title: Cardio-ankle vascular index for evaluating immunosuppressive therapy in a patient with aortitis syndrome.
abstract: Aortitis syndrome is a chronic vasculitis that leads to arterial wall thickening and stiffening in large elastic arteries. However, there are no established markers for assessing arterial stiffening in aortitis syndrome. The cardio-ankle vascular index (CAVI) has recently been utilized to assess arterial stiffening that is associated with atherosclerosis-related diseases. We hypothesized that CAVI can be applicable for assessing alterations in arterial stiffness during immunosuppressive therapy for aortitis syndrome. A 69-year-old woman with a 2-month history of recurrent fever, fatigue, and malaise, showed intense 18F-fluorodeoxyglucose (18F-FDG) uptake in the thoracic aorta and common carotid arteries in 18F-FDG-positron emission tomography. These clinical and imaging findings resulted in the diagnosis of aortitis syndrome. The patient also showed the elevated CAVIs on both sides (right, 10.3; left, 10.4) (normal value for her age, 9.1 +/- 0.8), indicating the arterial stiffness due to aortitis syndrome. The patient was treated for 34 weeks with immunosuppressive therapy, which included oral prednisolone and methotrexate. C-reactive protein (from 4.24 to 0.49 mg/dL) and immunoglobulin G (from 2,627 to 1,524 mg/dL) were decreased by 7 weeks after initiation of the treatment. The decrease in these inflammatory parameters suggests the effectiveness of the immunosuppressive therapy. In addition, after the 34-week treatment, the CAVIs on both sides (right, 9.3; left, 9.2) were within the normal range. These data indicate that the immunosuppressive therapy ameliorates the degree of arterial stiffness. In conclusion, CAVI may be a promising marker for evaluating the effectiveness of immunosuppressive therapy in patients with aortitis syndrome.
authors.affiliation: Department of Integrated Medicine, Kagawa University, Kita-gun, Kagawa, Japan. masugata@med.kagawa-u.ac.jp
authors.forename: Hisashi
authors.initials: H
authors.lastname: Masugata
authors.forename: Shoichi
authors.initials: S
authors.lastname: Senda
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Dobashi
authors.forename: Takashi
authors.initials: T
authors.lastname: Himoto
authors.forename: Koji
authors.initials: K
authors.lastname: Murao
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Okuyama
authors.forename: Michio
authors.initials: M
authors.lastname: Inukai
authors.forename: Naohisa
authors.initials: N
authors.lastname: Hosomi
authors.forename: Masakazu
authors.initials: M
authors.lastname: Kohno
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Nishiyama
authors.forename: Takeaki
authors.initials: T
authors.lastname: Kohno
authors.forename: Fuminori
authors.initials: F
authors.lastname: Goda
mesh_terms: D000368:Aged; D000842:Ankle / Q000098:blood supply; D015415:Biomarkers / Q000032:analysis*; D001783:Blood Flow Velocity; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000502:physiology*; D005260:Female; D006801:Humans; D007165:Immunosuppression Therapy / Q000379:methods*; D008727:Methotrexate; D011239:Prednisolone; D013625:Takayasu Arteritis / Q000175:diagnosis* / Q000188:drug therapy* / Q000276:immunology; D016896:Treatment Outcome; D017539:Tunica Intima / Q000033:anatomy & histology; D014463:Ultrasonography; D014655:Vascular Resistance
chemical_list: D015415:Biomarkers; D011239:Prednisolone; D008727:Methotrexate