Liver vascular lesions

The liver shows the following types of toxic response steatosis (fatty liver), cytotoxic damage, cholestatic damage, cirrhosis, vascular lesions, liver tumors, and proliferation of peroxisomes. 

An interesting report by P an and Jegier noted an increase in serum trypsin protein esterase in association with pulmonaiy vascular lesions in rabbits chronically exposed to ozone at 0.4 ppm. This serum a,-macroglobulin, which is synthesized in the liver, has been reported to be increased in human vascular disorders, but its physiologic significance is unknown. 

Figure 15-4 In silico subtraction method for mechanistic study to compare the hepatic gene expression profile induced by compound X to other compounds that induce hepatic APR secondary to inflammation at sites other than the liver. In the proposed simple model, compound X-induced gene expression change has two components. One is vasculitis specific the other is acute phase response (APR) specific. By subtracting the APR specific component, we might select candidate genes that are specifically associated with the hepatic vascular lesion Diclofenac known to induce APR without triggering vasculitis in liver is used to subtract genes activated by hepatic APR from the compound X response.

CHRONIC HEALTH RISKS irritation of skin and mucous membranes dermatitis rhinitis pharyngitis conjunctivitis skin lesions hyper-pigmentation gangrene of the extremities vascular lesions exfoliation herpes appearance of small corns or warts increased risk of nonmelanoma skin cancer lung cancer bladder and liver cancer tumors of mouth, esophagus, larynx, bladder, para nasal sinus liver or kidney damage lower than normal birth weights. 

Fig. 17.1a,b. Angiosarcoma. Ultrasound findings, a Documentation of two hypoechoic lesions (arrows) in the liver with cystic areas and dorsal increased signal in B-mode imaging, h Color coded imaging refers to central non-vascular lesions (arrows) with hypervascularity in the periphery of the lesions and feeding vessels... 

Microscopic investigation of the mice from group I revealed the presence of vessel congestion, small numerous intralobular and perivenular infiltrates, moderate focal protein-hydropic degeneration combined with polymorphism of hepatocyte nuclei and inconstant lymphoid infiltration of portal tracts. Marked activation of histiomacrophage elements — hepatic macrophages must be emphasized. Homotypic moderate inflammatory alterations remained in the liver on Days 3, 5, 7 and 10. The presence of inflammatory mononuclear infiltration in the walls of central veins, typical for a viral infection, reflects a massive lesion of the vascular... 

The minimal lethal dose in mice by subcutaneous injection was 180mg/kg animals developed progressive cyanosis and dyspnea before death at autopsy there were degenerative lesions in the liver, kidneys, and other organs, with evidence of vascular damage. ... 

Exposure to allylamine in industries synthesizing pharmaceuticals and other commercial products is a known occurrence. Allylamines are known to cause adverse effects, especially to the liver, kidney, heart and/or blood vascular systems in experimental humans. It has been reported that exposure to methyl-, ethyl-, heptyl-, and allylamines results in severe pathologic lesions of the above-mentioned vital organs in animals and humans.72 High doses of allylamines are always associated with the induction of fatal cardiovascular injury.72,73... 

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