Chitotriosidase proved to be a biomarker with good sensitivity and specificity that is easily detected in serum. It can be proposed in clinical practice to identify progressive patients requiring close follow-up, to detect relapses and to evaluate the effects of therapy.

No abstract

A crucial pathogenetic role of serum amyloid A (SAA) in granulomatous inflammation of sarcoidosis has recently been reported. In this study we analyzed SAA expression in detail, starting from proteomic analysis of serum of sarcoidosis patients. We also used the faster ELISA method that enabled us to examine a greater number of samples. Serum concentrations of SAA were significantly higher in sarcoidosis patients than controls (p<0.001), inversely correlated with FEV(1) and significantly higher in patients with subacute onset requiring prolonged and multiple steroid treatments (class 6 SCAC) than in patients with subacute onset not requiring therapy (class 4 SCAC) (p<0.001). Our results suggest that serum amyloid A could be a suitable marker of sarcoidosis: its serum concentrations are significantly higher in sarcoidosis patients than controls, the protein is only expressed in gels of sarcoidosis patients and not in healthy subjects, and the SAA1 isoforms could match the unidentified biomarker of sarcoidosis reported in a previous proteomic study by another group. The effectiveness of SAA as a clinical biomarker of sarcoidosis should now be investigated in a large prospective study.

Calgranulins are small calcium-binding proteins with several immunological functions involved in inflammatory processes. Calgranulin A is reported to be mainly associated with acute inflammation while calgranulin B seems to play a role in chronic inflammatory disorders. In this study we used a proteomic approach to analyse calgranulin B expression in bronchoalveolar lavage (BAL) from a group of patients with different interstitial lung diseases. Two dimensional electrophoresis analysis of BAL was performed in 11 idiopathic pulmonary fibrosis patients, nine sarcoidosis patients, 11 with systemic sclerosis patients and five healthy controls. Significantly higher (p<0.001) calgranulin B percentage volumes were observed in BAL from IPF patients than controls and other ILD patients. This result sustains the hypothesis that calgranulin B could be involved in chronic lung diseases, probably through increased expression and enhanced activation of alveolar polymorphonuclear cells related to idiopathic pulmonary fibrosis. Quantitative analysis by an easier method applied to a larger population will be necessary to determine whether calgranulin B could be a good marker of disease severity.

Chitotriosidase and sIL-2R are two markers of sarcoidosis of different origin, the values of which show a correlation in these patients; they are easily detectable in serum and could be useful clinical markers of progression.