Brian W. Christman

TL;DR: Pulmonary arterial hypertension has a multifactorial pathobiology and recent genetic and pathophysiologic studies have emphasized the relevance of several mediators in this condition, including prostacyclin, nitric oxide, ET-1, angiopoietin- 1, serotonin, cytokines, chemokines, and members of the transforming-growth-factor-beta superfamily.

TL;DR: An increase in the release of the vasoconstrictor thromboxane A2, suggesting the activation of platelets, occurs in both the primary and secondary forms of pulmonary hypertension.

TL;DR: Treatment with ibuprofen reduces levels of prostacyclin and thromboxane and decreases fever, tachycardia, oxygen consumption, and lactic acidosis, but it does not prevent the development of shock or the acute respiratory distress syndrome and does not improve survival.

TL;DR: The NF-kappa B pathway represents an attractive therapeutic target for strategies to control neutrophilic inflammation and lung injury and treatment with the antioxidant N-acetylcysteine 1 h before endotoxin resulted in decreased lung NF- kappa B activation in a dose-dependent manner and diminished cytokine-induced neutrophil chemoattractant mRNA expression in lung tissue.

TL;DR: The treating physician needs to be vigilant in diagnosing and treating bacterial infections in cirrhosis early, in order to prevent the development and downward spiral of the sepsis syndrome.