scholarly journals Changes Over Time in COVID-19 Severity and Mortality in Patients Undergoing Cancer Treatment in the United States: Initial Report From the ASCO Registry

2021 ◽  
Author(s):  
Kathryn F. Mileham ◽  
Suanna S. Bruinooge ◽  
Charu Aggarwal ◽  
Alicia L. Patrick ◽  
Christiana Davis ◽  
...  

PURPOSE: People with cancer are at increased risk for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. ASCO's COVID-19 registry promotes systematic data collection across US oncology practices. METHODS: Participating practices enter data on patients with SARS-CoV-2 infection in cancer treatment. In this analysis, we focus on all patients with hematologic or regional or metastatic solid tumor malignancies. Primary outcomes are 30- and 90-day mortality rates and change over time. RESULTS: Thirty-eight practices provided data for 453 patients from April to October 2020. Sixty-two percent had regional or metastatic solid tumors. Median age was 64 years. Forty-three percent were current or previous cigarette users. Patients with B-cell malignancies age 61-70 years had twice mortality risk (hazard ratio = 2.1 [95% CI, 1.3 to 3.3]) and those age > 70 years had 4.5 times mortality risk (95% CI, 1.8 to 11.1) compared with patients age ≤ 60 years. Association between survival and age was not significant in patients with metastatic solid tumors ( P = .12). Tobacco users had 30-day mortality estimate of 21% compared with 11% for never users (log-rank P = .005). Patients diagnosed with SARS-CoV-2 before June 2020 had 30-day mortality rate of 20% (95% CI, 14% to 25%) compared with 13% (8% to 18%) for those diagnosed in or after June 2020 ( P = .08). The 90-day mortality rate for pre-June patients was 28% (21% to 34%) compared with 21% (13% to 28%; P = .20). CONCLUSION: Older patients with B-cell malignancies were at increased risk for death (unlike older patients with metastatic solid tumors), as were all patients with cancer who smoke tobacco. Diagnosis of SARS-CoV-2 later in 2020 was associated with more favorable 30- and 90-day mortality, likely related to more asymptomatic cases and improved clinical management.

Author(s):  
Elliot Friedman ◽  
Beth LeBreton ◽  
Lindsay Fuzzell ◽  
Elizabeth Wehrpsann

By many estimates the majority of adults over age 65 have two or more chronic medical conditions (multimorbidity) and are consequently at increased risk of adverse functional outcomes. Nonetheless, many older adults with multimorbidity are able to maintain high levels of function and retain good quality of life. Research presented here is designed to understand the influences that help ensure better functional outcomes in these older adults. This chapter presents findings that draw on data from the Midlife in the United States study. The independent and interactive contributions of diverse factors to multimorbidity and changes in multimorbidity over time are reviewed. The degree that multimorbidity increases risk of cognitive impairment and disability is examined. The role of inflammation as a mediator is considered. Multimorbidity is increasingly the norm for older adults, so better understanding of factors contributing to variability in multimorbidity-related outcomes can lead to improved quality of life.


2020 ◽  
Vol 7 (Supplement_1) ◽  
pp. S150-S150
Author(s):  
Michael R Hovan ◽  
Vanessa Cedarbaum ◽  
Thomas Kirn ◽  
Thomas Kirn

Abstract Background Carbapenem-Resistant Enterobacteriales (CRE) bacteremia is associated with significant morbidity and mortality. CRE were assigned a threat level of “urgent” in the 2019 CDC report on antibiotic resistance in the United States. We attempted to identify predictors of 30-day mortality in patients with CRE bacteremia. Methods We performed a chart review of 146 patients with CRE bacteremia from January 2010 - July 2019. CRE was defined using the current CDC definition. Electronic medical records were reviewed to obtain clinical characteristics and outcomes including prior antibiotic use, comorbidities, prior location, treatment, hospital course, microbiological data and outcomes including in-hospital mortality. Results Of 146 patients included for analysis, the overall 30-day mortality rate was 36.3%. Patients admitted from a healthcare facility including outside hospitals, rehab, nursing homes, and LTACs had a 49.1% (29/59) 30-day mortality rate compared to 27.5% (24/87) for those admitted from home (RR=1.78, 95% CI 1.16–2.73, p=.0082). Patients with a Pitt bacteremia score ≥ 4 had a greater 30-day mortality rate (42.6%, 26/61) compared to those with a Pitt bacteremia score < 4 (17.6%, 15/85) (RR=2.92, 95% CI 1.40–4.16, p=.0015). Patients that received inactive empiric therapy had a 30-day mortality rate of 36% (36/100) compared to 36.9% (17/46) in those that received active empiric therapy (RR=.9741, 95% CI .6155-1.59, p=.9109). Patients with isolates determined to have a meropenem MIC ≥ 4 had a 30-day mortality rate of 40.2% (37/92) while those with an MIC < 4 had a 30-day mortality rate of 30.2% (16/53) (RR=1.33, 95% CI .8250–2.1513, p=.2408). A pulmonary source of bacteremia was associated with an increased risk of 30-day mortality (64.3%, 9/14) compared to all other sources of bacteremia (34.8%, 31/89) (RR=1.85, 95% CI 1.39–2.99, p=.0129). No other infection source was associated with an increased 30-day mortality rate. Conclusion Admission from a healthcare facility, Pitt bacteremia score ≥ 4, and pulmonary source of bacteremia were associated with increased risk of 30-day mortality. Interestingly, administration of active empiric therapy was not associated with a decreased mortality risk. Meropenem MIC was not predictive of 30-day mortality. Disclosures All Authors: No reported disclosures


2015 ◽  
Vol 33 (21) ◽  
pp. 2376-2383 ◽  
Author(s):  
Anna E. Coghill ◽  
Meredith S. Shiels ◽  
Gita Suneja ◽  
Eric A. Engels

Purpose Despite advances in the treatment of HIV, HIV-infected people remain at increased risk for many cancers, and the number of non–AIDS-defining cancers is increasing with the aging of the HIV-infected population. No prior study has comprehensively evaluated the effect of HIV on cancer-specific mortality. Patients and Methods We identified cases of 14 common cancers occurring from 1996 to 2010 in six US states participating in a linkage of cancer and HIV/AIDS registries. We used Cox regression to examine the association between patient HIV status and death resulting from the presenting cancer (ascertained from death certificates), adjusting for age, sex, race/ethnicity, year of cancer diagnosis, and cancer stage. We included 1,816,461 patients with cancer, 6,459 (0.36%) of whom were HIV infected. Results Cancer-specific mortality was significantly elevated in HIV-infected compared with HIV-uninfected patients for many cancers: colorectum (adjusted hazard ratio [HR], 1.49; 95% CI, 1.21 to 1.84), pancreas (HR, 1.71; 95% CI, 1.35 to 2.18), larynx (HR, 1.62; 95% CI, 1.06 to 2.47), lung (HR, 1.28; 95% CI, 1.17 to 1.39), melanoma (HR, 1.72; 95% CI, 1.09 to 2.70), breast (HR, 2.61; 95% CI, 2.06 to 3.31), and prostate (HR, 1.57; 95% CI, 1.02 to 2.41). HIV was not associated with increased cancer-specific mortality for anal cancer, Hodgkin lymphoma, or diffuse large B-cell lymphoma. After further adjustment for cancer treatment, HIV remained associated with elevated cancer-specific mortality for common non–AIDS-defining cancers: colorectum (HR, 1.40; 95% CI, 1.09 to 1.80), lung (HR, 1.28; 95% CI, 1.14 to 1.44), melanoma (HR, 1.93; 95% CI, 1.14 to 3.27), and breast (HR, 2.64; 95% CI, 1.86 to 3.73). Conclusion HIV-infected patients with cancer experienced higher cancer-specific mortality than HIV-uninfected patients, independent of cancer stage or receipt of cancer treatment. The elevation in cancer-specific mortality among HIV-infected patients may be attributable to unmeasured stage or treatment differences as well as a direct relationship between immunosuppression and tumor progression.


PLoS ONE ◽  
2019 ◽  
Vol 14 (3) ◽  
pp. e0213209 ◽  
Author(s):  
Alok A. Khorana ◽  
Katherine Tullio ◽  
Paul Elson ◽  
Nathan A. Pennell ◽  
Stephen R. Grobmyer ◽  
...  

2019 ◽  
Vol 96 (2) ◽  
pp. 121-123 ◽  
Author(s):  
Jami S Leichliter ◽  
Patricia J Dittus ◽  
Casey E Copen ◽  
Sevgi O Aral

ObjectivesWithin the context of rising rates of reportable STIs in the USA, we used national survey data to examine temporal trends in high-risk factors that indicate need for STI/HIV preventive services among key subpopulations with disproportionate STI rates.MethodsWe used data from the 2002 (n=12 571), 2006–2010 (n=22 682) and 2011–2015 (n=20 621) National Survey of Family Growth (NSFG). NSFG is a national probability survey of 15–44 year olds living in US households. We examined STI risk factors among sexually active men who have sex with men (MSM) and Hispanic, non-Hispanic black, 15–19 year old, 20–24 year old, and 25–29 year old women who have sex with men (WSM) and men who have sex with women (MSW). Risk behaviours included: received money or drugs for sex, gave money or drugs for sex, partner who injected drugs, partner who has HIV, non-monogamous partner (WSM, MSW only) and male partner who had sex with other men (WSM only). Endorsement of any of these behaviours was recoded into a composite variable focusing on factors indicating increased STI risk (yes/no). We used chi-squares and logistic regression (calculating predicted marginals to estimate adjusted prevalence ratios (aPRs)) to examine STI risk factors over time among the key subpopulations.ResultsFrom 2002 to 2011–2015, reported STI risk factors did not change or declined over time among key subpopulations in the USA. In adjusted analyses comparing 2002 to 2011–2015, we identified significant declines among WSM: Hispanics (aPR=0.84 (0.68–1.04), non-Hispanic blacks (aPR=0.69 (0.58–0.82), adolescents (aPR=0.71 (0.55–0.91) and 25–29 year olds (aPR=0.76 (0.58–0.98); among MSW: Hispanics (aPR=0.53 (0.40–0.70), non-Hispanic blacks (aPR=0.74 (0.59–0.94) and adolescents (aPR=0.63 (0.49–0.82); and among MSM (aPR=0.53 (0.34–0.84).ConclusionsWhile reported STIs have increased, STI risk factors among key subpopulations were stable or declined. Condom use related to these risk factors, sexual mixing patterns and STI testing should be examined.


PLoS ONE ◽  
2019 ◽  
Vol 14 (4) ◽  
pp. e0215108
Author(s):  
Alok A. Khorana ◽  
Katherine Tullio ◽  
Paul Elson ◽  
Nathan A. Pennell ◽  
Stephen R. Grobmyer ◽  
...  

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 1747-1747
Author(s):  
Susan O'Brien ◽  
Andrew John Davies ◽  
Ian W. Flinn ◽  
Ajay K Gopal ◽  
Thomas J. Kipps ◽  
...  

Abstract BACKGROUND Chronic lymphocytic leukemia (CLL) and indolent non-Hodgkin lymphoma (iNHL) are B-cell malignancies associated with neutropenia, anemia and thrombocytopenia.The etiology of impaired hematopoiesis is not well understood, however the bone marrow leukemia/lymphoma cell infiltrates that often occur with these diseases is thought to contribute. In studies evaluating the selective PI3Kd inhibitor idelalisib (IDL) in B-cell malignancies, hematologic responses across all 3 lineages were observed in a majority of patients (pts) with baseline (BL) cytopenias. This post hoc analysis reports hemogram changes in pts with relapsed or refractory (R/R) CLL/iNHL treated with IDL in two pivotal studies and describes trends in hematologic parameters over time during IDL treatment in pts with or without BL cytopenias. METHODS In phase 3 study 312-0116 (NCT01539512), frail pts with R/R CLL were randomized to receive a combination of 8 doses of rituximab (R) with IDL 150 mg BID or placebo (P). In phase 2 study 101-09 (NCT01282424), pts with refractory iNHL received IDL 150 mg BID. In both studies, IDL was continued until disease progression (PD) or unacceptable toxicity. Trial inclusion criteria allowed enrollment of pts with BL cytopenias of any grade (CLL) or grade ˂3 (iNHL). Hematologic profiles for pts in each study were categorized as normal or abnormal (any grade of cytopenia) at BL. In the iNHL study, pts with PD at the first assessment were excluded from this analysis to avoid confounding by underlying uncontrolled disease. RESULTS A total of 345 pts participated in the 2 trials. The overall response rates of IDL-treated patients in the CLL and iNHL studies were 81% and 57%, respectively. For pts with CLL on IDL+R (n=110), BL cytopenias (grade ≥1) included anemia (76%), thrombocytopenia (62%), and neutropenia (34%). For pts with iNHL on IDL-mono (n=115), BL cytopenias included anemia (50.4%), thrombocytopenia (64.3%), and neutropenia (75.7%). We present changes in hemoglobin (Hgb), platelet (PLT), or neutrophil (ANC) counts over time (BL, peak, and time to peak) in pts with an abnormal BL hemogram in Table 1. Median hematologic lab values over time were unchanged in pts with normal hemograms at BL. Among patients with BL cytopenia, anemia and thrombocytopenia improved over time in pts with CLL and iNHL while on treatment with IDL. For pts with CLL, the magnitude of improvement was larger for pts in the IDL+R arm compared to those in the P+R arm. For pts in the IDL+R arm, median peak values of Hgb and PLT were observed within 6 months of IDL initiation. For pts with iNHL, median peak values for Hgb and PLT were observed within 3 months. ANC remained stable over time in CLL, and increased in iNHL. CONCLUSIONS Idelalisib treatment was associated with improvement in Hgb and PLT counts in this population of pts with R/R CLL or iNHL. In those pts with BL anemia or thrombocytopenia, peak improvement in Hgb or PLT values occurred early in treatment (≤3 months for iNHL and ≤6 months for CLL). Disclosures O'Brien: Gilead: Research Funding. Davies:Gilead: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding. Flinn:Cephalon, Inc; Teva Pharmaceutical Industries Ltd; Genentech, inc; Gilead: Research Funding. Gopal:Spectrum, Pfizer, BioMarin, Cephalon/Teva, Emergent/Abbott. Gilead, Janssen., Merck, Milennium, Piramal, Seattle Genetics, Giogen Idec, BMS: Research Funding; Gilead, Spectrum, Pfizer, Janssen, Seattle Genetics: Consultancy; Millennium, Seattle Genetics, Sanofi-Aventis: Honoraria. Kipps:Pharmacyclics Abbvie Celgene Genentech Astra Zeneca Gilead Sciences: Other: Advisor. Salles:Celgene Corporation; Roche and Gilead Sciences: Research Funding; Calistoga Pharmaceuticals, Inc.; Celgene Corporation; Genentech, Inc.; Janssen Pharmaceutica Products, L.P.; Roche: Consultancy; Celgene Corporation; Roche: Speakers Bureau. Newcomb:Gilead: Employment. Waldapfel:Gilead: Employment. Zhang:Gilead: Employment. Stilgenbauer:Gilead: Honoraria, Research Funding.


2014 ◽  
Vol 32 (27) ◽  
pp. 3033-3038 ◽  
Author(s):  
Mohummad Minhaj Siddiqui ◽  
Kathryn M. Wilson ◽  
Mara M. Epstein ◽  
Jennifer R. Rider ◽  
Neil E. Martin ◽  
...  

Purpose Conflicting reports remain regarding the association between vasectomy, a common form of male contraception in the United States, and prostate cancer risk. We examined prospectively this association with extended follow-up and an emphasis on advanced and lethal disease. Patients and Methods Among 49,405 US men in the Health Professionals Follow-Up Study, age 40 to 75 years at baseline in 1986, 6,023 patients with prostate cancer were diagnosed during the follow-up to 2010, including 811 lethal cases. In total, 12,321 men (25%) had vasectomies. We used Cox proportional hazards models to estimate the relative risk (RR) and 95% CIs of total, advanced, high-grade, and lethal disease, with adjustment for a variety of possible confounders. Results Vasectomy was associated with a small increased risk of prostate cancer overall (RR, 1.10; 95% CI, 1.04 to 1.17). Risk was elevated for high-grade (Gleason score 8 to 10; RR, 1.22; 95% CI, 1.03 to 1.45) and lethal disease (death or distant metastasis; RR, 1.19; 95% CI, 1.00 to 1.43). Among a subcohort of men receiving regular prostate-specific antigen screening, the association with lethal cancer was stronger (RR, 1.56; 95% CI, 1.03 to 2.36). Vasectomy was not associated with the risk of low-grade or localized disease. Additional analyses suggested that the associations were not driven by differences in sex hormone levels, sexually transmitted infections, or cancer treatment. Conclusion Our data support the hypothesis that vasectomy is associated with a modest increased incidence of lethal prostate cancer. The results do not appear to be due to detection bias, and confounding by infections or cancer treatment is unlikely.


Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 3148-3148
Author(s):  
Elizabeth Kander ◽  
Qiuhong Zhao ◽  
Tracy Wiczer ◽  
John C. Byrd ◽  
Jennifer A. Woyach ◽  
...  

Abstract BACKGROUND: Ibrutinib is an irreversible inhibitor of BTK in the B-cell receptor signaling cascade and is widely used to treat chronic lymphocytic leukemia (CLL) and other B-cell malignancies. Ibrutinib also inhibits the tyrosine kinase Tec in platelets, which may be one of the mechanisms of its bleeding toxicity. This makes concomitant use of anticoagulation (AC) or antiplatelet agents challenging, which is a common delimma as many patients taking ibrutinib are elderly and have increased risks of venous and arterial thromboses. The incidence of thrombosis in patients taking ibrutinib is unknown, and we hypothesized that the risk of thrombosis may be reduced during ibrutinib treatment. Therefore, we conducted a single-institution retrospective cohort study to determine the incidence and type of both arterial and venous thromboses during ibrutinib treatment and their management. METHODS: We reviewed medical records of all patients treated with ibrutinib for a hematological malignancy at the Ohio State University between 6/1/2010 and 3/31/2016. Baseline patient and disease characteristics were captured at time of starting ibrutinib. All thrombotic events occurring at any time during treatment with ibrutinib and within three days of its discontinuation were recorded. Time to thrombosis was calculated from the date of starting ibrutinib to the date of thrombosis or censored at the last assessment date, treating discontinuation of ibrutinib or death prior to thrombosis as competing risks. The cumulative incidence of thrombosis was estimated and the Fine and Gray regression models accounting for competing riskes were used to examine the association between patient characteristics and risk of thrombosis. RESULTS: The cohort included 565 patients. Median age was 65 (range 23->89) years and 70.3% (397/565) were men. The majority of patients had CLL (73.6%, 416/565). Other diagnoses included mantle cell lymphoma (9.9%, 56/565), indolent B-cell malignancies (8.1%, 46/565), and aggressive lymphomas (8.3%, 47/565). Median number of prior treatments was 3 (range 0-18) and 6.5% (37/565) of patients were treatment naïve. Prior to ibrutinib, 144 of 565 patients (25.5%) had a history of thrombosis. Sixty-four (11.3%, 64/565) patients had only venous thromboses, 66 (11.7% 66/565) had only arterial thromboses, and 14 patients had both. Concurrently with ibrutinib, 193 (34.2%) patients received antiplatelet agents, 16 (2.8%) patients received AC, and 31 (5.5%) patients received both. Total ibrutinib exposure for the cohort was 1,429 person-years with a median exposure of 2.39 (range 0-7.36) years per patient. A second antineoplastic agent was given with ibrutinib in 30.8% (174/565) of cases, including an immunomodulatory drug in 24 (4.2%, 24/565) patients. During ibrutinib treatment, 22 of 565 (3.9%) patients experienced 24 acute thrombotic events, mostly arterial (Table 1). The incidence of thrombosis was 1.7 (95% CI 1.1-2.5) per 100 person-years of ibrutinib exposure. Of the venous thromboses, 87.5% (7/8) were deep vein thromboses and developed at a median of 7.5 (range 0.5-75.3) months after starting ibrutinib. Of the arterial thromboses, the majority were acute cerebrovascular accidents (37.5%, 6/16) and developed at a median of 27.4 (range 0.4 - 56.6) months after starting ibrutinib. Thrombosis treatment is summarized in Table 1. After thrombosis, ibrutinib was discontinued or held in the majority of cases (75%, 18/24). One patient developed a recurrent thrombosis while on ibrutinib and AC. There were six bleeding events, 3 major (based on ISTH criteria) and 3 minor: all were taking ibrutinib and most were on AC (2 patients on antiplatelet, 1 on AC, 2 on both, 1 on neither). On univariable analysis, the only factors associated with significant (p<0.05) and substantial (HR >2) increased risk of venous thrombosis were prior venous (HR 4.73, CI: 1.06-21.11) and arterial (HR 15.66, CI: 3.07-79.87) thromboses. Antiplatelet use was not significantly associated with either thrombus type. CONCLUSIONS: The cumulative incidence of thrombosis during ibrutinib treatment was low (1.7 per 100 person-years), with the majority being arterial. Prior thrombosis was associated with increased venous thrombosis risk. There are more bleeding than thrombotic complications after patients develop thromboses on ibrutinib, and optimal treatment strategies for this population requires further investigation. Disclosures Kander: AstraZeneca: Consultancy. Wang:Daiichi Sankyo: Consultancy, Other: Travel.


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