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Chronic Inflammation Resources

The role of chronic inflammation in wellness and the development and progression of chronic disease is becoming more evident every day. Information sources from peer-reviewed medical publications to social media continue to be filled with new information. We are dedicated to sharing information pertaining to chronic inflammation from reliable sources.

First Experience Addressing the Prognostic Utility of Novel Urinary Biomarkers in Patients With COVID-19

"Urinary 11-dh-TxB2 is a marker of whole-body inflammation and TxA2 biosynthesis contributed by platelet, leukocytes, and endothelial cells [5]."

"Among COVID-19 patients in our study, we found significantly elevated levels of u11-dh-TxB2 in patients with events compared with patients without events, and higher u11-dh-TxB2 levels were associated with prolonged hospitalization, death, and mechanical ventilation requirement. These observations highlight the potential prognostic utility of u11-dh-TxB2 in patients with COVID-19. This is in line with the observations of systemic cytokine storm, endothelial dysfunction, and elevated thrombotic risk in COVID-19."

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Targeting the eicosanoid pathway in hepatocellular carcinoma

"The role of inflammation has long been recognized as one of the major factors contributing to initiation and progression of various solid and non-solid malignancies, including hepatocellular carcinoma.  Studies in humans have consistently shown that COX-2 and PGE2 play an oncogenic role in hepatocellular carcinoma."

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Aspirin triggers antiinflammatory 15-epi-lipoxin A4 and inhibits thromboxane in a randomized human trial

"Local aspirin-triggered 15-epilipoxinA4 production may not only account for aspirin’s anti-inflammatory and antineutrophil actions in vivo, but could be a sensitive new means to directly assess aspirin as well as other acetylation-based anti-inflammatory treatments."

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Aspirin blocks formation of metastatic intravascular niches by inhibiting platelet-derived COX-1/thromboxane A2

"COX-1 activity and Thromboxane A2 production in platelets contribute to the generation of a permissive early metastatic niche.  Aspirin reduces metastasis through the inhibition of platelet COX-1 and its product Thromboxane A2."

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Abstract 34: High urinary thromboxane B2 associates with lethal prostate cancer in African American men and inversely correlates with aspirin use

"Systemic low-grade inflammation is a candidate risk factor for prostate cancer in African American men, potentially contributing to lethal prostate cancer development.  Men with high urine thromboxane B2 were more likely to be diagnosed with prostate cancer metastasis compared to men with low urine thromboxane B2.  In this study, high urine thromboxane B2 was associated with all-cause mortality and prostate cancer mortality in African American men. Aspirin may reduce lethal prostate cancer in African American Men."

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International COVID-19 thrombosis biomarkers colloquium: COVID-19 diagnostic tests

"The stable urinary metabolite of thromboxane A2 (TxA2), urinary 11-dehydro thromboxane B2 (u 11-dh TxB2) has been used as a marker of platelet activation and also response to aspirin therapy. U 11-dh TxB2, in addition to platelet COX-1 activity, also reflects a low-grade inflammatory process of atherosclerosis and activation of inflammatory white cells thus reflecting the whole-body inflammatory state [35]. "

"... an inadequate therapeutic aspirin response (> 1520 pg/mg creatinine) was observed in 91% of COVID-19 patients on 81 mg daily aspirin [18]. The frequency of thromboinflammation (> 4200 pg/mg creatinine) was highest in COVID-19 patients not on aspirin (81%) and lower on 81 mg daily (55%). "

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Bedside thromboelastography to rapidly assess the pharmacodynamic response of anticoagulants and aspirin in COVID-19: evidence of inadequate therapy in a predominantly minority population

"In COVID-19 patients, u11-dh TxB2 was lower in aspirin-treated patients than patients not on aspirin (3760 ± 2295 versus 13,125 ± 11,474 pg/mg creatinine, p = 0.003). An inadequate therapeutic aspirin response was observed in 91% of COVID-19 patients on 81 mg daily aspirin and 50% of patients on ≥ 162 mg daily aspirin (Fig. 1b). The frequency of thromboinflammation was highest in COVID-19 patients not on aspirin (81%) and lower on 81 mg daily (55%) and lowest on ≥ 162 mg daily aspirin (25%)."

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Glucocorticoids Impair Platelet Thromboxane Biosynthesis in Community—Acquired Pneumonia

“Previous reports suggest that community-acquired pneumonia (CAP) is associated with an enhanced risk of myocardial infarction (MI) and that enhanced platelet activation may play a role.  Aims of this study were to investigate if urinary excretion of 11-dehydro-thromboxane (Tx) B2, a reliable marker of platelet activation in vivo, was elevated in CAP and whether glucocorticoid administration reduced platelet activation”.
“Compared to controls, CAP patients showed significantly higher levels of 11-dehydro-TxB2.  A COX regression analysis showed that 11-dehydro-TxB2 independently predicted MI.  CAP patients treated with glucocorticoids showed significantly lower levels of 11-dehydro-TxB2 compared to untreated ones”.

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2218-PUB: Increased Platelet Reactivity Is Associated with Inflammation and Arterial Stiffness in Subjects with Prediabetes

"We investigated markers of platelet reactivity and low-grade inflammation, and their association with early markers of vascular disease in subjects with prediabetes and new onset type 2 diabetes (NDOM)."

"Platelet reactivity was evaluated as 11-dehydrothromboxane B2 urinary levels (TXB2)"

"TXB2 urinary levels were independently associated with hs-CRP, fibrinogen and HbA1c in multiple regression analysis."

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Digoxin and Platelet Activation in Patients with Atrial Fibrillation: In Vivo and In Vitro Study

"Digoxin use was shown to be associated with an increased risk of cardiovascular events in atrial fibrillation (AF). We hypothesized that digoxin may affect cardiovascular risk by increasing platelet activation. Urinary excretion of 11-dehydro-thromboxane B2 (TxB2), a marker of platelet activation, and serum digoxin concentration (SDC) were measured. Patients in the upper tertile of SDC showed higher 11-dehydro-TxB2 compared with non-digoxin users. In vitro study showed an increased basal platelet activation in patients with AF compared with healthy subjects."

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