Environmental pollution as a cause of papillary fibroelastoma: hints for a new etiological hypothesis?
Known mechanisms of cardiovascular damage generated by environmental pollution are cross linked with described papillary fibroelastomas' etiological cascade. Evidence is suggested for a common origin. These results provide intriguing but inconclusive insights into pathophysiological pathways that may link exposure to environmental pollution and development of papillary fibroelastomas.
These results provide evidence that procalcitonin acts as a modulator that augments the inflammatory response triggered by agonists like lipopolysaccharide, tumor necrosis factor-alpha, and interferon-gamma. Although not effective as a single stimulus, it might contribute to the detrimental outcome following excessive activation of the inflammatory cascade.