Patients with sleep apnea were 1.67 times more likely to develop glaucoma than patients without apnea, according to a study that compared more than 1000 apnea patients with more than 6000 age-matched participants. The study was published in the August issue of Ophthalmology.

Ching-Chun Lin, MA, from the Graduate Institute of Biomedical Informatics, College of Medical Science and Technology, Taipei Medical University, Taiwan, and colleagues relied on data from the Taiwan Longitudinal Health Insurance Database 2000, matching 1012 apnea patients aged 40 years and older with 6072 control patients of similar age, sex, and urbanization. A patient was considered to have apnea only if there were a record of him or her undergoing a sleep study. The researchers counted a glaucoma diagnosis only if the patient were prescribed medication.

“The fact that the authors required this [evidence of diagnosis] really increases the validity of their results,” Ahmad A. Aref, MD, assistant professor of ophthalmology, University of Illinois Eye and Ear Infirmary, Chicago, told Medscape Medical News. Dr. Aref, who authored a review on glaucoma and sleep earlier this year was not involved in the current study.

“Armed now with this study, clinicians should start to question their patients about sleep apnea,” Dr. Aref said. “I would treat it like other established risk factors for glaucoma, such as having a family member with glaucoma, or having high eye pressure, or being of African-American race. I would start to think seriously about grouping sleep apnea with those more established risk factors.”

Lin and colleagues found that the incidence rate of open-angle glaucoma among patients diagnosed with apnea was 11.26 per 1000 person years (95% confidence interval [CI], 8.61 – 14.49) compared with 6.76 per 1000 person years (95% CI, 5.80 – 7.83) for patients without an obstructive sleep apnea (OSA) diagnosis.

The adjusted hazard ratio (HR) for a glaucoma diagnosis within 5 years of being diagnosed with apnea was 1.67 (95% CI, 1.30 – 2.17; P < .001) after adjusting for monthly income, geographic region, diabetes, hypertension, heart disease, obesity, hyperlipidemia, renal disease, hypothyroidism, and number of outpatient visits for ophthalmologic care.

The adjusted HR for a glaucoma diagnosis among women in the 5 years after a sleep apnea diagnosis was 1.55 (95% CI, 1.04 – 2.31). For men, the adjusted HR was 1.45 (95% CI, 1.02 – 2.16).

“This study gives the most evidence to date that sleep apnea is a risk factor for OAG,” Parag Gokhale, MD, from Virginia Mason Medical Center, Seattle, Washington, told Medscape Medical News in an email. Dr. Gokhale, the spokesman for the American Academy of Ophthalmology, was not involved in the current research. Among the study’s strengths, he said, was the researchers’ decision to control for other possible causes of glaucoma, something several previous studies failed to do.

In this study, participants in the OSA group had higher levels of hypertension (P < .001), diabetes (P < .001), heart disease (P < .001), hyperlipidemia (P < .001), obesity (P < .001), renal disease (P < .001), and migraine (P < .001), the researchers found. Prevalence of hypothyroidism was equal in each group.

W. Christopher Winter, MD, medical director, Martha Jefferson Hospital Sleep Medicine Center, Charlottesville, Virginia, says this study should influence sleep specialists to include eye health in the list of concerns for apnea patients.

“With the risk [for glaucoma] 3 to 5 years out as high as it is, recommending a baseline eye exam would be a good thing. Eye exams, if your vision is good, usually fall by the wayside. I think I would add that,” Dr. Winter said.

The authors noted several limitations to the current study including a lack of severity information, such as apnea-hypopnea index scores or respiratory disturbance index scores, which would have allowed them to determine whether risk for glaucoma increased with the severity of the sleep apnea.

Source: Ophthalmology

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0����east-font-family:”Times New Roman”; color:black’> ABCG2 (p<0.01), the group writes. In the 134 patients on atorvastatin, explainable blood-level variability was split between two polymorphisms in SLCO1B1 (p<0.01 and p<0.05, respectively) and the activity of cytochrome P3A (CYP3A). The analyses were adjusted for gender, age, body mass index, ethnicity, statin dose, and time from last dose, and echo a 2008 study which concluded that two SLCO1B1 variants were associated with simvastatin-related myopathy, as reported by heartwire . The screening concept is currently being applied to simvastatin therapy at least at one major center.

The group retrospectively tested their ideas, looking at the relationships between genotypic and clinical variables and statin dose, in a validation cohort of 579 patients taking either drug in a primary care setting in the US and at a referral clinic in Canada.

The group found that the transporter genotypes that raise statin concentrations were homogeneously distributed among patients taking a range of atorvastatin and rosuvastatin dosages. That is, the prescribing physicians, armed primarily with their clinical judgment to decide dosage levels, failed to achieve optimal dosing with respect to serum drug levels. But it seemed to be only patients receiving the highest dosages who showed higher-than-safe serum levels according to genotype- and age-based criteria.

“Although we didn’t quite get to the sample size we needed, it did seem like people with the wrong genetic makeup are more likely to stop a statin or switch to [another dyslipidemia drug],” Kim said, at least among patients on the highest statin dosages.

The group’s proposed management algorithm recommends a maximum statin dosage that will result in plasma concentrations below the 90th percentile (reflecting an assumption that 10% of patients will have statin-related muscle issues) based on patient age and transporter-related genotype.

The algorithm is based on data predominantly from whites; the group cautions that some other ethnicities, “particularly Asians,” have increased sensitivity to statins.

Source: medscape.com