Diabetes Treatment and Progression of Benign Prostatic Hyperplasia in Community-dwelling Black and White Men
Article Outline
Objective
To conduct a study to determine whether diabetes treatment is associated with benign prostatic hyperplasia (BPH)/lower urinary tract symptoms (LUTS) and progression in black and white men. Diabetes has been associated with BPH and LUTS in aging men.
Methods
Using the Olmsted County Study of Urinary Symptoms and Health Status among Men and the Flint Men's Health Study, we examined how the use of medical therapy (eg, insulin regimens, oral hypoglycemics) related to changes in LUTS severity, maximal urinary flow rate measured by uroflowmetry, prostate volume determined by transrectal ultrasonography, and serum prostate-specific antigen concentrations.
Results
Of the 2226 men participating in the Olmsted County Study of Urinary Symptoms and Health Status among Men and the Flint Men's Health Study, 186 men reported a history of diabetes, 76.9% of whom were treated with medical therapy. Overall, the men with diabetes had significantly greater odds of moderate/severe LUTS (age- and race-adjusted odds ratio 1.37, 95% confidence interval 1.00-1.87) compared with those without diabetes. However, among the diabetic men, those not taking medication had greater odds of moderate/severe LUTS than those taking medication. This association among men not taking medication was seen for 5 of the 7 individual symptoms. The prostate volume and prostate-specific antigen level were not significantly associated with diabetes treatment. No significant differences were observed for the annual change in BPH characteristics by diabetes treatment status.
Conclusion
These findings suggest that the presence of diabetes and subsequent poor glycemic control might be less related to prostate growth and more to the dynamic components of lower urinary tract function. Additional evaluations of the associations between glycemic control and BPH progression are warranted.
Benign prostatic hyperplasia (BPH) is the most common benign neoplasm in American men. Marked by the progressive development of lower urinary tract symptoms (LUTS), its prevalence increases with age and >6.5 million Americans meet the criteria for treatment. In 2010 alone, 4.5 million visits to physicians' offices were made for BPH and >87 000 BPH-related surgeries were performed. Exclusive of medical therapy, the direct costs of BPH treatment are >$1.3 billion annually.1
To help lessen the disease's substantial public health burden, interventions are needed that can prevent the development of BPH, as well as symptom progression in men with mild/moderate LUTS. Accumulating evidence has indicated an association between diabetes and BPH. In a previous cross-sectional baseline comparison,2 we observed that diabetic men reported more moderate/severe American Urological Association Symptom Index (AUASI) scores than nondiabetic men. Insofar as glycemic control is associated with a decreased risk of BPH, high-risk groups could be targeted with diabetes treatment plans to reduce the incidence of this common condition.
To explore this possibility, we used the data from 2 cohort studies of community-dwelling men: the Olmsted County Study of Urinary Symptoms and Health Status among Men (OCS) and the Flint Men's Health Study (FMHS). We leveraged the longitudinal nature of the OCS and the FMHS to determine whether treatment of diabetes (glycemic control) was associated with the progression of BPH in 2 racially diverse populations.
Material and Methods
Study Population
Details on subject selection for the OCS and FMHS have been previously published.3, 4 In brief, the OCS and FMHS are population-based, prospective cohort studies established to evaluate the natural history of BPH in white and black male residents of Olmsted County, Minnesota, and Genesee County, Michigan, respectively.
In the OCS, 2115 of 3874 eligible white men aged 40-79 years in 1990 without a history of prostate cancer or surgery or other conditions known to interfere with voiding, including diabetic neuropathy leading to lower limb amputation, completed the self-administered AUASI.5 A detailed urologic examination, including uroflowmetry, transrectal ultrasonography, and serum prostate-specific antigen (PSA) measurement, was conducted on a 25% random subsample (476 [89%] of 537). All the men in the cohort have been followed up biennially since 1990. At each round of follow-up, all men completed the same protocol. Men who died or were lost to follow-up during the course of the study were replaced during rounds 2 and 3, resulting in 2447 study participants and 634 subsample participants to date.
Using the same criteria and protocol described, 730 of 943 eligible black men completed an interview-administered questionnaire in 1996 in the FMHS. Of these, 369 men underwent the comprehensive urologic examination, including, just as in the OCS, uroflowmetry, transrectal ultrasonography, serum PSA measurement, and self-administered AUASI, and were deemed to be free of prostate cancer. At 4 years after baseline (2000), the 369 men who participated in the baseline clinical examination were recontacted and invited to complete the same study protocol. Of the 369 men, 186 (50%) were available and agreed to participate in the follow-up examination.
The study population for the present analyses was limited to those from rounds 4 (1996) and 6 (2000) of the OCS and the baseline (1996) and follow-up (2000) of the FMHS to provide temporal comparability. A total of 2140 men participated in round 4 of the OCS. Those with prostate cancer and/or treatment before round 4 were removed, leaving 1863 white men for the present report. Similarly, of the 369 black men who participated at baseline in the FMHS, 363 were free of prostate cancer and/or treatment before their baseline visit and were included in the present report for a total sample of 2226 men (1863 white and 363 black).
Measurements
Diabetes MellitusInformation on diabetes was gathered by questionnaire in the OCS and FMHS at baseline. The participants were asked whether they had ever been diagnosed by a physician to have diabetes mellitus and in which year they were diagnosed. Treatment of diabetes was defined by patient report of the use of oral diabetes medication or insulin.
Benign Prostatic HyperplasiaThe primary endpoints included the following clinical markers of BPH: LUTS severity, maximal urinary flow rate, prostate volume, and serum PSA concentrations. Specifically, LUTS severity was determined according to the AUASI score measured by self-administered questionnaires in the OCS and FMHS. The prostate volume, determined by transrectal ultrasonography, maximal urinary flow rate, measured by uroflowmetry, and serum PSA concentrations were collected during the clinical examination portions of the 2 studies. Although no single surrogate measure provides a definitive nonhistologic diagnosis of BPH, previous studies have demonstrated that these measures have adequate construct and predictive validity for BPH.6
Statistical Analysis
Because the FMHS urologic measurements were collected in 1996 and 2000, the corresponding 1996 and 2000 OCS measurements were used in these analyses as the baseline and 4-year follow-up measures. The characteristics of the study populations at baseline were compared by diabetes status using chi-square tests. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated to examine the associations of diabetes treatment status (nondiabetics, diabetics taking medication, and diabetics not taking medication) with the baseline BPH/LUTS characteristics. Multivariable logistic regression models were used to adjust for age and race. The empirical distribution of annual change (points/y) in the AUASI score was calculated by dividing the difference between the baseline and 4-year follow-up AUASI score by the number of years between the measurements. The annual percentage of change for the maximal urinary flow rate, prostate volume, and PSA concentration was calculated by dividing the difference between the baseline and 4-year follow-up measure by the product of the baseline measure and the interval between the 2 measures multiplied by 100 (for the percentage). Tests for differences were examined across diabetes treatment categories.
Results
Of the 2226 total participants (1863 white and 363 black men), 186 (8.4%) had a self-reported history of diabetes (Table 1). The mean age at baseline was 62.5 ± 10.4 years (standard deviation) and 57.5 ± 10.1 years in those with and without diabetes, respectively (P < .001). Overall, 78.8% of men were overweight/obese (body mass index ≥25 kg/m2), and men with diabetes were more likely to be overweight than were the men without diabetes (Table 1). Black men were also more likely to have a history of diabetes than the white men (P < .001). Data on the incidence of LUTS severity and progression overall by age and race can be found in the Appendix.
Table 1. Overall distribution of subject characteristics at baseline
| Characteristic | No Diabetes (n = 2,040) | Diabetes (n = 186) | P Value |
|---|---|---|---|
| Age (y) | <.001 | ||
 40-49 | 610(29.90) | 23(12.37) | |
| 50-59 | 696(34.12) | 57(30.65) | |
| 60-69 | 438(21.47) | 52(27.96) | |
| ≥70 | 296(14.51) | 54(29.03) | |
| Body mass index | <.001 | ||
| Normal (<25 kg/m2) | 409(22.00) | 22(12.79) | |
| Overweight (25-29 kg/m2) | 892(47.98) | 62(36.05) | |
| Obese (≥30 kg/m2) | 558(30.02) | 88(51.16) | |
| Race | <.001 | ||
| White (OCS cohort) | 1,741(85.34) | 122(65.59) | |
| Black (FMHS cohort) | 299(14.66) | 64(34.41) | |
| Diabetes medication use | |||
| Yes | |||
| White (OCS cohort) | — | 97(67.83) | |
| Black (FMHS cohort) | — | 46(32.17) |
In the bivariate analyses, we compared 3 groups of men: men taking medication to treat diabetes, men not taking medication to treat their diabetes, and nondiabetics. Overall, men with diabetes had significantly greater odds (age- and race-adjusted OR 1.37, 95% CI 1.00-1.87) of moderate/severe LUTS (AUASI score >7) compared with nondiabetics. However, diabetic men who were not taking medication had greater odds of moderate/severe LUTS than diabetic men who were taking medication (Table 2). Specifically, the frequency of irritative symptoms (AUASI score >3 for symptoms of urgency, frequency, and nocturia) was significantly greater among diabetic men, with the greatest effect observed among diabetic men not taking medication (age- and race-adjusted OR 2.04, 95% CI 1.08-3.86) compared with nondiabetics. On multivariable analyses adjusted for age and race, prostate volume and total PSA level were not significantly associated with diabetes treatment status at baseline (Table 2).
Table 2. Association between diabetes medication use and BPH/LUTS characteristics in community-dwelling white and black men at baseline
| Characteristic | No Diabetes (n = 2,040) | Diabetes | |
|---|---|---|---|
| No Medication (n = 43) | Medication (n = 143) | ||
| LUTS severity | |||
| Mild/none (AUASI score ≤7) | 1,276(62.92) | 19(45.24) | 73(51.77) |
| Moderate/severe (AUASI score >7) | 752(37.08) | 23(54.76) | 68(48.23) |
| Unadjusted OR (95% CI) | Reference | 2.05(1.11-3.80) | 1.58(1.12-2.23) |
| Age- and race-adjusted OR (95% CI) | Reference | 1.77(0.94-3.31) | 1.26(0.89-1.80) |
| Obstructive symptom score | |||
| ≤4 | 1,396(68.97) | 23(54.76) | 96(68.09) |
| >4 | 628(31.03) | 19(45.24) | 45(31.91) |
| Unadjusted OR (95% CI) | Reference | 1.84(0.99-3.40) | 1.04(0.72-1.50) |
| Age- and race-adjusted OR (95% CI) | Reference | 1.73(0.92-3.23) | 0.89(0.61-1.30) |
| Irritative symptom score | |||
| ≤3 | 1,217(60.04) | 16(37.21) | 63(44.37) |
| >3 | 810(39.96) | 27(62.79) | 79(55.63) |
| Unadjusted OR (95% CI) | Reference | 2.54(1.36-4.74) | 1.88(1.34-2.65) |
| Age- and race-adjusted OR (95% CI) | Reference | 2.04(1.08-3.86) | 1.46(1.02-2.08) |
| Maximal urinary flow rate (mL/s)⁎ | |||
| ≥12 | 427(84.55) | 14(82.35) | 27(69.23) |
| <12 | 78(15.45) | 3(17.65) | 12(30.77) |
| Unadjusted OR (95% CI) | Reference | 1.17(0.33-4.18) | 2.43(1.18-5.01) |
| Age- and race-adjusted OR (95% CI) | Reference | 0.96(0.26-3.51) | 1.99(0.91-4.34) |
| Prostate volume (cm3)⁎ | |||
| ≤30 | 406(64.75) | 12(48.00) | 30(50.85) |
| >30 | 221(35.25) | 13(52.00) | 29(49.15) |
| Unadjusted OR (95% CI) | Reference | 1.99(0.89-4.44) | 1.78(1.04-3.04) |
| Age- and race-adjusted OR (95% CI) | Reference | 1.85(0.80-4.27) | 1.53(0.86-2.72) |
| Total PSA (ng/mL)⁎ | |||
| ≤2.5 | 595(86.61) | 21(77.78) | 51(80.95) |
| >2.5 | 92(13.39) | 6(22.22) | 12(19.05) |
| Unadjusted OR (95% CI) | Reference | 1.85(0.73-4.70) | 1.52(0.78-2.96) |
| Age- and race-adjusted OR (95% CI) | Reference | 1.47(0.54-3.97) | 0.93(0.45-1.92) |
⁎ Measures from men with in-clinic examinations only (414 OCS men, all 363 FMHS men; 687 without diabetes, 27 with diabetes and no medication, and 63 with diabetes and medication). |
When assessing the associations between diabetes and individual symptoms (Table 3), 5 of the 7 individual symptoms were significantly (or marginally significant) greater among the diabetic men not taking medication (age- and race-adjusted OR range 1.82-2.40). Only the symptom of nocturia was also significantly greater among diabetics taking medication (age- and race-adjusted OR 2.22, 95% CI 1.52-3.23) compared with nondiabetics. Finally, no significant differences were observed for the annual change in BPH characteristics by diabetes treatment status (Table 4).
Table 3. Association between diabetes medication use and individual symptoms in community-dwelling white and black men at baseline
| Characteristic | No Diabetes (n = 2,040) | Diabetes | |
|---|---|---|---|
| No Medication (n = 43) | Medication (n = 143) | ||
| Frequency symptom score | |||
| ≤1 | 1,337(66.19) | 20(46.51) | 88(61.97) |
| >1 | 683(33.81) | 23(53.49) | 54(38.03) |
| Unadjusted OR (95% CI) | Reference | 2.25(1.23-4.13) | 1.20(0.85-1.71) |
| Age- and race-adjusted OR (95% CI) | Reference | 1.90(1.03-3.51) | 1.02(0.72-1.47) |
| Urgency symptom score | |||
| ≤1 | 1,369(67.67) | 23(54.76) | 90(63.83) |
| >1 | 654(32.33) | 19(45.24) | 51(36.17) |
| Unadjusted OR (95% CI) | Reference | 1.73(0.94-3.20) | 1.19(0.83-1.69) |
| Age- and race-adjusted OR (95% CI) | Reference | 1.82(0.97-3.42) | 1.08(0.75-1.57) |
| Nocturia symptom score | |||
| ≤1 | 1,532(76.03) | 20(46.51) | 67(48.20) |
| >1 | 483(23.97) | 23(53.49) | 72(51.80) |
| Unadjusted OR (95% CI) | Reference | 3.65(1.99-6.70) | 3.41(2.41-4.83) |
| Age- and race-adjusted OR (95% CI) | Reference | 2.40(1.26-4.60) | 2.22(1.52-3.23) |
| Incomplete emptying symptom score | |||
| ≤1 | 1,604(79.25) | 26(61.90) | 106(75.18) |
| >1 | 420(20.75) | 16(38.10) | 35(24.82) |
| Unadjusted OR (95% CI) | Reference | 2.35(1.25-4.42) | 1.26(0.85-1.88) |
| Age- and race-adjusted OR (95% CI) | Reference | 2.01(1.06-3.81) | 1.05(0.70-1.58) |
| Intermittency symptom score | |||
| ≤1 | 1,515(74.74) | 23(54.76) | 110(78.01) |
| >1 | 512(25.26) | 19(45.24) | 31(21.99) |
| Unadjusted OR (95% CI) | Reference | 2.45(1.32-4.53) | 0.83(0.55-1.26) |
| Age- and race-adjusted OR (95% CI) | Reference | 2.33(1.25-4.37) | 0.73(0.48-1.11) |
| Straining symptom score | |||
| ≤1 | 1,768(87.61) | 35(85.37) | 121(86.43) |
| >1 | 250(12.39) | 6(14.63) | 19(13.57) |
| Unadjusted OR (95% CI) | Reference | 1.21(0.51-2.91) | 1.11(0.67-1.83) |
| Age- and race-adjusted OR (95% CI) | Reference | 1.23(0.51-2.97) | 1.06(0.63-1.76) |
| Weak urinary stream symptom score | |||
| ≤1 | 1,265(62.65) | 24(55.81) | 93(65.96) |
| >1 | 754(37.35) | 19(44.19) | 48(34.04) |
| Unadjusted OR (95% CI) | Reference | 1.33(0.72-2.44) | 0.87(0.60-1.24) |
| Age- and race-adjusted OR (95% CI) | Reference | 1.43(0.76-2.69) | 0.79(0.54-1.15) |
Table 4. Change in BPH/LUTS characteristics over time by diabetes status in community-dwelling white and black men at baseline
| Annual Change | No Diabetes (n = 1,290) | Diabetes | P Value⁎ | |
|---|---|---|---|---|
| No Medication (n = 23) | Medication (n = 78) | |||
| AUASI score | 0.00(−0.25,0.56) | 0.00(−0.91,0.94) | 0.00(−0.91,1.31) | .89 |
| Prostate volume (%)† | 4.39(0.22,8.26) | 3.54(1.24,8.76) | 4.70(1.83,9.03) | .87 |
| Maximal urinary flow rate (%)† | −2.16(−6.20,2.10) | −4.20(−6.25,3.55) | −1.66(−3.20,5.86) | .53 |
| Total PSA (%)† | 4.90(−3.04,13.67) | 3.35(−1.31,11.26) | 3.41(−10.21,7.64) | .57 |
⁎ Kruskal-Wallis P value for test of differences across diabetes categories. |
† Measures of men with in-clinic examinations only: 364 without diabetes, 14 with diabetes and no medication, and 28 with diabetes and medication. |
Comment
Type 2 diabetes, which affects 90%-95% of people with diabetes, has been associated with bladder dysfunction, typically resulting in impairment of the detrusor.7, 8 Impaired detrusor function results in a lower maximal flow rate for any given level of bladder outlet resistance and can increase the postvoid residual urine volume and LUTS severity.7 BPH is also characterized by its presentation of LUTS, including a reduced maximal urinary flow rate and increased postvoid residual urine volume. The underlying pathophysiology, however, is different because BPH does not primarily impair detrusor function but enhances bladder outlet resistance by static and dynamic components.7 In a baseline examination of the present combined cohort, we previously reported significant differences in the presence of irritative LUTS in men with diabetes compared with men without diabetes. The present report expands on that analysis to assess the potential for the effect of glycemic control on BPH/LUTS measures by examining the associations between diabetes treatment and the measures of BPH and LUTS progression in community-dwelling black and white men.
Although several studies have examined the association between diabetes and BPH, the findings have been inconsistent. A series of cross-sectional studies from Sweden observed that physician-diagnosed type 2 diabetes, treated hypertension, obesity, low high-density lipoprotein cholesterol levels, and high insulin levels were significantly associated with the presence of BPH in a consecutive series of patients with LUTS referred for surgery.9, 10, 11 Furthermore, the Massachusetts Male Aging Study,12 the FMHS,13 and others14, 15 have consistently reported diabetes or glucose levels to be significantly associated with an increased risk of LUTS.
The positive associations described between measures of diabetes and BPH, however, have not been consistently observed across studies. Specifically, Boon et al16 examined men with physician-diagnosed diabetes and LUTS and those with LUTS only and found little difference in the prostate volume, maximal urinary flow rate, and postvoid residual urine volume. That study, however, relied on a control group from a referral population that did not meet the specified exclusion criteria for BPH and thus likely underestimated the effect of diabetes on LUTS. Furthermore, in contrast to their finding for BPH surgery, the Normative Aging Study found a nonsignificant inverse association between diabetes and clinical BPH.17 Finally, in several reports using data from the OCS, Burke et al18 and, in the baseline comparison of the present combined cohort, Sarma et al,2 observed that diabetic men reported more moderate/severe AUASI scores than did nondiabetic men. However, we found no differences in prostate volume, suggesting, perhaps, that the presence of diabetes might be less directly associated with prostate growth and more closely associated with the dynamic components of lower urinary tract function.
Importantly, some of these cited studies used markers of BPH (eg, transurethral resection of the prostate) to define the disease. These markers can be a poor endpoint for LUTS in diabetic men, whose LUTS could be a result of bladder dysfunction.19 Furthermore, the failure to differentiate LUTS from BPH, along with the lack of inclusion of additional clinical markers more specific to BPH, might have contributed to the confusing evidence now seen in the published data.19 Finally, these studies were limited by their inclusion of primarily white men, the lack of population-based samples,20, 21 and cross-sectional designs that the present examination of the FMHS and OCS have overcome.
In the present study, we observed that diabetes was significantly associated with increased symptom severity and that this effect was most prominent among men who reported not taking medication for their diabetes. An increased prostate volume, increased serum PSA levels, and decreased urinary flow rates were not significantly associated with diabetes treatment status and suggest that no strong evidence exists for an association between diabetes treatment and BPH across measures. Given the lack of evidence with measures more specific to prostatic disease, the association observed between diabetes and LUTS is likely attributed to diabetic neuropathy and was largely driven in the present study by the significant association observed specifically between diabetes and nocturia. Although nocturia might be a consequence of changes in bladder reservoir function and/or kidney function secondary to urinary tract obstruction, nocturia has been associated with diabetes in numerous reports.22, 23, 24
There are several mechanisms by which diabetes might influence BPH. The first is by changes in insulin concentrations, which could, in turn, influence sex hormone concentrations,25 sympathetic nerve activity, and/or the insulin-like growth factor axis and affect the growth of the prostate.10, 26 In addition, poorly controlled diabetes can cause osmotic diuresis, which can be associated with urinary frequency and nocturia and also affect LUTS by way of neuropathic mechanisms, influencing both motor and sensory nerves.27 This is supported by our findings that diabetic men who were not taking medication had greater odds of moderate/severe LUTS than did men without diabetes, including 5 of the individual symptoms. These associations were not seen in diabetic men who were taking medication, with the exception of the symptom of nocturia.
In addition, we did not observe statistically significant associations between diabetes treatment and more specific measures of BPH. However, the magnitude and direction of the associations observed across the spectrum of BPH measures suggest that, potentially, diabetes could influence not only the dynamic components of lower urinary tract function by way of the bladder but might also even influence prostate growth. This is evidenced specifically in the marginally positive association observed between diabetes and prostate volume, particularly among diabetic men not taking medication. This observation could be explained, in part, by the relationship between increasing insulin concentrations and insulin-like growth factor bioavailability, which has be found to be associated with prostate growth.28, 29 Furthermore, it is possible that conflicting effects exist for glycemic control on the prostate and bladder that would result in inconsistent findings across the measures of BPH. If diabetes slows down prostate growth by way of testosterone and growth factors, it might reduce the risk of obstructive LUTS but not necessarily mask the beneficial effects of glycemic control on the bladder, which would present with irritative symptoms.
Because both BPH and diabetes are highly prevalent conditions of significant burden in the United States, the potential of prostate and bladder disease as complications of poorly controlled diabetes warrants additional investigation in study populations with larger samples of men with diabetes and identifies a target for primary and secondary prevention.
Although this is 1 of the first studies to examine the association between diabetes treatment and the progression of clinical markers of BPH in a multiethnic population-based sample of men, several limitations should be considered. First, the present study relied on a self-reported history of physician-diagnosed diabetes and its treatment, which might have resulted in the inclusion of men with diabetes in the control group or vice versa. However, this misclassification is not likely to be differential by the markers of BPH and would most likely result in an underestimation of the association between the BPH markers and diabetes treatment. Second, although the findings revealed positive associations between diabetes treatment and various clinical markers of BPH, we could not exclude the possibility of chance as an explanation for our findings, because the 95% CIs for the multivariable estimates included the numeral 1. This could likely be attributed to the limited sample size available among the clinical subset over time. However, the present study is one of the few studies with comprehensive clinical data regarding measures of BPH and estimating the magnitude of the association between diabetes treatment and BPH progression is an important first step in determining whether such relationships indeed exist. These potential limitations are offset by the strengths of our study, including a longitudinal, population-based multiethnic sample of men with comprehensive set of clinical markers of BPH.
Conclusions
In the present community-based study of BPH and diabetes, we have demonstrated associations between diabetes treatment and increased LUTS, particularly irritative LUTS severity. Moreover, the magnitude of the association between irritative LUTS and diabetes was most pronounced in diabetic men who were not taking medication. Furthermore, no strong evidence was found for an association between diabetes and BPH across measures more specific to BPH (ie, prostate volume, PSA level). Taken together, our findings suggest that the presence of diabetes and subsequent poor glycemic control might be less related to prostate growth and more related to the dynamic components of lower urinary tract function. Additional evaluations of the associations among diabetes, glycemic control, and BPH progression are warranted.
Appendix
Table A1. Incidence rate per 1000 person-years of lower urinary tract symptom severity and progression overall and by race
| Age Group (y) | AUASI Score >7 | AUASI Increase ≥4 Points | ||
|---|---|---|---|---|
| OCS (White Men) | FMHS (Black Men) | OCS (White Men) | FMHS (Black Men) | |
| 40-49 | 44.8(38.0-52.3) | 19.9(2.4-71.5) | 49.6(43.3-56.5) | 23.8(6.5-61.0) |
| 50-59 | 58.1(51.8-64.9) | 48.4(20.9-95.3) | 64.7(58.9-70.9) | 40.2(19.3-74.0) |
| 60-69 | 72.9(63.8-82.9) | 107.3(53.6-192.1) | 82.4(74.4-91.2) | 64.6(33.4-112.8) |
| 70-79 | 109.8(93.2-128.6) | 74.6(24.2-173.8) | 105.9(93.4-119.7) | 120.6(34.1-141.8) |
| ≥80 | 174.5(128.2-232.0) | — | 128.3(99.3-163.3) | 153.9(3.9-853.9) |
| All | 65.7(61.5-70.1) | 59.0(38.5-86.5) | 72.3(68.5-76.2) | 49.3(34.5-68.3) |
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Funding Support: This research was supported by the Urologic Diseases in America Project.
PII: S0090-4295(11)02343-0
doi:10.1016/j.urology.2011.08.065
© 2012 Elsevier Inc. All rights reserved.
