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. Author manuscript; available in PMC: 2025 Nov 1.
Published in final edited form as: AIDS Care. 2024 Jul 30;36(11):1657–1667. doi: 10.1080/09540121.2024.2383875

Incidence of prostate cancer in Medicaid beneficiaries with and without HIV in 2001-2015 in 14 states

Filip Pirsl 1, Keri Calkins 1,2, Jacqueline E Rudolph 1, Eryka Wentz 1, Xiaoqiang Xu 3, Bryan Lau 1,4,5, Corinne E Joshu 1,4
PMCID: PMC11511642  NIHMSID: NIHMS2015199  PMID: 39079500

Abstract

Prostate cancer (PCa) incidence is reportedly lower in men with HIV compared to men without HIV for unknown reasons. We describe PCa incidence by HIV status in Medicaid beneficiaries, allowing for comparison of men with and without HIV who are similar with respect to socioeconomic characteristics and access to healthcare.Men (N=15,167,636) aged 18-64 with ≥7 months of continuous enrollment during 2001-2015 in 14 US states were retained for analysis. Diagnoses of HIV and PCa were identified using non-drug claims. We estimated cause-specific (csHR) comparing incidence of PCa by HIV status, adjusted for age, race-ethnicity, state of residence, year of enrollment, and comorbid conditions, and stratified by age and race-ethnicity.Hazard of PCa was lower in men with HIV than men without HIV (csHR=0.89; 95% CI: 0.80, 0.99), but varied by race-ethnicity, with similar observations among non-Hispanic Black (csHR=0.79; 95% CI: 0.69, 0.91) and Hispanic (csHR=0.85; 95% CI: 0.67, 1.09), but not non-Hispanic white men (csHR=1.17; 95% CI: 0.91, 1.50). Findings were similar in models restricted to men aged 50-64 and 40-49, but not in men aged 18-39.Reported deficits in PCa incidence by HIV status may be restricted to specific groups defined by age and race-ethnicity.

Keywords: HIV, Prostate cancer, Medicaid, Non-AIDS-defining cancers

SDG Keywords: reduced inequalities, good health and well-being

Introduction

People living with HIV (PLWH) are projected to age considerably, with increasing morbidity and mortality due to age-related conditions, including cardiovascular disease, cognitive decline, and cancer, with the latter estimated to currently account for up to one third of deaths in this population (Shiels et al., 2018; Althoff et al., 2015; Wong et al., 2018; Saylor et al., 2016; Engels et al., 2017; Morlat et al., 2014; Goehringer et al, 2017). PLWH are at elevated risk for numerous cancers compared to the general United States (US) population, including cancers of the anus, cervix, liver, and lung as well as lymphoma and Kaposi sarcoma (Shiels et al., 2018; Bedimo et al., 2009; Robbins et al., 2015; Patel et al., 2008; Hernandez-Ramirez et al., 2017). Conversely, it has been reported that incidence of breast and prostate cancer is lower among PLWH than in the general population (Bedimo et al., 2009; Robbins et al., 2015; Patel et al., 2008; Hernandez-Ramirez et al., 2017; Marcus et al., 2014; Shiels et al., 2010a; Coghill et al., 2018, Leapman et al., 2022). Despite these observations, prostate cancer is projected to account for the greatest proportion of cancer burden among PLWH as this population continues to age (Shiels et al., 2018).

Multiple differences exist between men with and without HIV that may contribute to the observed differences in incidence of prostate cancer. Several physiologic processes that have been reported to differ by HIV status, including testosterone metabolism and replacement (Wunder et al., 2007; Rochira et al., 2011; Bhatia R et al., 2015), diabetes (Brown et al., 2005a; Brown et al., 2005b; Rasmussen et al., 2012; Tien et al., 2008), and chronic inflammation (Zicari et al., 2019), may influence pathophysiology of prostate cancer. Testosterone is believed to be necessary for development of prostate cancer, although neither testosterone deficiency nor replacement have been associated with prostate cancer (Pienta et al., 2006; Mohr et al., 2001; Roddam et al., 2008; Cui et al., 2014). Diabetes has been associated with reduced risk of aggressive prostate cancer (Waters et al., 2009; Fall et al, 2013; Miller et al., 2021), and intraprostatic inflammation may promote development of prostate cancer (Sfanos et al., 2012), although it is unknown how HIV-related inflammation influences the prostate, if at all.

Differences by HIV status also exist in demographic characteristics that influence health outcomes. HIV disproportionately affects minority and socioeconomically disadvantaged communities (El-Sadr et al., 2010; Denning et al., 2019), resulting in differences in racial composition and healthcare coverage by HIV status. In 2019, an estimated 40% of PLWH in the US were non-Hispanic Black individuals, who account for only 12% of the general population (Centers for Disease Control and Prevention, 2021; US Census, 2021). Non-Hispanic Black men are also subject to numerous prostate cancer disparities, including greater incidence of any and advanced prostate cancer (Giaquinto et al., 2022; Siegel et al., 2020), lower likelihood of receiving appropriate treatment (Wang et al., 2016; Krishna et al., 2016), and greater prostate cancer-specific mortality (Williams et al., 2018; Dess et al., 2019; McKay et al., 2021) compared to other men, although differences are attenuated in settings of equal access to care. Racial disparities in prostate cancer in the general population may influence differences observed by HIV status, including more advanced stage at diagnosis of prostate cancer (Coghill et al, 2019; Shiels et al, 2015) and greater prostate cancer-specific mortality (Coghill et al, 2015) in men living with HIV compared to men without HIV. Moreover, healthcare for approximately 40% of PLWH is covered by Medicaid compared to 13% of the general population, where private insurance is most common (70%) (Kaiser Family Foundation, 2020; Kaiser Family Foundation, 2022), reflecting socioeconomic differences which may affect access to or engagement with healthcare.

Lastly, prostate cancer screening is a significant driver of detection of prostate cancer and extent of screening influences observed incidence rates (Kearns et al., 2018; Magnani et al., 2019). Prostate cancer screening has been reported to be higher among privately-insured men with HIV (Marcus et al., 2014) but not in lower income men with AIDS (Shiels et al, 2010a) compared to men without HIV, among US armed forces veterans with HIV compared to matched controls without HIV (Leapman et al., 2022), and in Medicaid beneficiaries with HIV compared to those without HIV (Pirsl et al., 2024). Current understanding is unable to explain lower incidence of prostate cancer in men with HIV, and the hypotheses described here may act in concert to yield these observations.

The objective of this study is to describe incidence of prostate cancer by HIV status in a large sample of Medicaid beneficiaries, allowing for comparison of men with HIV to men without HIV who are otherwise similar by socioeconomic characteristics and access to healthcare, effectively adjusting for these factors. We are also able to conduct comparisons stratified by race-ethnicity, which is implicated in multiple prostate cancer disparities in the general population, to describe any heterogeneity that exists by this characteristic. Findings of this study will complement the existing literature and contribute previously unreported descriptions of prostate cancer incidence accounting for key demographic characteristics of men with HIV, providing additional evidence for consideration of mechanisms underlying differences in prostate cancer incidence by HIV status.

Methods

Study Sample

Medicaid Analytic eXtract (MAX) data were obtained from the Centers for Medicare and Medicaid Services (CMS) for 2001-2015 for 14 US states. MAX data were available through 2015 for California, Georgia, New York, and Pennsylvania; through 2014 for Massachusetts, Ohio, Texas, and Washington; and through 2013 for Alabama, Colorado, Florida, Illinois, Maryland, and North Carolina. Data available for analysis included enrollment data and claims for inpatient care, outpatient care, and long-term therapy for beneficiaries aged 18-64. Beneficiaries with dual eligibility for Medicare or private insurance coverage were excluded to ensure all care received was captured in Medicaid claims. Enrollment was defined at the month level and beneficiaries were considered to be eligible in a month with at least 15 days of Medicaid coverage. Follow-up for states with MAX data through 2015 was administratively censored at the end of September 2015, immediately preceding the transition to ICD-10, and only ICD-9 codes were used to identify claims of interest.

Only beneficiaries’ first enrollment periods were considered, and beneficiaries could not re-enter and continue contributing person-time if re-enrollment was observed, as measures of interest could not be observed during a lapse in coverage. A six-month run-in period of continuous enrollment was implemented to exclude prevalent cases of any cancer, meaning beneficiaries needed at least seven months of continuous enrollment and to be cancer-free to be included in this analysis. The Johns Hopkins Bloomberg School of Public Health Institutional Review Board determined that this study represented a secondary analysis of existing Medicaid claims data and that it met criteria for exempt status.

Study Measures

HIV and covariates of interest were measured during the run-in period and tabulated at the start of the seventh month of continuous enrollment, henceforth referred to as baseline. Age, race-ethnicity, sex, and state of residence were obtained from the MAX personal summary file. Race-ethnicity was categorized as non-Hispanic white, non-Hispanic Black, Hispanic, and other or unknown race-ethnicity. Only beneficiaries for whom male sex was recorded were retained for this analysis. State was defined at baseline and fixed.

Men with HIV were identified using a modified version of the CMS chronic condition definition for HIV of at least one inpatient claim or at least two long-term or other care claims within a one-year period with ICD-9 code indicating diagnosis of HIV (042, 042.X, 079.53, 795.71, V08). The service start date of the first claim was used as the date of diagnosis of HIV. Prostate cancer, the outcome of interest, was identified using a similar algorithm, with ICD-9 codes indicating prostate cancer diagnosis (185.X, V10.46). We also identified diagnoses of comorbid conditions, specifically those included in the Charlson comorbidity index (Charlson et al., 1987; Quan et al., 2005; Quan et al., 2011). Codes used to identify the conditions are provided in Supplemental Materials.

Statistical Analysis

Men contributed follow-up time at risk beginning on the first day of the seventh month of continuous enrollment in Medicaid until earliest of diagnosis of prostate cancer, diagnosis of any other cancer, age 65, lapse in enrollment, recorded date of death, or end of data coverage for state of residence. We calculated incidence rates of prostate cancer per 100,000 person-years at risk, stratified by age and race-ethnicity. Age-stratified analyses used cutoffs of ages 40 and 50 years. The United States Preventive Services Task Force recommended initiation of prostate cancer screening at age 50 for most of the study period (US Preventive Services Task Force, 1994; Lin et al., 2008; Moyer; 2012), whereas the American Cancer Society had suggested initiation of screening in the 40s for high-risk men, namely Black men and men with family history of prostate cancer (von Eschenbach et al., 1997; Wolf et al., 2010). For age-stratified analyses, person-time contributed was additionally constrained by aging into and out of age strata.

Cox proportional hazard models were used to estimate the cause-specific hazard ratio (csHR) of prostate cancer in men with HIV compared to men without HIV. Due to the considerable difference in risk of death due to any cause by HIV status, we also estimated sub-distribution hazard ratios (sdHR) using a Fine and Gray model, to compare incidence of prostate cancer by HIV status allowing for death as a competing risk to occur. Lastly, we estimated and plotted cumulative incidence curves of prostate cancer by HIV status and 95% confidence intervals using the Aalen-Johansen estimator and Greenwood’s formula, respectively. All models used age as the time scale. The distribution of age in men with HIV differs from that of men without HIV in the general population (Shiels et al., 2010b; Shiels et al.; 2018) as well as men without HIV enrolled in Medicaid (Medicaid, 2022), requiring careful adjustment for age in analyses of cancer incidence in this population. Using age as the time scale is one way to control for these differences. HRs were estimated in all men, omitting men of other or unknown race-ethnicity, and separately among non-Hispanic white, non-Hispanic Black, and Hispanic men.; We additionally ran models stratified by age (18-39, 40-49, and 50-64). All models were adjusted for race-ethnicity, state of residence, calendar year of enrollment, and comorbid conditions (none, one, or two or more). All hazard ratio estimates presented henceforth are from adjusted models.

Results

Men with HIV were older at baseline (median age 43 (IQR: 36, 50) vs. 30 (IQR: 20, 44)), were more frequently non-Hispanic Black (43.1% vs. 18.2%), and had more often been diagnosed with at least one comorbid condition (32.0% vs. 10.7%) than men without HIV (Table 1). Over one quarter of men with HIV (26.2%) were aged 50 or older at enrollment compared to 16.7% of men without HIV.

Table 1:

Beneficiary Characteristics at Baseline

Characteristic HIV
N=112,498		 No HIV
N=15,055,138
Enrollment year
 2001 or earlier 30.4% 13.2%
 2002 5.9% 6.0%
 2003 5.0% 5.5%
 2004 4.6% 5.5%
 2005 4.3% 5.2%
 2006 3.8% 4.8%
 2007 3.3% 4.7%
 2008 4.4% 5.6%
 2009 5.0% 6.6%
 2010 5.0% 6.8%
 2011 4.8% 6.9%
 2012 4.4% 6.8%
 2013 4.0% 6.3%
 2014 13.0% 13.1%
 2015 2.0% 3.0%
Age
 Median (IQR) 43 (36, 50) 30 (20, 44)
 18-24 5.7% 37.1%
 25-29 6.3% 11.7%
 30-34 10.3% 10.2%
 35-39 15.8% 9.0%
 40-44 18.6% 8.1%
 45-49 17.1% 7.1%
 50-54 12.1% 6.3%
 55-59 6.8% 5.2%
 60-64 7.3% 5.3%
Race-ethnicity
 Non-Hispanic white 27.0% 33.7%
 Non-Hispanic Black 43.1% 18.2%
 Hispanic 20.5% 33.1%
 Other/Unknown 9.4% 15.0%
State
 Alabama 0.8% 1.0%
 California 21.7% 43.4%
 Colorado 0.5% 0.9%
 Florida 10.4% 4.3%
 Georgia 3.9% 2.2%
 Illinois 4.5% 4.3%
 Maryland 3.5% 2.1%
 Massachusetts 3.4% 3.4%
 New York 35.1% 19.0%
 North Carolina 3.5% 2.4%
 Ohio 2.9% 5.0%
 Pennsylvania 2.9% 4.9%
 Texas 4.8% 4.0%
 Washington 2.2% 3.1%
Comorbid condition
 0 68.0% 89.3%
 1 22.2% 7.5%
 2+ 9.8% 3.2%
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Baseline defined as first day of seventh month of enrollment following six-month run-in period; characteristics tabulated during run-in period; comorbid conditions considered listed in Supplemental Materials; abbreviations: IQR-interquartile range

We observed 366 cases of prostate cancer over 299,976 person-years among men with HIV and 17,224 cases over 22,298,914 person-years in men without HIV. Prostate cancer cases were predominantly observed among men aged 50-64, followed by men aged 40-49 and 18-39, and more frequently observed among non-Hispanic Black men, followed by Hispanic and non-Hispanic white men.

The cause-specific hazard of prostate cancer was lower among men with HIV compared to men without HIV (csHR=0.89; 95% CI: 0.80, 0.99); however, this association varied by age and race-ethnicity (Figure 1, Table 2). The hazard of prostate cancer was lower among non-Hispanic Black (csHR=0.79; 95% CI: 0.69, 0.91) and to a lesser extent among Hispanic (csHR=0.85; 95% CI: 0.67, 1.09) men with HIV compared to men without HIV. Conversely, non-Hispanic white men with HIV had a slightly higher (but not significantly different) hazard of prostate cancer compared to non-Hispanic White men without HIV (csHR=1.17; 95% CI: 0.91, 1.50). Results were consistent when estimating the sdHR, with minimal changes in estimates (Table 2).

Figure 1:

Figure 1:

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Cumulative Incidence of Prostate Cancer and Overall Survival by HIV Status in Men Aged 18-64 Stratified by Race-Ethnicity; insets are magnified curves for cumulative incidence of prostate cancer

Table 2:

Cause-Specific, Sub-Distribution Hazard Ratios of Prostate Cancer by HIV Status in Men Aged 18-64

Cases Person-time
(PY)		 IRa Beneficiaries Crudeb Adjustedc
csHR (95% CI) sdHR (95% CI) csHR (95% CI) sdHR (95% CI)
Overall
 No HIV 17,224 22,298,914.31 77.24 15,055,138 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 382 299,976.15 127.34 112,498 1.23 (1.11, 1.36) 1.19 (1.08, 1.32) 0.89 (0.80, 0.99) 0.87 (0.87, 0.96)
NHW, NHB, Hispanic
 No HIV 15,130 19,014,049.38 79.57 12,798,610 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 357 281,072.75 127.01 101,941 1.14 (1.03, 1.26) 1.11 (1.00, 1.23) 0.85 (0.77, 0.95) 0.83 (0.75, 0.92)
Non-Hispanic white
 No HIV 5,333 8,168,577.87 65.29 5,076,975 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 64 72,883.66 87.81 30,324 1.21 (0.95, 1.55) 1.19 (0.93, 1.52) 1.17 (0.91, 1.50) 1.14 (0.89, 1.46)
Non-Hispanic Black
 No HIV 6,826 4,614,123.25 147.94 2,736,867 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 226 136,837.93 165.16 48,503 0.83 (0.73, 0.95) 0.80 (0.70, 0.91) 0.79 (0.69, 0.91) 0.76 (0.67, 0.87)
Hispanic
 No HIV 2,971 6,231,348.25 47.68 4,984,768 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 67 71,351.16 93.90 23,114 1.05 (0.83, 1.34) 1.03 (0.81, 1.32) 0.85 (0.67, 1.09) 0.83 (0.65, 1.07)
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a

per 100,000 person-years

b

adjusted for age (time metric)

c

adjusted for age (time metric), race-ethnicity, state of residence, enrollment year, and comorbid conditions; abbreviations: CI-confidence interval, csHR-cause-specific hazard ratio, IR-incidence rate, NHB-non-Hispanic Black, NHW-non-Hispanic white, PY-person-years, sdHR-sub-distribution hazard ratio

In analyses stratified by age, similar results were observed among men aged 50-64 to those estimated among men aged 18-64, as most events occurred in this age category (Table 3, Supplemental Figure 1). Overall, the hazard of prostate cancer was lower among men with HIV (csHR=0.89; 95% CI: 0.80, 0.99). When stratified by race-ethnicity, the hazard of prostate cancer was lower among non-Hispanic Black (adjusted csHR=0.81; 95% CI: 0.70, 0.94) and Hispanic (csHR=0.80; 95% CI: 0.61, 1.06), but not non-Hispanic white (csHR=1.15; 95% CI: 0.88, 1.50), men with HIV compared to men without HIV (Table 3). The sdHR results remained similar.

Table 3:

Cause-Specific, Sub-Distribution Hazard Ratios of Prostate Cancer by HIV Status in Men Aged 50-64

Cases Person-time
(PY)		 IRa Beneficiaries Crudeb Adjustedc
csHR (95% CI) sdHR (95% CI) acsHR (95% CI) asdHR (95% CI)
Overall
 No HIV 16,007 5,418,742.81 295.40 2,945,505 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 332 108,867.34 304.96 41,603 1.22 (1.09, 1.36) 1.17 (1.05, 1.31) 0.89 (0.80, 0.99) 0.85 (0.77, 0.95)
NHW, NHB, Hispanic
 No HIV 14,012 4,446,608.25 315.12 2,341,829 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 311 102,146.14 304.47 37,923 1.14 (1.01, 1.27) 1.09 (0.98, 1.22) 0.85 (0.76, 0.96) 0.82 (0.73, 0.92)
Non-Hispanic white
 No HIV 4,974 2,233,446.25 222.71 1,153,935 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 55 25,097.74 219.14 10,732 1.19 (0.91, 1.55) 1.16 (0.89, 1.52) 1.15 (0.88, 1.50) 1.12 (0.86, 1.46)
Non-Hispanic Black
 No HIV 6,308 1,228,129.00 513.63 559,478 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 202 52,880.52 381.99 18,890 0.85 (0.74, 0.98) 0.81 (0.70, 0.93) 0.81 (0.70, 0.94) 0.77 (0.67, 0.89)
Hispanic
 No HIV 2,730 985,033.00 277.15 628,416 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 54 24,167.88 223.44 8,301 0.97 (0.74, 1.27) 0.94 (0.72, 1.23) 0.80 (0.61, 1.06) 0.78 (0.59, 1.02)
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a

per 100,000 person-years

b

adjusted for age (time metric)

c

adjusted for age (time metric), race-ethnicity, state of residence, enrollment year, and comorbid conditions; abbreviations: CI-confidence interval, csHR-cause-specific hazard ratio, IR-incidence rate, NHB-non-Hispanic Black, NHW-non-Hispanic white, PY-person-years, sdHR-sub-distribution hazard ratio

Among men aged 40-49, hazard of prostate cancer was also lower among men with HIV compared to men without HIV; however, this difference was attenuated compared to men aged over 50 (csHR=0.92; 95% CI: 0.68, 1.26) (Table 4, Supplemental Figure 2). When stratified by race-ethnicity, men with HIV had a lower hazard of prostate cancer compared to men without HIV among non-Hispanic Black men (csHR=0.68; 95% CI: 0.43, 1.06), while the hazard of prostate cancer was higher among men with HIV compared to men without HIV among non-Hispanic white (csHR=1.12; 95% CI: 0.53, 2.37) and Hispanic men (csHR=1.24; 95% CI: 0.69, 2.21). None of the differences by HIV status in this age group were statistically significant. No changes in results were observed when estimating the sdHR.

Table 4:

Cause-Specific, Sub-Distribution Hazard Ratios of Prostate Cancer by HIV Status in Men Aged 40-49

Cases Person-time
(PY)		 IRa Beneficiaries Crudeb Adjustedc
csHR (95% CI) sdHR (95% CI) csHR (95% CI) sdHR (95% CI)
Overall
 No HIV 1,062 4,376,172.00 24.27 2,736,466 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 43 116,470.90 36.92 49,401 1.43 (1.05, 1.93) 1.39 (1.03, 1.89) 0.92 (0.68, 1.26) 0.90 (0.66, 1.23)
NHW, NHB, Hispanic
 No HIV 973 3,656,230.88 26.61 2,276,711 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 40 109,660.72 36.48 45,392 1.28 (0.93, 1.75) 1.25 (0.91, 1.71) 0.88 (0.64, 1.21) 0.86 (0.62, 1.19)
Non-Hispanic white
 No HIV 312 1,672,119.12 18.66 982,198 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 7 29,985.88 23.34 13,768 1.23 (0.58, 2.59) 1.20 (0.57, 2.54) 1.12 (0.53, 2.37) 1.09 (0.52, 2.31)
Non-Hispanic Black
 No HIV 456 883,193.50 51.63 490,435 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 20 51,005.41 39.21 21,177 0.72 (0.46, 1.13) 0.71 (0.45, 1.10) 0.68 (0.43, 1.06) 0.66 (0.42, 1.03)
Hispanic
 No HIV 205 1,100,918.25 18.62 804,078 1.00 (reference) 1.00 (reference) 1.00 (reference) 1.00 (reference)
 HIV 13 28,669.43 45.34 10,447 2.15 (1.22, 3.76) 2.12 (1.21, 3.71) 1.24 (0.69, 2.21) 1.22c
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a

per 100,000 person-years

b

adjusted for age (time metric)

c

adjusted for age (time metric), race-ethnicity, state of residence, enrollment year, and comorbid conditions

c

unable to estimate standard error and confidence interval; abbreviations: CI-confidence interval, csHR-cause-specific hazard ratio, IR-incidence rate, NHB-non-Hispanic Black, NHW-non-Hispanic white, PY-person-years, sdHR-sub-distribution hazard ratio

Lastly, very few prostate cancer cases (n=7) were observed among men aged 18-39, resulting in imprecise model estimates. Overall, the hazard of prostate cancer was elevated among men with HIV compared to men without HIV (csHR=2.02; 95% CI: 0.93, 4.39), with similar results observed among non-Hispanic Black (csHR=1.81; 95% CI: 0.64, 5.10) and non-Hispanic white men (csHR= csHR=4.15; 95% CI: 0.99, 17.43) (Supplemental Table 1, Supplemental Figure 3). Due to the small number of cases, a Cox model could not be run among Hispanic men, nor could we run the Fine-Gray model among any race-ethnicity group.

Discussion

Men with HIV were found to have lower hazard of prostate cancer; however, heterogeneity in this association was observed by age and race-ethnicity. Among men aged 40 or older, the hazard of prostate cancer was largely lower in non-Hispanic Black, but higher in non-Hispanic white men with HIV compared to men without HIV. The relative hazard of prostate cancer by HIV status in Hispanic men varied by age category. Our results are congruent with previous reports of lower incidence of prostate cancer in men with HIV compared to men without HIV (Bedimo et al., 2009; Robbins et al., 2015; Patel et al., 2008; Hernandez-Ramirez et al., 2017; Marcus et al., 2014; Shiels et al., 2010a; Coghill et al., 2018), although the estimates we report indicate a smaller difference. We additionally report model estimates stratified by race-ethnicity and describe previously unreported differences in the association between HIV and incidence of prostate cancer by race-ethnicity.

Differences observed by HIV status and race-ethnicity may be explained in part by prostate cancer screening, a significant driver of the detection of prostate cancer (Kearns et al., 2018; Magnani et al., 2019). For most of the study period, guidelines recommended screening for men aged 50 or older, with some guidelines suggesting initiation of screening in the 40s for Black men and men with family history of prostate cancer (United States Preventive Services Task Force, 1994; Lin et al., 2008; Moyer, 2012; von Eschenbach et al., 1997; Wolf et al., 2010). It is possible that, among men in whom screening is not yet recommended, men with HIV are more likely to be screened and have prostate cancer detected due to increased engagement in HIV care. At ages for which screening is recommended, this difference due to care engagement is abrogated or even reversed by broad uptake of screening in men without HIV. The recommendation of earlier initiation of screening in Black men may contribute to a lower hazard of prostate cancer observed in non-Hispanic Black men with HIV beginning already in men in their 40s. In contrast, among Hispanic men with HIV, the hazard of prostate cancer was higher in the 40s, but lower beyond age 50, than in men without HIV. This explanation is not supported by findings in non-Hispanic white men, in whom the hazard of prostate cancer was consistently comparable by HIV status across age categories, although this may reflect different patterns of screening uptake or cancer detection in either or both HIV groups compared to non-Hispanic Black and Hispanic men.

Biological mechanisms may explain the reduced incidence of prostate cancer in men with HIV compared to men without HIV, such as those mediated by inflammatory processes or hormonal perturbations. However, further refinements may be needed to explain the heterogeneity in associations by race-ethnicity observed in this analysis. It is possible that prostate cancer disparities by race-ethnicity described in the general population exert an influence on and potentially interact with biological processes and characteristics that differ by HIV status, although what these interactions are is unclear.

This study was not without limitations, and findings of these analyses should be interpreted with the following considerations. This analysis was conducted in men aged 18-64 whereas approximately 60% of prostate cancer cases in the US are diagnosed in men aged 65 or older (National Cancer Institute, 2023). However, the proportion of PLWH in the US aged 65 or older was below 10% for much of the study period and only in more recent years have greater numbers of PLWH aged beyond 65 years (Shiels et al., 2018). Nevertheless, the findings of this study are not generalizable to individuals aged 65 and older in whom prostate cancer burden is highest.

The outcome of interest in this study was incidence of any prostate cancer, as neither stage nor grade at diagnosis could be determined from administrative claims data. Results of this analysis should be interpreted solely in the context of total prostate cancer. Prostate cancer-specific mortality in the first five years following diagnosis increases with grade and almost exclusively occurs among men with regional or distant disease at diagnosis. While prostate cancer is most commonly diagnosed at the local stage, (National Cancer Institute, 2023; Siegel et al., 2020) men with HIV have previously been found to be diagnosed with prostate cancer at more advanced stages (Coghill et al., 2019; Shiels et al., 2015), which are associated with adverse outcomes.

A six-month run-in period was implemented to exclude beneficiaries with prevalent cancer at enrollment, and only beneficiaries with evidence of HIV observed during this period were considered to have HIV for analysis. Inclusion of beneficiaries diagnosed with HIV later in enrollment in analysis as not having HIV likely attenuated our estimates, assuming these individuals experienced risks indicated by our results after being diagnosed with HIV. It is also possible that the run-in period did not exclude all prevalent cancers and that some events did not represent first primary cancers. Additionally, use of a six-month run-in period likely excluded beneficiaries experiencing “churn”, often defined as a temporary gap in Medicaid coverage due to inability to maintain continuous enrollment or a period of ineligibility, who receive less preventive care (Sugar et al, 2021) and may be less likely to have prostate cancer detected. Lastly, we were unable to measure and account for cancer risk factors, such as obesity and smoking, although these have been associated with fatal prostate cancer, not any prostate cancer (Rodriguez et al., 1997; Giovannucci et al., 2007; Calle et al., 2003; Wright et al., 2007; Cao et al., 2011); we also could not control for HIV-related factors, such as viral suppression and immune status.

This study was conducted among Medicaid beneficiaries enrolled in 14 US states over the period of 2001-2015. Medicaid provides health insurance for low-income adults, children, and people with disabilities, among others, in the US and insured an estimated monthly mean of 80 million individuals in 2022, including a disproportionately high number of medically underserved racial and ethnic minorities (Donohue et al, 2022). Approximately 40% of PLWH in the US are enrolled in Medicaid (Kaiser Family Foundation, 2020); thus, the results of this analysis reflect the experience of a significant proportion of men with HIV in the US. Our study benefits from comparing men with HIV to men without HIV who are otherwise similar with respect to socioeconomic characteristics and access to care, complementing prior congruent reports of lower incidence (Bedimo et al., 2009; Robbins et al., 2015; Patel et al., 2008; Hernandez-Ramirez et al., 2017; Marcus et al., 2014; Shiels et al., 2010a; Coghill et al., 2018), some of which were unable to make such direct comparisons. We were also able to estimate differences in prostate cancer incidence by HIV status stratified by race-ethnicity and identified heterogeneity in this association not previously reported. These results extend our understanding of prostate cancer in men with HIV to the Medicaid-insured population; however, existing evidence remains insufficient to identify underlying causes of differences in observed incidence of prostate cancer by HIV status. Further investigation, with particular emphasis on stage and grade at diagnosis, may provide sufficient evidence to support or exclude hypotheses explaining the differences by HIV status related to prostate cancer screening and detection, as well as biological mechanisms of prostate cancer development. The findings reported herein do not support changes in clinical practice but reiterate the need to elucidate targets of intervention to address disparities in prostate cancer outcomes by HIV status.

Prostate cancer diagnoses, related treatments, and subsequent side effects are significant sources of distress in older men in the general population (De Sousa et al., 2012). Men living with HIV already suffer adverse psychosocial effects following diagnosis of and living with HIV due to HIV-related stigma and lack of social support, and often experience dual burdens with the addition of a cancer diagnosis and its accompanying stressors (Knettel et al, 2021). This is exacerbated by cancer care disparities experienced by PLWH due to the preponderance of social barriers to cancer care among PLWH (Corrigan et al, 2020) as well as lack of evidence and guidelines for treating cancer in patients with HIV and associated provider uncertainty and stigma (Suneja et al, 2015). As PLWH continue to age and prostate cancer accounts for an increasing proportion of cancer burden in this population, it is imperative to generate evidence necessary to understand differences in prostate cancer that exist by HIV status and to improve care for men living with HIV diagnosed with prostate cancer.

Supplementary Material

Supp 1

Funding details:

This work was supported in part by NIH grants R01 CA250851, U01 AI069918, P30 CA006973, R01 AI170240, and by a 2018 and 2021 development grant from the Johns Hopkins University Center for AIDS Research, an NIH-funded program (1P30AI094189), which is supported by the following NIH Co-Funding and Participating Institutes and Centers: NIAID, NCI, NICHD, NHLBI, NIDA, NIA, NIGMS, NIDDK, NIMHD. F Pirsl was supported by the NCI Cancer Epidemiology, Prevention, and Control Grant (T32 CA0093140). This content does not necessarily represent the official views of the NIH and is the sole responsibility of the authors.

Footnotes

Disclosure statement:

The Johns Hopkins Bloomberg School of Public Health Institutional Review Board determined that this study represented a secondary analysis of existing Medicaid claims data and that it met criteria for exempt status. The authors have no conflicts of interest to disclose.

Data availability statement:

The data that support the findings of this study are available from Research Data Assistance Center (ResDAC). Restrictions apply to the availability of these data, which were used under license for this study.

References

  1. Althoff KN, McGinnis KA, Wyatt CM, Freiberg MS, Gilbert C, Oursler KK, Rimland D, Rodriguez-Barradas MC, Dubrow R, Park LS, Skanderson M, Shiels MS, Gange SJ, Gebo KA, Justice AC, Veterans Aging Cohort Study (VACS). (2015). Comparison of risk and age at diagnosis of myocardial infarction, end-stage renal disease, and non-AIDS-defining cancer in HIV-infected versus uninfected adults. Clinical Infectious Diseases, 60(4), 627–638. 10.1093/cid/ciu869 [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Bedimo RJ, McGinnis KA, Dunlap M, Rodriguez-Barradas MC, Justice AC (2010). Incidence of Non-AIDS-Defining Malignancies in HIV-Infected Vs. Non-Infected Patients in the HAART Era: Impact of Immunosuppression. Journal of Acquired Immune Deficiency Syndromes, 52(2), 203–208. 10.1097/QAI.0b013e3181b033ab [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Bhatia R, Murphy AB, Raper JL, Chamie G, Kitahata MM, Drozd DR, Mayer K, Napravnik S, Moore R, Achenbach C, Center for AIDS Research (CFAR) Network of Integrated Clinical Systems (CNICS). (2015). Testosterone replacement therapy among HIV-infected men in the CFAR Network of Integrated Clinical Systems. AIDS, 29(1), 77–81. 10.1097/QAD.0000000000000521 [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Brown TT, Li X, Cole SR, Kingsley LA, Palella FJ, Riddler SA, Chmiel JS, Visscher BR, Margolick JB, Dobs AS (2005). Cumulative exposure to nucleoside analogue reverse transcriptase inhibitors is associated with insulin resistance markers in the Multicenter AIDS Cohort Study. AIDS, 19(13), 1375–1383. 10.1097/01.aids.0000181011.62385.91 [DOI] [PubMed] [Google Scholar]
  5. Brown TT, Cole SR, Li X, Kingsley LA, Palella FJ, Riddler SA, Visscher BR, Margolick JB, Dobs AS (2005). Antiretroviral therapy and the prevalence and incidence of diabetes mellitus in the multicenter AIDS cohort study. Archives of Internal Medicine, 165(1), 1179–1184. 10.1001/archinte.165.10.1179 [DOI] [PubMed] [Google Scholar]
  6. Calle EE, Rodriguez C Walker-Thurmond K, Thun MJ (2003). Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. New England Journal of Medicine, 348(17), 1625–1638. 10.1056/NEJMoa021423 [DOI] [PubMed] [Google Scholar]
  7. Cao Y, Ma J (2011). Body mass index, prostate cancer-specific mortality, and biochemical recurrence: a systematic review and meta-analysis. Cancer Prevention Research (Philadelphia, PA), 4(4), 486–501. 10.1158/1940-6207.CAPR-10-0229 [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Centers for Disease Control and Prevention. (2021). Estimated HIV incidence and prevalence in the United States, 2015-2019. HIV Surveillance Supplemental Report 2021; 26(1): 123. https://www.cdc.gov/hiv/pdf/library/reports/surveillance/cdc-hiv-surveillance-supplemental-report-vol-26-1.pdf [Google Scholar]
  9. Charlson ME, Pompei P, Ales KL, MacKenzie CR (1987). A new method of classifying prognostic comorbidity in longitudinal studies: development and validation. Journal of Chronic Diseases, 40(5), 373–383. 10.1016/0021-9681(87)90171-8 [DOI] [PubMed] [Google Scholar]
  10. Coghill AE, Shiels MS, Suneja G, Engels EA (2015). Elevated Cancer-Specific Mortality Among HIV-Infected Patients in the United States. Journal of Clinical Oncology. 33(21):2376–2383 [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Coghill AE, Engels EA, Schymura MJ, Mahale P, Shiels MS (2018). Risk of Breast, Prostate, and Colorectal Cancer Diagnosis Among HIV-Infected Individuals in the United States. Journal of the National Cancer Institute, 110(9), 959–966. 10.1093/jnci/djy010 [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Coghill AE, Han X, Suneja G, Lin CC, Jemal A, Shiels MS (2019). Advanced stage at diagnosis and elevated mortality among US patients with cancer infected with HIV in the National Cancer Data Base. Cancer, 125(16), 2868–2876. 10.1002/cncr.32158 [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Corrigan KL; Knettel BA; Suneja G (2020). Inclusive Cancer Care: Rethinking Patients Living with HIV and Cancer. The Oncologist. 25(5):361–363. 10.1634/theoncologist.2019-0853 [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Cui Y, Zong H, Yan H, Zhang Y (2014). The effect of testosterone replacement therapy on prostate cancer: a systematic review and meta-analysis. Prostate Cancer and Prostatic Diseases, 17(2), 132–143. 10.1038/pcan.2013.60 [DOI] [PubMed] [Google Scholar]
  15. Denning P, DiNenno E (2019, December 11). Communities in Crisis: Is There a Generalized HIV Epidemic in Impoverished Urban Areas of the United States? Centers for Disease Control and Prevention. https://www.cdc.gov/hiv/group/poverty.html [Google Scholar]
  16. De Sousa A, Sonavane S, Mehta J (2012). Psychological aspects of prostate cancer: a clinical review. Prostate Cancer and Prostatic Diseases. 15(2):120–127. 10.1038/pcan.2011.66 [DOI] [PubMed] [Google Scholar]
  17. Dess RT, Hartman HE, Mahal BA, Soni PD, Jackson WC, Cooperberg MR, Amling CL, Aronson WJ, Kane CJ, Terris MK, Zumsteg ZS, Butler S, Osborne JR, Morgan TM, Mehra R, Salami SS, Kishan AU, Wang C, Schaeffer EM, Roach M 3rd, Pisansky TM, Shipley WU, Freedland SJ, Sandler HM, Halabi S, Feng F,Y, Dignam JJ, Nguyen PL, Schipper MJ, Sprat DE (2019). Association of Black Race With Prostate Cancer-Specific and Other-Cause Mortality. JAMA Oncology, 5(7), 975–983. 10.1001/jamaoncol.2019.0826 [DOI] [PMC free article] [PubMed] [Google Scholar]
  18. Donohue JM, Cole ES, James CV, Jarlenski M, Michener JD, Roberts ET (2022). The US Medicaid Program: Coverage, Finances, Reforms, and Implications for Health Equity. Journal of the American Medical Association, 328(11), 1085–1099. 10.1001/jama.2022.14791 [DOI] [PubMed] [Google Scholar]
  19. El-Sadr WM, Mayer KH, Hodder SL (2015). AIDS in America – Forgotten but Not Gone. New England Journal of Medicine, 362(11), 967–970. 10.1056/NEJMp1000069 [DOI] [PMC free article] [PubMed] [Google Scholar]
  20. Engels EA, Yanik EL, Wheeler W, Gill MJ, Shiels MS, Dubrow R, Althoff KN, Silverberg MJ, Brooks JT, Kitahata MM, Goedert JJ, Grover S, Mayor AM, Moore RD, Park LS, Rachlis A, Sigel K, Sterling TR, Thorne JE, Pfeiffer RM, North American AIDS Cohort Collaborations on Research and Design of the International Epidemiologic Databases to Evaluate AIDS. (2017). Cancer-Attributable Mortality Among People With Treated Human Immunodeficiency Virus Infection in North America. Clinical Infectious Diseases, 65(4), 636–643. 10.1093/cid/cix392 [DOI] [PMC free article] [PubMed] [Google Scholar]
  21. Fall K, Garmo H, Gudbjornsdottir S, Stattin P, Zethelius B (2013). Diabetes Mellitus and Prostate Cancer Risk; A Nationwide Case—Control Study within PCBaSe Sweden. Cancer Epidemiology, Biomarkers, and Prevention, 22(6), 1102–1109. 10.1158/1055-9965.EPI-12-1046 [DOI] [PubMed] [Google Scholar]
  22. Giaquinto AN, Miller KD, Tossas KY, Winn RA, Jemal A, Siegel RL (2022). Cancer statistics for African American/Black People 2022. CA: A Cancer Journal for Clinicians, 72(3), 202–229. 10.3322/caac.21718 [DOI] [PubMed] [Google Scholar]
  23. Giovannucci E, Liu Y, Platz EA, Stampfer MJ, Willett WC (2007). Risk factors for prostate cancer incidence and progression in the health professionals follow-up study. International Journal of Cancer, 121(7), 1571–1578. 10.1002/ijc.22788 [DOI] [PMC free article] [PubMed] [Google Scholar]
  24. Goehringer F, Bonnet F, Salmon D, Cacoub P, Paye A, Chene G, Morlat P, May T (2017). Causes of Death in HIV-Infected Individuals with Immunovirologic Success in a National Prospective Survey. AIDS Research and Human Retroviruses, 33(2), 187–193. 10.1089/AID.2016.0222 [DOI] [PubMed] [Google Scholar]
  25. Hernandez-Ramirez RU, Shiels MS, Dubrow R, Engels EA (2017). Cancer risk in HIV-infected people in the USA from 1996 to 2012: a population-based, registry-linkage study. Lancet HIV, 4(11), e495–e504. 10.1016/S2352-3018(17)30125-X [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. Kaiser Family Foundation. (2020, September 24). An Update on Insurance Coverage Among People with HIV in the United States. https://www.kff.org/report-section/an-update-on-insurance-coverage-among-people-with-hiv-in-the-united-states-findings/
  27. Kaiser Family Foundation. (2022). Health Insurance Coverage of the Population. https://www.kff.org/other/state-indicator/total-population
  28. Kearns JT, Holt SK, Wright JL, Lin DW, Lange PH, Gore JL (2018). PSA screening, prostate biopsy, and treatment and prostate cancer in the years surrounding the USPSTF recommendation against prostate cancer screening. Cancer, 124(13), 2733–2739. 10.1002/cncr.31337 [DOI] [PubMed] [Google Scholar]
  29. Knettel BA, Corrigan KL, Cherenack EM, Ho N, Carr S, Cahill J, Chino JP, Ubel P, Watt MH, Suneja G, (2021). HIV, Cancer, and Coping: The Cumulative Burden of a Cancer Diagnosis among People Living with HIV. Journal of Psychosocial Oncology. 39(6):734–748. 10.1080/07347332.2020.1867691 [DOI] [PMC free article] [PubMed] [Google Scholar]
  30. Krishna S, Fan Y, Jarosek S, Adejoro O, Chamie K, Konety B (2017). Racial Disparities in Active Surveillance for Prostate Cancer. Journal of Urology, 197(2), 342–349. 10.1016/j.juro.2016.08.104 [DOI] [PubMed] [Google Scholar]
  31. Leapman MS, Stone K, Wadia R, Park LS, Gibert CL, Goetz MB, Bedimo R, Rodriguez-Barradas M, Shebl F, Justice AC, Brown ST, Crothers K, Sigel KM (2022). Prostate Cancer Screening and Incidence Among Aging Persons Living with HIV. Journal of Urology, 207(2), 324–332. 10.1097/JU.0000000000002249 [DOI] [PMC free article] [PubMed] [Google Scholar]
  32. Lin K, Lipsitz R, Miller T, Janakiraman S, United States Preventive Services Task Force. (2008). Benefits and harms of prostate-specific antigen screening for prostate cancer: an evidence update for the U.S. Preventive Services Task Force. Annals of Internal Medicine, 149(3), 192–199. 10.7326/0003-4819-149-3-200808050-00009 [DOI] [PubMed] [Google Scholar]
  33. Magnani CJ, Li K, Seto T, McDonald KM, Blayney DW, Brooks JD, Hernandez-Boussard T (2019). PSA Testing Use and Prostate Cancer Diagnostic Stage After the 2012 U.S. Preventive Services Task Force Guideline Changes. Journal of the National Cancer Institute, 17(7), 795–803. 10.6004/jnccn.2018.7274 [DOI] [PMC free article] [PubMed] [Google Scholar]
  34. Marcus JL, Chao CR, Leyden WA, Xu L, Klein DB, Horberg MA, Towner WJ, Quesenberry CP Jr, Abrams DI, Van Den Eeden SK, Silverberg MJ (2014). Prostate cancer incidence and prostate-specific antigen testing among HIV-positive and HIV-negative men. Journal of Acquired Immune Deficiency Syndromes, 66(5), 495–502. 10.1097/QAI.0000000000000202 [DOI] [PubMed] [Google Scholar]
  35. McKay RR, Sarkar RR, Kumar A, Einck JP, Garraway IP, Lynch JA, Mundt AJ, Murphy JD, Stewart TF, Yamoah K, Rose BS Outcomes of Black men with prostate cancer treated with radiation therapy in the Veterans Health Administration. Cancer, 127(3), 403–411. 10.1002/cncr.33224 [DOI] [PubMed] [Google Scholar]
  36. Medicaid. (n. d.). Medicaid and CHIP Scorecard. https://www.medicaid.gov/state-overviews/scorecard/main
  37. Miller EA, Pinsky PF, Pierre-Victor D (2021). Differences in the relationship between diabetes and prostate cancer among Black and White non-Hispanic men. Cancer Causes and Control, 32(12), 1385–1393. 10.1007/s10552-021-01486-2 [DOI] [PubMed] [Google Scholar]
  38. Mohr BA, Feldman HA, Kalish LA, Longcope C, McKinlay JB (2001). Are serum hormones associated with the risk of prostate cancer? Prospective results from the Massachusetts Male Aging Study. Urology, 57(5), 930–935. 10.1016/s0090-4295(00)01116-x [DOI] [PubMed] [Google Scholar]
  39. Morlat P, Roussillon C, Henard S, Salmon D, Bonnet F, Cacoub P, Georget A, Aouba A, Rosenthal E, May T, Chauveau M, Diallo B, Costagliola D, Chene G, ANRS EN20 Mortalité 2010 Study Group. (2014). Causes of death among HIV-infected patients in France in 2010 (national survey): trends since 2000. AIDS, 28(8), 1181–1191. 10.1097/QAD.0000000000000222 [DOI] [PubMed] [Google Scholar]
  40. Moyer VA, United States Preventive Services Task Force. (2012). Screening for prostate cancer: U.S. Preventive Services Task Force recommendation statement. Annals of Internal Medicine, 157(2), 120–134. 10.7326/0003-4819-157-2-201207170-00459 [DOI] [PubMed] [Google Scholar]
  41. National Cancer Institute Surveillance, Epidemiology, and End Results Program. (2023). Cancer Stat Facts: Prostate Cancer. https://www.seer.cancer.gov/statfacts/html/prost.html
  42. Patel P, Hanson DL, Sullivan PS, Novak RM, Moorman AC, Tong TC, Holmberg SD, Brooks JT, Adult and Adolescent Spectrum of Disease Project and HIV Outpatient Study Investigators. (2008). Incidence of types of cancer among HIV-infected persons compared with the general population in the United States, 1992-2003. Annals of Internal Medicine, 148(10), 728–736. 10.7326/0003-4819-148-10-200805200-00005 [DOI] [PubMed] [Google Scholar]
  43. Pienta KJ, Bradley D (2006). Mechanisms underlying the development of androgen-independent prostate cancer. Clinical Cancer Research, 12(6), 1665–1671. 10.1158/1078-0432.CCR-06-0067 [DOI] [PubMed] [Google Scholar]
  44. Pirsl F, Calkins K, Rudolph JE, Wentz E, Xu X, Zhou Y, Lau B, Joshu CE (2024). Receipt of prostate-specific antigen test in Medicaid beneficiaries with and without HIV in 2001-2015 in 14 states. AIDS Research and Human Retroviruses. [online ahead of print]. 10.1089/AID.2023.0142 [DOI] [PMC free article] [PubMed] [Google Scholar]
  45. Quan H, Sundararajan V, Halfon P, Fong A, Burnand B, Luthi J-C, Saunders LD, Beck CA, Feasby TE, Ghali WA (2005). Coding algorithms for defining comorbidities in ICD-9-CM and ICD-10 administrative data. Medical Care, 43(11), 1130–1139. 10.1097/01.mlr.0000182534.19832.83 [DOI] [PubMed] [Google Scholar]
  46. Quan H, Li B, Couris CM, Fushimi K, Graham P, Hider P, Januel J-M, Sundararajan V (2011). Updating and validating the Charlson comorbidity index and score for risk adjustment in hospital discharge abstracts using data from 6 countries. American Journal of Epidemiology, 173(6), 676–682. 10.1093/aje/kwq433 [DOI] [PubMed] [Google Scholar]
  47. Rasmussen LD, Mathiesen ER, Kronborg G, Pederson C, Gerstoft J, Obel N (2012). Risk of diabetes mellitus in persons with and without HIV: a Danish nationwide population-based cohort study. PLoS One, 7(9), e44575. 10.1371/journal.pone.0044575 [DOI] [PMC free article] [PubMed] [Google Scholar]
  48. Robbins HA, Pfeiffer RM, Shiels MS, Li J, Hall HI, Engels EA (2015). Excess cancers among HIV-infected people in the United States. Journal of the National Cancer Institute, 107(4), dju503. 10.1093/jnci/dju503 [DOI] [PMC free article] [PubMed] [Google Scholar]
  49. Rochira V, Zirilli L, Orlando G, Santi D, Brigante G, Diazzi C, Carli F, Carani C, Guaraldi G (2011). Premature decline of serum total testosterone in HIV-infected men in the HAART-era. PLoS One, 6(12), e28512. 10.1371/journal.pone.0028512 [DOI] [PMC free article] [PubMed] [Google Scholar]
  50. Endogenous Hormones and Prostate Cancer Collaborative Group, Roddam AW, Allen NE, Appleby P, Key TJ (2008). Endogenous sex hormones and prostate cancer: a collaborative analysis of 18 prospective studies. Journal of the National Cancer Institute, 100(3), 170–183. 10.1093/jnci/djm323 [DOI] [PMC free article] [PubMed] [Google Scholar]
  51. Rodriguez C, Tatham LM, Thun MJ, Calle EE, Heath CW Jr (1997). Smoking and fatal prostate cancer in a large cohort of adult men. American Journal of Epidemiology, 145(5), 466–475. 10.1093/oxfordjournals.aje.a009129 [DOI] [PubMed] [Google Scholar]
  52. Saylor D, Dickens AM, Sacktor N, Haughey N, Slusher B, Pletnikov M, Mankowski JL, Brown A, Volsky DJ, McArthur JC (2016). HIV-associated neurocognitive disorder—pathogenesis and prospects for treatment. Nature Reviews Neurology, 12(4), 234–248. 10.1038/nrneurol.2016.27 [DOI] [PMC free article] [PubMed] [Google Scholar]
  53. Sfanos KS, De Marzo AM (2012). Prostate cancer and inflammation: the evidence. Histopathology, 60(1), 199–215. 10.1111/j.1365-2559.2011.04033.x [DOI] [PMC free article] [PubMed] [Google Scholar]
  54. Shiels MS, Goedert JJ, Moore RD, Platz EA, Engels EA (2010). Reduced risk of prostate cancer in U.S. Men with AIDS. Cancer Epidemiology, Biomarkers, and Prevention, 19(11), 2910–2915. 10.1158/1055-9965.EPI-10-0741 [DOI] [PMC free article] [PubMed] [Google Scholar]
  55. Shiels MS, Pfeiffer RM, Engels EA (2010). Age at cancer diagnosis among persons with AIDS in the United States. Annals of Internal Medicine, 153(7), 452–460. 10.7326/0003-4819-153-7-201010050-00008 [DOI] [PMC free article] [PubMed] [Google Scholar]
  56. Shiels MS, Copeland G, Goodman MT, Harrell J, Lynch CF, Pawlish K, Pfeiffer RM, Engels EA (2015). Cancer stage at diagnosis in patients infected with the human immunodeficiency virus and transplant recipients. Cancer, 121(12), 2063–2071. 10.1002/cncr.29324 [DOI] [PMC free article] [PubMed] [Google Scholar]
  57. Shiels MS, Islam JY, Rosenberg PS, Hall HI, Jacobson E, Engels EA (2018). Projected Cancer Incidence Rates and Burden of Incident Cancer Cases in HIV-Infected Adults in the United States Through 2030. Annals of Internal Medicine, 168(12), 866–873. 10.7326/M17-2499 [DOI] [PMC free article] [PubMed] [Google Scholar]
  58. Siegel DA, O’Neil ME, Richards TB, Dowling NF, Weir HK (2020). Prostate Cancer Incidence and Survival, by Stage and Race/Ethnicity – United States, 2001-2017. Morbidity and Mortality Weekly Report, 69(41), 1473–1480. 10.15585/mmwr.mm6941a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
  59. Sugar S, Peters C, De Lew N, Sommers B, Office of the Assistant Secretary for Planning and Evaluations, Office of Health Policy, United States Department of Health and Human Services. (April 2021). Medicaid Churning and Continuity of Care: Evidence and Policy Considerations Before and After the COVID-19 Pandemic. https://aspe.hhs.gov/sites/default/files/private/pdf/265366/medicaid-churning-ib.pdf [Google Scholar]
  60. Suneja G, Boyer M, Yehia BR, Shiels MS, Engels EA, Bekelman JE, Long JA (2015). Cancer Treatment in Patients With HIV Infection and Non-AIDS-Defining Cancers: A Survey of US Oncologists. Journal of Oncology Practice. 11(3):e380–e387. 10.1200/JOP.2014.002709 [DOI] [PMC free article] [PubMed] [Google Scholar]
  61. Tien PC, Schneider MF, Cole SR, Levine AM, Cohen M, DeHovitz J, Young M, Justman JE (2010). Antiretroviral Therapy Exposure and Insulin Resistance in the Women’s Interagency HIV Study. Journal of Acquired Immune Deficiency Syndromes, 49(4), 369–376. 10.1097/qai.0b013e318189a780 [DOI] [PMC free article] [PubMed] [Google Scholar]
  62. United States Census Bureau. (August 2021). Racial and Ethnic Diversity in the United States: 2010 Census and 2020 Census. http://www.census.gov/library/visualizations/interactive/racial-and-ethnic-diversity-in-the-united-states-2010-and-2020-census.html
  63. United States Preventive Services Task Force. (1994). Screening for prostate cancer: commentary on the recommendations of the Canadian Task Force on the Periodic Health Examination. The U.S. Preventive Services Task Force. American Journal of Preventive Medicine, 10(4), 187–193. [PubMed] [Google Scholar]
  64. von Eschenbach A, Ho R, Murphy GP, Cunningham M, Lins N (1997). American Cancer Society guideline for the early detection of prostate cancer: update 1997. CA: A Cancer Journal for Clinicians, 47(5), 261–264. 10.3322/canjclin.47.5.261 [DOI] [PubMed] [Google Scholar]
  65. Wang EH, Yu JB, Abouassally R, Meropol NJ, Cooper G, Shah ND, Williams SB, Gonzalez C, Smaldone MC, Kutikov A, Zhu H, Kim SP (2016). Disparities in Treatment of Patients With High-risk Prostate Cancer: Results From a Population-based Cohort. Urology, 95, 88–94. 10.1016/j.urology.2016.06.010 [DOI] [PubMed] [Google Scholar]
  66. Waters KM, Henderson BE, Stram DO, Wan P, Kolonel LN, Haiman CA (2009). Association of diabetes with prostate cancer risk in the multiethnic cohort. American Journal of Epidemiology, 169(8), 937–945. 10.1093/aje/kwp003 [DOI] [PMC free article] [PubMed] [Google Scholar]
  67. Williams VL, Awasthi S, Fink AK, Pow-Sang JM, Park JY, Gerke T, Yamoah K (2018). African-American men and prostate cancer-specific mortality: a competing risk analysis of a large institutional cohort, 1989-2015. Cancer Medicine, 7(5), 2160–2171. 10.1002/cam4.1451 [DOI] [PMC free article] [PubMed] [Google Scholar]
  68. Wolf AMD, Wender RC, Etzioni RB, Thompson IM, D’Amico AV, Volk RJ, Brooks DD, Dash C, Guessous I, Andrews K, DeSantis C, Smith RA, American Cancer Society Prostate Cancer Advisory Committee. (2010). American Cancer Society guideline for the early detection of prostate cancer: update 2010. CA: A Cancer Journal for Clinicians, 60(2), 70–98. 10.3322/caac.20066 [DOI] [PubMed] [Google Scholar]
  69. Wong C, Gange SJ, Moore RD, Justice AC, Buchacz K, Abraham AG, Rebeiro PF, Koethe JR, Martin JN, Horberg MA, Boyd CM, Kitahata MM, Crane HM, Gebo KA, Gill MJ, Silverberg MJ, Palella FJ, Patel P, Samji H, Thorne J, Rabkin CS, Mayor A, Althoff KN, North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD). (2018). Multimorbidity Among Persons Living with Human Immunodeficiency Virus in the United States. Clinical Infectious Diseases, 66(8), 1230–1238. 10.1093/cid/cix998 [DOI] [PMC free article] [PubMed] [Google Scholar]
  70. Wright ME, Chang S-C, Schatzkin A, Albanes D, Kipnis V, Mouw T, Hurwitz P, Hollenbeck A, Leitzmann MF (2007). Prospective study of adiposity and weight change in relation to prostate cancer incidence and mortality. Cancer, 109(4), 675–684. 10.1002/cncr.22443 [DOI] [PubMed] [Google Scholar]
  71. Wunder DM, Bersinger NA, Fux CA, Mueller NJ, Hischel B, Cavassini M, Elzi L, Schmid P, Bernasconi E, Mueller B, Furrer H, Swiss HIV Cohort Study. (2007). Hypogonadism in HIV-1-infected men is common and does not resolve during antiretroviral therapy. Antiviral Therapy, 12(2), 261–265. 10.1177/135965350701200215 [DOI] [PubMed] [Google Scholar]
  72. Zicari S, Sessa L, Cotugno N, Ruggiero A, Morrocchi E, Concato C, Rocca S, Zangari P, Manno EC, Palma P (2019). Immune Activation, Inflammation, and Non-AIDS Co-Morbidities in HIV-Infected Patients under Long-Term ART. Viruses, 11(3), 200. 10.3390/v11030200 [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supp 1
NIHMS2015199-supplement-Supp_1.docx (336.1KB, docx)

Data Availability Statement

The data that support the findings of this study are available from Research Data Assistance Center (ResDAC). Restrictions apply to the availability of these data, which were used under license for this study.

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