title: A Fever in Acute Aortic Dissection is Caused by Endogenous Mediators that Influence the Extrinsic Coagulation Pathway and Do Not Elevate Procalcitonin.
abstract: Objective A fever is observed in approximately one-third of cases of acute aortic dissection (AAD); however, the causes remain unclear. We investigated the mechanism of a fever in AAD by measuring the serum concentrations of inflammatory markers, mediators of coagulation and fibrinolysis, and procalcitonin, a marker of bacterial infection. Methods We retrospectively studied 43 patients with medically treated AAD without apparent infection. Patients were divided into those with (Group A; n=19) and without (Group B; n=24) a maximum body temperature >38°C. We established which patients fulfilled the criteria for systemic inflammatory response syndrome (SIRS), and its relationship with a fever was examined. Mediators of inflammation, coagulation and fibrinolysis were compared by a univariate analysis. Factors independently associated with a fever were established by a multivariate analysis. Results The criteria for SIRS were fulfilled in a greater proportion of patients in Group A (79%) than in Group B (42%, p=0.001). There was no difference in the procalcitonin concentration between Groups A and B (0.15±0.17 ng/mL vs. 0.11±0.12 ng/mL, respectively; p=0.572). Serum procalcitonin concentrations lay within the normal range in all patients in whom it was measured, which showed that the fever was caused by endogenous mediators. On the multivariate analysis, there was a borderline significant relationship between a fever and the prothrombin time-International Normalized Ratio (p=0.065), likely reflecting the extrinsic pathway activity initiated by tissue factor. Conclusion Our findings suggest that a fever in AAD could be caused by SIRS, provoked by endogenous mediators that influence the extrinsic coagulation pathway without elevating the serum procalcitonin concentration.
authors.affiliation: Division of Cardiovascular Intensive Care, Nippon Medical School Hospital, Japan.
authors.forename: Yoshie
authors.initials: Y
authors.lastname: Inoue Arita
authors.forename: Koichi
authors.initials: K
authors.lastname: Akutsu
authors.forename: Takeshi
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Kawanaka
authors.forename: Mitsunobu
authors.initials: M
authors.lastname: Kitamura
authors.forename: Hiroshige
authors.initials: H
authors.lastname: Murata
authors.forename: Hideki
authors.initials: H
authors.lastname: Miyachi
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Hosokawa
authors.forename: Keiji
authors.initials: K
authors.lastname: Tanaka
authors.forename: Wataru
authors.initials: W
authors.lastname: Shimizu
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001014:Aortic Aneurysm / Q000150:complications*; D015415:Biomarkers; D001777:Blood Coagulation / Q000502:physiology; D002116:Calcitonin / Q000378:metabolism; D005260:Female; D005334:Fever / Q000209:etiology*; D005342:Fibrinolysis / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011517:Prothrombin Time; D012189:Retrospective Studies; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology*
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D002116:Calcitonin