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Effect of Trilostane on Hormone and Serum Electrolyte Concentrations in Dogs with Pituitary‐Dependent Hyperadrenocorticism

BACKGROUND: The effects of trilostane on key hormones and electrolytes over 24 hours in dogs with pituitary‐dependent hyperadrenocorticism (PDH) are unknown. OBJECTIVES: To determine the plasma concentration of cortisol, endogenous adrenocorticotropic hormone (ACTH), aldosterone, sodium, potassium,...

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Published in:Journal of veterinary internal medicine 2014-01, Vol.28 (1), p.160-165
Main Authors: Griebsch, C, Lehnert, C, Williams, G.J, Failing, K, Neiger, R
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creator Griebsch, C
Lehnert, C
Williams, G.J
Failing, K
Neiger, R
description BACKGROUND: The effects of trilostane on key hormones and electrolytes over 24 hours in dogs with pituitary‐dependent hyperadrenocorticism (PDH) are unknown. OBJECTIVES: To determine the plasma concentration of cortisol, endogenous adrenocorticotropic hormone (ACTH), aldosterone, sodium, potassium, and ionized calcium concentrations, and plasma renin activity over a 24‐hour period after administration of trilostane to dogs with well‐controlled PDH. ANIMALS: Nine dogs (mean age 9.3 ± 0.67 years, mean weight 31.9 ± 6.4 kg) with confirmed PDH. METHODS: Prospective study. Thirty days after the first administration of trilostane, blood samples were taken at −30, 0 (baseline), 15, 30, 60, and 90 minutes, and 2, 3, 4, 6, 8, 12, 16, 20, and 24 hours after administration of trilostane and plasma concentration of cortisol, endogenous ACTH, aldosterone, sodium, potassium, ionized calcium, and renin activity were determined. RESULTS: Cortisol concentrations decreased significantly (P 
doi_str_mv 10.1111/jvim.12268
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OBJECTIVES: To determine the plasma concentration of cortisol, endogenous adrenocorticotropic hormone (ACTH), aldosterone, sodium, potassium, and ionized calcium concentrations, and plasma renin activity over a 24‐hour period after administration of trilostane to dogs with well‐controlled PDH. ANIMALS: Nine dogs (mean age 9.3 ± 0.67 years, mean weight 31.9 ± 6.4 kg) with confirmed PDH. METHODS: Prospective study. Thirty days after the first administration of trilostane, blood samples were taken at −30, 0 (baseline), 15, 30, 60, and 90 minutes, and 2, 3, 4, 6, 8, 12, 16, 20, and 24 hours after administration of trilostane and plasma concentration of cortisol, endogenous ACTH, aldosterone, sodium, potassium, ionized calcium, and renin activity were determined. RESULTS: Cortisol concentrations decreased significantly (P &lt; .001) 2–4 hours after trilostane administration. From baseline, there was a significant (P &lt; .001) increase in endogenous ACTH concentrations between hours 3–12, a significant increase (P &lt; .001) in aldosterone concentration between hours 16–20, and a significant (P &lt; .001) increase in renin activity between hours 6–20. Potassium concentration decreased significantly (P &lt; .05) between hours 0.5–2. CONCLUSION AND CLINICAL IMPORTANCE: Treatment with trilostane did not cause clinically relevant alterations in plasma aldosterone and potassium concentration. Results suggest that in dogs with PDH, the optimal time point for an ACTH‐stimulation test to be performed is 2–4 hours after trilostane dosing. Future studies are necessary to establish interpretation criteria for a 2‐ to 4‐hour postpill ACTH‐stimulation test.</description><identifier>ISSN: 0891-6640</identifier><identifier>EISSN: 1939-1676</identifier><identifier>DOI: 10.1111/jvim.12268</identifier><identifier>PMID: 24341822</identifier><language>eng</language><publisher>United States: J.B. Lippincott</publisher><subject>Adrenal gland ; Adrenocortical Hyperfunction - blood ; Adrenocortical Hyperfunction - drug therapy ; Adrenocortical Hyperfunction - physiopathology ; Adrenocortical Hyperfunction - veterinary ; Adrenocorticotropic Hormone - blood ; aldosterone ; Aldosterone - blood ; Animals ; blood serum ; calcium ; Calcium - blood ; corticotropin ; cortisol ; Dihydrotestosterone - administration &amp; dosage ; Dihydrotestosterone - analogs &amp; derivatives ; Dihydrotestosterone - pharmacokinetics ; Dihydrotestosterone - therapeutic use ; Dog Diseases - blood ; Dog Diseases - drug therapy ; Dog Diseases - physiopathology ; Dogs ; electrolytes ; Enzyme Inhibitors - administration &amp; dosage ; Enzyme Inhibitors - pharmacokinetics ; Enzyme Inhibitors - therapeutic use ; Female ; Hormones ; Hydrocortisone - blood ; hyperadrenocorticism ; Hypercortisolism ; Male ; medicine ; Original ; Plasma ; potassium ; Potassium - blood ; Prospective Studies ; renin ; sodium ; Sodium - blood ; Treatment</subject><ispartof>Journal of veterinary internal medicine, 2014-01, Vol.28 (1), p.160-165</ispartof><rights>Copyright © 2013 by the American College of Veterinary Internal Medicine</rights><rights>Copyright © 2013 by the American College of Veterinary Internal Medicine.</rights><rights>2014. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5108-c06c0f5061d3725fa474a3e86903117db66575fdcbd18593bcb378711bc244963</citedby><cites>FETCH-LOGICAL-c5108-c06c0f5061d3725fa474a3e86903117db66575fdcbd18593bcb378711bc244963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4895538/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4895538/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,11562,27924,27925,46052,46476,53791,53793</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjvim.12268$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24341822$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Griebsch, C</creatorcontrib><creatorcontrib>Lehnert, C</creatorcontrib><creatorcontrib>Williams, G.J</creatorcontrib><creatorcontrib>Failing, K</creatorcontrib><creatorcontrib>Neiger, R</creatorcontrib><title>Effect of Trilostane on Hormone and Serum Electrolyte Concentrations in Dogs with Pituitary‐Dependent Hyperadrenocorticism</title><title>Journal of veterinary internal medicine</title><addtitle>J Vet Intern Med</addtitle><description>BACKGROUND: The effects of trilostane on key hormones and electrolytes over 24 hours in dogs with pituitary‐dependent hyperadrenocorticism (PDH) are unknown. OBJECTIVES: To determine the plasma concentration of cortisol, endogenous adrenocorticotropic hormone (ACTH), aldosterone, sodium, potassium, and ionized calcium concentrations, and plasma renin activity over a 24‐hour period after administration of trilostane to dogs with well‐controlled PDH. ANIMALS: Nine dogs (mean age 9.3 ± 0.67 years, mean weight 31.9 ± 6.4 kg) with confirmed PDH. METHODS: Prospective study. Thirty days after the first administration of trilostane, blood samples were taken at −30, 0 (baseline), 15, 30, 60, and 90 minutes, and 2, 3, 4, 6, 8, 12, 16, 20, and 24 hours after administration of trilostane and plasma concentration of cortisol, endogenous ACTH, aldosterone, sodium, potassium, ionized calcium, and renin activity were determined. RESULTS: Cortisol concentrations decreased significantly (P &lt; .001) 2–4 hours after trilostane administration. From baseline, there was a significant (P &lt; .001) increase in endogenous ACTH concentrations between hours 3–12, a significant increase (P &lt; .001) in aldosterone concentration between hours 16–20, and a significant (P &lt; .001) increase in renin activity between hours 6–20. Potassium concentration decreased significantly (P &lt; .05) between hours 0.5–2. CONCLUSION AND CLINICAL IMPORTANCE: Treatment with trilostane did not cause clinically relevant alterations in plasma aldosterone and potassium concentration. Results suggest that in dogs with PDH, the optimal time point for an ACTH‐stimulation test to be performed is 2–4 hours after trilostane dosing. Future studies are necessary to establish interpretation criteria for a 2‐ to 4‐hour postpill ACTH‐stimulation test.</description><subject>Adrenal gland</subject><subject>Adrenocortical Hyperfunction - blood</subject><subject>Adrenocortical Hyperfunction - drug therapy</subject><subject>Adrenocortical Hyperfunction - physiopathology</subject><subject>Adrenocortical Hyperfunction - veterinary</subject><subject>Adrenocorticotropic Hormone - blood</subject><subject>aldosterone</subject><subject>Aldosterone - blood</subject><subject>Animals</subject><subject>blood serum</subject><subject>calcium</subject><subject>Calcium - blood</subject><subject>corticotropin</subject><subject>cortisol</subject><subject>Dihydrotestosterone - administration &amp; dosage</subject><subject>Dihydrotestosterone - analogs &amp; derivatives</subject><subject>Dihydrotestosterone - pharmacokinetics</subject><subject>Dihydrotestosterone - therapeutic use</subject><subject>Dog Diseases - blood</subject><subject>Dog Diseases - drug therapy</subject><subject>Dog Diseases - physiopathology</subject><subject>Dogs</subject><subject>electrolytes</subject><subject>Enzyme Inhibitors - administration &amp; dosage</subject><subject>Enzyme Inhibitors - pharmacokinetics</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Female</subject><subject>Hormones</subject><subject>Hydrocortisone - blood</subject><subject>hyperadrenocorticism</subject><subject>Hypercortisolism</subject><subject>Male</subject><subject>medicine</subject><subject>Original</subject><subject>Plasma</subject><subject>potassium</subject><subject>Potassium - blood</subject><subject>Prospective Studies</subject><subject>renin</subject><subject>sodium</subject><subject>Sodium - blood</subject><subject>Treatment</subject><issn>0891-6640</issn><issn>1939-1676</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNp9kU9v0zAchiMEYmVw4QOAJW5IGXb8L7kgTW3XDG0DaRscLcdxOpfELra7rRIHPgKfkU-CR7YKLvhiS35-j1_5zbKXCB6gtN6trs1wgIqClY-yCapwlSPG2eNsAssK5YwRuJc9C2EFYUEp5U-zvYJggsqimGTf512nVQSuAxfe9C5EaTVwFtTODy4dpW3BufabAcz7BHrXb6MGU2eVttHLaJwNwFgwc8sAbky8Ap9M3Jgo_fbXj58zvda2TSSot2vtZeu1dcr5aJQJw_PsSSf7oF_c7_vZ5dH8YlrnJx8Xx9PDk1xRBMtcQaZgRyFDLeYF7SThRGJdsgpihHjbMEY57VrVtKikFW5Ug3nJEWpUQUjF8H72fvSuN82g2zF5L9beDCmmcNKIf2-suRJLdy1IWVGKyyR4cy_w7ttGhyhWbuNtyiwwTH_NcEWKRL0dKeVdCF53uxcQFHdNibumxJ-mEvzq70w79KGaBKARuDG93v5HJT58Pj59kObjjAlR3-5mpP8qGMecii9nC4FP6yk_my1EnfjXI99JJ-TSmyAuzwuIKISIIEIQ_g1Yhbpa</recordid><startdate>201401</startdate><enddate>201401</enddate><creator>Griebsch, C</creator><creator>Lehnert, C</creator><creator>Williams, G.J</creator><creator>Failing, K</creator><creator>Neiger, R</creator><general>J.B. Lippincott</general><general>Blackwell Publishing Ltd</general><general>John Wiley &amp; Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>FBQ</scope><scope>BSCLL</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>K9.</scope><scope>5PM</scope></search><sort><creationdate>201401</creationdate><title>Effect of Trilostane on Hormone and Serum Electrolyte Concentrations in Dogs with Pituitary‐Dependent Hyperadrenocorticism</title><author>Griebsch, C ; Lehnert, C ; Williams, G.J ; Failing, K ; Neiger, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5108-c06c0f5061d3725fa474a3e86903117db66575fdcbd18593bcb378711bc244963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adrenal gland</topic><topic>Adrenocortical Hyperfunction - blood</topic><topic>Adrenocortical Hyperfunction - drug therapy</topic><topic>Adrenocortical Hyperfunction - physiopathology</topic><topic>Adrenocortical Hyperfunction - veterinary</topic><topic>Adrenocorticotropic Hormone - blood</topic><topic>aldosterone</topic><topic>Aldosterone - blood</topic><topic>Animals</topic><topic>blood serum</topic><topic>calcium</topic><topic>Calcium - blood</topic><topic>corticotropin</topic><topic>cortisol</topic><topic>Dihydrotestosterone - administration &amp; dosage</topic><topic>Dihydrotestosterone - analogs &amp; derivatives</topic><topic>Dihydrotestosterone - pharmacokinetics</topic><topic>Dihydrotestosterone - therapeutic use</topic><topic>Dog Diseases - blood</topic><topic>Dog Diseases - drug therapy</topic><topic>Dog Diseases - physiopathology</topic><topic>Dogs</topic><topic>electrolytes</topic><topic>Enzyme Inhibitors - administration &amp; dosage</topic><topic>Enzyme Inhibitors - pharmacokinetics</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Female</topic><topic>Hormones</topic><topic>Hydrocortisone - blood</topic><topic>hyperadrenocorticism</topic><topic>Hypercortisolism</topic><topic>Male</topic><topic>medicine</topic><topic>Original</topic><topic>Plasma</topic><topic>potassium</topic><topic>Potassium - blood</topic><topic>Prospective Studies</topic><topic>renin</topic><topic>sodium</topic><topic>Sodium - blood</topic><topic>Treatment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Griebsch, C</creatorcontrib><creatorcontrib>Lehnert, C</creatorcontrib><creatorcontrib>Williams, G.J</creatorcontrib><creatorcontrib>Failing, K</creatorcontrib><creatorcontrib>Neiger, R</creatorcontrib><collection>AGRIS</collection><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of veterinary internal medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Griebsch, C</au><au>Lehnert, C</au><au>Williams, G.J</au><au>Failing, K</au><au>Neiger, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Trilostane on Hormone and Serum Electrolyte Concentrations in Dogs with Pituitary‐Dependent Hyperadrenocorticism</atitle><jtitle>Journal of veterinary internal medicine</jtitle><addtitle>J Vet Intern Med</addtitle><date>2014-01</date><risdate>2014</risdate><volume>28</volume><issue>1</issue><spage>160</spage><epage>165</epage><pages>160-165</pages><issn>0891-6640</issn><eissn>1939-1676</eissn><abstract>BACKGROUND: The effects of trilostane on key hormones and electrolytes over 24 hours in dogs with pituitary‐dependent hyperadrenocorticism (PDH) are unknown. OBJECTIVES: To determine the plasma concentration of cortisol, endogenous adrenocorticotropic hormone (ACTH), aldosterone, sodium, potassium, and ionized calcium concentrations, and plasma renin activity over a 24‐hour period after administration of trilostane to dogs with well‐controlled PDH. ANIMALS: Nine dogs (mean age 9.3 ± 0.67 years, mean weight 31.9 ± 6.4 kg) with confirmed PDH. METHODS: Prospective study. Thirty days after the first administration of trilostane, blood samples were taken at −30, 0 (baseline), 15, 30, 60, and 90 minutes, and 2, 3, 4, 6, 8, 12, 16, 20, and 24 hours after administration of trilostane and plasma concentration of cortisol, endogenous ACTH, aldosterone, sodium, potassium, ionized calcium, and renin activity were determined. RESULTS: Cortisol concentrations decreased significantly (P &lt; .001) 2–4 hours after trilostane administration. From baseline, there was a significant (P &lt; .001) increase in endogenous ACTH concentrations between hours 3–12, a significant increase (P &lt; .001) in aldosterone concentration between hours 16–20, and a significant (P &lt; .001) increase in renin activity between hours 6–20. Potassium concentration decreased significantly (P &lt; .05) between hours 0.5–2. CONCLUSION AND CLINICAL IMPORTANCE: Treatment with trilostane did not cause clinically relevant alterations in plasma aldosterone and potassium concentration. Results suggest that in dogs with PDH, the optimal time point for an ACTH‐stimulation test to be performed is 2–4 hours after trilostane dosing. Future studies are necessary to establish interpretation criteria for a 2‐ to 4‐hour postpill ACTH‐stimulation test.</abstract><cop>United States</cop><pub>J.B. Lippincott</pub><pmid>24341822</pmid><doi>10.1111/jvim.12268</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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subjects Adrenal gland
Adrenocortical Hyperfunction - blood
Adrenocortical Hyperfunction - drug therapy
Adrenocortical Hyperfunction - physiopathology
Adrenocortical Hyperfunction - veterinary
Adrenocorticotropic Hormone - blood
aldosterone
Aldosterone - blood
Animals
blood serum
calcium
Calcium - blood
corticotropin
cortisol
Dihydrotestosterone - administration & dosage
Dihydrotestosterone - analogs & derivatives
Dihydrotestosterone - pharmacokinetics
Dihydrotestosterone - therapeutic use
Dog Diseases - blood
Dog Diseases - drug therapy
Dog Diseases - physiopathology
Dogs
electrolytes
Enzyme Inhibitors - administration & dosage
Enzyme Inhibitors - pharmacokinetics
Enzyme Inhibitors - therapeutic use
Female
Hormones
Hydrocortisone - blood
hyperadrenocorticism
Hypercortisolism
Male
medicine
Original
Plasma
potassium
Potassium - blood
Prospective Studies
renin
sodium
Sodium - blood
Treatment
title Effect of Trilostane on Hormone and Serum Electrolyte Concentrations in Dogs with Pituitary‐Dependent Hyperadrenocorticism
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