Subclinical atherosclerosis evolution during 5 years of anti-TNF-alpha treatment in psoriatic arthritis patients.


Journal

Clinical and experimental rheumatology
ISSN: 0392-856X
Titre abrégé: Clin Exp Rheumatol
Pays: Italy
ID NLM: 8308521

Informations de publication

Date de publication:
Historique:
received: 11 02 2020
accepted: 07 04 2020
pubmed: 27 5 2020
medline: 11 2 2021
entrez: 27 5 2020
Statut: ppublish

Résumé

Our aim was to evaluate subclinical atherosclerosis progression during 5 years of anti-tumour necrosis factor (TNF)-α treatment in psoriatic arthritis (PsA) patients. Thirty-two consecutive PsA patients starting TNF-α inhibitors were enrolled and evaluated at baseline (T0), 2 years (FU1) and 5 years (FU2) of treatment. Arterial structural properties were evaluated by B-mode ultrasound of mean carotid intima-media thickness (mean-IMT) and maximum IMT (M-MAX) in each segment (common, bulb, internal), bilaterally. Endothelial function was assessed by post-occlusion flow-mediated dilation (FMD) of the brachial artery using high-sensitivity ultrasonography. Treatment response was studied through DAS28 (disease activity score) and inflammatory biomarkers (C-reactive protein, TNF-α, osteoprotegerin). Metrologic and metabolic data were collected. At T1, a significant decrease of DAS28 (4.2±0.7 vs. 2.3±0.8, p<0.001) and CRP (11.25±9.16 vs. 2.91±1.72, p<0.01) was observed. Efficacy was preserved at FU2 (DAS28 2.4±0.9, CRP 2.73±2.51; p=ns vs. FU1). Systolic blood pressure and BMI remained stable throughout the follow-up, while diastolic blood pressure decreased significantly from FU1 to FU2 (80±10 vs. 74±7 mmHg, p=0.001). From T0 to FU1 there was an increase of IMT-mean and M-MAX (0.7±0.1 vs. 0.9±0.4 and 0.9±0.2 vs. 1.1±0.4, p<0.01). At FU2, IMT-mean and M-max did not change significantly (0.9±0.3 and 1.1±0.3, p=ns vs. FU1). No significant variation in FMD values was observed during the study period. A slight progression of subclinical atherosclerosis in PsA was observed in the first 2 years of anti-TNF-α treatment. This process seemed to decelerate in follow-up extension to 5 years.

Identifiants

pubmed: 32452348
pii: 15329
doi: 10.55563/clinexprheumatol/3qiqk3
doi:

Substances chimiques

Tumor Necrosis Factor-alpha 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

158-161

Auteurs

Augusta Ortolan (A)

Rheumatology Unit, Department of Medicine DIMED, University of Padova, Italy.

Roberta Ramonda (R)

Rheumatology Unit, Department of Medicine DIMED, University of Padova, Italy. roberta.ramonda@unipd.it.

Mariagrazia Lorenzin (M)

Rheumatology Unit, Department of Medicine DIMED, University of Padova, Italy.

Raffaele Pesavento (R)

Clinica Medica 3, Department of Medicine DIMED, University of Padova, Italy.

Alice Spinazzè (A)

Clinica Medica 3, Department of Medicine DIMED, University of Padova, Italy.

Mara Felicetti (M)

Rheumatology Unit, Department of Medicine DIMED, University of Padova, Italy.

Chiara Nardin (C)

Medicina Interna I, Ospedale Ca Foncello, Treviso, Italy.

Marcello Rattazzi (M)

Medicina Interna I, Ospedale Ca Foncello, Treviso, Italy.

Andrea Doria (A)

Rheumatology Unit, Department of Medicine DIMED, University of Padova, Italy.

Massimo Puato (M)

Clinica Medica 3, Department of Medicine DIMED, University of Padova; and Dipartimento di Medicina, Ospedaledi Mirano, Venezia, Italy.

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