Aims: To determine whether systemic hypertension and glaucoma might coexist mo re often than expected, with possible implications for treatment. Methods: Case -control study using general practitioner database of pati...Aims: To determine whether systemic hypertension and glaucoma might coexist mo re often than expected, with possible implications for treatment. Methods: Case -control study using general practitioner database of patients with glaucoma ma tched with controls for age and sex. Results: Hypertension was significantly mor e common in the 27 080 patients with glaucoma (odds ratio 1.29, 95%confidence i ntervals 1.23 to 1.36, p< 0.001) than in controls. Treatment by oral βblockade appeared to protect from risk (odds ratio 0.77, 95%CI 0.73 to 0.83, p < 0.0001) , but oral calcium channel antagonists or angiotensin converting enzyme (ACE) in hibitors did not (odds ratios 1.34, 1.24 to 1.44 and 1.16 1.09-1.24, respective ly, p < 0.0001 in each case). Oral corticosteroid treatment was associated with enhanced risk (odds ratio 1.78, 1.61 to 1.96). Conclusion: Common pathogenetic m echanisms in ciliary and renal tubular epithelia may explain coincidence of glau coma and systemic hypertension. The choice of cardiovascular treatment, could su bstantially influence glaucoma incidence, with βblockade protecting and ACE inh ibitors or calcium channel blockers not affecting underlying risk.展开更多
文摘Aims: To determine whether systemic hypertension and glaucoma might coexist mo re often than expected, with possible implications for treatment. Methods: Case -control study using general practitioner database of patients with glaucoma ma tched with controls for age and sex. Results: Hypertension was significantly mor e common in the 27 080 patients with glaucoma (odds ratio 1.29, 95%confidence i ntervals 1.23 to 1.36, p< 0.001) than in controls. Treatment by oral βblockade appeared to protect from risk (odds ratio 0.77, 95%CI 0.73 to 0.83, p < 0.0001) , but oral calcium channel antagonists or angiotensin converting enzyme (ACE) in hibitors did not (odds ratios 1.34, 1.24 to 1.44 and 1.16 1.09-1.24, respective ly, p < 0.0001 in each case). Oral corticosteroid treatment was associated with enhanced risk (odds ratio 1.78, 1.61 to 1.96). Conclusion: Common pathogenetic m echanisms in ciliary and renal tubular epithelia may explain coincidence of glau coma and systemic hypertension. The choice of cardiovascular treatment, could su bstantially influence glaucoma incidence, with βblockade protecting and ACE inh ibitors or calcium channel blockers not affecting underlying risk.
