title: Infliximab, a TNF-α inhibitor, reduces 24-h ambulatory blood pressure in rheumatoid arthritis patients.
abstract: Tumour necrosis factor-alpha (TNF-α) is an important mediator in the pathogenesis of rheumatoid arthritis (RA) and hypertension. TNF-α inhibitors improve clinical symptoms and inhibit joint destruction in RA, but their effect on blood pressure (BP) has not been fully investigated. We measured 24-h BP using an ambulatory BP monitor in 16 RA patients treated with a TNF-α inhibitor, infliximab, to investigate its influence on BP and its association with the regulatory factors of BP and renin-angiotensin-aldosterone and sympathetic nervous systems. Infliximab significantly reduced the 24-h systolic BP (SBP) from 127.4±21.8 to 120.1±23.4 mm Hg (P<0.0001). Particularly, morning BP (0600-0800 h) decreased from 129.7±19.7 to 116.9±13.4 mm Hg (P<0.0001), and daytime BP decreased from 131.8±15.1 to 122.5±13.7 mm Hg (P<0.0001). Infliximab significantly reduced the plasma level of norepinephrine and plasma renin activity (PRA) (from 347.5±180.7 to 283.0±181.8 pg ml(-1) and 2.6±2.7 to 2.1±2.9 ng ml(-1) h(-1), respectively) but did not significantly reduce the plasma levels of dopamine and epinephrine. The reduction in morning SBP correlated with the reduction in the norepinephrine level (P<0.05) but not with that in PRA and inflammatory parameters related to RA. This study shows the effect of infliximab on ambulatory BP, especially daytime BP, which may be partly accounted for by the reduction of sympathetic nerve activity after infliximab treatment.
authors.affiliation: Department of Internal Medicine (I), Osaka Medical College, Takatsuki, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Yoshida
authors.affiliation: Department of Internal Medicine (I), Osaka Medical College, Takatsuki, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Takeuchi
authors.affiliation: Department of Internal Medicine (I), Osaka Medical College, Takatsuki, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kotani
authors.affiliation: Department of Internal Medicine (I), Osaka Medical College, Takatsuki, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Yamamoto
authors.affiliation: Department of Internal Medicine (I), Osaka Medical College, Takatsuki, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hata
authors.affiliation: Department of Internal Medicine (I), Osaka Medical College, Takatsuki, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Nagai
authors.affiliation: Department of Internal Medicine (I), Osaka Medical College, Takatsuki, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Shoda
authors.affiliation: Department of Pharmacology, Osaka Medical College, Takatsuki, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Takai
authors.affiliation: Department of Internal Medicine (I), Osaka Medical College, Takatsuki, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Makino
authors.affiliation: Department of Internal Medicine (I), Osaka Medical College, Takatsuki, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Hanafusa
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D018660:Blood Pressure Monitoring, Ambulatory; D002940:Circadian Rhythm; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000187:drug effects; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D012083:Renin; D009638:Norepinephrine