Plasma beta endorphin in cirrhosis and renal failure

Article Abstract:

Amino acids from the diet and endogenous sources (produced within the body) are synthesized into linear molecules called peptides, which range in size from two or three amino acids to hundreds of amino acids. Some of the physiological and biochemical properties of these substances are dependent on their size. It has been reported that the liver is important in the degradation of relatively small peptides (with less than eight amino acids), and that levels of oligopeptides such as methionine and leucine encephalon are increased in patients with degenerative liver diseases such as hepatitis. The role of the liver in the metabolism of larger peptides is not as well characterized. To investigate how the liver affects the metabolism of the larger peptide beta endorphin (with 31 amino acids), levels of this peptide were measured in the blood of patients with severe cirrhosis, mild cirrhosis, and kidney failure (the kidney is important in the excretion of peptides into the urine). Groups of patients with unrelated diseases and healthy controls were also assessed. Blood concentrations of beta endorphin were not altered at all in patients with either severe or mild cirrhosis, nor were they different in the patients with nonliver disease and healthy controls. However, levels of beta endorphin were increased more than two-fold in patients with chronic kidney failure, as would be expected, inasmuch as other peptides of similar size are known to be excreted from the blood into the urine. Hence, the liver seems to play a much less important role in the elimination of larger peptides such as beta endorphin than it does with smaller molecules. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Peptides, Chronic kidney failure, Beta-endorphin, Beta endorphin

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Incidence of large oesophageal varices in patients with cirrhosis: application to prophylaxis of first bleeding

Article Abstract:

The increase in size of large varices, or twisted, dilated veins, in the esophagus of patients with chronic cirrhosis of the liver is often an event signalling the onset of variceal bleeding. It has been suggested that administration of beta blockers can prevent or delay the onset of this bleeding in cirrhotic patients with varices, but often the first indication of varices is the bleeding, which is fatal in one out of three first-time episodes. Thus, it is important to know the rate of development of varices in cirrhotic patients, and the factors associated with this development. A prospective study was carried out in 84 patients diagnosed as having cirrhosis of the liver. The patients were predominantly male alcoholics, and their average age was 54 years. Endoscopic evaluation (viewing the inner surface of the esophagus with a fiberoptic viewing device) was performed at the onset of the study, and at least one additional time from 1 to 36 months later. The follow-up evaluations indicated that patients with no or moderate varices had a 31 percent or 70 percent likelihood, respectively, of developing large varices within a two-year period. Based on the estimation of a 10 percent risk of developing bleeding varices with no medical intervention, it is recommended that cirrhotic patients with no varices be screened endoscopically every other year, while those with moderate varices should be screened annually. (Consumer Summary produced by Reliance Medical Information, Inc.)

Care and treatment, Prevention, Complications and side effects, Gastrointestinal bleeding, Gastrointestinal hemorrhage, Esophageal varices

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Nodular regenerative hyperplasia mimicking cirrhosis of the liver

Article Abstract:

A case is reported of a 47-year-old man with symptoms of liver cirrhosis, a chronic degenerative liver disease. The patient had a history of a kidney disorder and a submassive liver necrosis (cell death) of unknown cause, from which he had recovered. Between the ages of 45 and 47, the patient had episodes of hepatic encephalopathy (nervous system impairment caused by liver failure) often associated with peritonitis (bacterial infection of the abdominal wall). He also had poor function of the portal vein, which carries blood from the abdominal organs to the liver. The patient was given a liver transplant, and analysis of the diseased liver showed nodular regenerative hyperplasia (NRH) rather than cirrhosis. Branches of the portal vein showed evidence of old clots. NRH is distinguished by multiple nodules, containing both hyperplastic (overgrown) and atrophic (wasting) liver cells, which spread throughout the liver. Central liver veins, important for liver function, may be absent or closed, but the fibrosis or inflammation typical of cirrhosis is not present. The patient's symptoms, including encephalopathy, were not typical of NRH. It is possible that the old liver disease resulted in portal vein clotting, which probably contributed to the medical picture. The study points out that medical diagnosis without cellular studies of the diseased liver can be misleading. (Consumer Summary produced by Reliance Medical Information, Inc.)

Diagnosis, Liver diseases, Liver

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