Abstract
Abstract: :
Purpose: Homocysteine can induce vascular injury, and alterations of extracellular matrix metabolism due to dysregulation of matrix metalloproteinases and their inhibitors, and contributes to neuronal cell death by different mechanisms. Moderate hyperhomocysteinemia has been found in patients with primary and secondary open–angle glaucoma due to pseudoexfoliation. Pseudoexfoliation syndrome is a clinically significant systemic disorder of the extracellular matrix, which represents not only the most common identifiable cause of open–angle glaucoma, but also a risk factor for cardiovascular disease. This study was performed to determine the homocysteine level in aqueous humor of patients with pseudoexfoliation glaucoma (PEXG). Patients and Methods: Total plasma homocysteine, vitamins relevant in its metabolism (folate, B12, B6), and total homocysteine of aqueous humor were determined in 30 patients with PEXG (age:72.8±6.8 years, 17 female, 13 male), and 31 controls with cataract (age: 71.8±9.3 years., 18 female, 13 male). Patients with any commonly known other risk factors for hyperhomocysteinemia were excluded. The control group was matched to the study group by age, gender and concurrent diagnosis of systemic hypertension. Results: Significantly raised plasma homocysteine levels were found in patients with PEXG (15.53µmol/l ± 7.76, Mann–Whitney–U–test, Z=–2.55, p = 0.01) as compared with the control group (11.82µmol/l ± 3.56). Homocysteine was also identified in all aqueous humor samples. The homocysteine level was raised twofold in PEXG samples (2.51µmol/l ± 1.41, Mann–Whitney–U–test, Z=–5.18, p<0.001), as compared with the control group (1.26µmol/l ± 0.80). Plasma and aqueous humor homocysteine levels were correlated in PEXG patients (Spearman rho, r=0.46, p=0.025), but not in the control patients. Conclusions: The present study revealed elevated homocysteine plasma levels and aqueous humor levels in patients with PEXG. Therefore, increased levels of homocysteine in patients with PEXG may have important implications for understanding the pathogenesis of PEX glaucoma.
Keywords: clinical laboratory testing • extracellular matrix • trabecular meshwork