BPH is a complex and highly prevalent disease in men older than 50 years and it may lead to aggravation in the quality of life of suffering men [1
]. Previous studies have shown that BPH is associated with several etiologic factors that may influence the prostate pathophysiology [12
Recently, many studies have also shown that components of MS (central obesity, hypertension, NIDDM, hyperlipidemia, low HDL-C, hypertriglyceridemia) are risk factors for BPH development and that these components may play a part in BPH pathogenesis [12
]. Hammarsten and Hogstedt [13
] reported that men with MS had a significantly larger PV and faster annual BPH growth rates than did men without MS. In particular, central obesity, NIDDM, hypertension, low HDL-C, and high fasting insulin level are risk factors in the development of BPH [14
]. Ozden et al. [4
] demonstrated that PV was positively correlated with central obesity, as represented by WC, but that overall obesity measured by BMI was not correlated with PV. There was no significant relationship between obesity-related parameters and LUTS [18
]. The present study illustrated that patients with high WC, high SBP/DBP, high TG, low HDL-C, and high FPG level had a significantly larger PV.
The serum PSA level test is a screening tool that is the most widely used marker for the early detection of prostate cancer and is used in the management of the disease after the diagnosis of BPH [19
]. The serum PSA level may be influenced by many factors, such as age, BMI, PV, and prostate disease [19
]. Han et al. [9
] reported trends for a positive association between older age, diastolic BP, and the serum PSA level, whereas BMI, HDL, and FBG correlated negatively with the serum PSA level. We demonstrated that patients with central obesity, high SBP/DBP, high TG, low HDL-C, and high FPG had a significantly higher serum PSA level than did patients without these conditions.
Although several investigators have observed a significant association between BPH and MS or its components, others have opposing opinions. Gupta et al. [17
] suggested that there were no significant relationships between BPH and MS, weight, BMI, lipid level, or thyroid hormone status. Jeong et al. [8
] suggested that MS was not associated with PSA level in a screened population. Among the risk factors for MS, BP, WC, and FPG were independently associated with serum PSA levels [8
]. Unfortunately, the relationships between PV, serum PSA level, and components of MS have not been clearly established and there is no consensus on the basis of recent results.
However, in the present study, most of the metabolic components were significantly related to larger PVs and a higher serum PSA level. Also, patients with more numerous MS components had increased serum PSA levels and PV. In general, MS develops as a result of westernized diet and lifestyle, which are in turn are related with obesity and insulin resistance [21
]. Central obesity also contributes to insulin resistance [22
]. Adipose tissue secretes several substances (adipocytokines), and these substances can induce insulin resistance. Several reports have suggested that insulin resistance with hyperinsulinemia is related to prostate enlargement [21
]. Hypertension was also associated with BPH/LUTS in several animal models and epidemiologic studies. Golomb et al. [23
] reported that spontaneously hypertensive rats develop BPH-like features with aging in the absence of any inductive exogenous agents. Similar to obesity, the relationship between BPH and dyslipidemia has been documented in several epidemiologic studies [24
]. Hammarsten et al. [10
] examined the data of 158 men and reported that individuals with a low HDL-C level had a larger PV and a higher annual BPH growth rate than did individuals with a high HDL-C level. Hyperinsulinemia contributes to activation of the sympathetic nerve system and leads to an increased level of catecholamine in the tissue [25
]. It may also contribute to MS development and increased smooth muscle tone of the prostate, leading to severe LUTS [24
]. These observations suggest that components of MS may interact to increase the risk of BPH. As seen in the above mentioned studies, each study reported different results for the relationship between MS components and PSA. These differences can be attributed to the different sample sizes and different selection process of the study subjects. Also, there are several studies confirming a correlation between the serum PSA level and PV [25
]. PV is strongly related to serum PSA and age in men with symptomatic BPH and in whom prostate cancer has been excluded. PSA can also be used as an aid to estimate the degree of prostate enlargement [28
]. In summary, because patients with MS components have a larger PV than do patients without MS components, larger PV is related to a high serum PSA level.
Possible limitations of our study should be considered. This study reported a different result for the relationship between PSA and MS components from the result of Jeong et al. [8
]. The small sample size may have influenced the difference in results. Our study was not community-based; however, the subjects were healthy and were applicants for a routine health screening. Therefore, the serum PSA levels of our study subjects may not be significantly different from the serum PSA levels of a community-based population. In addition, prostate biopsy was not performed in all study subjects. The presence of undiagnosed prostate cancer could have confounded our results. Therefore, a prospective, community-based study including prostate biopsy is necessary to verify whether MS influences the accuracy of the serum PSA level test and PV measurement.