Background Patients with cancer may be at high risk of adverse outcomes from SARS-CoV-2 infection. We analyzed a cohort of patients with cancer and COVID-19 reported to the COVID-19 and Cancer Consortium (CCC19) to identify prognostic clinical factors, including laboratory measurements and anti-cancer therapies. Patients and Methods Patients with active or historical cancer and a laboratory-confirmed SARS-CoV-2 diagnosis recorded between March 17-November 18, 2020 were included. The primary outcome was COVID-19 severity measured on an ordinal scale (uncomplicated, hospitalized, admitted to intensive care unit, mechanically ventilated, died within 30 days). Multivariable regression models included demographics, cancer status, anti-cancer therapy and timing, COVID-19-directed therapies, and laboratory measurements (among hospitalized patients). Results 4,966 patients were included (median age 66 years, 51% female, 50% non-Hispanic white); 2,872 (58%) were hospitalized and 695 (14%) died; 61% had cancer that was present, diagnosed, or treated within the year prior to COVID-19 diagnosis. Older age, male sex, obesity, cardiovascular and pulmonary comorbidities, renal disease, diabetes mellitus, non-Hispanic Black race, Hispanic ethnicity, worse ECOG performance status, recent cytotoxic chemotherapy, and hematologic malignancy were associated with higher COVID-19 severity. Among hospitalized patients, low or high absolute lymphocyte count, high absolute neutrophil count, low platelet count, abnormal creatinine, troponin, LDH, and CRP were associated with higher COVID-19 severity. Patients diagnosed early in the COVID-19 pandemic (January-April 2020) had worse outcomes than those diagnosed later. Specific anti-cancer therapies (e.g. R-CHOP, platinum combined with etoposide, and DNA methyltransferase inhibitors) were associated with high 30-day all-cause mortality. Conclusions Clinical factors (e.g. older age, hematological malignancy, recent chemotherapy) and laboratory measurements were associated with poor outcomes among patients with cancer and COVID-19. Although further studies are needed, caution may be required in utilizing particular anti-cancer therapies.

This study adds to the growing evidence that psychological factors contribute to IBD symptom flares. There was no support for differential rates of use of NSAIDS, antibiotics, or for the occurrence of (non-enteric) infections related to IBD flares.

Non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics, enteric or other systemic infections, and stress have all been reported to be potential triggers of inflammatory bowel disease (IBD). Although a mechanism of triggering a flare of IBD can be hypothesized for each factor, the associations of these factors with flares of IBD remains confusing. In this review, we analyze the literature that explores these associations. There is some evidence to support an association between NSAID use and flares but little data to associate antibiotic use directly with flares. An important connection between antibiotic use and an exacerbation of symptoms is through the development of Clostridium difficile infections. However, for all enteric infections, including C. difficile, it is unclear whether these infections simply trigger symptoms in patients with IBD that resolve on resolution of the infection, or whether they truly trigger a flare of intestinal inflammation that outlasts the infection. There is a paucity of evidence that other systemic infections trigger flares of IBD. Although there is strong evidence for an association between perceived stress levels and flares, there is a weaker association between a simple accounting of stressful life events and flares. Much of the literature is limited by a lack of adequate control groups and failure to report on base rates in the population under study (i.e., NSAIDs and antibiotic use, occurrence of infections, and stress levels). More large population-based matched cohort or case crossover studies and a continued emphasis on prospective designs are needed to better explore these potential associations. Clinical implications given the current state of knowledge are discussed.

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