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Published on: June 16, 2020
Antibodies to carbonic anhydrase in patients with connective tissue diseases: relationship with lung involvement
D Caccavo1, A Afeltra, A Rigon
1Department of Internal Medicine, Immunology and Infectious Diseases, University of Bari, Bari, Italy. caccavo@midim.uniba.it
Insights
Antibodies to carbonic anhydrase (ACAI and ACAII) are present in over 30% of patients with connective tissue diseases. Higher ACAI levels correlate with lung involvement, suggesting a potential role in disease pathogenesis.
Area of Science:
- Immunology
- Rheumatology
- Pulmonology
Background:
- Connective tissue diseases (CTD) encompass a range of autoimmune disorders.
- Lung involvement is a significant complication in CTD patients.
- Antibodies to carbonic anhydrase I and II (ACAI and ACAII) are implicated in autoimmune conditions.
Purpose of the Study:
- To evaluate the prevalence of ACAI and ACAII in CTD patients.
- To investigate the association between ACAI/ACAII and lung involvement assessed by High-Resolution CT (HRCT).
Main Methods:
- ELISA was used to detect ACAI and ACAII in 96 CTD patients (RA, PA, AS, SLE, SS, SSc).
- Lung involvement was quantified using a validated HRCT score.
- Patients were categorized based on HRCT scores predictive of interstitial lung disease.
Main Results:
- ACAI and/or ACAII were detected in 31.2% of CTD patients, significantly higher than controls.
- Prevalence was notably elevated in Rheumatoid Arthritis, Psoriatic Arthritis, Systemic Lupus Erythematosus, and Systemic Sclerosis.
- Positive correlations were observed between HRCT scores and C-reactive protein (CRP) or ACAI levels.
- Patients with significant lung involvement (HRCT score ≥ 10) exhibited higher CRP and ACAI levels.
- Inverse correlations were found between HRCT scores and C3/C4 complement fractions, with lower levels in patients with lung involvement.
Conclusions:
- ACAI and/or ACAII are prevalent in CTD patients, particularly those with RA, PA, SLE, and SSc.
- Elevated ACAI levels are associated with lung involvement in CTD.
- Lower complement levels (C3, C4) in patients with lung involvement suggest a potential immune-complex-mediated mechanism contributing to pulmonary complications.
Abstract:
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.
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