Hyperadrenocorticism in a dog due to ectopic secretion of adrenocorticotropic hormone
Spontaneous hyperadrenocorticism in dogs is known to be the result of excessive secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland or excessive autonomous glucocorticoid secretion by an adrenocortical tumor. Here, we report on an 8-year-old German shepherd dog in which ACTH-depen...
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| Veröffentlicht in: | Domestic animal endocrinology 2005-04, Vol.28 (3), p.338-348 |
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| creator | Galac, S. Kooistra, H.S. Voorhout, G. van den Ingh, T.S.G.A.M. Mol, J.A. van den Berg, G. Meij, B.P. |
| description | Spontaneous hyperadrenocorticism in dogs is known to be the result of excessive secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland or excessive autonomous glucocorticoid secretion by an adrenocortical tumor. Here, we report on an 8-year-old German shepherd dog in which ACTH-dependent hyperadrenocorticism was a result of ectopic ACTH secretion and could be related to an abdominal neuroendocrine tumor. Hyperadrenocorticism was diagnosed on the basis of the history, clinical signs, and elevated urinary corticoid/creatinine ratios (UCCRs; 236 and 350
×
10
−6; reference range |
| doi_str_mv | 10.1016/j.domaniend.2004.11.001 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67503579</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0739724004001468</els_id><sourcerecordid>67503579</sourcerecordid><originalsourceid>FETCH-LOGICAL-c393t-35f9bd3b87848983bdc49d7bd0c9f744a6096b6b5886d77de94c77183f5c753a3</originalsourceid><addsrcrecordid>eNqFkEFPHCEYhkljo6v1LygnbzN-LDDA0Zi2mph40D0TBr6xbHaGLcw28d-L3Y3tzROX5_le8hByyaBlwLrrdRvS6KaIU2iXAKJlrAVgX8iCaWUaACmOyAIUN41aCjghp6WsAUBV-5icMKk66JRYkNXd6xazCxmn5FOeo49lpHGijob0QsMO6Zwo-jlto6cFfcY5pommgf4vpTn_BX6lPKYJv5Gvg9sUPD-8Z2T14_vz7V3z8Pjz_vbmofHc8LnhcjB94L1WWmijeR-8MEH1AbwZlBCuA9P1XS-17oJSAY3wSjHNB-mV5I6fkav93W1Ov3dYZjvG4nGzcROmXbGdksClMhVUe9DnVErGwW5zHF1-tQzse1G7th9F7XtRy5itRat5cZjY9SOGf94hYQUu98DgknUvORa7elpWE8BoqQVU4mZPYE3xJ2K2xdcdjyHmWrYOx0-_8QaNRpXb</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67503579</pqid></control><display><type>article</type><title>Hyperadrenocorticism in a dog due to ectopic secretion of adrenocorticotropic hormone</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Galac, S. ; Kooistra, H.S. ; Voorhout, G. ; van den Ingh, T.S.G.A.M. ; Mol, J.A. ; van den Berg, G. ; Meij, B.P.</creator><creatorcontrib>Galac, S. ; Kooistra, H.S. ; Voorhout, G. ; van den Ingh, T.S.G.A.M. ; Mol, J.A. ; van den Berg, G. ; Meij, B.P.</creatorcontrib><description>Spontaneous hyperadrenocorticism in dogs is known to be the result of excessive secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland or excessive autonomous glucocorticoid secretion by an adrenocortical tumor. Here, we report on an 8-year-old German shepherd dog in which ACTH-dependent hyperadrenocorticism was a result of ectopic ACTH secretion and could be related to an abdominal neuroendocrine tumor. Hyperadrenocorticism was diagnosed on the basis of the history, clinical signs, and elevated urinary corticoid/creatinine ratios (UCCRs; 236 and 350
×
10
−6; reference range <10
×
10
−6). The UCCR remained elevated (226
×
10
−6) after three oral doses of dexamethasone (0.1
mg/kg body weight) at 8-h intervals. Ultrasonography revealed two equivalently enlarged adrenal glands, consistent with adrenocortical hyperplasia. Plasma ACTH concentration was clearly elevated (159 and 188
ng/l; reference range 5–85
ng/l). Computed tomography (CT) revealed that the pituitary was not enlarged. These findings were interpreted as indicating dexamethasone-resistant pituitary-dependent hyperadrenocorticism. Transsphenoidal hypophysectomy was performed but within 2 weeks after surgery, there was exacerbation of the clinical signs of hyperadrenocorticism. Plasma ACTH concentration (281
ng/l) and UCCRs (1518 and 2176
×
10
−6) were even higher than before surgery. Histological examination of the pituitary gland revealed no neoplasia. Stimulation of the pituitary with corticotropin-releasing hormone did not affect plasma ACTH and cortisol concentrations. Treatment with trilostane was started and restored normocorticism. CT of the pituitary fossa, 10 months after hypophysectomy, revealed an empty sella. Hence, it was presumed that there was ectopic secretion of ACTH. CT of the abdomen revealed a mass in the region of the pancreas and a few nodules in the liver. Partial pancreatectomy with adjacent lymph node extirpation was performed and the liver nodules were biopsied. Histological examination revealed a metastasized neuroendocrine tumor. Abdominal surgery was not curative and medical treatment with trilostane was continued. At 18 months after the abdominal surgery, the dog is still in good condition. In conclusion, the combination of (1) severe dexamethasone-resistant hyperadrenocorticism with elevated circulating ACTH levels, (2) definitive demonstration of the absence of pituitary neoplasia, and (3) an abdominal neuroendocrine tumor allowed the diagnosis of ectopic ACTH secretion.</description><identifier>ISSN: 0739-7240</identifier><identifier>EISSN: 1879-0054</identifier><identifier>DOI: 10.1016/j.domaniend.2004.11.001</identifier><identifier>PMID: 15760674</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Abdominal Neoplasms - secretion ; Abdominal Neoplasms - veterinary ; ACTH ; ACTH Syndrome, Ectopic - complications ; ACTH Syndrome, Ectopic - diagnosis ; ACTH Syndrome, Ectopic - veterinary ; adrenal cortex ; Adrenocortical Hyperfunction - etiology ; Adrenocortical Hyperfunction - veterinary ; adrenocortical hyperplasia ; Adrenocorticotropic Hormone - blood ; Adrenocorticotropic Hormone - secretion ; Animals ; antineoplastic agents ; Canine ; corticotropin ; corticotropin-releasing hormone ; Corticotropin-Releasing Hormone - pharmacology ; Cortisol ; Cushing syndrome ; Cushing's syndrome ; dexamethasone ; disease diagnosis ; Dog Diseases - diagnosis ; Dog Diseases - etiology ; Dog Diseases - surgery ; Dogs ; drug therapy ; hormone secretion ; Hydrocortisone - blood ; hyperadrenocorticism ; Liver - diagnostic imaging ; Male ; neoplasms ; Neuroendocrine tumor ; Neuroendocrine Tumors - secretion ; Neuroendocrine Tumors - veterinary ; Tomography, X-Ray Computed - veterinary ; trilostane ; Ultrasonography - veterinary ; urinary corticoid/creatinine ratio</subject><ispartof>Domestic animal endocrinology, 2005-04, Vol.28 (3), p.338-348</ispartof><rights>2004 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c393t-35f9bd3b87848983bdc49d7bd0c9f744a6096b6b5886d77de94c77183f5c753a3</citedby><cites>FETCH-LOGICAL-c393t-35f9bd3b87848983bdc49d7bd0c9f744a6096b6b5886d77de94c77183f5c753a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.domaniend.2004.11.001$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15760674$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Galac, S.</creatorcontrib><creatorcontrib>Kooistra, H.S.</creatorcontrib><creatorcontrib>Voorhout, G.</creatorcontrib><creatorcontrib>van den Ingh, T.S.G.A.M.</creatorcontrib><creatorcontrib>Mol, J.A.</creatorcontrib><creatorcontrib>van den Berg, G.</creatorcontrib><creatorcontrib>Meij, B.P.</creatorcontrib><title>Hyperadrenocorticism in a dog due to ectopic secretion of adrenocorticotropic hormone</title><title>Domestic animal endocrinology</title><addtitle>Domest Anim Endocrinol</addtitle><description>Spontaneous hyperadrenocorticism in dogs is known to be the result of excessive secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland or excessive autonomous glucocorticoid secretion by an adrenocortical tumor. Here, we report on an 8-year-old German shepherd dog in which ACTH-dependent hyperadrenocorticism was a result of ectopic ACTH secretion and could be related to an abdominal neuroendocrine tumor. Hyperadrenocorticism was diagnosed on the basis of the history, clinical signs, and elevated urinary corticoid/creatinine ratios (UCCRs; 236 and 350
×
10
−6; reference range <10
×
10
−6). The UCCR remained elevated (226
×
10
−6) after three oral doses of dexamethasone (0.1
mg/kg body weight) at 8-h intervals. Ultrasonography revealed two equivalently enlarged adrenal glands, consistent with adrenocortical hyperplasia. Plasma ACTH concentration was clearly elevated (159 and 188
ng/l; reference range 5–85
ng/l). Computed tomography (CT) revealed that the pituitary was not enlarged. These findings were interpreted as indicating dexamethasone-resistant pituitary-dependent hyperadrenocorticism. Transsphenoidal hypophysectomy was performed but within 2 weeks after surgery, there was exacerbation of the clinical signs of hyperadrenocorticism. Plasma ACTH concentration (281
ng/l) and UCCRs (1518 and 2176
×
10
−6) were even higher than before surgery. Histological examination of the pituitary gland revealed no neoplasia. Stimulation of the pituitary with corticotropin-releasing hormone did not affect plasma ACTH and cortisol concentrations. Treatment with trilostane was started and restored normocorticism. CT of the pituitary fossa, 10 months after hypophysectomy, revealed an empty sella. Hence, it was presumed that there was ectopic secretion of ACTH. CT of the abdomen revealed a mass in the region of the pancreas and a few nodules in the liver. Partial pancreatectomy with adjacent lymph node extirpation was performed and the liver nodules were biopsied. Histological examination revealed a metastasized neuroendocrine tumor. Abdominal surgery was not curative and medical treatment with trilostane was continued. At 18 months after the abdominal surgery, the dog is still in good condition. In conclusion, the combination of (1) severe dexamethasone-resistant hyperadrenocorticism with elevated circulating ACTH levels, (2) definitive demonstration of the absence of pituitary neoplasia, and (3) an abdominal neuroendocrine tumor allowed the diagnosis of ectopic ACTH secretion.</description><subject>Abdominal Neoplasms - secretion</subject><subject>Abdominal Neoplasms - veterinary</subject><subject>ACTH</subject><subject>ACTH Syndrome, Ectopic - complications</subject><subject>ACTH Syndrome, Ectopic - diagnosis</subject><subject>ACTH Syndrome, Ectopic - veterinary</subject><subject>adrenal cortex</subject><subject>Adrenocortical Hyperfunction - etiology</subject><subject>Adrenocortical Hyperfunction - veterinary</subject><subject>adrenocortical hyperplasia</subject><subject>Adrenocorticotropic Hormone - blood</subject><subject>Adrenocorticotropic Hormone - secretion</subject><subject>Animals</subject><subject>antineoplastic agents</subject><subject>Canine</subject><subject>corticotropin</subject><subject>corticotropin-releasing hormone</subject><subject>Corticotropin-Releasing Hormone - pharmacology</subject><subject>Cortisol</subject><subject>Cushing syndrome</subject><subject>Cushing's syndrome</subject><subject>dexamethasone</subject><subject>disease diagnosis</subject><subject>Dog Diseases - diagnosis</subject><subject>Dog Diseases - etiology</subject><subject>Dog Diseases - surgery</subject><subject>Dogs</subject><subject>drug therapy</subject><subject>hormone secretion</subject><subject>Hydrocortisone - blood</subject><subject>hyperadrenocorticism</subject><subject>Liver - diagnostic imaging</subject><subject>Male</subject><subject>neoplasms</subject><subject>Neuroendocrine tumor</subject><subject>Neuroendocrine Tumors - secretion</subject><subject>Neuroendocrine Tumors - veterinary</subject><subject>Tomography, X-Ray Computed - veterinary</subject><subject>trilostane</subject><subject>Ultrasonography - veterinary</subject><subject>urinary corticoid/creatinine ratio</subject><issn>0739-7240</issn><issn>1879-0054</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEFPHCEYhkljo6v1LygnbzN-LDDA0Zi2mph40D0TBr6xbHaGLcw28d-L3Y3tzROX5_le8hByyaBlwLrrdRvS6KaIU2iXAKJlrAVgX8iCaWUaACmOyAIUN41aCjghp6WsAUBV-5icMKk66JRYkNXd6xazCxmn5FOeo49lpHGijob0QsMO6Zwo-jlto6cFfcY5pommgf4vpTn_BX6lPKYJv5Gvg9sUPD-8Z2T14_vz7V3z8Pjz_vbmofHc8LnhcjB94L1WWmijeR-8MEH1AbwZlBCuA9P1XS-17oJSAY3wSjHNB-mV5I6fkav93W1Ov3dYZjvG4nGzcROmXbGdksClMhVUe9DnVErGwW5zHF1-tQzse1G7th9F7XtRy5itRat5cZjY9SOGf94hYQUu98DgknUvORa7elpWE8BoqQVU4mZPYE3xJ2K2xdcdjyHmWrYOx0-_8QaNRpXb</recordid><startdate>20050401</startdate><enddate>20050401</enddate><creator>Galac, S.</creator><creator>Kooistra, H.S.</creator><creator>Voorhout, G.</creator><creator>van den Ingh, T.S.G.A.M.</creator><creator>Mol, J.A.</creator><creator>van den Berg, G.</creator><creator>Meij, B.P.</creator><general>Elsevier Inc</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20050401</creationdate><title>Hyperadrenocorticism in a dog due to ectopic secretion of adrenocorticotropic hormone</title><author>Galac, S. ; Kooistra, H.S. ; Voorhout, G. ; van den Ingh, T.S.G.A.M. ; Mol, J.A. ; van den Berg, G. ; Meij, B.P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-35f9bd3b87848983bdc49d7bd0c9f744a6096b6b5886d77de94c77183f5c753a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Abdominal Neoplasms - secretion</topic><topic>Abdominal Neoplasms - veterinary</topic><topic>ACTH</topic><topic>ACTH Syndrome, Ectopic - complications</topic><topic>ACTH Syndrome, Ectopic - diagnosis</topic><topic>ACTH Syndrome, Ectopic - veterinary</topic><topic>adrenal cortex</topic><topic>Adrenocortical Hyperfunction - etiology</topic><topic>Adrenocortical Hyperfunction - veterinary</topic><topic>adrenocortical hyperplasia</topic><topic>Adrenocorticotropic Hormone - blood</topic><topic>Adrenocorticotropic Hormone - secretion</topic><topic>Animals</topic><topic>antineoplastic agents</topic><topic>Canine</topic><topic>corticotropin</topic><topic>corticotropin-releasing hormone</topic><topic>Corticotropin-Releasing Hormone - pharmacology</topic><topic>Cortisol</topic><topic>Cushing syndrome</topic><topic>Cushing's syndrome</topic><topic>dexamethasone</topic><topic>disease diagnosis</topic><topic>Dog Diseases - diagnosis</topic><topic>Dog Diseases - etiology</topic><topic>Dog Diseases - surgery</topic><topic>Dogs</topic><topic>drug therapy</topic><topic>hormone secretion</topic><topic>Hydrocortisone - blood</topic><topic>hyperadrenocorticism</topic><topic>Liver - diagnostic imaging</topic><topic>Male</topic><topic>neoplasms</topic><topic>Neuroendocrine tumor</topic><topic>Neuroendocrine Tumors - secretion</topic><topic>Neuroendocrine Tumors - veterinary</topic><topic>Tomography, X-Ray Computed - veterinary</topic><topic>trilostane</topic><topic>Ultrasonography - veterinary</topic><topic>urinary corticoid/creatinine ratio</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Galac, S.</creatorcontrib><creatorcontrib>Kooistra, H.S.</creatorcontrib><creatorcontrib>Voorhout, G.</creatorcontrib><creatorcontrib>van den Ingh, T.S.G.A.M.</creatorcontrib><creatorcontrib>Mol, J.A.</creatorcontrib><creatorcontrib>van den Berg, G.</creatorcontrib><creatorcontrib>Meij, B.P.</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Domestic animal endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Galac, S.</au><au>Kooistra, H.S.</au><au>Voorhout, G.</au><au>van den Ingh, T.S.G.A.M.</au><au>Mol, J.A.</au><au>van den Berg, G.</au><au>Meij, B.P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperadrenocorticism in a dog due to ectopic secretion of adrenocorticotropic hormone</atitle><jtitle>Domestic animal endocrinology</jtitle><addtitle>Domest Anim Endocrinol</addtitle><date>2005-04-01</date><risdate>2005</risdate><volume>28</volume><issue>3</issue><spage>338</spage><epage>348</epage><pages>338-348</pages><issn>0739-7240</issn><eissn>1879-0054</eissn><abstract>Spontaneous hyperadrenocorticism in dogs is known to be the result of excessive secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland or excessive autonomous glucocorticoid secretion by an adrenocortical tumor. Here, we report on an 8-year-old German shepherd dog in which ACTH-dependent hyperadrenocorticism was a result of ectopic ACTH secretion and could be related to an abdominal neuroendocrine tumor. Hyperadrenocorticism was diagnosed on the basis of the history, clinical signs, and elevated urinary corticoid/creatinine ratios (UCCRs; 236 and 350
×
10
−6; reference range <10
×
10
−6). The UCCR remained elevated (226
×
10
−6) after three oral doses of dexamethasone (0.1
mg/kg body weight) at 8-h intervals. Ultrasonography revealed two equivalently enlarged adrenal glands, consistent with adrenocortical hyperplasia. Plasma ACTH concentration was clearly elevated (159 and 188
ng/l; reference range 5–85
ng/l). Computed tomography (CT) revealed that the pituitary was not enlarged. These findings were interpreted as indicating dexamethasone-resistant pituitary-dependent hyperadrenocorticism. Transsphenoidal hypophysectomy was performed but within 2 weeks after surgery, there was exacerbation of the clinical signs of hyperadrenocorticism. Plasma ACTH concentration (281
ng/l) and UCCRs (1518 and 2176
×
10
−6) were even higher than before surgery. Histological examination of the pituitary gland revealed no neoplasia. Stimulation of the pituitary with corticotropin-releasing hormone did not affect plasma ACTH and cortisol concentrations. Treatment with trilostane was started and restored normocorticism. CT of the pituitary fossa, 10 months after hypophysectomy, revealed an empty sella. Hence, it was presumed that there was ectopic secretion of ACTH. CT of the abdomen revealed a mass in the region of the pancreas and a few nodules in the liver. Partial pancreatectomy with adjacent lymph node extirpation was performed and the liver nodules were biopsied. Histological examination revealed a metastasized neuroendocrine tumor. Abdominal surgery was not curative and medical treatment with trilostane was continued. At 18 months after the abdominal surgery, the dog is still in good condition. In conclusion, the combination of (1) severe dexamethasone-resistant hyperadrenocorticism with elevated circulating ACTH levels, (2) definitive demonstration of the absence of pituitary neoplasia, and (3) an abdominal neuroendocrine tumor allowed the diagnosis of ectopic ACTH secretion.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15760674</pmid><doi>10.1016/j.domaniend.2004.11.001</doi><tpages>11</tpages></addata></record> |
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| ispartof | Domestic animal endocrinology, 2005-04, Vol.28 (3), p.338-348 |
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| subjects | Abdominal Neoplasms - secretion Abdominal Neoplasms - veterinary ACTH ACTH Syndrome, Ectopic - complications ACTH Syndrome, Ectopic - diagnosis ACTH Syndrome, Ectopic - veterinary adrenal cortex Adrenocortical Hyperfunction - etiology Adrenocortical Hyperfunction - veterinary adrenocortical hyperplasia Adrenocorticotropic Hormone - blood Adrenocorticotropic Hormone - secretion Animals antineoplastic agents Canine corticotropin corticotropin-releasing hormone Corticotropin-Releasing Hormone - pharmacology Cortisol Cushing syndrome Cushing's syndrome dexamethasone disease diagnosis Dog Diseases - diagnosis Dog Diseases - etiology Dog Diseases - surgery Dogs drug therapy hormone secretion Hydrocortisone - blood hyperadrenocorticism Liver - diagnostic imaging Male neoplasms Neuroendocrine tumor Neuroendocrine Tumors - secretion Neuroendocrine Tumors - veterinary Tomography, X-Ray Computed - veterinary trilostane Ultrasonography - veterinary urinary corticoid/creatinine ratio |
| title | Hyperadrenocorticism in a dog due to ectopic secretion of adrenocorticotropic hormone |
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