Diabetes & Metabolism 37 (2011) 139–143

Original article

Statin therapy and cataract in type 2 diabetes

M.P. Hermans a,∗ , S.A. Ahn b , M.F. Rousseau b
a Service d’endocrinologie et nutrition, cliniques universitaires St.-Luc, avenue Hippocrate 10, 1200 Bruxelles, Belgium
b Département de cardiologie, cliniques universitaires St.-Luc, université catholique de Louvain,

avenue Hippocrate 10, 1200 Brussels, Belgium

Received 3 June 2010; received in revised form 5 September 2010; accepted 6 September 2010
Available online 8 December 2010

Abstract
Background. – It was recently reported that the prolonged use of statins may predispose to incident cataract in the general population. Cataract
is a frequent comorbidity of diabetes, and statins are widely prescribed in patients with type 2 diabetes (T2D) both for primary and secondary
cardiovascular prevention. For this reason, this study aimed to assess whether or not the use of statins was associated with an increased prevalence
of cataract in such a high-risk population and, conversely, whether or not there was greater usage of statins, or any other lipid-lowering drugs, in
T2D patients with cataract.
Patients and methods. – This was a cross-sectional analysis of 780 T2D outpatients, with a mean age (± 1 SD) of 64 ± 12 years and diabetes
duration of 13 ± 9 years. Diabetic retinopathy (DR) was found in 23%, and cataract was diagnosed in 16.8% (n = 131). Age and diabetes duration
of the patients with cataract were significantly higher than those of patients without cataract (n = 649): 75 ± 9 vs 62 ± 11 years, and 20 ± 11 vs
12 ± 8 years, respectively (both P < 0.0001). HbA1c was non-significantly higher in the cataract group: 7.75 ± 1.55% vs 7.57 ± 1.49% (NS).
Results. – Statins, fibrates and/or ezetimibe use did not differ between patients with and without cataract, nor was cataract prevalence higher
in statin users (n = 435) vs non-users (n = 345). Statin use in patients with cataract was not higher than in cataract-free subgroups with mean age
(n = 218) or with both mean age and diabetes duration (n = 161) similar to those of patients with cataract.
Conclusion. – In this cross-sectional analysis of a large diabetic population at very high risk of both DR and cataract, chronic therapy with statins
was not cataractogenic, and the presence of cataract was not associated with more statin or other lipid-lowering drug use. This suggests that the
benefits of statin therapy in T2D may far outweigh any potential ocular drawbacks as a side effect which, in any case, were not supported by our
findings.
© 2010 Elsevier Masson SAS. All rights reserved.

Keywords: Statin; Fibrate; Ezetimibe; Side-effects; Cataract; Retinopathy; Type 2 diabetes

Résumé
Traitement par statine et cataracte dans le diabète de type 2.
But. – Il a été récemment rapporté que l’usage prolongé de statines pourrait prédisposer à la survenue de cataractes dans la population générale.
La cataracte est une co-morbidité fréquente du diabète, et la prescription de statines largement recommandée aux patients diabétiques de type 2
(DT2), tant en prévention cardiovasculaire primaire que secondaire. Nous avons analysé si l’utilisation de statines était associée à une prévalence
accrue de cataracte dans cette population à haut risque, et inversement, si les patients DT2 souffrant de cataracte étaient plus souvent traités par
statines ou par d’autres agents hypolipémiants.
Méthodes. – Analyse transversale de 780 patients ambulatoires avec DT2; l’âge moyen (± 1 DS) était de 64 ± 12 ans, et la durée du diabète de
13 ± 9 ans. Une rétinopathie diabétique (RD) était présente chez 23 % des patients. Une cataracte était diagnostiquée dans 16,8 % de la cohorte
(n = 131). L’âge et la durée du diabète des patients avec cataracte étaient significativement supérieurs à ceux des patients sans cataracte (n = 649),
respectivement 75 ± 9 versus 62 ± 11 ans, et 20 ± 11 versus 12 ± 8 ans (P à chaque fois inférieur à 0,0001). L’HbA1c était non-significativement
plus élevée dans le groupe avec cataracte: 7,75 ± 1,55 % versus 7,57 ± 1,49 %.

∗ Corresponding author. Tel.: +32 0 2 764 54 75; fax: +32 0 2 764 54 18.
E-mail address: michel.hermans@diab.ucl.ac.be (M.P. Hermans).

1262-3636/$ – see front matter © 2010 Elsevier Masson SAS. All rights reserved.
doi:10.1016/j.diabet.2010.09.005

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 140 M.P. Hermans et al. / Diabetes & Metabolism 37 (2011) 139–143

Résultats. – L’utilisation de statines, de fibrates et/ou d’ézétimibe n’était pas différente entre les patients avec ou sans cataracte. La prévalence
de cataracte n’était pas plus élevée chez les utilisateurs de statines (n = 435) versus les non-utilisateurs (n = 345). La prescription de statines chez
les patients avec cataracte n’était pas supérieure à celle de sous-groupes de patients sans cataracte d’âge moyen similaire (n = 218), ou à la fois
d’âge et de durée de diabète similaires (n = 161) à ceux des patients avec cataracte.
Conclusions. – Dans cette étude transversale d’une population de patients avec DT2 à haut risque à la fois de RD et de cataracte, l’usage chronique
de statines ne paraît pas cataractogène, et la présence de cataracte n’est pas associée à une utilisation accrue de statines ou d’autres hypolipémiants.
Ces observations suggèrent que les bénéfices d’un traitement par statines chez des patients DT2 dépassent largement le risque théorique d’effet
délétère sur le cristallin, qui n’est d’ailleurs pas étayé dans cette étude.
© 2010 Elsevier Masson SAS. Tous droits réservés.

Mots clés : Statine ; Fibrate ; Ézétimibe ; Effets secondaires ; Cataracte ; Rétinopathie ; Diabète de type 2

1. Introduction 2. Patients and methods

Lens opacification leading to cataract is a frequent comor-
bidity of diabetes, as adults with type 2 diabetes (T2D) are five
times more often affected than the general population (60%
vs 12%). While juvenile diabetic cataract is rare, adult-onset,
mostly cortical cataract in T2D patients is similar to age-related
cataract in the general population, except for an earlier onset
and greater prevalence [1,2]. Major risk factors for cataract in
T2D include hyperglycaemia, diabetes duration and the pres-
ence of diabetic retinopathy (DR), although specific risk factors
or markers may differ according to cataract subtype. Smoking,
for example, is associated with nuclear opacities, whereas ultra-
violet radiation increases the risk for cortical opacities, and high
blood pressure (BP) and corticosteroids raise the odds for sub-
capsular cataract. Various pathophysiological mechanisms are
involved in cataract formation, including osmosis-driven lens
overhydration triggered by the polyol pathway (mostly ascribed
to juvenile cataract), lens protein glycation and an excess of free
radicals, with the latter being particularly associated with the
nuclear subset of age-related cataract [3–5].
The presence of statins in the human lens following lipid-
lowering therapy has been demonstrated, although the effects
of statins on cataract genesis/protection are poorly documented
and widely debated [6,7]. Klein et al. [3] reported an inverse
association between statin use and nuclear cataract incidence,
but not cortical or posterior subcapsular cataract, in a general
US population. Recently, an increased risk of all-type cataract
was suggested in a group of new statin users of both genders, who
were relatively young at baseline and mostly without diabetes,
followed over a 6-year observational period in UK-based general
practices [8].
T2D is an ideal condition in which to assess the potential
beneficial/detrimental effects of statins or other lipid-lowering
drugs (LLD) on cataract, as T2D patients have a high prevalence
of atherogenic dyslipidaemia as part of the associated metabolic
syndrome, and also exhibit an increased incidence/prevalence
of both hyperglycaemia- and age-related cataract(s). Also, most
T2D patients are de facto eligible for low-density lipoprotein
(LDL)-lowering therapy with statins as per the current stan-
dards of care [9]. Thus, the aim of the present study was to
assess whether or not the use of statins is associated with an
increased prevalence of cataract and, conversely, whether or not
T2D patients with cataract are more often using a statin and/or
other LLD.
This was a cross-sectional analysis of medical records from
780 consecutive adult (aged > 18 years; 84% Caucasian) outpa-
tients with T2D, defined according to the Expert Committee on
the Diagnosis and Classification of Diabetes [10]. The diagnosis
of cataract (cortical, nuclear and/or subcapsular) was estab-
lished by an ophthalmologist during annual or biannual retinal
checkups. Patients receiving chronic therapy with systemic cor-
ticosteroids were excluded from the analysis. In patients with
previous lens surgery for cataract, lens extraction was consid-
ered a surrogate for cataract prevalence. Cataract was diagnosed
in 16.8% of the total study cohort (n = 131; Catar(+) group). DR
was diagnosed following mydriatic fundus examination, with
conventional fluorescein (fluo) angiography if deemed neces-
sary by an in-house ophthalmologist. DR was classified as mild,
moderate or severe and as non-proliferative or proliferative.
Mean age and diabetes duration of patients in the Catar(+)
group were significantly higher than those of patients with-
out cataract (n = 649): 75 ± 9 vs 62 ± 11 years, and 20 ± 11 vs
12 ± 8 years, respectively (both P < 0.0001). Age and diabetes
duration are major confounders of cataract incidence, as both
increase the likelihood of statin treatment for primary, secondary
or equivalent-secondary cardiovascular disease (CVD) preven-
tion. For this reason, Catar(+) patients were compared with a
cataract-free group [Catar(–), n = 218], representing the upper
tertile of the age distribution of those without cataract (n = 216),
plus two adjacent patients from the 66th percentile for rounding.
The following parameters were recorded: age; gender; known
diabetes duration; family history (diabetes, CVD); CVD med-
ications; and body mass index (BMI). The presence of the
metabolic syndrome (MetS) was defined according to Ameri-
can Heart Association/National Heart, Lung, and Blood Institute
(AHA/NHLBI) criteria [11]. Hypertension was defined as sys-
tolic BP ≥ 140 mmHg and/or diastolic BP ≥ 90 mmHg and/or
treatment with BP-lowering drug(s) for high BP. Coronary artery
disease (CAD) was defined as a medical history of myocar-
dial infarction, angioplasty, stents, revascularization surgery
and/or significant coronary stenosis confirmed by angiography.
Peripheral artery disease (PAD) was defined as a medical his-
tory of lower-limb claudication and/or ischaemic diabetic foot,
angioplasty, stents, revascularization surgery and/or significant
lower-limb artery stenosis, confirmed by Doppler ultrasonogra-
phy and/or angiography. Stroke was defined according to UK
Prospective Diabetes Study (UKPDS) criteria: any neurologi-

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 M.P. Hermans et al. / Diabetes & Metabolism 37 (2011) 139–143 141

cal deficit lasting ≥ 1 month, with no distinction made between Table 1

ischaemic, embolic and haemorrhagic strokes [12]. In patients Patients’ characteristics.
with multiple CVD events, only the first was considered in the No cataract Cataract P
prevalence data. n 218 131 ∼
The following biological variables were also measured: Age (years) 75 (6) 75 (9) ∼
HbA1c (measured by chromatography; normal range: 4–6%); Males:females (%) 62:38 57:43 NS
fasting lipids; apolipoproteins A-I and B100 (with LDL Diabetes duration (years) 16 (10) 20 (11) 0.0006
cholesterol [LDL-C] calculated by Friedewald’s formula, and Smokinga 51 - 40 - 9 51 - 40 - 9 NS
BMI (kg.m−2 ) 28.5 (5.5) 28.1 (5.3) NS
non-high-density lipoprotein (HDL)-C calculated by subtract- HOMA S (%) 59 (37) 56 (31) NS
ing HDL-C from total C); high-sensitivity C-reactive protein Metabolic syndromeb (%) 80 81 NS
(hs CRP); fibrinogen; serum urate; serum cystatin C; plasma Hypertension (%) 91 92 NS
homocysteine; and albuminuria. Normo-, micro- and macroal- Systolic BP (mmHg) 143 (20) 144 (21) NS
buminuria were defined as urinary albumin excretion < 30 Diastolic BP (mmHg) 77 (10) 77 (11) NS
Retinopathy (%) 25 42 0.0009
(normoalbuminuria), 30–299 (microalbuminuria) and ≥ 300 Background (%) 23 38 0.0070
(macroalbuminuria) ␮g.mg creatinine−1 . Glomerular filtration Proliferative (%) 2 5 NS
rate was estimated (eGFR) using the Modified Diet in Renal Dis-
Peripheral polyneuropathy (%) 27 43 0.0022
ease (MDRD) formula [13]. The computer-based homoeostasis Creatinine (mg.dl−1 ) 1.12 (0.46) 1.25 (0.79) NS
model assessment (HOMA) model (see www.dtu.ox.ac.uk) was eGFRc (ml.min−1 1.73 m2 ) 70 (23) 66 (27) NS
used to assess insulin sensitivity, ␤-cell function, and the hyper- Albuminuria (alb.) (␮g.mg creatinine−1 ) 72 (211) 149 (305) 0.0116
bolic product and its loss rate, as previously described [14–18]. Normo- vs. micro-/macro-alb. (%) 67–33 49–51 0.0007
IIEF-5 erectile function (score/25) 11 (8) 8 (8) 0.0099
The study was performed in accordance to the World Health
Organization’s standards of Good Clinical Practice. Results are expressed as means (1 SD) or proportions (%); BMI: body mass
(Quetelet’s) index; BP: blood pressure; eGFR: estimated glomerular filtration
rate; HOMA: homeostatic model assessment; HOMA-S: insulin sensitivity;
3. Statistical analyses
IIEF-5: International Index of Erectile Function 5-items questionnaire; NS: non
significant.
Results were presented as means ± 1 standard deviation (SD) a Never - former - current smokers.
b NCEP ATP III definition.
or as proportions. The significance of differences between means
c Modified diet in renal disease (MDRD) formula.
was assessed by Student’s t test or by Welch’s test for datasets
with significant differences in SD, and by Fisher’s exact test for
differences in proportions (using GraphPad InStatTM software). diabetes duration [longer by a mean of 4 years in Catar(+)],
Results were considered significant or non-significant (NS) for and in DR and polyneuropathy prevalence [1.7 and 1.6 times
P < or ≥ 0.05, respectively. higher, respectively, in Catar(+)]. The degree and prevalence of
albuminuria were also higher in the Catar(+).
4. Results HbA1c was non-significantly higher (by a mean of 0.3%) in
Catar(+): 7.75 ± 1.55% vs 7.57 ± 1.49% in Catar(–). Men with
The mean age of our total T2D cohort (n = 780) was 64 ± 12 cataract also scored lower (by a mean of 3 points) on the five-item
years, with a diabetes duration of 13 ± 9 years. The MetS was version of the International Index of Erectile Function (IIEF-5)
present in 78%, and a history of hypertension in 84%. Mean questionnaire. For glucose-lowering therapies, 56%, 47%, 5%
HbA1c was 7.6 ± 1.5%, total C was 176 ± 40 mg.dL−1 , LDL- and 47% of the Catar(–) group were being treated with met-
C was 97 ± 34 mg.dL−1 , HDL-C was 47 ± 14 mg.dL−1 and formin, ␤-cell stimulant, glitazone and/or insulin, respectively,
triglycerides were 169 ± 119 mg.dL−1 . LLD were prescribed vs 54%, 42%, 8% and 58% of Catar(+) patients (NS except
to 67% as statins (56%), fibrates (21%) and/or ezetimibe (3%). for insulin, which was P = 0.0364; Table 1). HOMA for ␤-cell
In statin users, pravastatin was being used by 4%, simvastatin by function (HOMA-B) was higher in the Catar(–): 61 ± 41% vs
54%, atorvastatin by 22% and rosuvastatin by 20%. Macroan- 53 ± 33% in the Catar(+) (P = 0.0465), as was also (but not sig-
giopathy was present in 32% as CAD (23%), PAD (9%) and/or nificantly) the hyperbolic product (BxS): 29 ± 17% vs 26 ± 16%
stroke (8%). With microangiopathy, DR was diagnosed in 23% in Catar(+) (NS). The BxS loss rate was significantly lower
(n = 182), of whom 21% were non-proliferative (n = 163) and in the Catar(–): 1.05 ± 0.28%/year vs 1.13 ± 0.29%/year in the
2% (n = 19) were proliferative. Lower-limb diabetic neuropathy Catar(+) (P = 0.0112). Neither lipid values nor systemic CVD
was documented in 26%. risk biomarkers (fibrinogen, urate, cystatin C and homocysteine)
Age and diabetes duration are major confounders for cataract differed significantly between groups, except for hs CRP, which
incidence, as they increase the odds of being treated with statins was higher by a mean of 55% in the Catar(+) (Table 2).
for primary, secondary or equivalent-secondary CVD preven- LLD use in the entire cohort was analyzed according to
tion. On comparing Catar(+) patients with cataract-free Catar(–) cataract status and ongoing statin therapy. No significant dif-
subjects of similar mean age (n = 218; Table 1), there were no ferences were found in statin, fibrate or ezetimibe use between
significant differences in smoking history, BMI, insulin sensitiv- the Catar(–) and Catar(+) groups (Fig. 1, left). Intraclass distri-
ity, hypertension, MetS prevalence, BP values or eGFR. There butions of statin use in the Catar(–) vs Catar(+) groups were:
were, however, significant differences between the groups in fluvastatin: 2% vs 0%; pravastatin: 6% vs 2%; simvastatin: 47%

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 142 M.P. Hermans et al. / Diabetes & Metabolism 37 (2011) 139–143

Table 2 not differ between patients with and without cataract. In fact,
Laboratory values. in the age-comparable cataract-free subgroup, statin use was
No cataract Cataract P significantly higher than in patients with cataract. Such an anti-
n 218 131 ∼
cataractogenic association with statins may be a reflection of
HbA1c (%) 7.45 (1.25) 7.75 (1.55) NS beneficial pleiotropic effects with statins such as antioxidant
activities [19]. As expected, significant associations were found
Cholesterol (mg.dl−1 ) 175 (43) 175 (35) NS between cataract prevalence and age, diabetes duration, DR,
LDL-C (mg.dl−1 ) 94 (35) 95 (29) NS polyneuropathy, erectile dysfunction and/or albuminuria, which
Non-HDL-C (mg.dl−1 ) 127 (41) 126 (35) NS
HDL-C (mg.dl−1 ) 48 (13) 49 (14) NS
is in keeping with the present paradigm of shared underlying risk
Apolipoprotein A-I (mg.dl−1 ) 151 (30) 154 (29) NS factors for cataract, diabetic eye disease and microangiopathy
Apolipoprotein B100 (mg.dl−1 ) 90 (27) 87 (24) NS in non-ocular target organs [1–5,20,21]. However, conflicting
Triglycerides 170 (110) 155 (109) NS associations between statin use and cataract have been reported,
hsCRP (mg.dl−1 ) 0.31 (0.42) 0.48 (0.85) 0.0340 albeit in mostly non-diabetic populations [3,8,22,23].
Fibrinogen (mg.dl−1 ) 331 (85) 330 (70) NS
Uric acid (mg.l−1 ) 5.7 (1.6) 5.6 (1.8) NS
Patients with cataract had longer diabetes duration and non-
Cystatin C (mg.dl−1 ) 0.96 (0.36) 1.03 (0.37) NS significantly higher HbA1c , a combination likely to have brought
Homocysteine (␮mol.l−1 ) 14.2 (5.7) 15.3 (5.5) NS about a greater risk of hyperglycaemia over time. This may
Results expressed as means (1 SD); C: cholesterol; hsCRP: high-sensitivity C-
partly explain the more frequent end-organ damage seen in
reactive protein; HDL: high density lipoprotein; LDL: low-density lipoprotein; patients with cataract, who also presented with significantly
NS: non significant. higher prevalences of DR, albuminuria, polyneuropathy and
erectile dysfunction. In addition, residual ␤-cell function was
vs 55%; atorvastatin: 22% vs 25%; and rosuvastatin: 23% vs lower in patients with cataract, who also had significantly lower
18% (all NS). On analyzing the cohort by statin therapy, cataract hyperbolic product, both of which are likely to raise HbA1c
prevalence was non-significantly lower—by an absolute 4%—in and, consequently, prompt the initiation of aggressive glucose-
statin users (Fig. 1, right). LLD use was also assessed in Catar(–) lowering therapies. More frequent use of exogenous insulin in
subgroups of those with comparable mean age (n =218) or with cataract patients may have contributed to reducing the discrep-
both comparable age and diabetes duration (n = 161). In the age- ancy in current metabolic control between groups. Otherwise,
comparable subgroup, statin use was significantly higher in the there were no differences in inflammatory or lipid markers
Catar(–) vs Catar(+): 63% vs 51%, respectively (P = 0.0327), between groups, except for a significantly higher hs CRP level
whereas fibrate and ezetimibe use did not differ between these observed in T2D patients with cataract, as has been previ-
groups. Also, LLD use did not differ between the age- and dia- ously reported for age-related cataract in the general population
betes duration-comparable Catar(–) vs Catar(+): 58%, 22% and [4].
3% vs 51%, 22% and 4% for statin, fibrate and ezetimibe use, The findings of our present study in T2D adults do not support
respectively (data not shown). an association between the use of statins and presence of cataract,
nor do they demonstrate a different pattern of distribution of
5. Discussion currently used LLD in T2D patients with or without cataract.
Curiously, however, Hippisley-Cox and Coupland [8] mentioned
This cross-sectional study of a large cohort of T2D patients that statin use was linked to cataract risk, and cited a report by
failed to suggest any association between statin therapy and the Klein et al. [3] in which the sole significant difference between
presence of cataract. In addition, the type of statin used did statin users and non-users was a lower odds ratio for develop-
ing nuclear cataracts. Furthermore, their comparison of statin
users and non-users did not adjust for the plausible likelihood
of unequal distribution/exposure to major risk factors for new-
onset cataract at either baseline or during the observation period.
Thus, comorbidities associated with impaired fasting glucose,
impaired glucose tolerance, the MetS, T2D or an age-related
increase in CVD all had the potential to promote new-onset
statin therapy as well as to contribute to cataract incidence.
The overall prevalence of documented cataract in the present
study was low, despite the fact that most of our patients were
elderly and, therefore, had substantial exposure to hypergly-
caemia over their mean diabetes duration. Other than biases due
to gross misdiagnoses and markedly reduced life expectancy
associated with cataract affecting the cross-sectional demo-
graphics, both of which are unlikely or implausible scenarios,
Fig. 1. Use of lipid-lowering drugs (LLD) in 780 type 2 diabetic (T2D) patients
without (n = 649) and with (n = 131) cataract (all non-significant, NS) (left); such low prevalences of documented cataract in the medical
and prevalence of cataract in T2D patients treated with (n = 435) and without record may arise, in part, from less extensively reported find-
(n = 345) a statin drug (right). ings of subclinical lens opacities in an older population referred

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 M.P. Hermans et al. / Diabetes & Metabolism 37 (2011) 139–143
by endocrinologists who are focused on DR or maculopathy
screening and treatment.
However, the present study has several limitations related
to its cross-sectional design, heterogeneity of the statins pre-
scribed and/or statin exposures, lack of data on the time intervals
between statin prescription and cataract diagnosis or vice versa,
and the restricted applicability of these observations to a Cau-
casian T2D population. In addition, the retrospective diagnosis
of cataract was based on ophthalmologists’ records, and not
systematically diagnosed according to a protocol-defined, gold
standard classification. This may also have contributed to the
relatively low cataract prevalence in spite of the mean age of
the cohort [20]. Furthermore, no subanalyses were performed
between cataract subtypes and statin use although, based on the
demographics of our T2D cohort, the majority of patients most
likely had cortical subtypes of lens opacities [21]. Finally, the
size of our cohort did not allow adjusting for other, non-age-
related risk factors for cataract such as previous steroid use,
occupation and myopia.
T2D is an ideal condition for assessing the potentially detri-
mental and beneficial effects of statins on cataract, as the current
guidelines recommend prescribing a statin in most cases for
primary and secondary CVD prevention. Also, T2D patients
have high incidences and prevalences of both hyperglycaemia-
and age-related cataracts. Nevertheless, our present data do not
demonstrate an association between statins and cataract. Thus,
from this large cross-sectional analysis of a diabetic population
at high risk for both DR and cataract, it is possible to conclude
that chronic therapy with statins is not cataractogenic, and that
the presence of cataract is not associated with greater use of
statins or any other LLD.
Conflict of interest statement
The authors report no conflict of interest.
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