International multicenter study comparing COVID-19 in patients with cancer to patients without cancer: impact of risk factors and treatment modalities on survivorship
- The University of Texas MD Anderson Cancer Center, United States
- The University of Texas Health Science Center at Houston, United States
- Hospital Israelita Albert EinsteinUniversidade Metropolitana de Santos, Brazil
- UT MD Anderson Cancer Center, United States
- Community Health Network, United States
- Gustave Roussy, Université Paris-Saclay, France
- Cooper University Health Care, United States
- Unidad de Enfermedades Infecciosas, Servicio de Medicina Interna, Hospital Universitario, Spain
- Department of Hematology Oncology, Baptist Health, United States
- Ohio Health, United States
- St. Luke's International Hospital, Japan
- Hospital Israelita Albert Einstein, Brazil
- Banner MD Anderson Cancer Center, United States
- Banner MD Anderson, United States
- Tan Tock Seng Hospital, Singapore
- Rafik Hariri University Hospital, Lebanon
- Hospital Universitario Puerta de Hierro-Majadahonda, Spain
- St. Lukes Hospital, United States
- The Catholic University of Korea, Republic of Korea
- Peter MacCallum Cancer Centre, Australia
- Houston Methodist, United States
- The University of Texas MD Anderson Cancer Center,
Abstract
Background: In this international multicenter study we aimed to determine the independent risk factors associated with increased 30-day mortality and the impact of cancer and novel treatment modalities in a large group of patients with and without cancer with COVID-19 from multiple countries.
Methods: We retrospectively collected de-identified data on a cohort of patients with and without cancer diagnosed with COVID-19 between January and November 2020, from 16 international centers.
Results: We analyzed 3966 COVID-19 confirmed patients, 1115 with cancer and 2851 nwithout cancer patients. Patients with cancer were more likely to be pancytopenic, and have a smoking history, pulmonary disorders, hypertension, diabetes mellitus, and corticosteroid use in the preceding two weeks (p≤0.01). In addition, they were more likely to present with higher inflammatory biomarkers (D-dimer, ferritin and procalcitonin), but were less likely to present with clinical symptoms (p≤0.01). By country-adjusted multivariable logistic regression analyses, cancer was not found to be an independent risk factor for 30-day mortality (p=0.18) whereas lymphopenia was independently associated with increased mortality in all patients, and in patients with cancer. Older age (≥65 years) was the strongest predictor of 30-day mortality in all patients(OR=4.47, p<0.0001). Remdesivir was the only therapeutic agent independently associated with decreased 30-day mortality ()(OR=0.64, p=0.036). Among patients on low-flow oxygen at admission, patients who received remdesivir had a lower 30-day mortality rate than those who did not (5.9% vs 17.6%; p=0.03).
Conclusions: Increased 30-day all-cause mortality from COVID-19 was not independently associated with cancer but was independently associated with lymphopenia often observed in hematolgic malignancy. Remdesivir, particularly in patients with cancer receiving low-flow oxygen, can reduce 30-day all-cause mortality.
Funding: National Cancer Institute, National Institutes of Health.
Data availability
We are unable to share the data given our restriction policy and the fact that this study includes data from 16 centers from the five continents and we have no agreement in place to share data.*Thank you for indicating that you are unable to make this data publicly available and providing some further information regarding this. Exceptions to our usual data sharing policy are subject to editorial approval, as per our data availability policy [https://submit.elifesciences.org/html/elife_author_instructions.html#policies]. To enable the editors to make an informed decision, please can you provide further information on the data sharing plan for your manuscript. This information should be added to your data availability statement (found in the Submission Information section of the submission form). Some of these points may already be covered, however please ensure that the statement covers the following:- Please provide an explanation of why the data cannot be shared.We are unable to share our data given the restrictive policy of our institution. We also do not have the permission to share data from the other institutions that participated in this study- Please describe how an interested researcher would be able to access the original data e.g. Who would they need to contact? Do they need to apply or submit a project proposal? If so, who would assess this proposal (e.g. a data access committee or IRB)? Are there any restrictions on who can access the data e.g. could commercial research be performed on the data?Given that this study involves data from 16 centers from the five continents, we have no agreement to share data.- Please provide any code or software that you have used to analyse the data.The analyses were performed using SAS version 9.3 (SAS Institute Inc., Cary, NC).- Please provide access to all materials and data for which the restrictions do not apply. For instance, would it be possible to share a deidentified version of the dataset? If not, would you be able to share processed version of the dataset e.g. an Excel sheet with numbers used to plot the graphs and charts in your manuscript?We are unable to share the data.
Article and author information
Author details
Cielito Reyes-Gibby
Anne-Marie Chaftari
Funding
National Cancer Institute
- Issam I Raad
NIH Clinical Center
- Issam I Raad
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Human subjects: This study (Protocol # 2020-0437) was approved by the institutional review board at MD Anderson Cancer Center and the institutional review boards of the collaborating centers. A patient waiver of informed consent was obtained.
Copyright
© 2023, Raad et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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International multicenter study comparing COVID-19 in patients with cancer to patients without cancer: impact of risk factors and treatment modalities on survivorship
eLife 12:e81127.
https://doi.org/10.7554/eLife.81127
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Testicular microcalcifications consist of hydroxyapatite and have been associated with an increased risk of testicular germ cell tumors (TGCTs) but are also found in benign cases such as loss-of-function variants in the phosphate transporter SLC34A2. Here, we show that fibroblast growth factor 23 (FGF23), a regulator of phosphate homeostasis, is expressed in testicular germ cell neoplasia in situ (GCNIS), embryonal carcinoma (EC), and human embryonic stem cells. FGF23 is not glycosylated in TGCTs and therefore cleaved into a C-terminal fragment which competitively antagonizes full-length FGF23. Here, Fgf23 knockout mice presented with marked calcifications in the epididymis, spermatogenic arrest, and focally germ cells expressing the osteoblast marker Osteocalcin (gene name: Bglap, protein name). Moreover, the frequent testicular microcalcifications in mice with no functional androgen receptor and lack of circulating gonadotropins are associated with lower Slc34a2 and higher Bglap/Slc34a1 (protein name: NPT2a) expression compared with wild-type mice. In accordance, human testicular specimens with microcalcifications also have lower SLC34A2 and a subpopulation of germ cells express phosphate transporter NPT2a, Osteocalcin, and RUNX2 highlighting aberrant local phosphate handling and expression of bone-specific proteins. Mineral disturbance in vitro using calcium or phosphate treatment induced deposition of calcium phosphate in a spermatogonial cell line and this effect was fully rescued by the mineralization inhibitor pyrophosphate. In conclusion, testicular microcalcifications arise secondary to local alterations in mineral homeostasis, which in combination with impaired Sertoli cell function and reduced levels of mineralization inhibitors due to high alkaline phosphatase activity in GCNIS and TGCTs facilitate osteogenic-like differentiation of testicular cells and deposition of hydroxyapatite.
