Abstract 1767P
Background
There is growing evidence that cancer patients may be more susceptible to contracting coronavirus disease 2019 (COVID-19) infection, show a more aggressive course and associate a poorer prognosis than the general population. An unbalanced inflammatory response and systemic coagulopathy seem to define the pathological hallmark underlying severe presentations. However, the complex immune cell interplay and the role of the tumor-associated pro-coagulative state in COVID-19 remain a challenge.
Methods
We prospectively evaluated cancer patients presenting to the emergency department of the Hospital Clínico San Carlos (Madrid, Spain) with severe pneumonia, and compared a comprehensive coagulation and immunological profile from blood samples on admission between those with SARS-CoV-2 positive and negative RT-PCR tests.
Results
14 patients with suspected COVID-19 and receiving in-hospital care were prospectively followed. SARS-CoV-2 RT-PCR was positive on admission in 6 patients, and negative on admission and on re-test in 8 patients. Peripheral blood samples were drawn on admission. In spite of the modest sample size, patients with SARS-CoV-2 positive showed higher levels of D-dimer (median 6,355 vs. 1,964 ng/ml, p=0.025), a decreased CD4+/CD8+ ratio (1.2 vs. 2.2, p=0.17) at the expense of CD4+ T lymphocytopenia (305 vs. 467, p=0.18), and NK cell expansion (17 vs. 9%, p=0.13). Several monocyte activation markers were found to be elevated in RT-PCR positive patients, including CD86 (2.8-fold increase in classic monocytes, p=0.06) and CCR2 (2.9-fold in intermediate monocytes, p=0.17; 11-fold in non-classic monocytes, p=0.03).
Conclusions
In cancer patients presenting with severe SARS-CoV-2 positive pneumonia, the infection may cause a hypercoagulable state, as suggested by higher levels of D-dimer, and unleash a pro-inflammatory response. Marked CD4+ T lymphocytopenia and NK expansion may reflect lymphocyte exhaustion and dysregulated cytotoxicity. Monocyte activation and recruitment also seem to be strongly upregulated.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
Hospital Clínico San Carlos.
Funding
Cris Cancer Foundation.
Disclosure
All authors have declared no conflicts of interest.