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Serologic Evaluation of Clinical and Subclinical Secondary Hepatic Amyloidosis in Rhesus Macaques (Macaca mulatta). [Erratum: 2009 June, v. 59, no. 3, p. 220.]
Secondary hepatic amyloidosis in nonhuman primates carries a grave prognosis once animals become clinically ill. The purpose of this study was to establish serologic parameters that potentially could be used to identify rhesus macaques undergoing subclinical development of secondary hepatic amyloido...
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Published in: | Comparative medicine 2009-04, Vol.59 (2), p.168-173 |
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description | Secondary hepatic amyloidosis in nonhuman primates carries a grave prognosis once animals become clinically ill. The purpose of this study was to establish serologic parameters that potentially could be used to identify rhesus macaques undergoing subclinical development of secondary hepatic amyloidosis. A retrospective analysis was completed by using serum biochemical profiles from 26 histologically diagnosed amyloidotic macaques evaluated at 2 stages of disease, clinical and subclinical (3 to 32 mo prior to clinical signs of disease). Standard serum biochemistry values for cases were compared with institutional age- and gender-specific references ranges by construction of 95% confidence intervals for the difference between means. In addition, 19 histologically diagnosed amyloidotic macaques and 19 age-matched controls were assayed for changes in various parameters by using routinely banked, frozen (-80 °C) sera available from clinical and subclinical time points. Clinically amyloidotic animals displayed increased levels of alkaline phosphatase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyltranspeptidase, and macrophage colony-stimulating factor and significantly decreased quantities of albumin and total cholesterol. Subclinical amyloidotic animals displayed increased levels of alkaline phosphatase, aspartate aminotransferase, lactate dehydrogenase, and serum amyloid A and decreased concentrations of albumin and total cholesterol. The serologic parameters studied indicate a temporal relationship of these factors not previously described, show a clear pattern of disease progression, and could be useful in subclinical disease detection. |
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[Erratum: 2009 June, v. 59, no. 3, p. 220.]</title><source>PubMed (Medline)</source><source>IngentaConnect Journals</source><creator>MacGuire, Jamus G ; Christe, Kari L ; Yee, JoAnn L ; Kalman-Bowlus, Alexis L ; Lerche, Nicholas W</creator><creatorcontrib>MacGuire, Jamus G ; Christe, Kari L ; Yee, JoAnn L ; Kalman-Bowlus, Alexis L ; Lerche, Nicholas W</creatorcontrib><description>Secondary hepatic amyloidosis in nonhuman primates carries a grave prognosis once animals become clinically ill. The purpose of this study was to establish serologic parameters that potentially could be used to identify rhesus macaques undergoing subclinical development of secondary hepatic amyloidosis. A retrospective analysis was completed by using serum biochemical profiles from 26 histologically diagnosed amyloidotic macaques evaluated at 2 stages of disease, clinical and subclinical (3 to 32 mo prior to clinical signs of disease). Standard serum biochemistry values for cases were compared with institutional age- and gender-specific references ranges by construction of 95% confidence intervals for the difference between means. In addition, 19 histologically diagnosed amyloidotic macaques and 19 age-matched controls were assayed for changes in various parameters by using routinely banked, frozen (-80 °C) sera available from clinical and subclinical time points. Clinically amyloidotic animals displayed increased levels of alkaline phosphatase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyltranspeptidase, and macrophage colony-stimulating factor and significantly decreased quantities of albumin and total cholesterol. Subclinical amyloidotic animals displayed increased levels of alkaline phosphatase, aspartate aminotransferase, lactate dehydrogenase, and serum amyloid A and decreased concentrations of albumin and total cholesterol. The serologic parameters studied indicate a temporal relationship of these factors not previously described, show a clear pattern of disease progression, and could be useful in subclinical disease detection.</description><identifier>ISSN: 1532-0820</identifier><identifier>EISSN: 2769-819X</identifier><identifier>PMID: 19389309</identifier><language>eng</language><publisher>United States: American Association for Laboratory Animal Science</publisher><subject>Amyloidosis - blood ; Amyloidosis - diagnosis ; Amyloidosis - pathology ; Amyloidosis - veterinary ; Animals ; Blood Chemical Analysis ; blood chemistry ; disease course ; disease detection ; disease diagnosis ; Disease Progression ; enzymes ; Female ; Humans ; Immunoassay ; liver ; Liver - enzymology ; Liver Diseases - blood ; Liver Diseases - diagnosis ; Liver Diseases - pathology ; Liver Diseases - veterinary ; Macaca mulatta ; Macrophage Colony-Stimulating Factor - blood ; Male ; metabolic diseases ; Monkey Diseases - blood ; Monkey Diseases - diagnosis ; Monkey Diseases - pathology ; monkeys ; Nonhuman Primate Models ; Retrospective Studies ; Serologic Tests ; signs and symptoms (animals and humans) ; temporal variation</subject><ispartof>Comparative medicine, 2009-04, Vol.59 (2), p.168-173</ispartof><rights>American Association for Laboratory Animal Science 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2703146/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2703146/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,53725,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19389309$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MacGuire, Jamus G</creatorcontrib><creatorcontrib>Christe, Kari L</creatorcontrib><creatorcontrib>Yee, JoAnn L</creatorcontrib><creatorcontrib>Kalman-Bowlus, Alexis L</creatorcontrib><creatorcontrib>Lerche, Nicholas W</creatorcontrib><title>Serologic Evaluation of Clinical and Subclinical Secondary Hepatic Amyloidosis in Rhesus Macaques (Macaca mulatta). [Erratum: 2009 June, v. 59, no. 3, p. 220.]</title><title>Comparative medicine</title><addtitle>Comp Med</addtitle><addtitle>Comp Med</addtitle><description>Secondary hepatic amyloidosis in nonhuman primates carries a grave prognosis once animals become clinically ill. The purpose of this study was to establish serologic parameters that potentially could be used to identify rhesus macaques undergoing subclinical development of secondary hepatic amyloidosis. A retrospective analysis was completed by using serum biochemical profiles from 26 histologically diagnosed amyloidotic macaques evaluated at 2 stages of disease, clinical and subclinical (3 to 32 mo prior to clinical signs of disease). Standard serum biochemistry values for cases were compared with institutional age- and gender-specific references ranges by construction of 95% confidence intervals for the difference between means. In addition, 19 histologically diagnosed amyloidotic macaques and 19 age-matched controls were assayed for changes in various parameters by using routinely banked, frozen (-80 °C) sera available from clinical and subclinical time points. Clinically amyloidotic animals displayed increased levels of alkaline phosphatase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyltranspeptidase, and macrophage colony-stimulating factor and significantly decreased quantities of albumin and total cholesterol. Subclinical amyloidotic animals displayed increased levels of alkaline phosphatase, aspartate aminotransferase, lactate dehydrogenase, and serum amyloid A and decreased concentrations of albumin and total cholesterol. The serologic parameters studied indicate a temporal relationship of these factors not previously described, show a clear pattern of disease progression, and could be useful in subclinical disease detection.</description><subject>Amyloidosis - blood</subject><subject>Amyloidosis - diagnosis</subject><subject>Amyloidosis - pathology</subject><subject>Amyloidosis - veterinary</subject><subject>Animals</subject><subject>Blood Chemical Analysis</subject><subject>blood chemistry</subject><subject>disease course</subject><subject>disease detection</subject><subject>disease diagnosis</subject><subject>Disease Progression</subject><subject>enzymes</subject><subject>Female</subject><subject>Humans</subject><subject>Immunoassay</subject><subject>liver</subject><subject>Liver - enzymology</subject><subject>Liver Diseases - blood</subject><subject>Liver Diseases - diagnosis</subject><subject>Liver Diseases - pathology</subject><subject>Liver Diseases - veterinary</subject><subject>Macaca mulatta</subject><subject>Macrophage Colony-Stimulating Factor - blood</subject><subject>Male</subject><subject>metabolic diseases</subject><subject>Monkey Diseases - blood</subject><subject>Monkey Diseases - diagnosis</subject><subject>Monkey Diseases - pathology</subject><subject>monkeys</subject><subject>Nonhuman Primate Models</subject><subject>Retrospective Studies</subject><subject>Serologic Tests</subject><subject>signs and symptoms (animals and humans)</subject><subject>temporal variation</subject><issn>1532-0820</issn><issn>2769-819X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNp1ktGKEzEUhgdR3Lr6CporUWhLcjIzabwQl9J1lZUF64IgEs5kMt0smaROJoXdl_FVnbGt6IW5OeeQn-_nT86DbAKilLMFk18fZhNWcJjRBdCT7EmMt5SClBQeZydM8oXkVE6yn2vTBRc2VpPVDl3C3gZPQkOWznqr0RH0NVmnSh_ntdHB19jdkQuzHeSanLV3Ltg6RBuJ9eTzjYkpkk-o8UcykbwaO42kTQ77Hl_PybdV12Gf2jcEKJXkY_JmSnZzUsgp8WFO-JRs5wSAzr8_zR416KJ5dqin2fX56svyYnZ59f7D8uxy1uRM9DNNC820YDUiGE1p0QhArOoKZaFzEFWeVxWKaqjaGMqrnEKZc1pyiTWC5qfZ2z13m6rW1Nr4vkOntp1th6gqoFX_3nh7ozZhp0BQzvJyALw8ALowxu5Va6M2zqE3IUVVClbyHGAQPv_b6Y_F8U8Gwbu9wPrNYIbqNqTOD-EVosOodKvGZ1P09ymODQWFXT82YkBc_Qdh9YEy7sa4GmpXSA8DERhdMKEYA65q02ByveqxU5t7FUfiiz2xwaBw09mortdAGaesBJ6Xgv8C9OPBHA</recordid><startdate>20090401</startdate><enddate>20090401</enddate><creator>MacGuire, Jamus G</creator><creator>Christe, Kari L</creator><creator>Yee, JoAnn L</creator><creator>Kalman-Bowlus, Alexis L</creator><creator>Lerche, Nicholas W</creator><general>American Association for Laboratory Animal Science</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090401</creationdate><title>Serologic Evaluation of Clinical and Subclinical Secondary Hepatic Amyloidosis in Rhesus Macaques (Macaca mulatta). [Erratum: 2009 June, v. 59, no. 3, p. 220.]</title><author>MacGuire, Jamus G ; Christe, Kari L ; Yee, JoAnn L ; Kalman-Bowlus, Alexis L ; Lerche, Nicholas W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-f417t-c05c1c71daa2ec005f72aabdba95c427b44bba7bb44cee03b4026430639ada2c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Amyloidosis - blood</topic><topic>Amyloidosis - diagnosis</topic><topic>Amyloidosis - pathology</topic><topic>Amyloidosis - veterinary</topic><topic>Animals</topic><topic>Blood Chemical Analysis</topic><topic>blood chemistry</topic><topic>disease course</topic><topic>disease detection</topic><topic>disease diagnosis</topic><topic>Disease Progression</topic><topic>enzymes</topic><topic>Female</topic><topic>Humans</topic><topic>Immunoassay</topic><topic>liver</topic><topic>Liver - enzymology</topic><topic>Liver Diseases - blood</topic><topic>Liver Diseases - diagnosis</topic><topic>Liver Diseases - pathology</topic><topic>Liver Diseases - veterinary</topic><topic>Macaca mulatta</topic><topic>Macrophage Colony-Stimulating Factor - blood</topic><topic>Male</topic><topic>metabolic diseases</topic><topic>Monkey Diseases - blood</topic><topic>Monkey Diseases - diagnosis</topic><topic>Monkey Diseases - pathology</topic><topic>monkeys</topic><topic>Nonhuman Primate Models</topic><topic>Retrospective Studies</topic><topic>Serologic Tests</topic><topic>signs and symptoms (animals and humans)</topic><topic>temporal variation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MacGuire, Jamus G</creatorcontrib><creatorcontrib>Christe, Kari L</creatorcontrib><creatorcontrib>Yee, JoAnn L</creatorcontrib><creatorcontrib>Kalman-Bowlus, Alexis L</creatorcontrib><creatorcontrib>Lerche, Nicholas W</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Comparative medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MacGuire, Jamus G</au><au>Christe, Kari L</au><au>Yee, JoAnn L</au><au>Kalman-Bowlus, Alexis L</au><au>Lerche, Nicholas W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serologic Evaluation of Clinical and Subclinical Secondary Hepatic Amyloidosis in Rhesus Macaques (Macaca mulatta). [Erratum: 2009 June, v. 59, no. 3, p. 220.]</atitle><jtitle>Comparative medicine</jtitle><stitle>Comp Med</stitle><addtitle>Comp Med</addtitle><date>2009-04-01</date><risdate>2009</risdate><volume>59</volume><issue>2</issue><spage>168</spage><epage>173</epage><pages>168-173</pages><issn>1532-0820</issn><eissn>2769-819X</eissn><abstract>Secondary hepatic amyloidosis in nonhuman primates carries a grave prognosis once animals become clinically ill. The purpose of this study was to establish serologic parameters that potentially could be used to identify rhesus macaques undergoing subclinical development of secondary hepatic amyloidosis. A retrospective analysis was completed by using serum biochemical profiles from 26 histologically diagnosed amyloidotic macaques evaluated at 2 stages of disease, clinical and subclinical (3 to 32 mo prior to clinical signs of disease). Standard serum biochemistry values for cases were compared with institutional age- and gender-specific references ranges by construction of 95% confidence intervals for the difference between means. In addition, 19 histologically diagnosed amyloidotic macaques and 19 age-matched controls were assayed for changes in various parameters by using routinely banked, frozen (-80 °C) sera available from clinical and subclinical time points. Clinically amyloidotic animals displayed increased levels of alkaline phosphatase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyltranspeptidase, and macrophage colony-stimulating factor and significantly decreased quantities of albumin and total cholesterol. Subclinical amyloidotic animals displayed increased levels of alkaline phosphatase, aspartate aminotransferase, lactate dehydrogenase, and serum amyloid A and decreased concentrations of albumin and total cholesterol. 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subjects | Amyloidosis - blood Amyloidosis - diagnosis Amyloidosis - pathology Amyloidosis - veterinary Animals Blood Chemical Analysis blood chemistry disease course disease detection disease diagnosis Disease Progression enzymes Female Humans Immunoassay liver Liver - enzymology Liver Diseases - blood Liver Diseases - diagnosis Liver Diseases - pathology Liver Diseases - veterinary Macaca mulatta Macrophage Colony-Stimulating Factor - blood Male metabolic diseases Monkey Diseases - blood Monkey Diseases - diagnosis Monkey Diseases - pathology monkeys Nonhuman Primate Models Retrospective Studies Serologic Tests signs and symptoms (animals and humans) temporal variation |
title | Serologic Evaluation of Clinical and Subclinical Secondary Hepatic Amyloidosis in Rhesus Macaques (Macaca mulatta). [Erratum: 2009 June, v. 59, no. 3, p. 220.] |
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