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We characterized trends in statin eligibility and subsequent statin initiation among people with HIV (PWH) from 2001 to 2017 and identified predictors of statin initiation between 2014 and 2017.PWH participating in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) enrolled in 12 US cohorts collecting data on statin eligibility criteria/prescriptions from 2001 to 2017.We determined the annual proportion eligible for statins, initiating statins, and median waiting time (from statin eligibility to initiation). Eligibility was defined using ATP III guidelines (2001-2013) and ACC/AHA guidelines (2014-2017). We assessed initiation predictors in 2014-2017 among statin-eligible PWH using Poisson regression, estimating adjusted prevalence ratios (aPRs) with 95% confidence intervals (95% CIs).Among 16,409 PWH, 7386 (45%) met statin eligibility criteria per guidelines (2001-2017). From 2001 to 2013, statin eligibility ranged from 22% to 25%. Initiation increased from 13% to 45%. In 2014, 51% were statin-eligible, among whom 25% initiated statins, which increased to 32% by 2017. Median waiting time to initiation among those we observed declined over time. Per 10-year increase in age, initiation increased 46% (aPR 1.46, 95% CI: 1.29 to 1.67). Per 1-year increase in calendar year from 2014 to 2017, there was a 41% increase in the likelihood of statin initiation (aPR 1.41, 95% CI: 1.25 to 1.58).There is a substantial statin treatment gap, amplified by the 2013 ACC/AHA guidelines. Measures are warranted to clarify reasons we observe this gap, and if necessary, increase statin use consistent with guidelines including efforts to help providers identify appropriate candidates.

BACKGROUND: Optimal management of noncommunicable diseases, including diabetes mellitus (DM), is crucially important as people with HIV (PWH) live longer with antiretroviral therapy. Our objective was to assess patient-level and clinic-level factors associated with achieving hemoglobin A1c (HbA1c) ≤7.0% among PWH and DM. SETTING: The DC Cohort, an observational clinical cohort of PWH, followed from 2011 to 2019 at 12 sites in Washington, DC. METHODS: Among PWH with diagnosed DM and elevated HbA1c (>7.0%), we examined the association between achieving HbA1c ≤7.0% and demographic and clinical factors, including time-updated medication data, and clinic-level factors related to services and structure. A multilevel marginal extended Cox regression model was generated to identify factors associated with time to HbA1c ≤7.0%. RESULTS: Over half (52.3%) of 419 participants achieved HbA1c ≤7.0%. Individual-level factors associated with HbA1c ≤7.0% included a diagnosis of DM after enrollment and a longer time since HIV diagnosis [hazard ratio (HR) = 2.65 and 1.13, P < 0.05 for both]. Attending a clinic with an endocrinologist was associated with the outcome [adjusted HR (aHR) = 1.41 95% confidence interval (CI): (1.01 to 1.97)]. In addition, comparing clinics that treat everyone, refer everyone or have a mix of treating and referring, showed an association between attending a clinic that treats everyone [aHR = 1.52 95% CI: (1.21 to 1.90)] or a clinic that refers everyone [aHR = 2.24 95% CI: (1.63 to 3.07)] compared with clinics with a mix in achieving glycemic control. CONCLUSION: Multiple factors are associated with achieving glycemic control in an urban cohort of PWH. Determining if specific services or structures improve DM outcomes may improve health outcomes for PWH and DM.

OBJECTIVE: To evaluate associations of mood, anxiety, stress-/trauma-related, and psychotic disorders, both treated and untreated, with duration of unsuppressed HIV viral load (VL) among persons living with HIV (PLWH). SETTING: The DC Cohort, an observational clinical cohort of PLWH followed from 2011–2018 at 14 sites in Washington, DC. METHODS: Among PLWH ≥18 years old who received primary care at their HIV clinic, we determined in a time-updated manner whether participants had diagnoses and pharmacologic prescriptions for mood, anxiety, stress-/trauma-related, and/or psychotic disorders. Associations between psychiatric disorders/treatments and the proportion of subsequent days with VL ≥200 copies/mL were assessed using multivariable Poisson regression with generalized estimating equations. RESULTS: Among 5,904 participants (median age 51; 70% male; 82% Black), 45% had ≥1 psychiatric disorder, including 38% with mood disorders (50% treated), 18% with anxiety or stress-/trauma-related disorders (64% treated), and 4% with psychotic disorders (52% treated). Untreated major depressive disorder (adjusted rate ratio=1.17; 95% confidence interval: 1.00–1.37), untreated other/unspecified depressive disorder (1.23; 1.01–1.49), untreated bipolar disorder (1.39; 1.15–1.69), and treated bipolar disorder (1.25; 1.02–1.53) (vs. no mood disorder) predicted more time with VL ≥200 copies/mL. Treated anxiety disorders (vs. no anxiety disorder) predicted less time (0.78; 0.62–0.99). Associations were weaker and non-significant for treated depressive disorders (vs. no mood disorder) and untreated anxiety disorders (vs. no anxiety disorder). CONCLUSIONS: PLWH with depressive and bipolar disorders, particularly when untreated, spent more time with unsuppressed VL than PLWH without a mood disorder. Treatment of mood disorders may be important for promoting sustained viral suppression.

It is not known whether immune dysfunction is associated with increased risk of death after cancer diagnosis in persons with HIV (PWH). AIDS-defining illness (ADI) can signal significant immunosuppression. Our objective was to determine differences in cancer stage and mortality rates in PWH with and without history of ADI.PWH with anal, oropharynx, cervical, lung cancers, or Hodgkin lymphoma diagnoses from January 2000 to December 2009 in the North American AIDS Cohort Collaboration on Research and Design were included.Among 81,865 PWH, 814 had diagnoses included in the study; 341 (39%) had a history of ADI at time of cancer diagnosis. For each cancer type, stage at diagnosis did not differ by ADI (P0.05). Mortality and survival estimates for cervical cancer were limited by n = 5 diagnoses. Adjusted mortality rate ratios showed a 30%-70% increase in mortality among those with ADI for all cancer diagnoses, although only lung cancer was statistically significant. Survival after lung cancer diagnosis was poorer in PWH with ADI vs. without (P = 0.0001); the probability of survival was also poorer in those with ADI at, or before other cancers although not statistically significant.PWH with a history of ADI at lung cancer diagnosis had higher mortality and poorer survival after diagnosis compared to those without. Although not statistically significant, the findings of increased mortality and decreased survival among those with ADI (vs. without) were consistent for all other cancers, suggesting the need for further investigations into the role of HIV-related immune suppression and cancer outcomes.

BACKGROUND It is unknown if a survival gap remains between HIV-infected and HIV-uninfected individuals with access to care. METHODS We conducted a cohort study within Kaiser Permanente California during 1996-2011, using abridged life tables to estimate the expected years of life remaining ("life expectancy") at age 20. RESULTS Among 24,768 HIV-infected and 257,600 HIV-uninfected individuals, there were 2229 and 4970 deaths, with mortality rates of 1827 and 326 per 100,000 person-years, respectively. In 1996-1997, life expectancies at age 20 for HIV-infected and HIV-uninfected individuals were 19.1 and 63.4 years, respectively, corresponding with a gap of 44.3 years (95% confidence interval: 38.4 to 50.2). Life expectancy at age 20 for HIV-infected individuals increased to 47.1 years in 2008 and 53.1 years by 2011, narrowing the gap to 11.8 years (8.9-14.8 years) in 2011. In 2008-2011, life expectancies at age 20 for HIV-infected individuals ranged from a low of 45.8 years for blacks and 46.0 years for those with a history of injection drug use to a high of 52.2 years for Hispanics. HIV-infected individuals who initiated antiretroviral therapy with CD4 ≥500 cells per microliter had a life expectancy at age 20 of 54.5 years in 2008-2011, narrowing the gap relative to HIV-uninfected individuals to 7.9 years (5.1-10.6 years). For these HIV-infected individuals, the gap narrowed further in subgroups with no history of hepatitis B or C infection, smoking, drug/alcohol abuse, or any of these risk factors. CONCLUSIONS Even with early treatment and access to care, an 8-year gap in life expectancy remains for HIV-infected compared with HIV-uninfected individuals.

BACKGROUND We investigated whether the reported lower incidence of prostate cancer in HIV-positive men is a result of confounding factors or reduced screening. METHODS We conducted a cohort study of 17,424 HIV-positive and 182,799 HIV-negative men enrolled in Kaiser Permanente (KP). Subjects were followed from the first KP enrollment after January 01, 1996 for KP Northern California (KPNC) and January 01, 2000 for KP Southern California until the earliest of prostate cancer diagnosis, loss to follow-up, or December 31, 2007. Poisson regression was used to compare cancer rates by HIV status adjusting for age, race, smoking, alcohol/drug abuse, overweight/obesity, and diabetes. For the KPNC subset, we analyzed additional available data by HIV status on testosterone deficiency, and on prostate-specific antigen (PSA) tests as a proxy for cancer screening. RESULTS The prostate cancer incidence rate was 102/100,000 person-years in HIV-positive men (n = 74 cases) and 131/100,000 person-years in HIV-negative men (n = 1195 cases), with an adjusted rate ratio of 0.73 (95% confidence interval: 0.57 to 0.92; P = 0.008). The reduced risk among HIV-positive men was greater for higher-stage cancers, which are less likely to be biased by screening differences than lower-stage cancers. In the KPNC subset, more HIV-positive (90.8%) than HIV-negative men (86.2%) received a PSA test by age 55 (P < 0.001). Decreased risk for HIV-positive men remained when examined only among those with a previous PSA test, and with adjustment for testosterone deficiency (rate ratio = 0.55; 95% confidence interval: 0.39 to 0.80; P = 0.001). CONCLUSIONS Prostate cancer incidence rates are lower in HIV-positive compared with HIV-negative men, which is not explained by screening differences or the risk factors evaluated.

Background We sought to clarify the association of HIV infection and immunodeficiency on myocardial infarction (MI) risk. Methods We conducted a cohort study from 1996 to 2009 of HIV-positive (HIV) and demographically matched HIV-negative (HIV) Kaiser Permanente California health plan members. Rate ratios (RRs) were obtained from Poisson regression models comparing MI incidence rates between HIV (overall and stratified by recent and nadir CD4 count, and recent HIV RNA levels) and HIV subjects, adjusting for age, sex, calendar era, race/ethnicity, census-based socioeconomic status, smoking, alcohol/drug abuse, overweight/obesity, diabetes, hypertension, and lipid-lowering therapy. Among HIV subjects, we also evaluated the independent association of CD4, HIV RNA, and antiretroviral therapy (ART) use. Results The study population included 22,081 HIV and 230,069 HIV subjects. The crude MI incidence rate per 100,000 person-years was 283 and 165 for HIV and HIV subjects, respectively, with an adjusted RR of 1.4 [95% confidence interval (CI): 1.3 to 1.6]. Compared with HIV subjects (reference), MI rates were similar for HIV subjects with recent CD4 ≥500 cells per microliter (RR = 1.18; 95% CI: 0.96 to 1.45) and those with nadir CD4 ≥500 cells per microliter (RR = 0.85; 95% CI: 0.55 to 1.33). Among HIV subjects, nadir CD4 was the only HIV-specific factor associated with MIs (RR per 100 cells = 0.88; 95% CI: 0.81 to 0.96), whereas recent CD4 and HIV RNA, prior ART use, and duration of protease inhibitors and nonnucleoside reverse transcriptase inhibitors were not associated with MIs. Conclusion HIV subjects with recent or nadir CD4 ≥500 cells per microliter had similar MI rates compared with HIV subjects. Lower nadir CD4, in particular, seems to be independently associated with MIs. These results strengthen recommendations for earlier ART initiation.

To better characterize the long-term effects of tenofovir on renal function in a large managed care organization.We performed a retrospective cohort analysis in Kaiser Permanente for years 2002 to 2005 comparing renal function among antiretroviral naïve patients initiating a tenofovir-containing regimen (964 patients) or tenofovir-sparing regimens (683 patients). We evaluated glomerular filtration rate (GFR, [Modification of Diet in Renal Disease equation]), serum creatinine, and the development of renal proximal tubular dysfunction. We report multivariable hazard ratios (HR, Cox modeling) and linear outcomes (repeated measures) with predictors retained if P0.10 (backward selection). Potential predictor variables included in multivariate models were age, sex, Black race, baseline laboratories (including CD4 count), history of diabetes mellitus, hypertension, malignancy, hepatitis, and concurrent medications.Overall, tenofovir-exposed patients had a larger relative decline in GFR through 104 weeks (-7.6 mL/min/1.73 m(2) relative to tenofovir-sparing, P0.001); the degree of the difference varied by baseline GFR, with the greatest effect seen in those patients with GFR greater than 80 mL/min/1.73 m(2). Tenofovir-exposed patients had greater development of proximal tubular dysfunction over time (at 52 wk: HR(adjusted) = 1.95 [P = 0.01] and at 104 wk: HR(adjusted) = 5.23 [P = 0.0004]) and had greater risk of medication discontinuation (HR(adjusted) = 1.21, P = 0.02), especially as renal function worsened. Viral control and CD4 count changes were similar between the two groups.Tenofovir is associated with greater effect on decline in renal function and a higher risk of proximal tubular dysfunction in antiretroviral naïve patients initiating antiretroviral therapy.

To determine the impact of depression on highly active antiretroviral therapy (HAART) adherence and clinical measures and investigate if selective serotonin reuptake inhibitors (SSRIs) improve these measures.Retrospective cohort study.In 2 large health maintenance organizations, we measured the effects of depression (with and without SSRI use) on adherence and changes in viral and immunologic control among HIV-infected patients starting a new HAART regimen. HAART adherence, HIV RNA levels, and changes in CD4 T-cell counts through 12 months were measured.A total of 3359 patients were evaluated; 42% had a depression diagnosis, and 15% used SSRIs during HAART. Depression without SSRI use was associated with significantly decreased odds of achievingor =90% adherence to HAART (odds ratio [OR] = 0.81, 95% confidence interval [CI]: 0.70 to 0.98; P = 0.03). Depression was associated with significantly lower odds of an HIV RNA level500 copies/mL (OR = 0.77, 95% CI: 0.62 to 0.95; P = 0.02). Depressed patients compliant with SSRI medication (80% adherence to SSRI) had HAART adherence and viral control statistically similar to nondepressed HIV-infected patients taking HAART. Comparing depressed with nondepressed HIV-infected patients, CD4 T-cell responses were statistically similar; among depressed patients, those compliant with SSRI had statistically greater increases in CD4 cell responses.Depression significantly worsens HAART adherence and HIV viral control. Compliant SSRI use is associated with improved HIV adherence and laboratory parameters.