Abstract
Red cell distribution width (RDW), one of the biomarkers used to measure vascular
ageing, is known to correspond with cardiovascular diseases. As coronary artery dis‐
ease and erectile dysfunction (ED) are both caused by the same shared pathophysi‐
ology, in this study, we compared the RDW values of men diagnosed with ED and
those of healthy controls. Ninety‐nine patients who were diagnosed with ED were
included in the study. The control group consists of 100 men who presented to our
outpatient clinic. Patients' fasting blood glucose, triglyceride, total cholesterol and
LDL cholesterol levels were significantly higher in men diagnosed with ED. While the
mean RDW value was 13.49 ± 1.52 in men with ED, it was 12.91 ± 1.13 in the con‐
trol group. When RDW values were compared between the two groups, the RDW
values of men with ED were found to be statistically significantly higher. Multivariate
analyses showed that only the patients' body mass index, fasting blood sugar, triglyc‐
eride (TG), low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol
levels (HDL‐C), TG/HDL‐C ratio and RDW levels' relationship with ED was statisti‐
cally significant. Although some studies have shown that RDW may be related to
some diseases such as cardiovascular diseases and cancer, this appears to be the first
study demonstrating a relationship between RDW and ED. RDW can be utilised as a
predictor for the determination of the presence and monitoring of the severity of ED.
KEYWORDS
erectile dysfunction, IIEF‐5, red cell distribution, TG/HDL ratio
2 of 6 | DURSUN et al.
has been proven in many studies. Several other adult studies have
also demonstrated a relationship between RDW and cancer, diabe‐
tes mellitus, kidney disease, liver disease and complex community‐
acquired pneumonia (Evans & Jehle, 1991; Montagnana & Danese,
2016).
That a strong correlation exists between erectile dysfunction
(ED) and coronary artery disease has been widely discussed, with
endothelial dysfunction and vascular ageing being described as
the underlying pathophysiology (Gandaglia et al., 2013; Gazzaruso,
Coppola, & Giustina, 2011). RDW, one of the biomarkers used to
measure vascular ageing, is known to correspond with cardiovas‐
cular diseases (Balistreri et al., 2019). As coronary artery disease
and ED are both caused by the same shared pathophysiology, it was
hypothesised that it might be possible to utilise RDW as a parame‐
ter in predicting and evaluating ED. To the best of our knowledge,
a study examining the relationship between ED and RDW has not
yet been conducted. In this context, the present study compares
the RDW values of men diagnosed with ED and those of healthy
controls.
2 | PATIENTS AND METHODS
The present study was planned prospectively, following approval
from the local ethics committee. Ninety‐nine patients who were
admitted to our urology clinic between April 2018 and November
2018 and were diagnosed with ED were included in the study. The
control group consisting of 100 men who presented to our outpa‐
tient clinic excluded the presence of ED or any other systemic dis‐
ease and only included healthy participants. The study and control
group were both made up of sexually active men over 40 years of
age. All the participants had been in a regularly heterosexual re‐
lationship over the last 6 months. Those patients diagnosed with
mood disorders and/or undergoing treatment for depression were
not included in the present study. The men who have anaemia were
excluded from the study (exclusion criterion was a haemoglobin
count of <13.0 g/dl). Patients with anatomical penile deformities,
history of previous pelvic or spinal cord surgery, congestive heart
failure, chronic renal failure, Peyronie's disease, thyroid disease,
stroke and malignancy were also excluded. Finally, those patients
who previously received medical treatment for ED were excluded
from the study.
All patients in both the study group and the control group under‐
went an extensive sexual and medical evaluation as well as a complex
physical and genital examination prior inclusion. Sociodemographic
features such as age, height and weight were recorded. The pres‐
ence of ED was assessed by means of the five‐point version of the
International Erectile Function Index (IIEF‐5), and the IIEF‐5 ques‐
tionnaire was completed by all patients. Those patients who scored
21 points or less in the İİEF‐5 questionnaire were included in the
study group.
Fasting peripheral blood samples were obtained from all pa‐
tients, and fasting blood glucose, total cholesterol, LDL cholesterol,
HDL and triglyceride levels were measured biochemically in these
samples using standard assays. Follicle‐stimulating hormone (FSH),
luteinising hormone (LH) and total testosterone levels were mea‐
sured for the evaluation of hormone levels. An automatic blood cell
count (ADVIA Hematology System, Siemens Healthcare Diagnostics)
was used to determine parameters, including the RDW value, in the
complete blood count.
Statistical analysis was performed using SPSS (SPSS Inc.), with
the Shapiro–Wilk test used to calculate the normality of data dis‐
tribution. While normally distributed numerical variables were
expressed as mean ± standard deviations, data demonstrating
non‐normal distribution were expressed with median ± quarterly
values (IQR). Categorical variables were expressed as numbers
and percentages. Student's t test, Mann–Whitney U test and chi‐
square tests were utilised for final statistical analysis of data ob‐
tained. Correlation between Spearman's correlation coefficient
was used to evaluate the correlation between the non‐normally
distributed data. The differences were considered significant at
p < .05.
3 | RESULTS
No statistically significant difference was found between the
two groups in terms of age (50.67 ± 12.0 data 51.57 ± 8.13 years;
p = .69). The mean body mass index was found to be 29.64 ± 3.57
in ED and 24.50 ± 2.79 in non‐ED (p = .01). Patients' fasting blood
glucose, triglyceride, total cholesterol and LDL cholesterol levels
were significantly higher in men diagnosed with ED (p = .0001).
Total testosterone levels were also significantly lower in men with
ED (p = .004). While the mean RDW value was 13.49 ± 1.52 in
men with ED, it was 12.91 ± 1.13 in the control group. When RDW
values were compared between the two groups, the RDW values
of men with ED were found to be statistically significantly higher.
(p = .0001). Another biochemical marker, the TG/HDL‐cholesterol
ratio, was significantly higher in men with ED compared to the
control group (p = .001). All haematological and biochemical re‐
sults are shown in Table 1.
Univariate and multivariate logistic regression analyses were
conducted to determine the potential confounders for erectile
dysfunction. Although univariate analyses revealed that BMI, FBS,
TG, TC, LDL‐C, HDL‐C level, TG/HDL‐c ratio, WBC, Hct and RDW
levels were associated with the presence of ED, multivariate anal‐
yses showed that only the patients' BMI (1.362 OR [1.088–1.705],
p = .007), FBS (1.228, OR [1.128–1.337], p = .00001), TG (1.020
OR [1.010–1.030], p = .001), LDL‐C (1.046 OR [1.032–1.060],
p = .00001), HDL‐C levels (0.923 OR [0.860–0.990], p = .025), TG/
HDL‐C ratio (1.102 OR [1.015–1.196], p = .01) and RDW levels' (1.086
OR [1.014–1.194], p = .0001) relationship with ED were statistically
significant. The details are demonstrated in Table 2.
Figure 1 demonstrates the ROC curve for RDW to predict ED.
The calculated area under the curve (AUC) with confidence intervals
(CI) for ED was 0.658 (0.581–0.735).
| DURSUN et al. 3 of 6
4 | DISCUSSION
There are many causes of erectile dysfunction. However, trauma and
drug‐related causes, in addition to such organic causes as those in‐
volving neurogenic, vascular, anatomical and hormonal factors, make
up more than 80% of the aetiology of ED (Celik, Ipekci, Akarken,
Ekin, & Koksal, 2014; Hatzimouratidis et al., 2010; Yafi et al., 2016).
Simple and easily determinable markers can contribute greatly to
predicting the presence of and management of ED, which is com‐
monly encountered in clinical practice. It is for this purpose that
RDW, a marker strongly associated with atherosclerosis, ischaemic
heart disease, acute and chronic heart failure, hypertension, inflam‐
matory bowel disease and various cancers, was studied in terms of
its relationship to ED. To our knowledge, the present study is the
first study to research their correlation.
Red cell distribution width, used in the differential diagnosis
of anaemia, is a quantitative measure of variability in the size of
circulating erythrocytes and recently has been affirmed as a prog‐
nostic index for cardiovascular disease. It is believed that chronic
inflammation, endothelial dysfunction and oxidative stress all con‐
tribute to the development and progression of ED, reducing the
number of red blood cells, thereby causing an increased eryth‐
ropoietin production and leading to an increase in RDW. A study
conducted by Förhecz et al. demonstrated that in patients suffer‐
ing from heart failure, high RDW levels correlate with the eleva‐
tion of CRP, erythropoietin, interleukin‐6, tumour necrosis factor
(TNF) alpha and beta, and TNF receptors levels. This study, there‐
fore, confirmed the association of RDW with chronic inflammation
(Förhécz et al., 2009). Metabolic diseases cause chronic low‐grade
inflammation, a well‐known risk factor for sexual dysfunction in
both sexes (Maiorino, Bellastella, Giugliano, & Esposito, 2018).
In a study carried out by Arana Rosainz Mde et al. with patients
diagnosed with type 2 diabetes mellitus (DM) and nonsymptom‐
atic coronary artery disease, ED was found to be concurrent to
systemic endothelial dysfunction and a low‐grade inflammatory
response (Araña Rosaínz Mde et al., 2011). RDW, which is associ‐
ated with inflammation, was found to be higher in patients with ED
compared with patients in the control group.
In a cross‐sectional study of 15,343 nondiabetic adults with
large series, RDW was found to be positively and independently
associated with haemoglobin A1c (HbA1c; Veeranna, Zalawadiya,
Panaich, Ramesh, & Afonso, 2012). In another study, increased RDW
values were associated with diabetic complications and higher RDW
values were observed in patients with diabetic ketoacidosis (Liu, Jin,
Ma, Bai, & Xu, 2013; Malandrino, Wu, Taveira, Whitlatch, & Smith,
2012). In contrast, unlike the results of the prior mentioned studies,
Patients with ED
(n = 89) Control group (n = 100) p Values
Age (year) 50.67 ± 12.0 51.57 ± 8.13 .69a
Height (cm) 169.74 ± 6.01 164.11 ± 5.73 .77a
Weight (kg) 77.61 ± 10.70 65.72 ± 5.41 .0001*
,a
BMI (kg/m2
) 26.94 ± 3.57 24.50 ± 2.79 .01*
,a
FBS (mg/dl) 104.20 (63–480) 82.0 (67–102) .0001*
,b
Triglyceride (mg/dl) 183.46 (55–439) 124.0 (82–147) .0001*
,b
TC (mg/dl) 181.0 (86–363) 158.0 (124–195) .0001*
,b
LDL‐C (mg/dl) 119.45 ± 35.61 83.59 ± 21.44 .0001*
,a
HDL‐C (mg/dl) 42.98 ± 9.10 37.76 ± 7.38 .005a
TG/HDL ratio 4.25 (1.22–11.41) 3.22 (1.92–6.48) .001b
WBC (103
/mm3
) 8.56 ± 2.48 7.65 ± 1.24 .0001*
,a
PLT (×109
/L) 259.46 ± 55.37 275.61 ± 53.06 .48a
RDW 13.49 ± 1.52 12.91 ± 1.13 .0001*
,b
Hct (%) 45.40 (5.4–52.6) 43.50 (5.4–51.6) .0001*
,b
Testosterone (ng/ml) 3.56 (0.03–8.46) 4.25 (2.81–7.23) .004*
,b
FSH (mIU/ml) 5.27 (1.85–26.28) 6.36 (3.32–11.0) .099b
LH (mIU/ml) 5.55 (2.21–24.32) 4.61 (1.96–8.12) .0001*
,b
Abbreviations: BMI, body mass index; FBS, fasting blood sugar; FSH, follicle‐stimulating hormone;
Hct, haematocrit; HDL‐C, high‐density lipoprotein cholesterol; LDL‐C, low‐density lipoprotein
cholesterol; LH, luteinising hormone; PLT, platelet count; RDW, red cell distribution; TC, total
cholesterol; TG/HDL, triglyceride/high‐density lipoprotein cholesterol; WBC, white blood cell.
a
Student's t test. b
Mann–Whitney U test.
*Statistically significant.
TABLE 1 Clinical and demographic
features of the patients stratified by
erectile dysfunction
4 of 6 | DURSUN et al.
the Malmo Diet and Cancer Study, which involved a 14‐year follow‐
up of 26,709 participants aged 45 years and older, reported that
high RDW values were associated with reduced diabetic risk fac‐
tors (Engström et al., 2014). In the present study, high RDW values
appeared to correlate with diabetes and fasting blood glucose and
RDW levels were significantly higher in men with ED.
While the association between RDW and cardiovascular dis‐
ease was first reported in 2009 by Fukuta et al., the role of RDW in
diseases such as diabetes and its complications (including kidney
disease, liver disease, cancer) are continuing to be investigated to
this day (Felker et al., 2007). In a recent study by Abrahan, Ramos,
Cunanan, Tiongson, and Punzalan (2018), a meta‐analysis of 13
trials involving 10,410 patients with acute coronary syndrome,
low RDW values were found to be significantly associated with re‐
duced risk for cardiovascular events (RR 0.56, [95% CI 0.51–0.61],
P & lt; 0.00001, I
2 = 91%). In 2013, Emans et al. examined 17,533
European adults and showed that high RDW values correlate with
physical inactivity. In a subsequent study, it was shown that ex‐
ercise rapidly reduces RDW values (Lippi et al., 2014). In 2015,
Loprinzi et al. assessed the relationship between RDW values,
physical activity (measured objectively, using an accelerometer)
and daily diet models. They observed that not diet but physical
activity was inversely related to RDW levels and, as a result, con‐
cluded that regular exercise can help prevent cardiovascular dis‐
ease and mortality by altering RDW. In 2018, a different group
investigated the effects of cigarette smoking and water‐pipe
smoking on biochemical properties such as RDW in a representa‐
tive population sample obtained from a cohort study. Interestingly,
after multivariate analysis, RDW was significantly higher in smok‐
ers compared to nonsmokers and among water‐pipe smokers
TABLE 2 Logistic regression analysis of confounding factors for erectile dysfunction
Univariate analysis Multivariate analysis
p OR
95% CI
p OR
95% CI
Lower Upper Lower Upper
Age .543 0.991 0.964 1.020 .017*
BMI .00001* 1.269 1.148 1.404 .007* 1.362 1.088 1.705
FBS .00001* 1.174 1.118 1.232 .00001* 1.228 1.128 1.337
TG .00001* 1.034 1.021 1.046 .001* 1.020 1.010 1.030
TC .00001* 1.030 1.018 1.042 .078 0.975 0.875 1.082
LDL‐C .00001* 1.046 1.032 1.060 .00001* 1.046 1.032 1.060
HDL‐C .00001* 1.084 1.041 1.127 .025* 0.923 0.860 0.990
TG/HDL ratio .00001* 1.571 1.255 1.967 .01* 1.102 1.015 1.196
RDW .004* 1.466 1.130 1.902 .0001* 1.086 1.014 1.194
WBC .002* 1.290 1.095 1.520 .125 0.984 0.912 1.098
Hct .014* 1.088 1.017 1.165 .157 0.912 0.802 1.026
Abbreviations: BMI, body mass index; FBS, fasting blood sugar; Hct, haematocrit; HDL‐C, high‐density lipoprotein cholesterol; LDL‐C, low‐density
lipoprotein cholesterol; TC, total cholesterol; TG, triglyceride; WBC, white blood cell.
*Statistically significant.
FIGURE 1 Red cell distribution width‐erectile dysfunction
(RDW‐ED) ROC curve
Area Under the Curve
Test Result Variable(s): RDW
Area Std. Error
a Asymptotic Sig.b Asymptotic 95% Confidence
Interval
Lower Bound Upper Bound
,658 ,039 ,000 ,581 ,735
The test result variable(s): RDW has at least one tie between the positive actual
| DURSUN et al. 5 of 6
compared to cigarette smokers (Saffar Soflaei et al., 2018). A re‐
view of the impact of physical activity on endothelium and ED
revealed that endothelial damage was closely associated with ED
and was also associated with cardiovascular disease (CVD). On the
other hand, it is stated that physical activity is an important clinical
strategy in the prevention and treatment of CVDs and ED, mainly
due to its improvement of endothelial function (Leoni, Fukushima,
Rocha, Maifrino, & Rodrigues, 2014). In another review examin‐
ing the effect of smoking on ED, the risk caused by smoking in
the development of ED was found to be higher in smokers com‐
pared to age and comorbidities. As a result of several studies, it
has been concluded that smoking worsens erectile functions by
disrupting vascular mechanisms (Kovac, Labbate, Ramasamy, Tang,
& Lipshultz, 2015). The present study is in support of this data and
similarly demonstrates high RDW levels are associated with ED.
In our study, we found that the mean body mass index was found
to be 29.64 ± 3.57 in ED and 24.50 ± 2.79 in non‐ED. High BMI has
been shown to associate with erectile dysfunction in previous cross‐
sectional and prospective studies (Bacon et al., 2006; Larsen, Wagner,
& Heitmann, 2007). Another biochemical marker, the TG/HDL‐choles‐
terol ratio, was significantly higher in men with ED compared to the
control group in our study. Similarly, the previous study showed that the
TC/HDL‐C ratio was significantly related to the risk of ED. The relation
between serum lipid and ED was stronger in patients with such a high
ratio (Roumeguère, Wespes, Carpentier, Hoffmann, & Schulman, 2003).
When interpreting the results of the present study, it is important
for some potential limitations to be taken into consideration. As a cross‐
sectional study, this study does not provide us with information on the
temporal relationships between RDW measurements and the presence
of ED. In addition, the present study does not include an analysis of the
smoking history or the insulin resistance status of the participant with
ED. Similarly, ruling out the possibility that other unmeasured features
confuse the relationship between RDW and ED is not possible. Finally,
this study only includes Turkish males and the results may not be gener‐
alised to males from other racial or ethnic backgrounds. Also, the pres‐
ent study only discusses the correlation of elevated RDW levels with
the presence of sexual dysfunction in males not females.
In closing, this study shows that RDW is associated with ED.
Although some studies have shown that RDW may be related to some
diseases such as cardiovascular diseases and cancer, this appears to
be the first study demonstrating a relationship between RDW and ED.
Red cell distribution width can be utilised as a predictor for the
determination of the presence and monitoring of the severity of ED.
Nonetheless, well‐designed studies with larger sample sizes are re‐
quired for a better understanding of this relationship.
ORCID
Murat Dursun https://orcid.org/0000-0001-9115-7203
Serhan Cimen https://orcid.org/0000-0002-6612-0166
Muhammed Sulukaya https://orcid.org/0000-0002-4674-908X
Huseyin Besiroglu https://orcid.org/0000-0002-7459-584X
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