Antibodies to carbonic anhydrase in patients with connective tissue diseases: relationship with lung involvement.
The aim of this study is to evaluate the presence of antibodies to carbonic anhydrase I and/or II (ACAI and ACAII) in patients affected by connective tissue diseases (CTD) and to investigate their association with lung involvement evaluated by High resolution CT scan (HRCT). Ninety-six patients affected by CTD were studied, i.e. 33 rheumatoid arthritis (RA), 8 psoriatic arthritis (PA), 8 ankylosing spondilitis (AS), 23 Systemic Lupus Erythematosus (SLE), 10 Sjogren Syndrome (SS), and 14 Systemic Sclerosis (SSc). ACA were detected by ELISA. The lung involvement was evaluated by means of a previously described HRCT score. According to a receiver operator characteristic curve, patients were divided into those with HRCT score > or = 10 and those with HRCT score < 10, where HRCT score > or = 10 was predictive of interstitial lung disease. ACAI and/or ACAII were detected in 30/96 patients (31.2%) (P < 0.0001 in comparison with controls). In particular, the prevalence of ACAI and/or ACAII was significantly higher in patients with RA (P = 0.002), PA (P < 0.0001), SLE (P = 0.0003) and SSc (P < 0.0001). A positive correlation was found between HRCT scores and CRP or ACAI levels (P = < 0.0001 and P = 0.004, respectively). Thirty-nine of 96 patients (40.6%) showed a HRCT score > or = 10 and both their CRP and ACAI levels were significantly higher when compared with patients showing a HRCT score less than 10 (P < 0.0006 and P = 0.0009, respectively). Moreover, C3 and C4 complement fractions inversely correlated with HRCT scores (P = 0.0004 and P < 0.0001, respectively) and lower values of C3 and C4 complement fractions were found in patients with HRCT score > or = 10 than in those with HRCT score less than 10 (P = 0.014 and P = 0.007, respectively). Due to the lower levels of complement fractions detected in patients with HRCT score > or = 10, a possible immune-complex-mediated pathogenic mechanism of lung involvement could be suggested.
Caccavo
D
D
Department of Internal Medicine, Immunology and Infectious Diseases, University of Bari, Bari, Italy. caccavo@midim.uniba.it
Afeltra
A
A
Rigon
A
A
Vadacca
M
M
Zobel
B B
BB
Zennaro
D
D
Arcarese
L
L
Buzzulini
F
F
Pellegrino
N M
NM
Amoroso
A
A
D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000097:blood*; D002097:C-Reactive Protein / Q000032:analysis; D002256:Carbonic Anhydrases / Q000276:immunology*; D003176:Complement C3 / Q000032:analysis; D003181:Complement C4 / Q000032:analysis; D003240:Connective Tissue Diseases / Q000150:complications / Q000276:immunology*; D005260:Female; D006801:Humans; D008171:Lung Diseases / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D014057:Tomography, X-Ray Computed
D001323:Autoantibodies; D003176:Complement C3; D003181:Complement C4; D002097:C-Reactive Protein; D002256:Carbonic Anhydrases