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Anti-carbonic anhydrase antibodies in iron deficiency anemia. | LitMetric

AI Article Synopsis

  • Elevated oxidative stress in patients with iron deficiency anemia (IDA) leads to higher levels of autoantibodies against carbonic anhydrase I and II compared to healthy controls.
  • The study involved 40 IDA patients and 40 healthy individuals, measuring autoantibodies and oxidative stress markers like malondialdehyde (MDA).
  • There is a noted correlation between anti-CA I autoantibody levels and key iron-related blood parameters, suggesting these autoantibodies could be significant in diagnosing and potentially treating IDA.

Article Abstract

Objectives: Studies on experimental animals have shown that elevated oxidative stress in erythrocytes leads to the formation of autoantibodies against carbonic anhydrase (CA) and anemia. This study investigated the presence of CA I and II autoantibodies in patients with iron deficiency anemia (IDA).

Methods: Forty patients with IDA and 40 healthy controls were included in the study. Serum CA I and II autoantibody levels were analyzed using enzyme-linked immunosorbent assay. Serum malondialdehyde (MDA) levels were also measured in order to evaluate oxidative stress.

Results: CA I and II antibody titers in patients with IDA were higher than those in the controls (P = 0.005 and 0.010, respectively). A weak negative correlation was determined between anti-CA I antibody titers and ferritin, iron and mean cell volume (MCV) levels (P = 0.013, 0.042, and 0.021, respectively). Serum MDA levels were also significantly higher in the IDA group (P < 0.001). At an anti-CA I cut-off point of 0.155 absorbance unit (ABSU), sensitivity was 70% and specificity 65%. At an anti-CA II cut-off point of 0.088 ABSU, sensitivity was 60% and specificity 75%.

Discussion And Conclusion: In conclusion, an immune response against CA I and II develops in IDA. CA I autoantibodies are correlated with hematological parameters used in the diagnosis of IDA and have the potential to be used in treatment.

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Source
http://dx.doi.org/10.1179/1607845414Y.0000000204DOI Listing

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