High blood levels of chromogranin A in giant cell arteritis identify patients refractory to corticosteroid treatment

G Di Comite¹, P Previtali¹, C M Rossi¹, G Dell’Antonio¹, P Rovere-Querini¹, L Praderio¹, L Dagna¹, A Corti², C Doglioni¹, A Maseri¹, M G Sabbadini¹, A A Manfredi¹

¹ Departments of Medicine, Cardiology and Pathology, H San Raffaele Scientific Institute & Vita-Salute San Raffaele University, Milano, Italy
² Department of Oncology and IIT Network Research Unit of Molecular Neuroscience, H San Raffaele Scientific Institute & University, Milano, Italy

Correspondence to:
A A Manfredi, H San Raffaele, DIBIT 3A1, via Olgettina 58, 20132 Milano, Italy; manfredi.angelo@hsr.it

Accepted 24 March 2008

The first 150 words of the full text of this article appear below.

Giant cell arteritis (GCA) rapidly responds to high-dose corticosteroids. However, smouldering arterial inflammation can persist despite the absence of symptoms and altered acute phase reactants. In patients that are refractory, symptoms relapse during steroid tapering and vascular complications may develop. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level are not sensitive enough markers to detect refractory disease.¹ The neuroendocrine system regulates innate and acquired immune responses, influencing cytokine synthesis and limiting tissue damage via release of neurotransmitters and peptides in peripheral tissues. Chromogranin A in particular is a candidate marker linking neurogenic inflammation and vascular inflammation.² We investigated by ELISA, as described previously,³ the levels of circulating chromogranin A in 40 consecutive patients with GCA (table 1), classified according to the 1990 American College of Rheumatology (ACR) criteria,⁴ and 40 healthy control participants. All patients had been initially treated with oral prednisone (0.75–1 mg/kg). The initial . . . [Full text of this article]

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