Risk of Cataract in Patients Treated With Statins

Schlienger, Raymond G.; Haefeli, Walter E.; Jick, Hershel; Meier, Christoph

doi:10.1001/archinte.161.16.2021

Cited by 65 publications

(46 citation statements)

References 35 publications

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“…However, such a method has been extensively used in several studies (22,23), and it has been validated against medical records and pill counts, suggesting that pharmacy records are closely correlated (r ϭ 0.92) with the quantity of prescribed doses consumed (24).…”

Section: Filippi and Associatesmentioning

confidence: 99%

Effects of an Automated Electronic Reminder in Changing the Antiplatelet Drug–Prescribing Behavior Among Italian General Practitioners in Diabetic Patients

Filippi¹,

Sabatini²,

Badioli³

et al. 2003

Diabetes Care

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OBJECTIVE—To evaluate whether an electronic reminder integrated into a routine computer system increases the use of antiplatelet drugs for diabetic patients among Italian general practitioners (GPs). RESEARCH DESIGN AND METHODS—A randomized controlled trial was carried out among 300 GPs and their patients selected from the Health Search Database. Among these, 150 GPs (intervention group) received instructions to activate an electronic reminder plus a letter summarizing the beneficial effects of antiplatelet drugs in diabetic patients with at least one additional cardiovascular risk factor (“high risk”), whereas the other 150 GPs (control group) received only the letter. The electronic reminder, integrated into a standard software system for the management of the daily clinical practice, was displayed when every participating GP opened the medical record of diabetic patients aged ≥30 years. Only high-risk diabetic patients were included in the analysis. Patients were considered under antiplatelet treatment if they received two or more prescriptions at baseline and during the follow-up. RESULTS—We selected 15,343 high-risk diabetic patients, 7,313 belonging to GPs of the control group and 8,030 belonging to GPs of the intervention group. Overall, 1,672 patients (22.9%) of the control group and 1,886 (23.5%) patients of the intervention group received antiplatelet drugs at baseline (P = N.S.). At the end of the follow-up, the number of treated patients was significantly increased in the intervention group (odds ratio 1.99, 95% CI 1.79–2.22) versus the control group. The effect of the electronic reminder was more relevant among those patients with one or more cardiovascular risk factors but without previous cardiovascular diseases (CVDs), compared with those with CVDs. CONCLUSIONS—These findings provide evidence for the effect of an electronic reminder in affecting the prescriptive behavior of GPs.

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Section: Filippi and Associatesmentioning

confidence: 99%

Effects of an Automated Electronic Reminder in Changing the Antiplatelet Drug–Prescribing Behavior Among Italian General Practitioners in Diabetic Patients

Filippi¹,

Sabatini²,

Badioli³

et al. 2003

Diabetes Care

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show abstract

“…Genetically based deficiencies in mevalonate kinase (2), ⌬ 8, ⌬ 7-sterol isomerase (emapomil binding protein) (3) , 3 ␤ -hydroxysterol ⌬ 7-reductase (4), and 3 ␤ -hydroxysterol ⌬ 24-reductase (5) can result in human cataracts. Pharmacological inhibition of desmosterol reductase (6) or oxidosqualene cyclase (OSC) (7,8) causes cataracts in rodents, and inhibition of HMGCoA reductase by statins can induce cataracts in rats (9) and increase the risk of cataracts in humans (10). Simvastatin was shown to cause rapid lens damage and induce the formation of cataracts in Chbb:Thom rats (9).…”

mentioning

confidence: 99%

“…Simvastatin was shown to cause rapid lens damage and induce the formation of cataracts in Chbb:Thom rats (9). Simvastatin treatment also tripled the risk of cataracts in humans who concomitantly received two or more courses of erythromycin (10). Erythromycin can block statin catabolism and greatly increase its blood levels (11).…”

mentioning

confidence: 99%

Direct perturbation of lens membrane structure may contribute to cataracts caused by U18666A, an oxidosqualene cyclase inhibitor

Cenedella

Jacob²,

Borchman

et al. 2004

Journal of Lipid Research

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Induction of cataracts in experimental animals is a common toxic feature of oxidosqualene cyclase (OSC) inhibitors. U18666A has been shown to produce irreversible lens damage within a few weeks of treatment. Drug actions, besides reducing the availability of cholesterol, could contribute to cataract formation. Cholesterol added to cultures of lens epithelial cells could only partially overcome the growth-inhibiting effects of U18666A. In view of this finding and the fact that U18666A and other OSC inhibitors are highly lipophilic cationic tertiary amines, we tested the hypothesis that the cataractogenic effect of U18666A is related to direct perturbation of lens membrane structure and function. Based on changes in the anisotropy of fluorescent probes, U18666A incorporated into bovine lens lipid model membranes increased membrane structural order and, using small-angle x-ray diffraction, U18666A was shown to intercalate into the lens lipid model membranes and produce a broad condensing effect on membrane structure. Also, exposure of cultured lens epithelial cells and intact rat lenses to U18666A induced apoptosis. Induction of apoptosis may begin by intercalation of U18666A into cell membranes. By increasing membrane structural order, U18666A may also increase light scatter, thus directly contributing to lens opacification. -Cenedella, R.

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“…Although the results of clinical safety trials collec-tively show no higher risk of cataracts in statin-treated patients [as reviewed in ref. (1)], simvastatin use in one study was associated with an increased incidence of cortical cataracts after 2 years of treatment (21), and simvastatin was recently reported to increase the risk of cataracts in patients concomitantly taking erythromycin (22). Animal studies also indicated high ocular safety of statins since cataracts were seen in dogs only after 1 or more years of treatment with high doses (16) and no reports of statin cataracts in rodents had been previously reported.…”

mentioning

confidence: 99%

“…Polymorphism in one of more of the enzymes in the sterol synthesis pathway, in the numerous proteins that mediate the pleiotropic actions of the statins (52), or in the enzymes that metabolize statins could influence the ocular safety of these drugs. Schlienger et al (22) recently reported that "concomitant use of erythromycin and simvastatin may increase the risk for cataracts" in humans. Erythromycin, along with other drugs, can inhibit the cytochrome P-450 enzymes that metabolize simvastatin and increase its serum levels (53) and, thus, risk for toxicities.…”

mentioning

confidence: 99%

Discordant expression of the sterol pathway in lens underlies simvastatin-induced cataracts in Chbb

Cenedella

Kuszak

Al-Ghoul

et al. 2003

Journal of Lipid Research

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Simvastatin rapidly induced cataracts in young Chbb:Thom (CT) but not Sprague Dawley (SD) or Hilltop Wistar (HW) rats. Oral treatment for 14 but not 7 days committed CT rat lenses to cataract formation. The cholesterol to phospholipid molar ratio in lenses of treated CT rats was unchanged. Differences between strains in serum and ocular humor levels of simvastatin acid poorly correlated with susceptibility to cataracts. No significant differences were found between rat strains in the capacity of simvastatin acid to inhibit lens-basal sterol synthesis. Prolonged treatment with simvastatin comparably elevated HMG-CoA reductase protein and enzyme activity in lenses of both cataract resistant and sensitive strains. However, in contrast to SD and HW rats, where sterol synthesis was markedly increased, sterol synthesis in CT rat lenses remained at baseline. Discordant expression of sterol synthesis in CT rats may be due to inadequate upregulation of lens HMG-CoA synthase. HMGCoA synthase protein levels, and to a much lesser extent mRNA levels, increased in lens cortex of SD but not CT rats. Because upregulation of the sterol pathway may result in increased formation of isoprene-derived anti-inflammatory substances, failure to upregulate the pathway in CT rat lenses may reflect an attenuated compensatory response to injury that resulted in cataracts.-Cenedella, R. J., J. R. Kuszak, K. J. AlGhoul, S. Qin, and P. S. Sexton. Discordant expression of the sterol pathway in lens underlies simvastatin-induced cataracts in Chbb:Thom rats. J. Lipid Res. 2003. 44: 198-211.

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Risk of Cataract in Patients Treated With Statins

Abstract: Our study provides evidence that long-term use of therapeutic statin doses does not increase the risk of developing cataract. Concomitant use of erythromycin and simvastatin may increase the cataract risk.

Cited by 65 publications

References 35 publications

Effects of an Automated Electronic Reminder in Changing the Antiplatelet Drug–Prescribing Behavior Among Italian General Practitioners in Diabetic Patients

Effects of an Automated Electronic Reminder in Changing the Antiplatelet Drug–Prescribing Behavior Among Italian General Practitioners in Diabetic Patients

Direct perturbation of lens membrane structure may contribute to cataracts caused by U18666A, an oxidosqualene cyclase inhibitor

Discordant expression of the sterol pathway in lens underlies simvastatin-induced cataracts in Chbb

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