Continuous cardiac output and hemodynamic monitoring: high temporal correlation between plasma TNF-alpha and hemodynamic changes during a sepsis-like state in cancer immunotherapy.
Through continuous cardiac output monitoring, we investigated the temporal relationship between hemodynamic changes and plasma cytokines in a cancer patient who developed collateral sepsis to immunotherapy. A 52-year-old male with metastatic renal cell carcinoma received interleukin-2 (IL-2) infusion completing 72 h of administration. The patient developed 3 sepsis-like states including systemic inflammatory response syndrome (SIRS), shock, and multiple organ dysfunction syndrome (MODS). Hemodynamic parameters including systemic vascular resistance index (SVRI), left ventricular stroke work index (LVSWI) and cardiac index (CI) were measured over 60 h. Peripheral blood was drawn when SVRI dropped 20% in the patient and plasma cytokines including TNF-alpha, IL-6 and IL-1beta were measured using ELISA. After 60 h of immunotherapy, the patient showed a 63.4% decrease in SVRI, 54.5% decrease in LVSWI and 65.4% increase in CI. The evaluation of systemic cytokines revealed different kinetic patterns: (i) a sustained increase in TNF-alpha levels through all 3 sepsis-like states; (ii) IL-6 increased preferentially during SIRS and shock, while up/down-responses were found during MODS; (iii) IL-1beta was undetectable during the entire study period. A high temporal relationship between hemodynamic changes and plasma TNF-alpha, but not IL-6, was found. Although there are factors other than cytokines that can alter vascular resistance, this finding could represent an approach to evaluate the course of hemodynamia and probably the systemic cytokine expression after IL-2 administration in renal cancer.
Caorsi
Carlos
C
Intensive Care Unit, Clínica Las Condes, Santiago, Chile.
Quintana
Enrique
E
Valdés
Sergio
S
Muñoz
Carlos
C
D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000009:adverse effects; D002292:Carcinoma, Renal Cell / Q000150:complications / Q000473:pathology / Q000628:therapy; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D007167:Immunotherapy / Q000009:adverse effects*; D007376:Interleukin-2 / Q000008:administration & dosage / Q000009:adverse effects; D007680:Kidney Neoplasms / Q000150:complications / Q000556:secondary / Q000628:therapy; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D000970:Antineoplastic Agents; D007376:Interleukin-2; D014409:Tumor Necrosis Factor-alpha