Circulating and tissue endothelin immunoreactivity in advanced atherosclerosis

Article Abstract:

The development of an atherosclerotic plaque within an artery is a complicated process involving many factors. In the progression of an atherosclerotic plaque, the endothelial cells lining the artery are damaged, and the underlying smooth muscle cells proliferate inappropriately, contributing to the obstruction of the artery. The proliferation of these smooth muscle cells might result from stimulation by growth factors or from other compounds that exert growth-factor like properties. One such substance is endothelin. Endothelin is released by endothelial cells and causes blood vessels to constrict. Laboratory experiments suggest, however, that endothelin may stimulate cell growth as well. A study was conducted to determine if endothelin might play a role in the progression of atherosclerotic plaques. Amounts of endothelin in the blood were measured in 100 normal subjects and in 40 patients with advanced atherosclerosis. The results showed that the average levels of endothelin in the patients with atherosclerosis were over twice those found in the normal subjects. Furthermore, among the patients with atherosclerosis, an impressive correlation was found between the amount of endothelin in an individual patient's blood and the number of places in the patient's body affected by atherosclerosis. It is, of course, impossible to determine from these data whether the increased amounts of endothelin contribute to the progression of the atherosclerosis or are merely a consequence of the atherosclerotic process. Nevertheless, the findings raise the possibility that growth-factor-like effects exerted by endothelin on the smooth muscle cells of damaged arteries may contribute to the progression of atherosclerosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, Development and progression, Endothelin, Atherosclerosis

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Long-term outcome of hepatitis C infection after liver transplantation

Article Abstract:

Liver transplant recipients with hepatitis C virus (HCV) infection appear to be at greater risk of liver damage than recipients without HCV infection. Cirrhosis of the liver associated with HCV infection is a major reason for liver transplantation. Researchers compared 149 HCV-infected liver transplant recipients to 623 recipients without HCV infection, obtaining liver biopsies from 39 HCV-infected and 91 uninfected recipients five years after transplantation. Although rates of survival and graft rejection were similar between the two groups after five years, the biopsies showed that the HCV-infected group had a significantly higher risk of mild to moderate chronic hepatitis and of cirrhosis. When HCV types were determined in 100 recipients, infection with HCV type 1b was significantly associated with greater damage to the transplanted liver. The extent of HLA tissue matching between donor and recipient did not appear to have an effect on liver damage.

Risk factors, Liver, Graft rejection, Liver transplantation, Liver cirrhosis, Hepatitis, Hepatitis C virus

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