Tumors cardiovascular system

Boekstegers, P., Weidenhofer, S., Zell, R, et al. (1994). Repeated administration of a F(ab )2 fragment of an anti-tumor necrosis factor a monoclonal antibody in patients with severe sepsis Effects on the cardiovascular system and cytokine levels. Shock la, 1237-1245. 

There is emerging evidence that OSA may be a pro-inflammatory disorder with elevated circulating cytokines [60]. Abdominal visceral fat is a major reservoir of cytokines, and obesity is a leading risk factor for the presence of OSA [60], The mechanism(s) whereby pro-inflammatory cytokines are elevated in OSA is not fully elucidated, but may be related to the excessive sympathetic nervous system activation notable in OSA. Tumor necrosis factor (TNF)-a and interleukin (IL)-6 levels are elevated in OSA [61,62] and the circadian rhythm of TNF-a is disrupted in OSA [63]. IL-6 levels are higher again in OSA patients with systemic hypertension compared to normotensive apneics [60], IL-6 levels return to normal in OSA patients treated effectively with CPAP [64]. Other mediators of inflammation elevated in OSA include intercellular adhesion molecule-1 and C-reactive protein, the latter being synthesized primarily in hepatocytes in response to IL-6 [60], The presence of these and other pro-inflammatory cytokines may link to the increased prevalence of cardiovascular morbidity in OSA. 

Finally, in addition to the issues of costs and secondary events, treatment is also lacking for many more at-risk patients who cannot undergo successful angioplasty. These patients, who may have either diffuse, nonstentable, bifurcated lesions, or multivessel disease (i.e., diabetics), are not benefiting as much from DES, and improved treatments here also remain a clear clinical need. Often there is a systemic and local activation of the immune response, followed by a consequent local vascular incident. The role of the systemic immune response in these individuals, as well as in cardiovascular patients in general, is evidenced by the numerous reports of correlation of disease with increases in plasma markers such as CRB tumor necrosis factor, and even circulating white cell counts (87-89). 

The toxicity of elliptinium in rat kidneys has been found to be dose dependent (272,273). Elliptinium induces cardiovascular effects (mainly systemic hypotension) in dogs owing to the release of histamine (vasodilation) and catecholamines (tachycardia) (274). Similar effects were found in guinea pigs (275). Speculation was raised that the antitumor properties of elliptinium may be due to an increase of histamine, since this compound is known to slow tumor growth in animals (274). 

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