No previous study has evaluated systematically the relationship between metabolic syndrome (MetS) and prostate-related symptoms
and signs in young infertile men. We studied 171 (36.5 ± 8.3-years-old) males of infertile couples. MetS was defi ned based on the
National Cholesterol Education Program Third Adult Treatment Panel. All men underwent hormonal (including total testosterone (TT)
and insulin), seminal (including interleukin-8 (IL-8), seminal plasma IL-8 (sIL-8)), scrotal and transrectal ultrasound evaluations.
Because we have previously assessed correlations between MetS and scrotal parameters in a larger cohort of infertile men, here, we
focused on transrectal features. Prostate-related symptoms were assessed using the National Institutes of Health Chronic Prostatitis
Symptom Index (NIH-CPSI) and the International Prostate Symptom Score (IPSS). Twenty-two subjects fulfi lled MetS criteria. In an
age-adjusted logistic ordinal model, insulin levels increased as a function of MetS components (Wald = 29.5, P < 0.0001) and showed
an inverse correlation with TT (adjusted r = -0.359, P < 0.0001). No association between MetS and NIH-CPSI or IPSS scores was
observed. In an age-, TT-, insulin-adjusted logistic ordinal model, an increase in number of MetS components correlated negatively
with normal sperm morphology (Wald = 5.59, P < 0.02) and positively with sIL-8 levels (Wald = 4.32, P < 0.05), which is a marker
of prostate infl ammation, with prostate total and transitional zone volume assessed using ultrasound (Wald = 17.6 and 12.5, both
P < 0.0001), with arterial peak systolic velocity (Wald = 9.57, P = 0.002), with texture nonhomogeneity (hazard ratio (HR) = 1.87
(1.05–3.33), P < 0.05), with calcifi cation size (Wald = 3.11, P < 0.05), but not with parameters of seminal vesicle size or function.
In conclusion, in males of infertile couples, MetS is positively associated with prostate enlargement, biochemical (sIL8) and
ultrasound-derived signs of prostate infl ammation but not with prostate-related symptoms, which suggests that MetS is a trigger
for a subclinical, early-onset form of benign prostatic hyperplasia.

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