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Erectile Dysfunction in Turkish Diabetics

cander2014
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20 views6 pages

Erectile Dysfunction in Turkish Diabetics

cander2014
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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METABOLIC SYNDROME AND RELATED DISORDERS ORIGINAL ARTICLE

Volume X, Number X, 2014


 Mary Ann Liebert, Inc.
Pp. 1–6
DOI: 10.1089/met.2013.0150

Prevalence and Correlates of Erectile Dysfunction


in Type 2 Diabetes Mellitus:
A Cross-Sectional Single-Center Study
Among Turkish Patients

Soner Cander, MD,1 Soner Coban, MD,2 Sakir Altuner, MD,3 Ozen Oz Gul, MD,1
Zeynel Abidin Yetgin, MD,4 Aysen Akkurt, MD,5 Hakan Ucar, MD,4 and Ercan Tuncel, MD 5

Abstract
Objective: The aim of this study was to evaluate prevalence of erectile dysfunction (ED) in patients with type 2
diabetes mellitus (T2DM) in relation to vascular and neurogenic correlates.
Methods: A total of 116 males including T2DM patients [n = 68; mean age, 56.7 (5.8) years] and age-matched
healthy controls [n = 48; mean age, 57.0 (6.6) years] were included in this cross-sectional single-center study.
Data on anthropometrics, blood biochemistry, concomitant hypertension, hyperlipidemia, and coronary artery
disease (CAD) were recorded in each subject along with measurement of carotid artery intima media thickness
(CIMT) and evaluation of erectile dysfunction (ED) via International Index of Erectile Function (IIEF-5)
Questionnaire. A univariate analysis was performed to determine the relationship of cardiovascular risk factors
and diabetes-related complications to ED.
Results: Patient and control groups were similar in terms of percentage patients with hyperlipidemia (51.5%
and 39.6%, respectively) and CAD (33.8% and 22.9%, respectively), whereas concomitant hypertension was
more common (P = 0.05) and CIMT values were significantly higher (P = 0.020) in patients with T2DM
compared with controls. Polyneuropathy was noted in 46.2% of patients, nephropathy in 30.8%, and retinopathy
in 33.8%. ED scores were significantly lower in patients than controls [14.3 (7.3) vs. 18.2 (6.3), P = 0.004] with
a significantly higher percentage of patients than controls in the category of severe dysfunction (29.4 vs. 10.4%,
P = 0.014). Univariate analysis revealed that diabetic polyneuropathy was the only factor to be associated with
higher likelihood (93.3% in the presence and 60.0% in the absence of neuropathy) and severity (43.3% in the
presence and 14.3% in the absence of neuropathy) of ED (P = 0.004).
Conclusion: Findings from the present cross-sectional single-center study revealed the prevalence of ED to be
considerably higher in patients with T2DM than age-matched healthy controls, with identification of diabetic
polyneuropathy as the only risk factor associated with higher likelihood and more severe forms of ED.

Introduction factorial processes mediated by vascular and neurogenic fac-


tors, endothelial dysfunction, oxidative processes, and changes
in the nitric oxide system.4 Endothelial dysfunction has been
D efined as the inability to achieve, maintain, or
sustain an erection firm enough for sexual intercourse,1
erectile dysfunction (ED) has been reported to occur more
indicated as the key event in the pathophysiology of ED and,
importantly, men with penile vascular dysfunction have en-
commonly in diabetes than in the general population.2 The dothelial dysfunction in other vascular beds as well.5 Ac-
prevalence rate varies widely from 35% to 75% in different cordingly, disorders that lead to endothelial dysfunction and
cross-sectional studies, depending upon the methodology.3 vascular problems, the two factors also playing an important
Although not yet been fully clarified, the pathophysiology role in the pathogenesis of ED,6 have been shown to be asso-
of diabetic ED has been associated with complex and multi- ciated with ED.5,7,8 An impairment in both neurogenic and

1
Clinic of Endocrinology and Metabolism, 2Clinic of Urology, 3Clinic of Internal Medicine, and 4Clinic of Cardiology, Sevket Yilmaz
Training and Research Hospital, Bursa, Turkey.
5
Department of Endocrinology and Metabolism, Uludag University Faculty of Medicine, Bursa, Turkey.

1
2 CANDER ET AL.

endothelium-dependent relaxations was demonstrated in the Cardiologic assessments


corpus cavernosum of diabetic patients, and this is one of the
major organic causes of ED.9,10 Notably, several conventional CAD evaluation was based on echocardiography, elective
risk factors, including obesity and dyslipidemia, are also as- exercise electrocardiogram (ECG) testing, and, if necessary,
sociated with ED.11 Atherosclerosis is thought to be the most coronary angiography in diabetic patients. Patients with a
common cause of vasculogenic ED,12 which emphasizes a det- past history of bypass surgery or angioplasty and stent place-
rimental epidemiological link between ED, as an important ment intervention and myocardial infarction were also
marker of vascular disease throughout the arterial tree, and considered to have CAD.
coronary artery disease (CAD), stroke, and diabetes and ED.2,13 The CIMT measurement was used as a marker for CAD.
Largely on the basis of data from published studies con- CIMT was measured via high-resolution Duplex scanner
ducted in a western setup,3 ED has become a major concern (Siemens ACUSON X150 ultrasound system) with probe
affecting quality of life in millions of men with diabetes owing at a frequency of 10 MHz for a B scan based on average of
to the high incidence of ED and the increasing prevalence three consecutive measurements.
of type 2 diabetes mellitus (T2DM).9 In Turkey, as in other
countries, ED is a very common condition that increases in Diabetes-related complications
prevalence and severity with increasing age.14 Limited data are Polyneuropathy (deep tendon reflexes and Prick test),
available regarding the increased ED risk in T2DM as well as nephropathy (proteinuria of > 30 mg/day or high levels for
the role of conventional risk factors. Additionally, due to cul- creatinine), and retinopathy (ophthalmoscopic examination of
tural customs in Muslim countries such as Turkey, sexual retina) were assessed on the basis of medical history, physical
dysfunction is more commonly surrounded by social stigma, examination, and laboratory findings.
which may lead male patients to be less willing to discuss their
ED symptoms. Therefore, the present cross-sectional single- Erectile dysfunction
center study was designed to evaluate prevalence and correlates
of ED in patients with T2DM in Turkey to determine whether ED was evaluated via application of the five questions of the
vascular or neurogenic factors are responsible for ED. International Index of Erectile Function Questionnaire (IIEFQ)
via a face-to-face interview method. IIEF is one of the most
Methods frequently used forms for the patients applying with sexual
dysfunction. It is a standardized self-administered question-
Study population naire that addresses various sexual function domains: Erectile
A total of 116 males including T2DM patients [n = 68; function, orgasmic function, sexual desire, and overall satis-
mean age, 56.7 (5.8) years] and age-matched healthy controls faction. The original questionnaire includes 15 items related to
[n = 48; mean age, 57.0(6.6) years] were included in this cross- evaluation of ED for the last 4-week period,15 while an
sectional single-center study conducted between 2012 and abridged, five-item version (IIEFQ-5), which includes first
2013 at a tertiary care hospital located in Bursa, Turkey. five questions, deal with erectile function and overall satis-
Male patients aged 50–65 years having T2DM for more than faction has been validated for diagnostic purpose by National
1 year and age-matched healthy nondiabetic control subjects Institutes of Health (NIH).16 The IIEFQ-5 is scored on a five-
were included in the study. Subjects receiving any type of point Likert scale with a higher score indicating better sexual
medications for the treatment of ED or that may predispose for function. On the basis of the total score, the severity of sexual
ED, patients with past history of lower urinary tract surgery, dysfunction was classified into five categories (i.e., severe 5–
concomitant malignancy, chronic renal failure, chronic hepatic 7, moderate 8–11, mild to moderate 12–16, mild 17–21, and
failure, and co-morbid hormonal disorders that may cause hy- no ED 21–25).16 The Turkish version of the IIEF-5 was used
pogonadism or ED were excluded from the study. in the present study, which has been validated in Turkish
Written informed consent was obtained from each subject population to assess ED on the last 6 months.17
following a detailed explanation of the objectives and pro-
tocol of the study, which was conducted in accordance with Statistical analysis
the ethical principles stated in the Declaration of Helsinki Statistical analysis was made using computer software
and approved by the institutional ethics committee. SPSS version 11.0 (SPSS Inc. Chicago, IL). The chi-squared
test was used for the comparison of age- and gender-related
Study parameters differences in clinical practice. A univariate analysis was per-
Data on anthropometrics [body fat measurement and body formed to determine the relationship of cardiovascular risk
mass index (BMI, kg/m2)] via a Tanita body composition factors and diabetes related complications to ED. Data were
analyzer (Tanita SC 330), blood biochemistry including expressed as mean (standard deviation, SD), minimum-
prostate-specific antigen (PSA; ng/mL), free PSA (fPSA; maximum, and percent (%) where appropriate. P < 0.05 was
ng/mL), and total testosterone (T test; ng/dL), concomitant considered statistically significant.
hypertension, hyperlipidemia, CAD, carotid artery intima
media thickness (CIMT), prostate volume [via ultrasonogra- Results
phy (USG)], and ED were recorded in each subject. Duration Basic clinical features and blood biochemistry
of diabetes and diabetes-related complications, including
polyneuropathy, nephropathy, and retinopathy, were evalu- Mean (SD) duration of diabetes mellitus was 7.4 (6.9) years
ated in patients with T2DM. The relation of hypertension, in patients. Patients and control subjects were homogeneous in
hyperlipidemia, CAD, and diabetes-related complications to terms of age and anthropometrics and serum levels for PSA
ED were also evaluated via univariate analysis. (ng/mL), fPSA (ng/mL), and total T (ng/dL) (Table 1).
T2DM AND ERECTILE DYSFUNCTION 3

Table 1. Basic Clinical Characteristics and Laboratory Findings in Patients and Control Subjects
Total (n = 116) Type 2 diabetes (n = 68) Control (n = 48) P value
Basic characteristics Mean (SD)
Age (years) 56.8 (6.1) 56.7 (5.8) 57.0 (6.6) 0.819
Duration of diabetes (years) 7.4 (6.9) 7.4 (6.9) — —
HbA1c (%) 8.6 (2.0) 8.6 (2.0) — —
Height (cm) 169.5 (6.2) 168.9 (6.6) 170.4 (5.5) 0.153
Weight (kg) 82.8 (12.8) 82.5 (13.8) 83.3 (11.3) 0.468
Body mass index (kg/m2) 28.8 (3.9) 28.8 (4.3) 28.6 (3.3) 0.775
Waist circumference (cm) 101.0 (10.6) 101.0(11.2) 100.8 (9.8) 0.927
Hip circumference (cm) 102.2 (7.1) 102.0 (7.6) 102.4 (6.4) 0.778
Fat % 24.0 (6.2) 24.6 (6.5) 23.2 (5.6) 0.247
Smoking, n(%) 27 (23.3) 15 (22.1) 12 (25.0) 0.824
Blood biochemistry
PSA (ng/mL) 1.5 (2.1) 1.5 (2.6) 1.4 (1.4) 0.227
fPSA (ng/mL) 0.4 (0.4) 0.4 (0.4) 0.4 (0.4) 0.453
T-test (ng/dL) 345.2 (121.7) 334.8 (120.9) 360.5 (122.6) 0.273
FSH (IU/mL) 7.6 (4.8) 8.7 (5.4) 6.0 (3.4) 0.003
LH (IU/mL) 5.7 (2.9) 6.5 (3.1) 4.6 (2.2) 0.001
Prolactin (ng/mL) 9.1 (10.5) 10.6 (13.4) 7.0 (2.5) 0.018
TSH (IU/L) 2.0 (3.0) 1.9 (2.3) 2.1 (3.7) 0.076
Fasting blood glucose (mg/dL) 156.2 (89.0) 197.8 (93.5) 93.5 (13.0) <0.001
Creatinine (mg/dL) 0.9 (0.3) 1.0 (0.3) 0.9 (0.2) 0.074
ALT (U/L) 27.0 (15.4) 27.0 (14.6) 27.0 (16.6) 0.875
AST (U/L) 22.2 (9.2) 21.0 (9.8) 24.1 (7.9) 0.004
Total cholesterol (mg/dL) 200.2 (40.3) 198.1 (41.6) 203.5 (38.7) 0.486
HDL (mg/dL) 44.6 (9.8) 45.6 (10.1) 43.1 (9.1) 0.076
Triglycerides (mg/dL) 165.3 (90.7) 173.0 (101.6) 153.8 (71.1) 0.630
BUN (mmol/dL) 5.3 (1.5) 5.0 (1.4) 5.9 (1.4) 0.001
Protein volume 42.3 (23.7) 40.1 (19.5) 45.5 (28.6) 0.532
Cardiological findings n (%)
CIMT (mm) Mean (SD) 0.6 (0.2) 0.7 (0.2) 0.6 (0.2) 0.020
Hypertension 41 (35.3) 29 (42.6) 12 (25) 0.0501
Hyperlipidemia 54 (46.6) 35 (51.5) 19 (39.6) 0.2061
Coronary artery disease 34 (29.3) 23 (33.8) 11 (22.9) 0.2041
Diabetes-related complications n (%)
Polyneuropathy 30 (46.2) 30 (46.2) — —
Nephropathy 20 (30.8) 20 (30.8) — —
Retinopathy 22 (33.8) 22 (33.8) — —
Erectile dysfunction
Total score Mean (SD) 15.9 (7.1) 14.3 (7.3) 18.2 (6.3) 0.004
n (%)
Severe (scores 5–7) 25 (21.6) 20 (29.4) 5 (10.4) 0.014
Moderate (scores 8–11) 13 (11.2) 10 (14.7) 3 (6.3) 0.1581
Mild to moderate (scores 12–16) 14 (12.1) 6 (8.8) 8 (16.7) 0.1983
Mild (scores 17–21) 28 (24.1) 15 (22.1) 13 (27.1) 0.5356
None (scores 22–25) 36 (31) 17 (25.0) 19 (39.6) 0.0941
Age, waist circumference, hip circumference, total testosterone, total cholesterol, blood urea nitrogen, fat % variables were analyzed via
the Student t-test.
All other continuous variables were not normally distributed and compared with Mann–Whitney U-test.
Figures in bold are statistically significant.
1
Chi-squared test.
HbA1c, glycated hemoglobin; PSA, prostate-specific antigen; fPSA, free PSA; T-test, total testosterone FSH, follicle-stimulating
hormone; LH, luteinizing hormone; TSH, thyroid-stimulating hormone; ALT, alanine aminotransferase; AST, aspartate aminotransferase;
HDL, high-density lipoprotein; BUN, blood urea nitrogen; CIMT, carotid intima media thickness; SD, standard deviation.

Fasting blood glucose (mg/dL, P < 0.001), follicle-stimulating respectively) and CAD (33.8% and 22.9%, respectively),
hormone (FSH; IU/mL, P = 0.003), luteinizing hormone (LH; whereas concomitant hypertension was more common among
IU/mL, P = 0.001), and prolactin (ng/mL, P = 0.018) levels were diabetic patients than controls (42.6% and 25.0%, P = 0.050)
significantly higher in patients with T2DM with control subjects. (Table 1).
Serum levels for aspartate aminotransferase (AST; U/L, P =
0.001) and blood urea nitrogen (BUN; mmol/dL, P = 0.004) Diabetes-related complications
were significantly higher in controls than patients (Table 1).
Patient and control groups were similar in terms of per- Polyneuropathy was noted in 46.2% of patients, ne-
centage patients with hyperlipidemia (51.5% and 39.6%, phropathy in 30.8%, and retinopathy in 33.8% (Table 1).
4 CANDER ET AL.

Table 2. Univariate Analysis for the Correlates of Erectile Dysfunction


Erectile dysfunction categories*
Severe Moderate Mild to moderate Mild None Total
n (%) P value1
Overall 25 (21.6) 13 (11.2) 14 (12.1) 28 (24.1) 36 (31.0) 116 (100.0) —
Hypertensives 10 (24.4) 6 (14.6) 8 (19.5) 9 (22.0) 8 (19.5) 41(100.0) 0.076
Hyperlipidemics 11 (20.4) 6 (11.1) 10 (18.5) 16 (29.6) 11 (20.4) 54 (100.0) 0.383
CAD patients 8 (23.5) 6 (17.6) 4 (11.8) 9 (26.5) 7 (20.6) 34 (100.0) 0.193
Polyneuropathy 13 (43.3) 3 (10.0) 5 (16.7) 7 (23.3) 2 (6.7) 34 (100.0) 0.004
Nephropathy 8 (40.0) 2 (10.0) 2 (10.0) 2 (10.0) 6 (30.0) 20 (100.0) 0.465
Retinopathy 9 (40.9) 2 (9.1) 3 (13.6) 6 (27.3) 2 (9.1) 22 (100.0) 0.088
Figures in bold is statistically significant.
*Severe, score 5–7; moderate, score 8–11; mild to moderate, scores 12–16; mild, scores 17–21; none, scores 22–25.
1
Linear-by-linear association.
CAD, coronary artery disease.

Erectile dysfunction prevalence of ED in our control subjects (60.4%) seems


consistent with the previously reported rate in Turkey12 as
ED was determined in 75.0% of diabetic patients and in well as with the natural physiological course of aging on
60.4% of controls, with identification of severe ED in 29.4% sexual activity of an individual.3
of the overall patient population and 39.2% of patients with Given that severe ED was noted in 29.4% of overall dia-
ED, whereas only in 10.4% of controls. ED scores were sig- betic patients and 39.2% of diabetic patients with ED, our
nificantly lower in patients than controls [14.3 (7.3) vs. 18.2 findings are in strong agreement with the findings of a lon-
(6.3), P = 0.004] with a significantly higher percentage of gitudinal epidemiological study, the Massachusetts Male
patients than controls in the category of severe dysfunction Aging Study,20 in which men with treated diabetes were re-
(29.4 vs. 10.4%, P = 0.014) (Table 1). ported to have more than three times the probability of having
ED than men without diabetes.
Correlates of ED Although no difference was noted between patients and
Univariate analysis revealed that diabetic polyneuropathy controls in terms of the prevalence of CAD and CAD was
was the only significant factor associated with higher like- not a significant risk factor for ED in our study population,
lihood (93.3% in the presence and 60.0% in the absence of given the strong association reported in large epidemiolog-
neuropathy) and severity (43.3% in the presence and 14.3% ical studies between ED and future cardiovascular events,2
in the absence of neuropathy) of ED (P = 0.004; Table 2). significantly higher CIMT values in patients than controls in
No significant relationship of hypertension, hyperlipidemia, our study population seems to highlight the extremely det-
CAD, and other diabetes-related complications, including rimental epidemiological link between CAD, diabetes, and
nephropathy and retinopathy, to ED was noted (Table 2). ED emphasized in the past studies.2,21
Being a complex and multifactorial process,2 several risk
Discussion factors were identified for the development of ED in men with
diabetes,3 including higher age of the sample,20,22 longer du-
The present cross-sectional single-center study consider- ration of diabetes, poor glycemic control and BMI,23,24 pres-
ing the prevalence and correlates of ED in Turkish patients ence of microvascular complications,25 presence of co-morbid
with T2DM revealed a significantly higher prevalence of physical illnesses such as hypertension and dyslipidemia,
overall ED (75.0%) and severe ED (29.4%) in diabetic pa- sedentary lifestyle, and smoking habit.26
tients compared to age-matched healthy controls (60.4% and In our study sample, none of the co-morbid disorders,
10.4%, respectively). Given that polyneuropathy was the including hypertension, hyperlipidemia, and CAD, was as-
only correlate of risk for ED, our findings emphasize the sociated with increased risk for ED. Nonetheless, poly-
significant role of neurogenic rather than vascular factors in neuropathy was the only diabetes-related risk factor that
the development of ED. was significantly associated with an increased prevalence
The prevalence of overall and severe ED in the present of ED and the likelihood of the severe form of the disease.
study, which exceeds those noted in nondiabetic controls, This finding seems consistent with the consideration of au-
seems consistent with the statement that men suffering from tonomic neuropathy playing a major role in the development
diabetes are at higher risk of ED and experience a more of ED and being an independent cardiovascular risk factor.27
serious and therefore less tolerable form of ED than in men Notably, in diabetic patients, autonomic neuropathy has
without diabetes.2,18–20 been suggested to link ED to overt and silent CAD,28 which
Data from the first population-based study of the preva- may explain the lack of symptoms in patients with asymp-
lence and correlates of ED in Turkey revealed that in- tomatic CAD.2 Indeed, although traditionally affiliated with
creasing age was correlated with both increasing prevalence other microangiopathic complications, diabetic neuropathy
of any degree of ED as well as the severity of ED, with has been considered to be a multifactorial process in which
overall prevalence of ED as 69.2% and the prevalence of microvascular damage is only one aspect.29 Hence, our
moderate to severe ED cases as 36%.12 Hence, the overall findings are in line with the statement that microvascular
T2DM AND ERECTILE DYSFUNCTION 5

diabetic complications are more important risk factors for 5. Kaiser DR, Billups K, Mason C, et al. Impaired brachial
ED than macrovascular ones and the hypothesis that, in the artery endothelium-dependent and -independent vasodila-
complex pathogenesis of diabetic ED, diabetic neuropathy is tion in men with erectile dysfunction and no other clinical
at least an equal, if not more important, pathogenic causal cardiovascular disease. J Am Coll Cardiol 2004;43:
factor than macroangiopathy.29 179–184.
The present study has a number of limitations that should 6. Melman A, Gingell JC. The epidemiology and pathophys-
be taken into account in evaluating the results. First, rela- iology of erectile dysfunction. J Urol 1999;161:5–11.
tively low sample size might have prevented us from achiev- 7. Cartledge JJ, Eardley I, Morrison JF. Nitric oxide-mediated
ing the statistical significance concerning the correlates of ED corpus cavernosal smooth muscle relaxation is impaired in
as well as projecting results to the entire population. Second, ageing and diabetes. BJU Int 2001;87:394–401.
8. Montorsi P, Ravagnani PM, Galli S, et al. Association
the cross-sectional design made it impossible to establish any
between erectile dysfunction and coronary artery disease.
cause-and-effect relationships. Nevertheless given the likely
Role of coronary clinical presentation and extent of coro-
negative impact of cultural customs and social stigma on nary vessels involvement: The COBRA trial. Eur Heart J
patients’ willingness to discuss their symptoms about ED, our 2006;27:2632–2639.
findings emphasize the role of more comprehensive ques- 9. McCulloch DK, Campbell IW, Wu FC, et al. The preva-
tioning considering ED in male diabetic patients with neu- lence of diabetic impotence. Diabetalogia 1980;18:279–283.
ropathic complaints. 10. Saenz de Tejada I, Goldstein I, Azadzoi K, et al. Impaired
In conclusion, findings from the present cross-sectional neurogenic and endothelium-mediated relaxation of penile
single-center study revealed the prevalence of ED to be con- smooth muscle from diabetic men with impotence. N Engl J
siderably higher in patients with T2DM than in age-matched Med 1989;320:1025–1030.
healthy controls, with identification of diabetic polyneuro- 11. Ryan JG, Gajraj J. Erectile dysfunction and its association
pathy as the only risk factor associated with higher likeli- with metabolic syndrome and endothelial function among
hood and more severe forms of ED. Although our findings patients with type 2 diabetes mellitus. J Diabetes Compli-
emphasize that diabetic neuropathy is a more important cations 2012;26:141–147.
pathogenic factor than macroangiopathy and other micro- 12. Sullivan ME, Keoghane SR, Miller MA. Vascular risk
vascular diabetic complications, several mechanisms of ED factors and erectile dysfunction. BJU Int 2001;87:838–845.
have not yet been elucidated. There is a need for further 13. Kirby M, Jackson G, Simonsen U. Endothelial dysfunction
studies considering the particular nature of interrelated factors links erectile dysfunction to heart disease. Int J Clin Pract
in the pathogenesis of endothelial dysfunction-related ED in 2005;59:225–229.
T2DM. Given that ED was noted in three out of every four 14. Akkus E, Kadioglu A, Esen A, et al.; Turkish Erectile
diabetic patients in the present study, systematic screening for Dysfunction Prevalence Study Group. Prevalence and cor-
relates of erectile dysfunction in Turkey: A population-
ED in diabetic patients is strongly suggested so that the onset
based study. Eur Urol 2002;41:298–304.
of ED is not missed. ED marks the decisive aggravation stage
15. Rosen CR, Riley A, Wagner G, et al. The International
of diabetes and of its complications and offers a powerful Index of Erectile Function (IIEF): A multidimensional scale
motivator for patients to change their lifestyle and improve for assessment of erectile dysfunction. Urology 1997;49:
medication compliance. 822–830.
16. Rosen RC, Cappelleri JC, Gendrano N 3rd. The Interna-
Acknowledgments tional Index of Erectile Function (IIEF): A state-of-the-
We would like to acknowledge the reviewers for their science review. Int J Impot Res 2002;14:226–244.
helpful comments. We would also like to thank our col- 17. Turunc T, Deveci S, Guvel S, et al. The assessment of
Turkish validation with 5 question version of International
leagues at the Clinics of Endocrinology and Metabolism,
Index of Erectile Function (IIEF-5). Turkish J Urol 2007;
Clinics of Urology, Sevket Yilmaz Training and Research
33:45–49. [Article in Turkish]
Hospital. 18. Colson MH, Roussey G. Screening and managing erectile
dysfunction in diabetic patients. Sexologies 2013;22:e1–e8.
Author Disclosure Statement 19. Fedele D, Coscelli C, Santeusanio F, et al. Erectile dys-
The authors declare they have no conflict of interest. function in diabetic subjects in Italy. Gruppo Italiano Studio
Deficit Erettile nei Diabetici. Diabetes Care 1998;21:1973–
References 1977.
20. Feldman HA, Goldstein I, Hatzichristou DG, et al. Im-
1. NIH Consensus Development Panel on Impotence. JAMA potence and its medical and psychosocial correlates: Results
1993;270:83–90. of the Massachusetts Male Aging Study. J Urol 1994;151:
2. Phé V, Rouprêt M. Erectile dysfunction and diabetes: A 54–61.
review of the current evidence-based medicine and a syn- 21. Solomon H, Man JW, Wierzbicki AS, et al. Relation of
thesis of the main available therapies. Diabetes Metab erectile dysfunction to angiographic coronary artery dis-
2012;38:1–13. ease. Am J Cardiol 2003;91:230–231.
3. Dan A, Chakraborty K, Mondal M, et al. Erectile dysfunc- 22. Veves A, Webster L, Chen TF, et al. Aetiopathogenesis and
tion in patients with diabetes mellitus: Its magnitude, pre- management of impotence in diabetic males: Four year
dictors and their bio-psycho-social interaction: A study from experience from a combined clinic. Diabet Med 1995;12:
a developing country. Asian J Psychiatry 2013;7:58–65. 77–82.
4. Aslan Y, Sezgin T, Tuncel A, et al. Is type 2 diabetes 23. Romeo JH, Seftel AD, Madhun ZT, et al. Sexual function
mellitus a cause of severe erectile dysfunction in patients in men with diabetes type 2: Association with glycemic
with metabolic syndrome? Urology 2009;74:561–564. control. J Urol 2000;163:788–791.
6 CANDER ET AL.

24. Klein R, Klein BE, Lee KE, et al. Prevalence of self-re- 29. Kamenov ZA, Christov VG, Yankova TM. Erectile dys-
ported erectile dysfunction in people with long-term IDDM. function in diabetic men is linked more to microangiopathic
Diabetes Care 1996;19:135–141. complications and neuropathy than to macroangiopathic
25. Fedele D, Bortolotti A, Coscelli C, et al. Erectile dys- disturbances. JMHG 2007;4:64–73.
function in type 1 and type 2 diabetics in Italy. On behalf of
Gruppo Italiano Studio Deficit Erettile nei Diabetici. Int J
Epidemiol 2000;29:524–531. Address correspondence to:
26. Malavige LS, Levy JC. Erectile dysfunction in diabetes Soner Cander, MD
mellitus. J Sex Med 2009;6:1232–1247. Clinic of Endocrinology and Metabolism
27. Vinik AI, Maser RE, Mitchell BD, et al. Diabetic auto- Sevket Yilmaz Training and Research Hospital
nomic neuropathy. Diabetes Care 2003;26:1553–1579. 16230 Yildirim
28. Pegge NC, Twomey AM, Vaughton K, et al. The role of Bursa
endothelial dysfunction in the pathophysiology of erectile Turkey
dysfunction in diabetes and in determining response to
treatment. Diabet Med 2006;23:873–878. E-mail: drcander@gmail.com

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