Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pigment gallstones are defined as any dark brown-to-black stone, consisting of calcium salts of bilirubin, phosphate, carbonate and other anions, and can be separated into carbonate- and noncarbonate-containing groups. Pigment stones predominate in the rural Orient, in cirrhosis, and in elderly United States patients undergoing cholecystectomy. Clinical associations include bile duct obstruction, stasis, and possibly hemolysis. Of pigment stones, 50% are radioopaque and account for two-thirds of all opaque stones. The concentrations of bile salts, phospholipids,, cholesterol, and total bilirubin in bile are similar to normal levels, but the concentration of unconjugated bilirubin is increased in the bile of some patients. Increased unconjugated bilirubin in bile may be caused by increased hydrolysis of excreted conjugated bilirubin. Unconjugated bilirubin is solubilized by bile salts, but the interaction is primarily nonmicellar. Ionized calcium and pH are important determinants of solubility. Sulfated glycoproteins, excreted in increased amounts in patients with cholelithiasis, may be the site of pigment stone precipitation because these compounds bind calcium salts tightly. E coli is frequently cultured from pigment stones in Japan but not in the United States; thus, bacterial beta-glucuronidase may be important in stone formation in Japan but probably not in the West. Stasis leads to increased calcium secretion and to increases in the concentration of sparingly soluble compounds that may then precipitate. Incomplete emptying of the gallbladder may result in the same concentration process. Unsaturated fats and chronic vagal stimulation cause pigment stone formation in animals. At present, surgery is the only treatment for pigment lithiasis.
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PMID:Pigment gallstones. 31 81

The composition of pigment gallstones from patients with and without cirrhosis was compared. Carbonate-containing pigment stones were distinguished from noncarbonate stones by infrared spectroscopy. Calcium was the major cation of each stone group. The major anion in noncarbonate pigment stones was bilirubinate or phosphate, but was carbonate in carbonate stones. The composition of pigment stones from cirrhotic and noncirrhotic patients was similar except that significantly less carbonate was present in carbonate stones, and less pigment (bilirubinate) was present in noncarbonate stones from noncirrhotics. These data suggest that irrespective of the presence of cirrhosis, the formation of noncarbonate pigment stones involves the selective precipitation of calcium bilirubinate and phosphate, whereas carbonate stone formation involves the selective precipitation of calcium carbonate.
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PMID:Pigment gallstone composition in cirrhotic and noncirrhotic subjects. 71 46

Black and brown pigment gallstones are morphologically, compositionally, and clinically distinct. Black stones form primarily in the gallbladder in sterile bile and are associated with advanced age, chronic hemolysis, alcoholism, cirrhosis, pancreatitis, and total parenteral nutrition. Brown stones form not only within the gallbladder but also within the intrahepatic and extrahepatic ducts; they are uniformly infected with enteric bacteria and are usually associated with ascending cholangitis. Brown stones are related to juxtapapillary duodenal diverticula and are the predominant type of de novo common bile duct stones. Cholecystectomy is usually curative in black pigment stone disease, whereas stones often recur after cholecystectomy for brown stone disease. The pathogenesis of black stones is probably related to nonbacterial, nonenzymatic hydrolysis of bilirubin conjugates. At the pH of bile, this results in two monohydrogenated bilirubin anions that precipitate with calcium ions. Bilirubin monoconjugates that are increased in several conditions, such as Gilbert's syndrome and chronic hemolysis, may play a pivotal role in black stone formation as a source of unconjugated monohydrogenated bilirubin and as a possible co-precipitant with calcium. The precipitation of calcium carbonate and phosphate is influenced by local gallbladder factors. Brown pigment stones are formed in bile infected with enteric bacteria that elaborate hydrolytic enzymes: beta-glucuronidase, phospholipase A, and conjugated bile acid hydrolase. The resulting anions of bilirubin and fatty acids form insoluble calcium salts. We used nb/nb mice with a chronic hemolytic anemia as a model of hemolysis-induced black stone disease. The presence of 40% bilirubin monoconjugates in mouse gallstones indicated the importance of this moiety in the pathogenesis of black stones. Other data obtained by marrow transplantation experiments in mice revealed the relative importance of genotype versus the hemolytic anemia on determinants such as biliary bile acid composition and mucin secretory glands in the mouse gallbladder neck. Additional physical chemical studies of the interaction of unconjugated bilirubin in model bile solutions will be helpful in further delineating the pathogenesis of both black and brown pigment gallstones.
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PMID:Pigment gallstone disease. 202 17

This study examined the acid base disturbances in 18 adults with acute renal failure (ARF) from one of new aspects, which is lactate metabolism and pathophysiology. 10 patients (55%) of them were accompanied by lactic acidosis and 9 patients (90%) of those with lactic acidosis also had severe hepatic failure. Mortality of patients with lactic acidosis was 80%, and much higher than that of ARF (66.7%). Lactate, pyruvate, lactate-to-pyruvate ratio (L/P) were 76.7 +/- 15.66 mg/dl, 3.30 +/- 0.74 mg/dl and 19.9 +/- 1.41, respectively. All of them significantly raised, compared to values of healthy adults, patients with liver cirrhosis, chronic renal failure and diabetes mellitus. Arterial pH and HCO3- levels were 7.20 +/- 0.04 and 10.6 +/- 1.20 mEq/l. Anion gap (AG) was 30.0 +/- 3.66 mEq/l. Significant correlations of lactate with pH, HCO3-, AG and L/P were demonstrated, while correlations of lactate with BUN, CR and prothrombin time were not significantly observed. Lactic acidosis results from two mechanisms. One is lactate overproduction (e.g tissue hypoxia) and the other is lactate underutilization (e.g severe liver and/or renal failure). Whenever lactic acidosis occurred, both mechanisms were present simultaneously and continuously. Especially, the latter mechanism had a very important role on it, and seemed to decide the prognosis of the patients with lactic acidosis. Therapy of lactic acidosis was very difficult. First of all, we tried to improve the circulatory failure and severe acidemia (pH less than 7.20) not to fall into vicious cycle. Then, CAVH, if combined with alkali infusion, seemed to be the most useful technique in managing lactic acidosis with ARF.
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PMID:[Acute renal failure with lactic acidosis]. 221 21

A decrease in sodium, potassium and anion (HCO3)-activated erythrocyte ATPases is noted in patients with acute viral hepatitides A and B, chronic persisting hepatitis, liver cirrhosis, chronic cholecystitis and in HBs-antigen carriers, the reduction of HCO8-ATPase being more noticeable. A degree of expression of the above changes depends on the severity of a pathological process in the liver. The most serious changes are noted in liver cirrhosis. In this disease calcium ATPase activity is also on a decrease. Erythrocyte ATPase activity is lowered in chronic cholecystitis to a lesser degree. In patients with chronic persisting hepatitis and liver cirrhosis erythrocyte ATPase activity slightly increases, however it remains significantly lowered as compared to the control level. The determination of erythrocyte ATPase activity can be used for assessment of the status of patients with acute and chronic liver diseases.
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PMID:[Comparative characteristics of adenosine triphosphatase activity in the erythrocytes of patients with acute and chronic liver diseases, chronic cholecystitis and in HBs antigen carriers]. 295 84

The effect of hemolysis and infection/stasis on pigment gallstones was assessed by comparing the composition of stones from (1) U.S. patients without hemolysis or cirrhosis, (2) U.S. patients with sickle cell disease, and (3) Japanese patients with biliary infections. Gallstone composition was quantitated by infrared spectroscopy and chemical analyses. Gallstones from patients with sickle cell anemia contained more pigment, carbonate, calcium, and measured components than stones from U.S. patients without hemolysis (P less than 0.05). However, the similar types of calcium salts in black stones from patients with and without sickle cell anemia suggested that intermittent hemolysis may be a potential mechanism in the formation of black stones found in the general population. In Japanese patients with brown pigment stones, there was an absence of calcium carbonate, low levels of calcium phosphate, and the presence of calcium salts of fatty acids (P less than 0.05). Thus, the accompanying stasis and/or infection in this latter group was associated with the formation of a distinctive stone type and was not involved in the formation of the black stones. The similarly small proportion of cholesterol in each of these groups suggested that it was present due to coprecipitation rather than to cholesterol supersaturation.
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PMID:Pigment gallstone composition in patients with hemolysis or infection/stasis. 369 61

The transport of plasma albumin and newly made albumin into ascitic fluid was studied in eight patients with cirrhosis and ascites. The thoracic duct was cannulated in two patients and lymph collected over a period of 2 hr. Simultaneously albumin-(131)I and carbonate-(14)C were injected intravenously. The albumin-(131)I measured the transfer of plasma albumin into ascites and into thoracic duct lymph. The carbonate-(14)C, by labeling newly formed albumin, permitted the estimation of the transfer of newly formed albumin into plasma, ascites, and lymph. If the newly synthesized albumin entering ascites and thoracic duct lymph is delivered initially into the plasma, then the ratios of the albumin-(14)C and -(131)I in ascites and lymph compared with the content of albumin-(14)C and -(131)I in plasma would be identical. However, if some newly formed albumin is delivered directly into ascites or lymph, the ratio for albumin-(14)C would be higher than that for albumin-(131)I in lymph or ascites. The ratios of both labeled albumins found in ascites or lymph are expressed as per cent of the total plasma pool. In the eight patients studied 4.2-11.7% of the albumin-(14)C in plasma was found in ascites in 2 hr whereas only 0.4-2.2% of plasma albumin-(131)I entered in this same period. In the two patients studied during thoracic duct lymph drainage 6.1 and 13.5% of newly made albumin-(14)C appeared in lymph in 2 hr whereas only 2.8 and 3.8% of plasma albumin-(131)I was found in the lymph. In cirrhosis with ascites some newly formed albumin entered ascites and thoracic duct lymph by a direct pathway from the liver bypassing the systemic circulation.
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PMID:Albumin to ascites: demonstration of a direct pathway bypassing the systemic circulation. 582 72

So as to assess the effects of lithium carbonate on peripheral leucocyte levels of hepatic cirrhosis patients, 10 cirrhotic patients were studied with less than 4,500 leukocytes per cubic ml and without contraindications for lithium salts that were administered for three weeks at a dose of 90 mg daily. At the end of each week total peripheral leukocytes, differential formula, platelet count and serum lithium concentration determinations were made. In the basal stage, total leukocyte average was 3,400 +/- 527 (X +/- DE) and granulocyte average was 2,090 +/- 341. After the first week of lithium treatment a significant increase was observed in total leukocyte and granulocyte levels whose averages at the end of the third week of treatment were 4,800 +/- 1,052 (p less than 0.01) and 3,694 +/- 1,003 (p less than 0.001) respectively. There was no correlation between the magnitude of leukocyte increase and serum lithium levels obtained that ranged from 0.28 and 1.32 mEq/l. Three patients showed transient gross tremor and two suffered hepatic coma. We can conclude that lithium carbonate increases peripheral leucocytes at the expense of neutrophilia in patients with secondary granulocytopenia and hypersplenism resulting in liver cirrhosis.
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PMID:Effects of lithium carbonate on leucocytes of hepatic cirrhosis patients. 679 6

In 18 patients with acute myocardial infarction admitted to the Cardiological Care Department within 6 hours after the onset of chest pain, before administration of drugs and then in the 2nd, 3rd, 5th and 7th day, the levels of glucose, pyruvate, lactate in venous blood, the lactate/pyruvate ratio (L/P) and pH, actual hydrocarbons, PCO2 and PO2 in capillary arterialized were determined. Depending on the clinical status at admission the patients were classified into 2 groups: I--without complications (I class according to Killip-Kimbal; n = 10), and II--with complications (II-IV class of cardiac failure according to Killip-Kimbal and/or complex ventricular arrhythmias e.i. III-V class according to Lown and heart block of Mobitz--type II and III degree; n = 8). None of the patients had diabetes, chronic respiratory tract diseases, renal failure and liver cirrhosis. The control group consisted of 11 healthy persons. On the first day of myocardial infarction, the significant increase of blood glucose, lactate, pyruvate, as well as significant decrease of blood pH, HCO3- and PO2, and non significant increase of L/P ratio were observed in both groups as compared to the control group. Also there were non significant difference of the glucose, lactate, pyruvate L/P ratio and pH, PCO2 and HCO3- values between the I and II group on the first day of the acute myocardial infarction, with exception of the PO2, which was significantly lower in the group II. In the following days an increase of PO2 was observed. Since this effect coincided with a decrease of lactate concentration (significant only in the group II) it could be concluded, that the observed decrease of the lactate concentration resulted from the higher supply of oxygen. The obtained results have shown, that increase of glycaemia values and decrease of PO2 values may be considered as biochemical markers for hemodynamic complications of acute myocardial infarction.
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PMID:[Lactate metabolism in acute myocardial infarction]. 780 May 82

Gallstones form as a result of many disorders. Unphysiologic supersaturation, generally from hypersecretion of cholesterol, is essential for the formation of cholesterol gallstones. The other common abnormalities of the hepatobiliary system in gallstone patients are accelerated nucleation, gallbladder hypomotility, and the accumulation of mucin gel. An attempt is made here to relate hypersecretion of cholesterol and biliary supersaturation to the molecular basis of the associated phenomena. Supersaturation of bile with calcium hydrogen bilirubinate, the acid calcium salt of unconjugated bilirubin, is essential for pigment gallstone formation, but its magnitude remains undefined in model systems. Nucleation and the precipitation of calcium hydrogen bilirubinate with the polymerization of the pigment in the gallbladder, together with the deposition of the inorganic salts, calcium carbonate and phosphate, result in black pigment gallstone formation. On the basis of ex vivo muscle studies, gallbladder hypomotility is unlikely in patients with black pigment stones but is invariably present in patients with cholesterol stones. Pigment supersaturation in the gallbladder is the result of hepatic hypersecretion of bilirubin conjugates in hemolytic disorders and possibly enterohepatic cycling of unconjugated bilirubin in nonhemolytic states. Less common is bile salt hyposecretion from impaired synthesis in constitutional disorders and cirrhosis, and uncompensated interruption of the enterohepatic circulation in ileal dysfunction syndromes. Bile salt deficiency causes incomplete solubilization of unconjugated bilirubin and impaired binding of calcium ions. Stasis and anaerobic bacterial infection are responsible for brown pigment stones, which usually form in the bile ducts. In addition to the precipitation of calcium hydrogen bilirubinate that remains unpolymerized, there is also the deposition of the calcium salts of saturated fatty acids and free bile acids, both of which are the result of bacterial enzymatic hydrolysis of biliary lipids.
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PMID:Pathogenesis of gallstones. 848 Aug 73


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