macrotumor (ie, a tumor ≥ 10 mm in height), and 41 of the 73 (56%) dogs with neurologic abnormalities did not have a detectable pituitary tumor or had a pituitary microtumor. Vague signs of CNS dysfunction (ie, lethargy, inappetence, and mental dullness) were more specific for detection of pituitary macrotumors than were CNS-specific signs (ie, seizure or blindness).

Conclusions and Clinical Relevance—Results suggested that there was no apparent relationship between a pituitary tumor and development of neurologic abnormalities in dogs with PDH. In addition, neurologic abnormalities in dogs with pituitary macrotumors were often vague (ie, lethargy, inappetence, and mental dullness).

Abstract

Objective—To compare imaging findings in dogs with pituitary-dependent hyperadrenocorticism (PDH) that did or did not have neurologic abnormalities.

Design—Retrospective case series.

Animals—157 dogs with PDH that did (n = 73) or did not (84) have neurologic abnormalities.

Procedures—Medical records were reviewed for the presence and nature of clinical signs of CNS disease, and computed tomographic and magnetic resonance images were reviewed for evidence of a pituitary tumor.

Results—60 of the 84 (71%) dogs without neurologic abnormalities and 48 of the 73 (66%) dogs with neurologic abnormalities had a detectable pituitary tumor. However, 17 of the 84 (20%) dogs without neurologic abnormalities had a pituitary macrotumor (ie, a tumor ≥ 10 mm in height), and 41 of the 73 (56%) dogs with neurologic abnormalities did not have a detectable pituitary tumor or had a pituitary microtumor. Vague signs of CNS dysfunction (ie, lethargy, inappetence, and mental dullness) were more specific for detection of pituitary macrotumors than were CNS-specific signs (ie, seizure or blindness).

Conclusions and Clinical Relevance—Results suggested that there was no apparent relationship between a pituitary tumor and development of neurologic abnormalities in dogs with PDH. In addition, neurologic abnormalities in dogs with pituitary macrotumors were often vague (ie, lethargy, inappetence, and mental dullness).

In recent years, the management of dogs with PDH has improved, with the result that affected dogs may have a longer life expectancy than in the past, allowing more time for causative pituitary tumors to grow. It has been estimated that 10% to 30% of dogs with PDH will eventually develop a pituitary tumor large enough to cause neurologic signs.1 However, tumor size alone cannot be used to predict development of neurologic signs,2 and more information is needed on the size of pituitary tumors in dogs with PDH that do or do not have neurologic signs.

Neurologic abnormalities in dogs with PDH may be specific to the CNS (eg, circling, seizures, and blindness) or vague and nonspecific (eg, mental dullness, lethargy, poor appetite, and aimless pacing).3 Regardless, such abnormalities may prompt a recommendation for diagnostic imaging (ie, CT or MRI) to determine whether they are the result of a large pituitary tumor amenable to radiation therapy. Alternatively, diagnostic imaging may be performed to determine the likelihood of neurologic dysfunction in dogs with PDH that do not currently have neurologic signs. Arbitrarily, pituitary tumors have been classified as macrotumors if they are ≥ 10 mm in greatest diameter and as microtumors if they are < 10 mm in greatest diameter,4 with macrotumors considered more likely to cause neurologic signs than microtumors.

Previous studies2,5 have indicated that dogs with PDH that also have neurologic signs or CT or MRI evidence of a pituitary tumor have higher mean plasma endogenous ACTH concentrations than do dogs with PDH that do not have neurologic signs or have microtumors. In contrast, another study6 reported that there was no association between plasma endogenous ACTH concentration and tumor size in dogs with PDH. Therefore, the decision to perform radiation therapy in dogs with PDH is currently made on the basis of detection of neurologic signs in conjunction with size of any pituitary tumor identified by means of CT or MRI.

The purpose of the study reported here was to compare imaging findings and results of serum biochemical testing in dogs with PDH that did or did not have clinical signs of CNS disease.

Criteria for Selection of Cases

Medical records of all dogs examined at the University of California, Davis, Veterinary Medical Teaching Hospital between December 1, 1989, and August 18, 2005, in which a diagnosis of PDH had been made were reviewed. Dogs were included in the present study only if history and physical examination findings were consistent with a diagnosis of hyperadrenocorticism; serum biochemical testing, urinalysis, and bacterial culture of a urine sample had revealed at least 1 clinicopathologic abnormality suggestive of hyperadrenocorticism (ie, low or low-normal BUN concentration, high serum alkaline phosphatase and alanine aminotransferase activities, hypercholesterolemia, urine specific gravity < 1.020, or microbial growth); and results of at least 1 of 3 commonly used screening tests for hyperadrenocorticism (ie, low-dose dexamethasone suppression test, ACTH stimulation test, or measurement of urine cortisol-to-creatinine ratio) were abnormal. In addition, dogs were included in the present study only if hyperadrenocorticism had been confirmed to be of pituitary gland, rather than adrenal gland, origin on the basis of results of a low-dose dexamethasone suppression test (ie, serum cortisol concentration 4 hours after administration of a low dose of dexamethasone < 50% of the baseline concentration or < 1.0 μg/dL), an endogenous plasma ACTH concentration ≥ 45 pg/mL, or ultrasonographic detection of 2 adrenal glands of relatively equal size. Finally, dogs were included in the present study only if contrast-enhanced CTa,b or MRIc,d including, but not necessarily limited to, the pituitary gland region had been performed within 2 months of the diagnosis of PDH.

Procedures

Medical records review—Medical records of cases included in the present study were reviewed, and information was obtained regarding age, weight, the presence and nature of any neurologic abnormalities, results of clinicopathologic testing, and height of the pituitary gland or pituitary tumor on cross-sectional computed tomographic or magnetic resonance images.

Diagnostic imaging—In all dogs, cross-sectional CT or MRI of the entire brain had been performed to identify a cause for neurologic signs or to identify candidates for radiation therapy. Images were obtained before and between 1 and 5 minutes after IV contrast administration. Dynamic CT imaging of the pituitary gland was not performed in any dog. Cross-sectional images obtained at the level of the pituitary gland were examined for evidence of a pituitary mass and, if a mass was seen, the shape of the mass; for the presence and homogeneity of contrast enhancement; and for the presence of compression of surrounding brain tissue. Brain compression was defined as displacement of regional brain structures, dilatation of ventricular structures, or the presence of edema. All pituitary masses that were seen were arbitrarily categorized as tumors. The size of the pituitary gland or pituitary tumor was determined by measuring the height on transverse, postcontrast images. The presence of mineralization or other intracranial lesions was recorded.

Statistical analysis—Dogs were allotted to 2 groups on the basis of whether they did or did not have neurologic signs, and Student t tests were used to compare age, results of clinicopathologic testing, and size of the pituitary gland or pituitary tumor between groups. A value of P < 0.05 was considered significant. Standard equations were used to calculate sensitivity, specificity, positive predictive value, and negative predictive value of individual neurologic signs to predict whether dogs had a pituitary macrotumor (ie, a pituitary tumor ≥ 10 mm in greatest diameter).

Results

A total of 157 dogs met the criteria for inclusion in the study. Of these, 84 (54%) did not have any clinical signs other than those associated with hyperadrenocorticism and 73 (46%) had neurologic signs in addition to clinical signs associated with hyperadrenocorticism. One dog with neurologic signs had been included in a previous study.2 None of the dogs with neurologic signs had CT or MRI lesions, other than pituitary gland lesions, that could account for the neurologic signs.

Body weight for dogs without neurologic signs (median, 15.0 kg [29.9 lb]; range, 4.1 to 61 kg [9.0 to 134.2 lb]) was similar to body weight for dogs with neurologic signs (median, 13.6 kg [33.0 lb]; range, 3.7 to 46 kg [8.1 to 101.2 lb]). Mean age at the time of diagnostic imaging for dogs without neurologic signs (mean ± SD, 10.1 ± 2.2 years) was not significantly (P = 0.22) different from mean age for dogs with neurologic signs (10.5 ± 2.8 years). A variety of breeds were represented in both groups, with Australian Shepherds, Beagles, Boston Terriers, Cocker Spaniels, Dachshunds, Labrador Retrievers, Miniature Schnauzers, Shih Tzus, and Toy Poodles being most common.

Dogs with PDH but without neurologic signs— Computed tomography was performed in 42 of the 84 dogs with PDH that did not have neurologic signs, and MRI was performed in the other 42 (Figure 1). Sixty (71%) dogs (19 males and 41 females) had a detectable pituitary tumor, and 24 (29%) dogs (11 males and 13 females) did not. Mean ± SD height of the pituitary gland in the 24 dogs without a detectable tumor was 3.6 ± 0.2 mm (reference range for CT, 3.2 to 5.1 mm; reference range for MRI, 3 to 7.5 mm7,8). Mean height of the pituitary tumor in the 60 dogs with a detectable tumor was 8.5 ± 4.1 mm; height of the pituitary tumor was between 3 and 9 mm in 43 of the 60 (72%) dogs, between 10 and 14 mm in 11 (18%) dogs, between 15 and 20 mm in 5 (8%) dogs, and > 20 mm in 1 (2%) dog.

The pituitary tumor was round in 37 of 60 (61%) dogs with a pituitary tumor, irregular in 11 (18%), oval in 8 (13%), and pyramidal in 4 (7%). Forty-nine of 60 (82%) dogs with a pituitary tumor had homogeneous contrast enhancement, 10 (17%) had heterogeneous contrast enhancement, and 1 (2%) did not have contrast enhancement. Brain compression was identified in 11 (18%) of the dogs but was not identified in the other 49 (82%). Four (7%) dogs had evidence of mineralization of the pituitary tumor.

Figure 1—
Figure 1—

Axial postcontrast CT images of 2 dogs with PDH but no evidence of neurologic dysfunction. A—The pituitary gland (arrow) does not extend dorsal to the sella turcica and has normal contrast enhancement. B—A homogenously contrast-enhancing pyramidal mass (arrow) in the hypophyseal fossa extends dorsal to the sella turcica. Asymmetry of the lateral ventricles is evident.

Citation: Journal of the American Veterinary Medical Association 231, 7; 10.2460/javma.231.7.1081

Figure 2—
Figure 2—

Axial T1-weighted postcontrast magnetic resonance image of a dog with PDH and neurologic abnormalities. There is a homogenously contrast-enhancing irregularly shaped mass in the hypophyseal fossa (arrow) extending dorsal to the sella turcica. Overt brain compression is not evident.

Citation: Journal of the American Veterinary Medical Association 231, 7; 10.2460/javma.231.7.1081

Dogs with PDH and neurologic signs—Computed tomography was performed in 34 of the 73 dogs with PDH that also had neurologic signs, and MRI was performed in the other 39 (Figure 2). Forty-eight (66%) dogs (15 males and 33 females) had a detectable pituitary tumor, and 25 (34%) dogs (8 males and 17 females) did not. Mean ± SD height of the pituitary gland in the 25 dogs without a detectable tumor was 3.5 ± 0.1 mm. Mean height of the pituitary tumor in the 48 dogs with a detectable tumor was 13.3 ± 5.6 mm; height of the pituitary tumor was between 3 and 9 mm in 16 of the 48 (33%) dogs, between 10 and 14 mm in 11 (23%) dogs, between 15 and 20 mm in 12 (25%) dogs, and > 20 mm in 9 (19%) dogs.

The pituitary tumor was round in 25 of the 48 (52%) dogs with a pituitary tumor, irregular in 12 (25%), oval in 7 (15%), and pyramidal in 3 (6%). Thirty-four of the 48 (71%) dogs with a pituitary tumor had homogeneous contrast enhancement, and 14 (29%) had heterogeneous contrast enhancement. Brain compression was identified in 20 (42%) of the dogs but was not identified in the other 28 (58%). Twenty-three (48%) dogs had evidence of mineralization of the pituitary tumor.

Neurologic signs identified in dogs in this group were categorized as nonspecific, including mental dullness (indicating a change in the level of consciousness), inappetence, and lethargy, or CNS-specific (ie, seizures, circling, head tilt, cranial nerve deficits, blindness, ataxia, head pressing, or behavioral changes); many dogs had signs involving > 1 category. Of the 25 dogs with neurologic signs that did not have a detectable pituitary tumor, 1 had mental dullness, 1 had inappetence, 11 had lethargy, and 16 had CNS-specific signs (behavioral changes, 6; seizures, 4; cranial nerve deficits, 3; head pressing, 1; head tilt, 1; and blindness, 1). Of the 48 dogs with neurologic signs that did have a detectable pituitary tumor, 3 had mental dullness, 19 had inappetence, 19 had lethargy, and 28 had CNS-specific signs (seizures, 12; cranial nerve deficits, 4; behavioral changes, 4; circling, 3; head tilt, 2; blindness, 2; and ataxia, 1).

Group comparisons—Mean height of the pituitary gland for dogs without neurologic signs that did not have a tumor was not significantly different from mean height for dogs with neurologic signs that did not have a tumor. However, mean height of the pituitary tumor in the 60 dogs without neurologic signs was significantly (P < 0.001) less than mean height of the pituitary tumor in the 48 dogs with neurologic signs.

Table 1—

Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of using various neurologic signs used to predict a pituitary macrotumor (ie, a pituitary tumor ≥ 10 mm in height) in dogs with PDH.

Table 1—

When the 2 groups were compared, baseline plasma cortisol concentration (mean ± SD, 5.4 ± 3.7 μg/dL and 5.4 ± 2.8 μg/dL, respectively; P = 0.91), plasma cortisol concentration 4 hours after administration of a low dose of dexamethasone (3.3 ± 2.8 μg/dL and 3.1 ± 3.3 μg/dL, respectively; P = 0.90), and plasma cortisol concentration 8 hours after administration of a low dose of dexamethasone (4.1 ± 3.1 μg/dL and 4.2 ± 2.8 μg/dL, respectively; P = 0.93) were not significantly different between dogs without neurologic signs and dogs with neurologic signs. However, mean plasma endogenous ACTH concentration for dogs with neurologic signs (210.3 ± 342.5 pg/mL) was significantly (P = 0.02) higher than mean concentration for dogs without neurologic signs (113.9 ± 90.5 pg/mL).

Sensitivity and specificity of neurologic signs— Sensitivity of CNS-specific neurologic signs used for predicting whether dogs had a pituitary macrotumor (ie, a pituitary tumor ≥ 10 mm in greatest diameter) was low (Table 1). Specificity, however, was high for 2 of the nonspecific neurologic signs (inappetence and mental dullness).

Discussion

Results of the present study indicated that there was no apparent relationship between presence of a pituitary tumor and development of neurologic signs in dogs with PDH. Among dogs with a pituitary tumor, tumor size was significantly greater in dogs with neurologic signs than in dogs without. However, 17 of the 84 (20%) dogs without neurologic signs had a pituitary macrotumor (ie, a tumor ≥ 10 mm in height), and 41 of the 73 (56%) dogs with neurologic signs did not have a detectable pituitary tumor or had a pituitary microtumor (ie, a tumor < 10 mm in height).

Results of the present study also indicated that there was no apparent relationship between presence or size of a pituitary tumor and detection of CNS-specific signs (eg, seizures, circling, or ataxia). Observation of such CNS signs was not highly sensitive or specific for predicting the presence of a pituitary macrotumor in dogs with PDH. Presumably, dogs with CNS-specific signs in the present study that did not have a detectable pituitary tumor or had a pituitary microtumor had other causes for neurologic dysfunction, such as vestibular disease or idiopathic epilepsy, that were not associated with any visible lesions on computed tomographic or magnetic resonance images. In contrast, less specific neurologic signs (ie, lethargy, mental dullness, and inappetence) were highly specific for detection of a pituitary macrotumor in dogs with PDH, although none of these signs were particularly sensitive. Although these signs may be seen secondary to brain compression by a pituitary tumor, they might also be caused by a multitude of unrelated disorders.

The imaging appearance of pituitary tumors in dogs with neurologic signs in the present study suggested that CNS dysfunction may be related less to tumor size and perhaps more to how rapidly the tumor is growing. Potentially, adenomas or adenocarcinomas with a rapid growth rate might enlarge so quickly that the surrounding brain tissue does not have time to compensate for the lesion, whereas slowly growing tumors might be able to attain a larger size before causing neurologic signs to develop. Although pituitary adenocarcinomas are rare in people, there is reason to believe that these tumors are more rapidly growing than adenomas and result in more profound neurologic signs.

Use of CT to evaluate dogs with PDH has been described previously.9 Although CT involves the use of ionizing radiation, the good spatial resolution, ability to image in multiple planes, and relatively widespread availability make this imaging modality attractive as a way to evaluate dogs with PDH for the presence of pituitary tumors. In people, MRI is the preferred method of intracranial imaging. In comparison to CT, MRI has superior soft tissue resolution while still being capable of multiplanar imaging. As MRI becomes more widely available in the veterinary community, this imaging modality is likely to surpass CT as the method of choice for assessment of the pituitary region. In people, however, lesion detection rates are similar for the 2 modalities.10

The administration of contrast agents during CT and MRI allows for better assessment of lesion size and shape and increases the sensitivity and specificity of lesion detection.11 In the present study, the use of contrast agents allowed for better visualization of the pituitary gland but enhancement characteristics were not substantially different between dogs with and without neurologic signs. Dynamic CT and MRI techniques that allow visualization of contrast medium flowing into the pituitary gland parenchyma have been developed recently, and in people, these techniques appear to be useful for the detection of extremely small pituitary tumors.12 Dynamic CT in dogs has been described,13 and this technique shows promise for enhancing visibility of pituitary tumors. However, dynamic contrast studies were not performed on dogs in the present study.

Previous studies6,14,15 did not identify any breed predilections for development of pituitary macrotumors or neurologic signs. Duesberg et al14 reported that 11 of 13 dogs with PDH and neurologic signs weighed > 20 kg (44 lb) and concluded that CT or MRI of the brain may be indicated in large-breed dogs with PDH, as they may be predisposed to developing larger tumors. In the present study, we did not find any significant difference in body weight between dogs with and without neurologic signs, indicating that the presence of neurologic signs was not more common in larger dogs.

Although dogs in the present study with neurologic signs had significantly higher plasma endogenous ACTH concentrations than did dogs without neurologic signs, there were no significant differences between groups in regard to baseline plasma cortisol concentration or cortisol concentrations 4 and 8 hours after administration of a low dose of dexamethasone.

There were several limitations related to the retrospective nature of the present study. Importantly, results of a complete neurologic examination were not available for most of the dogs, although we believe it reasonable to assume that all neurologic abnormalities that were detected were recorded in the medical records. We also assumed that the neuroanatomic origin of neurologic signs that were recorded could potentially be attributable to the presence of a pituitary mass. Finally, at our institution, CSF analysis is not routinely performed in dogs with pituitary tumors. Thus, although results of CSF analysis may be of use in dogs with PDH, such data were not available for the present study.

In conclusion, results of the present study suggested that dogs with PDH that have or develop CNS-specific signs such as seizures or blindness should not be assumed to have a large pituitary tumor. In fact, it appeared that clinical signs associated with larger tumors were often vague and included lethargy, inappetence, and mental dullness. However, there was no evidence that results of biochemical testing were related to development of neurologic signs. Thus, it is imperative that dogs with PDH that have signs of neurologic dysfunction undergo confirmation of a pituitary tumor by means of diagnostic imaging.

ABBREVIATIONS

PDH

Pituitary-dependent hyperadrenocorticism

CT

Computed tomography

MRI

Magnetic resonance imaging

a.

GE 8800 whole body CT scanner or XI helical scanner, General Electric, Medical Systems Divisions, Milwaukee, Wis.

b.

Conray 400, Mallinckrodt Imaging, Tyco International Inc, Princeton, NJ.

c.

Signa 1.5 T, General Electric, Medical Systems Divisions, Milwaukee, Wis.

d.

Magnevist, Berlex Laboratories Inc, Wayne, NJ.

References

  • 1.

    Bertoy EH, Feldman EC & Nelson RW, et al. One-year follow-up evaluation of magnetic resonance imaging of the brain in dogs with pituitary-dependent hyperadrenocorticism. J Am Vet Med Assoc 1996;208:12681273.

    • Search Google Scholar
    • Export Citation
  • 2.

    Kipperman BS, Feldman EC & Dybdal NO, et al. Pituitary tumor size, neurologic signs, and relation to endocrine test results in dogs with pituitary-dependent hyperadrenocorticism: 43 cases (1980–1990). J Am Vet Med Assoc 1992;201:762767.

    • Search Google Scholar
    • Export Citation
  • 3.

    Feldman EC, Nelson RW. Canine and feline endocrinology and reproduction. Philadelphia: WB Saunders Co, 1987.

  • 4.

    Theon AP, Feldman EC. Megavoltage irradiation of pituitary macrotumors in dogs with neurologic signs. J Am Vet Med Assoc 1998;213:225231.

    • Search Google Scholar
    • Export Citation
  • 5.

    Bosje JT, Rijnberk A & Mol JA, et al. Plasma concentrations of ACTH precursors correlate with pituitary size and resistance to dexamethasone in dogs with pituitary-dependent hyperadrenocorticism. Domest Anim Endocrinol 2002;22:201210.

    • Search Google Scholar
    • Export Citation
  • 6.

    Nelson RW, Ihle SL, Feldman EC. Pituitary macroadenomas and macroadenocarcinomas in dogs treated with mitotane for pituitary-dependent hyperadrenocorticism: 13 cases (1981–1986). J Am Vet Med Assoc 1989;194:16121617.

    • Search Google Scholar
    • Export Citation
  • 7.

    Kippenes H, Gavin PR & Kraft SL, et al. Mensuration of the normal pituitary gland from magnetic resonance images in 96 dogs. Vet Radiol Ultrasound 2001;42:130133.

    • Search Google Scholar
    • Export Citation
  • 8.

    van der Vlugt-Meijer RH, Voorhout G, Meij BP. Imaging of the pituitary gland in dogs with pituitary-dependent hyperadrenocorticism. Mol Cell Endocrinol 2002;197:8187.

    • Search Google Scholar
    • Export Citation
  • 9.

    Mauldin GN, Burk RL. The use of diagnostic computerized tomography and radiation therapy in canine and feline hyperadrenocorticism. Probl Vet Med 1990;2:557564.

    • Search Google Scholar
    • Export Citation
  • 10.

    Thuomas KA. Pituitary microadenoma. MR appearance and correlation with CT. Acta Radiol 1999;40:663.

  • 11.

    Macpherson P, Hadley DM & Teasdale E, et al. Pituitary microadenomas. Does gadolinium enhance their demonstration? Neuroradiology 1989;31:293298.

    • Search Google Scholar
    • Export Citation
  • 12.

    Stadnik T, Spruyt D & van Binst A, et al. Pituitary microadenomas: diagnosis with dynamic serial CT, conventional CT and T1-weighted MR imaging before and after injection of gadolinium. Eur J Radiol 1994;18:191198.

    • Search Google Scholar
    • Export Citation
  • 13.

    van der Vlugt-Meijer RH, Meij BP, van den Ingh TS, et al. Dynamic computed tomography of the pituitary gland in dogs with pituitary-dependent hyperadrenocorticism. J Vet Intern Med 2003;17:773780.

    • Search Google Scholar
    • Export Citation
  • 14.

    Duesberg CA, Feldman EC & Nelson RW, et al. Magnetic resonance imaging for diagnosis of pituitary macrotumors in dogs. J Am Vet Med Assoc 1995;206:657662.

    • Search Google Scholar
    • Export Citation
  • 15.

    Sarfaty D, Carrillo JM, Peterson ME. Neurologic, endocrinologic, and pathologic findings associated with large pituitary tumors in dogs: eight cases (1976–1984). J Am Vet Med Assoc 1988;193:854856.

    • Search Google Scholar
    • Export Citation
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