The role of complement activation in the pathogenesis of Fuchs' dystrophy.

PURPOSE: Inflammation can be an etiologic factor of Fuchs' dystrophy according to previous studies. Our aim was to analyse the activation of the complement system in the aqueous humor in this pathological condition. METHODS: 100 µl aqueous humor sample was taken during keratoplasty of 11 Fuchs' dystrophic patients and during phacoemulsification surgery of 18 control patients. The samples were mixed with EDTA and stored at -80 °C. Concentrations of C1rC1sC1Inh and C3bBbP complexes as markers of the activation of the classical and alternative complement pathways, respectively, were measured with ELISA method. The results of the patient group and the control group were compared with statistical analysis (non-parametric Mann Whitney test). RESULTS: Both the concentrations of C1rC1sC1Inh [4.3 (3.2-20.2)AU/ml] and of C3bBbP [15.3 (7.8-22.6)AU/ml] were significantly higher in the Fuchs' dystrophic group than in the control group [C1rC1sC1Inh: 0.0 (0.0-5.6)AU/ml, C3bBbP: 1.4 (0.0-7.8)AU/ml]. The median value is shown along with the (25% and 75% percentiles). CONCLUSIONS: Based on our results, the complement system may be activated both through the classical and alternative pathways in the aqueous humor of the patients with Fuchs' dystrophy.

Complement activation in the aqueous humor of pseudophakic bullous keratopathy patients.

BACKGROUND/AIMS: According to some studies, inflammation is a potential etiological factor in pseudophakic bullous keratopathy (PBK). Our aim was to obtain information on the activation of the complement system in the aqueous humor in this disorder. METHODS: Aqueous humor samples were collected during keratoplasty of 12 PBK patients, as well as during phacoemulsification surgery of 18 control patients. The concentrations of the protein-protein complexes generated during complement activation (C1rC1sC1inh and C3bBbP) through the classical and alternative pathways, respectively, as well as of the C3 cleavage product C3a, were measured with ELISA methods. The correlation among the complement factors and between the duration of the edema, the stage of the disease, and the level of the complement activation products was examined. RESULTS: The concentration of C1rC1sC1inh, C3bBbP complex and C3a was significantly higher in the PBK group (p < 0.001) compared to the control group. In PBK patients, a correlation was found between the levels of the C1rC1sC1inh complex and C3a only. CONCLUSION: Our new findings indicate that in PBK the complement system is activated - via the classical pathway - in the aqueous humor. The activated complement may play a role in increased endothelial cell loss.