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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review of morbidity and mortality studies bearing on the hazards to physical health of chronic heavy alchol use indicates that such use carries a risk of premature death greatly exceeding normal expectancy. While the life style typical of many heavy drinker contributes to this risk, the effects of alcohol per se account for a substantial part of the excess mortality. The lowest level of consumption at which there is a significant increase in the death rate has yet to be determined. It is certainly below 120 g/day- the lower limit of consumption of most clinical alcoholics-and quite possibly below 35-60g: levels which appear to carry an increased likelihood of cirrhosis and certain cancers. On the other hand, the mortality experience of drinkers commonly identified as 'moderate' in the literature does not seem to differ notably from that of life-long abstainers. The relationship between heavy drinking and elevated mortality is exhibited in populations at large by the generally close covariation of cirrhosis death rates and per capita alcohol sales. There are also indications of co-variation between the latter and the excess of male over female general mortality in the middle age range.
Drug Alcohol Depend 1975 Sep
PMID:Heavy alcohol consumption and physical health problems: a review of the epidemiological evidence. 79 60

Derangements in glucose, amino acid and protein metabolism in patients with liver cirrhosis were examined with special reference to plasma levels of human growth hormone (HGH). Changes in blood glucose, IRI (immunoreactive insulin), HGH, FFA (free fatty acid) and plasma free amino acid levels were determined in controls and patients following either oral glucose load, protein feeding or intravenous arginine infusion. 1) In patients with liver cirrhosis, incidence of glucose intolerance after glucose tolerance test (GTT) was high and IRI levels were elevated in the fasting state as well as after glucose, protein or arginine loads. 2) Fasting levels of blood HGH were significantly higher in liver cirrhosis than in controls. GTT revealed that blood HGH levels decreased slightly during the rising phase of blood glucose, and conversely, increased during the falling phase of glucose (180 minutes after the glucose load) both in controls and in patients. In cirrhotic patients, marked increases in HGH levels were observed both 120 minutes after the protein load and 60 minutes after the arginine infusion. 3) Fasting levels of serum FFA were significantly higher in liver cirrhosis than in controls. Both controls and patients, however, showed a similar pattern of change in FFA levels following GTT or protein ingestion, i.e. a minimum value 120 minutes after the load and a gradual increase thereafter. 4) Fasting levels of plasma free amino acids were significantly higher in cirrhotic patients than in controls. After the glucose load, however, slight decrease was noted in some amino acid levels. All the amino acid levels examined were elevated following protein ingestion, particularly in cirrhotic patients. 5) A positive correlation was demonstrated in cirrhotic patients between total plasma free amino acids and maximal HGH responses following protein ingestion. Similar significant correlations were observed between the maximal HGH response and the plasma level of several amino acids such as His., Ser., Gly., Thr., Ala., and Ileu., respectively. 6) In cirrhotic patients, negative correlations were demonstrated between fasting levels of serum albumin and total plasma free amino acids or maximal HGH responses, respectively, after the protein ingestion. From these results it was inferred that derangements in the metabolism of protein and amino acids in cirrhotic patients may result in an increase in plasma free amino acid level which in turn stimulates HGH secretion. It was surmised that the HGH levels so elevated in the patients may cause FFA mobilization which in effect results in the glucose intolerance.
Hokkaido Igaku Zasshi 1975 Sep
PMID:[Studies on glucose, amino acid and protein metabolism in patients with liver cirrhosis in relation to plasma levels of human growth hormone (author's transl)]. 81 50

On the serum of 3790 patients (2131 women and 1659 male), aged from 3 days to 84 years, the RAC has been performed at the same time with the Mc Lagan's Kunkel's and Takata's reactions. The test of sulfobromophthalein's excretion has been performed in 246 of these patients. Between RAC and T.D., disagreement has been observed in 111 cases (- 2,9%). RAC positive and T.D. negative occurred in 68 cases; T.D. positive and RAC negative in the other 43. Repetition of the RAC on 100 sera (after complement inactivation at 56 degrees C for 30 min; after permanence at 4 degrees C for 7 days; after congealment at -18 degrees C) has always given the same results obtained on fresh sera. The complement, therefore, has no way influence on the RAC. The study of disagreeing cases has shown the RAC become positive for: 1) an apperance in serum of abnormal lipoproteins (chloestasis, cholangitis, some dislipemias), 2) a rise in gamma-M (biliary cirrhosis, macroglobulinaemia, lymphatic chronic leukema); 3) 1 and 2. It is always necessary to perform T.D. and RAC on the same serum, because these two test express different modification of the serum-proteins picture. Their agreement, or their disagreement, is very important in every single case, particularly in the diagnostic of jaundice and of bilary ducts pathology.
Quad Sclavo Diagn 1976 Sep
PMID:[On the chloranilic acid reaction (RAC) proposed by Closs (author's transl)]. 82 64

A specific, sensitive, and reproducible radioimmunoassay for human plasma thromboplastin antecedent (PTA, factor XI) has been developed with purified PTA and monospecific rabbit antiserum. Precise measurements of PTA antigen were possible for concentrations as low as 0.3% of that in normal pooled plasma. Normal plasma contained approximately 6 microgram PTA/ml. A good correlation (correlation coefficient 0.68) existed between the PTA procoagulant assays and radioimmunoassays among 50 normal adults (25 males and 25 females). PTA antigen was markedly reduced in plasma of 13 patients with congenital homozygous PTA deficiency (range less than 0.003-0.128 U/ml) and 9 patients with hepatic cirrhosis (0.35+/-0.17 U/ml), but was normal in those of 9 patients under treatment with warfarin, 8 patients with disseminated intravascular coagulation and 16 patients with other congenital clotting factor abnormalities, including prekallikrein deficiency (Fletcher trait) and high molecular weight kininogen deficiency (Fitzgerald trait).
Blood 1977 Sep
PMID:Plasma thromboplastin antecedent (PTA, factor XI): a specific and sensitive radioimmunoassay. 88 16

The peritoneovenous shunt of LeVeen can be safely performed under local anesthesia in patients with advanced cirrhosis and ascites. The results of the technique described have proved satisfactory in 25 diuretic resistant ascites in selected patients. The rapid, downhill course of the patient with severe hepatic encephalopathy or coma is probably unchanged by the presence of the valve. Eighteen surviving patients discharged with shunts in place are under continuing study.
Surg Gynecol Obstet 1977 Sep
PMID:Peritoneovenous shunting for ascites. 88 64

Two patients with hepatorenal syndrome were treated by insertion of a peritoneovenous shunt. The renal deficit was corrected rapidly in both cases. A 62-year-old woman with a slow onset syndrome with urine output of 100 to 150 ml/day and urinary sodium excretion of 1 mEq/day responded with large volume urinary output and sodium excretion. She is alive with minimal ascites 18 months after shunt. A 53-year-old man with severe nutritional cirrhosis, alcoholic hepatitis, and eventual massive necrosis was treated for bleeding esophageal varices by portacaval shunt. Postoperative massive ascites progressed to acute hepatorenal syndrome. Insertion of a peritoneovenous shunt reversed the renal deficit. HE eventually exsanguinated due to a hemorrhagic diathesis caused by massive hepatic necrosis.
Surgery 1977 Sep
PMID:Hepatorenal syndrome: reversal by peritoneovenous shunt. 88

A syndrome characterized by hypoxemia aggravated by exercise, orthodeoxia, hypocapnia, and evidence of hyperdynamic circulation, but otherwise normal indices of pulmonary air flow, volume, and distribution of ventilation has been observed as an infrequent complication of hepatic cirrhosis. An illustrative case is described, the features of which support the presence of a shunt or shunt-like mechanism consisting of low-resistance vascular communications within the lung. We suggest that this may represent the existence of a hepatopulmonary syndrome analogous to the hepatorenal syndrome.
Chest 1977 Sep
PMID:Exercise-aggravated hypoxemia and orthodeoxia in cirrhosis. 89 Dec 82

Endotoxin was measured by the Limulus assay in plasma and ascites in 46 patients with cirrhosis having demonstrable esophageal varices, of whom 29 had ascites and 17 did not. It was positive in ascitic fluid in 23 (79.3%) of the former group. In plasma, a positive test was obtained in 22 (75.9%) in the group with ascites and only 4 (23.5%) without ascites, the difference being significant (P less than 0.01). Of the 23 positive ascites specimens, 17 showed high titers (greater than or equal to 10(-3) microgram per ml). Hepatic uptake of 198Au colloid was markedly reduced in 11 of the 17 patients with endotoxemia who were studied by scanning. Death occurred within 6 months in 47.8% of the patients with a positive endotoxin test, whereas only 16.7% of those with a negative test died in the same period (P less than 0.05). No hypotension was noted in patients with toxemia and only 2 ran a fever above 37.5 degrees C. Development of tolerance to endotoxin is suspected. A follow-up study has demonstrated sustained endotoxemia in some of these patients.
Gastroenterology 1977 Sep
PMID:Detection of endotoxin in plasma and ascitic fluid of patients with cirrhosis: its clinical significance. 89 53

Transition from acute to chronic hepatitis has important prognostic and therapeutic implications. In 17 patients with acute viral hepatitis, observed during a period of 7 years, a liver biopsy showed changes compatible with chronic aggressive hepatitis and superimposed acute hepatitis. Follow-up biopsies showed normal liver in 14 cases, chronic persistent hepatitis in 1, and cirrhosis in 2. In 12 cases the initial biopsy which showed changes suggestive of chronicity was taken 1 month after onset of symptoms of acute hepatitis, or later. Cases developing chronic liver disease showed no characteristic clinical, laboratory, or histological features at the time of the first biopsy. If the diagnosis of chronic active hepatitis is based on histological findings alone in patients with prolonged acute hepatitis, the incidence of this condition will be grossly overestimated. The transition from acute to chronic hepatitis cannot be recognized with any degree of certainty by presently available methods.
Gastroenterology 1977 Sep
PMID:Significance of suspected "chronic aggressive hepatitis" in acute hepatitis. 89 54

A 61-year-old female presented with a right transudative pleural effusion in the absence of ascites and other stigmata of chronic liver disease. A diagnosis of cirrhosis with a secondary hydrothorax was eventually established; however, ascites could never be demonstrated clinically or radiographically until just before her death, when hypertonic saline was administered for symptomatic hyponatremia. Based on the autopsy finding of a 1-mm hole in the right diaphragm and her clinical course, a mechanism for the production of a cirrhotic pleural effusion in the absence of asictes is proposed.
Gastroenterology 1977 Sep
PMID:Cirrhotic pleural effusion in the absence of ascites. 89 57


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