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)

An investigation into the possible role of endotoxins in the pathogenesis of renal failure in cirrhosis and obstructive jaundice showed the two to be closely related. None of the patients with cirrhosis who had endotoxaemia had other evidence of Gram-negative infection at the time of the study, and the endotoxaemia was therefore probably due to impaired hepatic clearance of toxins normally absorbed from the gastrointestinal tract. In contrast, bacteriological evidence of Gram-negative infection was found in most of the patients with obstructive jaundice and endotoxaemia.
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PMID:Endotoxaemia and renal failure in cirrhosis and obstructive jaundice. 79 99

Sclerosing diseases of the biliary system encompass a spectrum ranging from primary sclerosing cholangitis (usually of the extrahepatic biliary tree) to primary biliary cirrhosis of the intrahepatic bile canaliculi. In a study of 35 patients with primary intra- and extrahepatic biliary sclerosis, age of onset, sex distribution, symptomatology, associated diseases, radiographic abnormalities and chemical profile were considered. The difficulty of differentiating sclerosing cholangitis and biliary cirrhosis from other causes of obstructive jaundice preoperatively was stressed, in addition to points of differential clinical and laboratory findings. The etiology of these entities as well as the possibility that they represent variant clinical manifestations of the same disease process were also considered. Mechanical and pharmacological treatment alternatives that were attempted included drainage procedures, the easiest and most widely used of which was the T-tube. However, this could prove to be a source of infection and should therefore be removed early, inasmuch as cholangitis represents a major cause of morbidity. Steroids have been used with varying effectiveness; subjective improvement was generally attained, although objective improvement has been difficult to document. When choleuretics and cholestyramine were administered, we noted significant palliation. Antibiotics were reserved for treatment of cholangitis. Until the underlying etiology of this rare malignant sclerosing process is found, only symptomatic treatment can be offered.
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PMID:Sclerosing cholangitis and primary biliary cirrhosis--a disease spectrum? 92 53

Long strictures of the intrapancreatic portion of the common bile duct were found in 6 patients with chronic pancreatitis. These strictures were responsible for painless obstructive jaundice, recurrent cholangitis, secondary biliary cirrhosis, and chronic abdominal pain difficult to distinguish from that caused by pancreatitis. Endoscopic retrograde cholangiopancreatography and intraoperative cholangiography were invaluable in making the diagnosis and in planning surgical correction. Decompression of the biliary tree by anastomosis of the gallbladder or common duct to the small intestine completely relieved symptoms and allowed liver function to improve significantly. Common duct stricture as a complication of chronic pancreatitis should be considered in the differential diagnosis of extrahepatic biliary obstruction and whenever surgical treatment of chronic pancreatitis is contemplated.
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PMID:Persistent obstructive jaundice, cholangitis, and biliary cirrhosis due to common bile duct stenosis in chronic pancreatitis. 94 56

The apparent well-being of some children who as neonates were believed to have obstructive jaundice prompted us to study the clinical course, histologic features and possible etiologic factors in 17 children with cholestasis in the neonatal period. During a follow-up period of five months to 22 years, all had signs of chronic cholestasis, but only four died (two from nonhepatic causes); the others live remarkably normal lives. Serial hepatic biopsies in 11 showed a variety of initial lesions, which progressed to hypoplasia of the intrahepatic bile ducts, increasing portal fibrosis and eventual cirrhosis. Although evidence of possible viral infection was found in only 10 cases, a hepatitis, beginning either before or after birth, appears to be a likely original cause. The histologic changes seen may represent different stages of one process, starting as cholestasis with or without evidence of hepatitis and progressing to obliteration or failure of normal growth of the intrahepatic bile ducts.
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PMID:Intrahepatic cholestasis in childhood. 95 76

A deficiency of the major serum alpha1-globulin, the alpha1-antitrypsin, was first described in five patients by Laurell and Eriksson in Sweden in 1963. It soon became obvious that severe alpha1-antitrypsin deficiency was familial, and highly associated with chronic lung disease, having its onset in the third or fourth decade of life. Since the early descriptions of this common deficiency state, it has become clearly associated with familial emphysema in some families, familial infantile cirrhosis in others, and occasionally with a combination of childhood lung and liver disease in siblings. For the pediatrician, severe alpha1-antitrypsin deficiency now enters into the differential diagnosis of both chronic pulmonary disease in childhood and obstructive jaundice in the newborn period; In addition, low levels of alpha1-antitrypsin in serum are characteristic of respiratory distress syndrome, and elevations of this protein may be found in a variety of clinical situations. The, alpha1-antitrypsin probably functions as a major control protein against the tissue-damaging effects of both endogenous and exogenous enzymes. This review will cover several basic and clinical features of this protein with respect to its importance in pediatrics.
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PMID:Basic and clinical aspects of the alpha1-antitrypsin. 109 21

Large amounts of bile acid sulfate were found in the urine of patients with hepatobiliary diseases. In patients with acute hepatitis, daily excretion of bile acid into urine was 68.24 plus or minus 51.80 mumoles per day, and the percentage of sulfated bile acid was 83.4 plus or minus 16.7%. In patients with chronic hepatitis and cirrhosis, a slight increase of urinary bile acid was observed (2.89 plus or minus 2.69 and 5.27 plus or minus 4.28 mumoles per day, respectively), and the percentage of sulfated bile acid was 73.9 plus or minus 28.6 and 44.6 plus or minus 30.4%, respectively. In patients with obstructive jaundice, a moderate increase of urinary bile acid was found (32.62 plus or minus 18.35 mumoles per day), and the percentage of sulfated bile acid was 58.3 plus or minus 22.6%. In patients with hepatobiliary diseases, the elevation of both levels of sulfated and nonsulfated bile acids in serum was observed. The percentage of sulfated bile acid was 9% in normal serum, and varied from zero to 82.8% in pathological sera. A remarkable increase of sulfated bile acid was found in patients with obstructive juandice and acute hepatitis, while a slight elevation was found in patients with chronic hepatitis and cirrhosis. Sulfated bile acid in bile was nonexistent or below 0.5% of total bile acid. According to these findings, the increased bile acid in serum of patients with hepatobiliary diseases might be more easily excreted into the urine as sulfated bile acid.
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PMID:Sulfated and nonsulfated bile acids in urine, serum, and bile of patients with hepatobiliary diseases. 111 56

Serum alkaline phosphatase activity was found to increase more markedly in patients with liver cirrhosis than in patients with peptic ulcer and this increase was found to be influenced by blood types. After testing several amino acids and bile acids, phenylalanine and cholic acid were chosen and their inhibitory effects upon serum alkaline phosphatase activity were studied in 66 patients with various liver diseases. It was found that the combination of both agents demonstrates different patterns of inhibition between the patients with liver cirrhosis and obstructive jaundice. This inhibitory effects were also variable among cases of different blood types. Basing upon the present observation, the possible source of the elevated alkaline phosphatase activity in liver cirrhosis was discussed.
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PMID:Inhibition of serum alkaline phosphatase activity by phenylalanine and cholic acid. 115 73

In an attempt to study the collagen formation in the liver occurring in association with obstructive jaundice, the authors carried out an experiment with liver slices from common bile duct-ligated rats. Hepatic collagen was fractionated into the neutral soluble, acid soluble and insoluble fractions, and the hydroxyproline synthesis rate of each fraction was measured using 14C-proline. Determination was also made for hexosamine content in the same liver tissue. The hydroxyproline content of hepatic collagen increased as biliary obstruction was prolonged, particularly from the 4th week, which is the transitional period of liver histology into biliary cirrhosis. The hexosamine content of hepatic collagen showed a similar tendency. The neutral soluble, acid soluble and insoluble collagen fractions all increased as biliary obstruction was prolonged. The collagenosynthetic activity of the neutral soluble fraction, attained a peak in 1 to 2 weeks of biliary obstruction, which indicates that collagen fibers are formed actively in the early stage of jaundice, although there is only a slight increase in the absolute amount of fibers developed then. Serum monoamine oxidase level tended to be parallel to collagenosynthetic activity but not to collagen content.
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PMID:Biochemical study of fibrosis in the rat liver in biliary obstruction. 115 83

Serum glutathione reductase activity was measured in various conditions including acute hepatitis, chronic hepatitis, liver cirrhosis, malignant neoplastic diseases, and obstructive jaundice. A statistically significant elevation of the enzyme activity was found in all of these clinical conditions above normal value, especially in patients with acute hepatitis, some liver cancer, and malignant biliary obstruction. Comparison with other liver function tests showed the existence of statistically significant correlations of serum glutathione reductase with SGOT, SGPT and alkaline phosphatase in acute hepatitis, and with alkaline phosphatase in cirrhosis. In parenchymatous liver disease, serial determination was found to be important. High values in obstructive jaundice suggest the malignant obstruction.
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PMID:Clinical significance of serum glutathione reductase in various clinical conditions, especially in liver diseases. 125 42

The simultaneous measurement of wedged hepatic venous pressure and portal venous pressure at 11 and 28 days following common bile duct and intrahepatic bile duct obstruction reveals a significant elevation of the portal pressure at 28 days which is due primarily to increased presinusoidal resistance to portal blood flow. Portal venograms performed prior to sacrifice revealed moderate narrowing of the portal vein radicles and delayed emptying at 11 days and severe morphological alterations at 28 days. These results confirm the findings of other investigators and help to explain why the hemodynamic alterations occur so rapidly in obstructive jaundice, well before the development of significant biliary cirrhosis.
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PMID:The location of increased resistance to portal blood flow in obstructive jaundice. 125 22


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