The clinical and molecular cardiometabolic fingerprint of an exploratory psoriatic arthritis cohort is associated with the disease activity and differentially modulated by methotrexate and apremilast
Autor
Arias de la Rosa, Iván
López-Montilla, María Dolores
Román-Rodríguez, Cristobal
Pérez Sánchez, Carlos
Gómez-García, Ignacio
López Medina, Eloísa Clementina
Ladehesa-Pineda, Lourdes
Ábalos-Aguilera, María del Carmen
Ruiz, Desireé
Patiño-Trives, Alejandra Mª
Luque-Tévar, María
Añón-Oñate, Isabel
Pérez-Galán, María José
Guzmán Ruiz, R.
Malagón, María M.
López-Pedrera, Ch.
Escudero Contreras, Alejandro
Collantes Estévez, Eduardo
Barbarroja, Nuria
Editor
WileyFecha
2022Materia
ApremilastCardiometabolic profile
Cardiovascular risk
Insulin resistance
Methotrexate
Obesity and disease activity
Psoriatic arthritis
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Objectives: (1) To evaluate clinical and molecular cardiovascular disease (CVD) signs and their relationship with psoriatic arthritis (PsA) features and (2) to identify a clinical patient profile susceptible to benefit from methotrexate (MTX) and/or apremilast regarding CVD risk. Methods: This cross-sectional study included 100 patients with PsA and 100 age-matched healthy donors. In addition, an exploratory cohort of 45 biologically naïve patients treated for 6 months with apremilast, MTX or combined therapy according to routine clinical practice was recruited. Extensive clinical and metabolic profiles were obtained. Ninety-nine surrogate CVD-related molecules were analysed in plasma and peripheral blood mononuclear cells (PBMCs). Hard cluster analysis was performed to identify the clinical and molecular phenotypes. Mechanistic studies were performed on adipocytes. Results: Cardiometabolic comorbidities were associated with disease activity and long-term inflammatory status. Thirty-five CVD-related proteins were altered in the plasma and PBMCs of PsA patients and were associated with the key clinical features of the disease. Plasma levels of some of the CVD-related molecules might distinguish insulin-resistant patients (MMP-3, CD163, FABP-4), high disease activity (GAL-3 and FABP-4) and poor therapy outcomes (CD-163, LTBR and CNTN-1). Hard cluster analysis identified two phenotypes of patients according to the rates of cardiometabolic comorbidities with distinctive clinical and molecular responses to each treatment. Conclusions: (1) Novel CVD-related proteins associated with clinical features could be emerging therapeutic targets in the context of PsA and (2) the pleiotropic action of apremilast could make it an excellent choice for the management of PsA patients with high CVD risk, targeting metabolic alterations and CVD-related molecules.
Fuente
Journal of Internal Medicine 291, 676-693 (2022)Versión del Editor
https://doi.org/10.1111/joim.13447Ítems relacionados
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