Prevalence Of Anemia In Patients With Pancreas, Liver And Biliary Cancers And Their Relationship With The Inflammatory Response

Thomé, M.G. Serna; Rosciano, A.E. Padilla; Pablo, Pedro Alberto Mendoza; Basave, Horacio Noe Lopez; Matus, Rolando García

doi:10.1016/j.hpb.2019.10.2367

Cited by 2 publications

(1 citation statement)

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“…[104][105][106] In patients with PDAC, iron deficiency rates of 60% and anemia rates of 30% at diagnosis have been reported. [105][106][107][108] Chemotherapy can cause or worsen anemia. PDAC patients are regularly treated with chemotherapy regimens containing one or more of the following chemotherapeutic agents; 5-fluorouracil, gemcitabine, irinotecan, nab-paclitaxel, and oxaliplatin, for which anemia incidences around 80 to 90% have been found.…”

Section: Red Blood Cellsmentioning

confidence: 99%

Cellular Components Contributing to the Development of Venous Thrombosis in Patients with Pancreatic Cancer

Willems,

Biesmans,

Campello

et al. 2023

Semin Thromb Hemost

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Pancreatic ductal adenocarcinoma (PDAC) is an aggressive type of cancer and has a poor prognosis. Patients with PDAC are at high risk of developing thromboembolic events, which is a leading cause of morbidity and mortality following cancer progression. Plasma-derived coagulation is the most studied process in cancer-associated thrombosis. Other blood components, such as platelets, red blood cells, and white blood cells, have been gaining less attention. This narrative review addresses the literature on the role of cellular components in the development of venous thromboembolism (VTE) in patients with PDAC. Blood cells seem to play an important role in the development of VTE. Altered blood cell counts, i.e., leukocytosis, thrombocytosis, and anemia, have been found to associate with VTE risk. Tumor-related activation of leukocytes leads to the release of tissue factor-expressing microvesicles and the formation of neutrophil extracellular traps, initiating coagulation and forming a scaffold for thrombi. Tissue factor-expressing microvesicles are also thought to be released by PDAC cells. PDAC cells have been shown to stimulate platelet activation and aggregation, proposedly via the secretion of podoplanin and mucins. Hypofibrinolysis, partially explained by increased plasminogen activator inhibitor-1 activity, is observed in PDAC. In short, PDAC-associated hypercoagulability is a complex and multifactorial process. A better understanding of cellular contributions to hypercoagulability might lead to the improvement of diagnostic tests to identify PDAC patients at highest risk of VTE.

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