ACTH-cortisol dissociation in patients with Kawasaki disease: a retrospective study
ACTH-cortisol dissociation is recognized in patients with critical illnesses. Cytokines, including tumor necrosis factor-α and interleukin-6 induce hypercortisolemia by enhancing the ACTH-independent synthesis and secretion of cortisol and by reducing cortisol breakdown. Subsequently, hypercortisole...
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| Veröffentlicht in: | Endocrine Journal 2021, Vol.68(6), pp.683-689 |
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| description | ACTH-cortisol dissociation is recognized in patients with critical illnesses. Cytokines, including tumor necrosis factor-α and interleukin-6 induce hypercortisolemia by enhancing the ACTH-independent synthesis and secretion of cortisol and by reducing cortisol breakdown. Subsequently, hypercortisolemia suppresses ACTH secretion by negative feedback inhibition. ACTH-cortisol dissociation in patients with systemic inflammatory diseases has not been reported. Here, we examined whether ACTH-cortisol dissociation is recognized in patients with Kawasaki disease (KD) associated with hypercytokinemia, as well as the possible cytokine involvement in ACTH-cortisol dissociation, retrospectively. The levels of serum cortisol, plasma ACTH, and cytokine-induced proteins, i.e., plasma C-reactive protein (CRP), serum ferritin, and urinary β2-microglobulin (U-β2MG), in 232 patients with KD were measured at diagnosis. Quartile groups based on cytokine-induced protein levels were formed (Q1, Q2, Q3, and Q4). We found a low median plasma ACTH [median (range): 8.9 ( |
| doi_str_mv | 10.1507/endocrj.EJ20-0533 |
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Cytokines, including tumor necrosis factor-α and interleukin-6 induce hypercortisolemia by enhancing the ACTH-independent synthesis and secretion of cortisol and by reducing cortisol breakdown. Subsequently, hypercortisolemia suppresses ACTH secretion by negative feedback inhibition. ACTH-cortisol dissociation in patients with systemic inflammatory diseases has not been reported. Here, we examined whether ACTH-cortisol dissociation is recognized in patients with Kawasaki disease (KD) associated with hypercytokinemia, as well as the possible cytokine involvement in ACTH-cortisol dissociation, retrospectively. The levels of serum cortisol, plasma ACTH, and cytokine-induced proteins, i.e., plasma C-reactive protein (CRP), serum ferritin, and urinary β2-microglobulin (U-β2MG), in 232 patients with KD were measured at diagnosis. Quartile groups based on cytokine-induced protein levels were formed (Q1, Q2, Q3, and Q4). We found a low median plasma ACTH [median (range): 8.9 (<2.0–332.0) pg/mL] but a high median serum cortisol level [median (range): 25.8 (1.4–99.8) μg/dL] in the entire study population. The median serum cortisol levels were significantly higher in the CRP-Q4, ferritin-Q4, and U-β2MG-Q4 groups than in the CRP-Q1, ferritin-Q2, and U-β2MG-Q1 groups, respectively (p < 0.01; p < 0.01; p < 0.001). The median plasma ACTH levels were significantly lower in the CRP-Q4 and ferritin-Q4 groups than in the CRP-Q1 and ferritin-Q1 groups, respectively (p < 0.001; p < 0.001). ACTH-cortisol dissociation was identified in patients with KD. Our findings suggest that inflammatory cytokines are involved in ACTH-independent hypercortisolemia in patients with KD. ACTH-cortisol dissociation in other systemic inflammatory diseases needs further investigation.]]></description><identifier>ISSN: 0918-8959</identifier><identifier>EISSN: 1348-4540</identifier><identifier>DOI: 10.1507/endocrj.EJ20-0533</identifier><identifier>PMID: 33536381</identifier><language>eng</language><publisher>Japan: The Japan Endocrine Society</publisher><subject>ACTH ; ACTH-cortisol dissociation ; Adrenocorticotropic hormone ; C-reactive protein ; Cortisol ; Cytokine ; Cytokines ; Feedback inhibition ; Ferritin ; Hormones ; Inflammatory diseases ; Interleukin 6 ; Kawasaki disease ; Mucocutaneous lymph node syndrome ; Plasma ; Population studies ; Tumor necrosis factor-α ; β2 Microglobulin</subject><ispartof>Endocrine Journal, 2021, Vol.68(6), pp.683-689</ispartof><rights>The Japan Endocrine Society</rights><rights>Copyright Japan Science and Technology Agency 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-50b62c07798837e94062c9d197ba580f0b0f81937c1804742a54b7478ba112523</citedby><cites>FETCH-LOGICAL-c526t-50b62c07798837e94062c9d197ba580f0b0f81937c1804742a54b7478ba112523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33536381$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aso, Keiko</creatorcontrib><creatorcontrib>Satoh, Mari</creatorcontrib><title>ACTH-cortisol dissociation in patients with Kawasaki disease: a retrospective study</title><title>Endocrine Journal</title><addtitle>Endocr J</addtitle><description><![CDATA[ACTH-cortisol dissociation is recognized in patients with critical illnesses. Cytokines, including tumor necrosis factor-α and interleukin-6 induce hypercortisolemia by enhancing the ACTH-independent synthesis and secretion of cortisol and by reducing cortisol breakdown. Subsequently, hypercortisolemia suppresses ACTH secretion by negative feedback inhibition. ACTH-cortisol dissociation in patients with systemic inflammatory diseases has not been reported. Here, we examined whether ACTH-cortisol dissociation is recognized in patients with Kawasaki disease (KD) associated with hypercytokinemia, as well as the possible cytokine involvement in ACTH-cortisol dissociation, retrospectively. The levels of serum cortisol, plasma ACTH, and cytokine-induced proteins, i.e., plasma C-reactive protein (CRP), serum ferritin, and urinary β2-microglobulin (U-β2MG), in 232 patients with KD were measured at diagnosis. Quartile groups based on cytokine-induced protein levels were formed (Q1, Q2, Q3, and Q4). We found a low median plasma ACTH [median (range): 8.9 (<2.0–332.0) pg/mL] but a high median serum cortisol level [median (range): 25.8 (1.4–99.8) μg/dL] in the entire study population. The median serum cortisol levels were significantly higher in the CRP-Q4, ferritin-Q4, and U-β2MG-Q4 groups than in the CRP-Q1, ferritin-Q2, and U-β2MG-Q1 groups, respectively (p < 0.01; p < 0.01; p < 0.001). The median plasma ACTH levels were significantly lower in the CRP-Q4 and ferritin-Q4 groups than in the CRP-Q1 and ferritin-Q1 groups, respectively (p < 0.001; p < 0.001). ACTH-cortisol dissociation was identified in patients with KD. Our findings suggest that inflammatory cytokines are involved in ACTH-independent hypercortisolemia in patients with KD. ACTH-cortisol dissociation in other systemic inflammatory diseases needs further investigation.]]></description><subject>ACTH</subject><subject>ACTH-cortisol dissociation</subject><subject>Adrenocorticotropic hormone</subject><subject>C-reactive protein</subject><subject>Cortisol</subject><subject>Cytokine</subject><subject>Cytokines</subject><subject>Feedback inhibition</subject><subject>Ferritin</subject><subject>Hormones</subject><subject>Inflammatory diseases</subject><subject>Interleukin 6</subject><subject>Kawasaki disease</subject><subject>Mucocutaneous lymph node syndrome</subject><subject>Plasma</subject><subject>Population studies</subject><subject>Tumor necrosis factor-α</subject><subject>β2 Microglobulin</subject><issn>0918-8959</issn><issn>1348-4540</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNpdkD1PwzAQhi0EgvLxA1hQJBaWgB1_hg1VpQUqMQCz5TguuKRxsR0q_j2OWjKw-HzSc6_uHgDOEbxGFPIb09ZO--X15LGAOaQY74ERwkTkhBK4D0awRCIXJS2PwHEISwgxpgQfgqNUMcMCjcDL3fh1lmvnow2uyWobgtNWRevazLbZOv1MG0O2sfEje1IbFdSn7TGjgrnNVOZN9C6sjY7222QhdvXPKThYqCaYs109AW_3k9fxLJ8_Tx_Gd_Nc04LFnMKKFRpyXgqBuSkJTG1Zo5JXigq4gBVcCFRirpGAhJNCUVJxwkWlECpogU_A1TZ37d1XZ0KUKxu0aRrVGtcFWRDBCMOI4YRe_kOXrvNt2k4WlHBGOeIoUWhL6XRS8GYh196ulP-RCMreuNwZl71x2RtPMxe75K5amXqY-FOcgOkWWIao3s0AqKRcN2aIZEKy_hmiB0J_KJ8w_At1uZXe</recordid><startdate>20210101</startdate><enddate>20210101</enddate><creator>Aso, Keiko</creator><creator>Satoh, Mari</creator><general>The Japan Endocrine Society</general><general>Japan Science and Technology Agency</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20210101</creationdate><title>ACTH-cortisol dissociation in patients with Kawasaki disease: a retrospective study</title><author>Aso, Keiko ; Satoh, Mari</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-50b62c07798837e94062c9d197ba580f0b0f81937c1804742a54b7478ba112523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>ACTH</topic><topic>ACTH-cortisol dissociation</topic><topic>Adrenocorticotropic hormone</topic><topic>C-reactive protein</topic><topic>Cortisol</topic><topic>Cytokine</topic><topic>Cytokines</topic><topic>Feedback inhibition</topic><topic>Ferritin</topic><topic>Hormones</topic><topic>Inflammatory diseases</topic><topic>Interleukin 6</topic><topic>Kawasaki disease</topic><topic>Mucocutaneous lymph node syndrome</topic><topic>Plasma</topic><topic>Population studies</topic><topic>Tumor necrosis factor-α</topic><topic>β2 Microglobulin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aso, Keiko</creatorcontrib><creatorcontrib>Satoh, Mari</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrine Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aso, Keiko</au><au>Satoh, Mari</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ACTH-cortisol dissociation in patients with Kawasaki disease: a retrospective study</atitle><jtitle>Endocrine Journal</jtitle><addtitle>Endocr J</addtitle><date>2021-01-01</date><risdate>2021</risdate><volume>68</volume><issue>6</issue><spage>683</spage><epage>689</epage><pages>683-689</pages><issn>0918-8959</issn><eissn>1348-4540</eissn><abstract><![CDATA[ACTH-cortisol dissociation is recognized in patients with critical illnesses. Cytokines, including tumor necrosis factor-α and interleukin-6 induce hypercortisolemia by enhancing the ACTH-independent synthesis and secretion of cortisol and by reducing cortisol breakdown. Subsequently, hypercortisolemia suppresses ACTH secretion by negative feedback inhibition. ACTH-cortisol dissociation in patients with systemic inflammatory diseases has not been reported. Here, we examined whether ACTH-cortisol dissociation is recognized in patients with Kawasaki disease (KD) associated with hypercytokinemia, as well as the possible cytokine involvement in ACTH-cortisol dissociation, retrospectively. The levels of serum cortisol, plasma ACTH, and cytokine-induced proteins, i.e., plasma C-reactive protein (CRP), serum ferritin, and urinary β2-microglobulin (U-β2MG), in 232 patients with KD were measured at diagnosis. Quartile groups based on cytokine-induced protein levels were formed (Q1, Q2, Q3, and Q4). We found a low median plasma ACTH [median (range): 8.9 (<2.0–332.0) pg/mL] but a high median serum cortisol level [median (range): 25.8 (1.4–99.8) μg/dL] in the entire study population. The median serum cortisol levels were significantly higher in the CRP-Q4, ferritin-Q4, and U-β2MG-Q4 groups than in the CRP-Q1, ferritin-Q2, and U-β2MG-Q1 groups, respectively (p < 0.01; p < 0.01; p < 0.001). The median plasma ACTH levels were significantly lower in the CRP-Q4 and ferritin-Q4 groups than in the CRP-Q1 and ferritin-Q1 groups, respectively (p < 0.001; p < 0.001). ACTH-cortisol dissociation was identified in patients with KD. Our findings suggest that inflammatory cytokines are involved in ACTH-independent hypercortisolemia in patients with KD. ACTH-cortisol dissociation in other systemic inflammatory diseases needs further investigation.]]></abstract><cop>Japan</cop><pub>The Japan Endocrine Society</pub><pmid>33536381</pmid><doi>10.1507/endocrj.EJ20-0533</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | ACTH ACTH-cortisol dissociation Adrenocorticotropic hormone C-reactive protein Cortisol Cytokine Cytokines Feedback inhibition Ferritin Hormones Inflammatory diseases Interleukin 6 Kawasaki disease Mucocutaneous lymph node syndrome Plasma Population studies Tumor necrosis factor-α β2 Microglobulin |
| title | ACTH-cortisol dissociation in patients with Kawasaki disease: a retrospective study |
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