Steroid Therapy Improves Endothelial Function in Patients with Biopsy-Proven Giant Cell Arteritis

CARLOS GONZALEZ-JUANATEY, JAVIER LLORCA, CARLOS GARCIA-PORRUA, AMALIA SANCHEZ-ANDRADE, JAVIER MARTÍN, and MIGUEL A. GONZALEZ-GAY

ABSTRACT.

Objective. Endothelial dysfunction has been found to be present in subjects with both small and medium-size blood vessel vasculitides. We assess whether endothelial dysfunction was also present in patients with biopsy-proven giant cell arteritis (GCA) and whether it might be improved following steroid treatment.

Methods. Endothelial function was determined in cross-sectional and longitudinal studies of 6 patients with biopsy-proven GCA diagnosed between January and May 2002 by measuring flow-mediated endothelial-dependent and independent vasodilatation (EDV and EIV) by brachial ultrasonography. Patients were assessed for endothelial function within 48 hours after the onset of steroid therapy, 4 weeks after the onset of steroid therapy, and 2 years after the disease diagnosis.

Results. EDV was significantly impaired in patients with GCA compared with 12 matched controls [mean 2.9%, median 2.45% (range 2.1% to 4.7%) vs mean 6.5%, median 6.6% (range 3.9% to 9.3%) in matched controls; p = 0.002]. However, no significant difference existed between patients and controls in EIV. Significant improvement of EDV after the suppression of inflammation was achieved. At Week 4 after the onset of steroid therapy all 6 patients showed enhanced responses (p = 0.028). This improvement of EDV was still present when steroid treatment was ended, 2 years after diagnosis.

Conclusion. Endothelial function is significantly impaired in individuals with active biopsy-proven GCA. The results highlight the importance of steroid therapy to improve endothelial function after suppression of the inflammation of GCA. (J Rheumatol 2006;33:74-8)

Key Indexing Terms:

GIANT CELL ARTERITIS
TEMPORAL ARTERY BIOPSY
ENDOTHELIAL DYSFUNCTION
FLOW-MEDIATED ENDOTHELIAL DEPENDENT VASODILATATION

---

From the Divisions of Rheumatology and Cardiology, Hospital Xeral-Calde, Lugo; Department of Preventive Medicine and Public Health, School of Medicine, University of Cantabria, Santander; and the Instituto de Parasitología y Biomedicina López Neyra, CSIC, Granada, Spain.

M.A. Gonzalez-Gay, MD, PhD; C. García-Porrua, MD, PhD; A. Sanchez-Andrade, MD, Division of Rheumatology; C. Gonzalez-Juanatey, MD, Division of Cardiology, Hospital Xeral-Calde; J. Llorca, MD, PhD, Department of Preventive Medicine and Public Health, School of Medicine, University of Cantabria; J. Martin, MD, PhD, Instituto de Parasitología y Biomedicina López Neyra, CSIC.

Address reprint requests to Dr. M.A. Gonzalez-Gay, Rheumatology Division, Hospital Xeral-Calde, c) Dr. Ochoa s/n, 27004 Lugo, Spain. E-mail: miguelaggay@hotmail.com

Accepted for publication August 31, 2005.

---