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

Numerous interactions between hormonal contraceptives and liver function have been described. Changed laboratory results do not represent obligatory pathologic conditions or hepatotoxi effects. Some of these changed results are transient, suggesting that liver cells are capable of adaptation. The use of oral contraceptives is contraindicated in the following liver diseases: - recurrent intrahepatic cholestasis (recurrent jaundice of pregnancy, Dubin-Johnson syndrome, Rotor syndrome); - acute disturbances of liver function. In general it is recommended that hormonal contraceptives should not be used by patients with biliary cirrhosis although some authors have stated that chronic disturbances of liver function did not appear to be aggravated by these agents. Impairment of carbohydrate and lipid metabolism needs careful control of the laboratory tests concerned. Due to its low frequency the increased risk of gallstones does not necessitate the withdrawal of the medication. Up to now the interrelationship between the use of contraceptive steroids and the induction of hepatic tumours has not been proven.
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PMID:[Liver function in hormonal contraception]. 82 25

Problems of pregnancy in patients with liver disease are discussed. The effects of pregnancy on the disease course are generally limited to triggering of intensifiying icterus and pruritus; intrahepatic cholestasis may also occur. Increased incidences of miscarriage and prematurity have been reported in patients with liver cirrhosis, chronic hepatitis, cholestasis, and Dubin-Johnson syndrome, which is hereditary, and viral hepatitis in early pregnancy (increased incidence of chromosome abnormalities). Liver diseases constitute a relative indication for abortion, depending on the general state of the mother's health and her desire for the child. Problems of diagnosis and treatment are also considered.
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PMID:[Pregnancy in liver diseases]. 112 34

A discussion is made of the basic peculiarties and differences in the clinico-laboratory profile in various forms of pre- and postmicrosome jaundice. The importance of direct to total bilirubin ratio, and of quantitative bilirubin and urobilinogen bodies' determination in the urine is stressed. Bile pigments conjugation by the hepatic cells and free bilirubin conversion to glucuronose may be also assayed by resorting to some additional tests. The test with N-acetyl-paraaminophenol (NAPA) provides for an indirect assessment of the liver's glucuronidase function and has a good informative value. It is optimally characterized by the percentage of free (non-conjugated) NAPA with respect to the total. The latter indicator is normal in chronic hepatitis and in Dubin-Johnson's syndrome, and is at the uppermost normal limit in hepatic cirrhosis and cholestatic jaundice. It is strongly increased (in the average three times with respect to normal values) in Gilbert's disease and posthepatitis hyperbilirubinemia (PHHB). It affords some information on the severity of the defect in transport of bile pigments in the mentioned affections. In hemolytic jaundice a normal percentage of free NAPA is usually found. Glucuronose conversion of bilirubin hardly plays an essential role in the pathogenesis of hyperbilirubinemia i the listed above diseases. This is also confirmed by the NAPA test, performed subsequent to novobiocin loading. The percentare of free NAPA under the conditions just outlined is furthermore increased in Gilbert's disease and PHHB, while in hemolytic jaundice it remains within normal limits. In Gibert's disease and PHHB, a strongly pronounced delay in the excretion of substances is noted. Not infrequently, a similar disorder is also observed in hepatic cirrhosis. It is interpreted as an expression of an overall disturbance in hepatic blood flow and function of the heavily affected hepatic parenchyma.
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PMID:[Study of liver glucuronidase function in indirect hyperbilirubinemia and liver cirrhosis]. 123 97

A 57-year-old man with hepatocellular carcinoma and liver cirrhosis combined with Dubin-Johnson syndrome was successfully treated by extensive right hepatic lobectomy. While the preoperative serum bilirubin level is one of the criteria in determining the indication for radical hepatic resection, it does not play a decisive role in the case of combined Dubin-Johnson syndrome.
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PMID:Hepatocellular carcinoma in a case of Dubin-Johnson syndrome treated successfully with right extended lobectomy. 626 Oct 27

In distinguishing normal from abnormal hepatic changes, the author described the expected changes in liver tests that occur during complicated pregnancy. This article reviews the forms of pre-existing liver disease that may affect or be affected by pregnancy, as well as liver diseases that tend to arise during pregnancy. Among the pre-existing liver diseases are autoimmune chronic active hepatitis, which may be activated by pregnancy and tends to be associated with an increased risk of still and premature births. Worsening of chronic hepatitis B and C has occasionally been observed. While some women with cirrhosis can sustain a normal pregnancy without any worsening of hepatic function, others develop liver failure; plus, women with cirrhosis are less fertile and have higher rates of both stillbirths and premature infants. Other liver disorders that may or may not be affected by pregnancy include Dubin-Johnson syndrome, Gilbert syndrome, benign recurrent intrahepatic cholestasis, Wilson's disease, hepatic adenomas, and focal nodular hyperplasia. Among the hepatic disorders that occur during pregnancy in normally healthy women and then resolve after delivery is intrahepatic cholestasis of pregnancy (also known as pruritus gravidarum, recurrent intrahepatic cholestasis of pregnancy, and obstetric hepatosis). Others include acute fatty liver of pregnancy and HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count), which may be part of the spectrum of disorders associated with pre-eclampsia/eclampsia. Pregnancy may also trigger the dissemination of herpes infection to the liver.
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PMID:Liver problems in pregnancy: part 2--managing pre-existing and pregnancy-induced liver disease. 973 96

Hepatocellular carcinoma (HCC) is the most common malignant tumor of males in the world, with an incidence of 1,000,000 new cases a year. It is endemic in Southeast Asia and Sub-Saharan Africa. Risk factors include chronic infection with hepatitis B virus (HBV) and hepatitis C virus (HCV), Aflatoxin B1 uptake, hemochromatosis, and alpha1 -antitripsin deficiency. Epidemiological studies provide evidence for the association of HCC with HBV infection. The incidence of HCC is high in regions hyperendemic for HBV. Chronic carrier state and maternal-infant transmission are important factors in the development of HCC. Evidence of direct oncogenic effect of H BV is well established, HCCs contain viral DNA sequences integrated into hepatocyte DNA that act as random insertional mutagens, and these sites are near genes involved in the control of proliferation and differentiation. The mechanism of hepatitis C virus in hepatocarcinogenesis is still imprecise but a high percentage of cases are related to this virus. Chronic alcohol consumption and cirrhosis are cofactors that increase the development of HCC in patients with chronic viral infection. In experimental carcinogenesis a multipotential element called oval cell proliferates in the early stages. The cellular events are accompanied by increased expression of several growth factors that enhance the survival of carcinogen-activated cells by suppressing apoptosis and increasing elements entering the cell cycle. Hepatic carcinogenesis is a complex process associated with accumulation of genetic and epigenetic changes that run through steps of initiation, promotion and progression. Activation of oncogenes of the "ras" family and others has been detected during chemically-induced HCC in rodents, but there is little evidence of such activation in human tumors. The role of tumor supressor genes such as retinoblastoma (RB) and P53 genes has been documented. Aflatoxin B1 that contaminates foods in endemic areas has a clear role in hepatocarcinogenesis. Metabolites of this toxin promote apurinic sites and G to T mutations in chromosomal DNA, the third base of codon 249 of the P53 gene is preferentially targeted to form aducts with aflatoxin B1, and this mutation has been specifically identified in HBV infection. Histological and cytological criteria for the diagnosis of HCC are well established and are based in architectural and cytological changes. An important issue is the diagnosis of liver "nodules" detected by image, from which small biopsies or aspiration material is obtained. Special studies such as reticulin, CD34, cytokeratin profile, and MOC-31 can be very useful for the differential diagnosis of primary and metastatic tumors. Telomerase activity has been found in HCC and negative in pericancerous tissue. It is more pronounced in poorly differentiated tumors and correlates with factors of clinical importance, such as prognosis and recurrences. Cells of well-differentiated HCC have an ultrastructural appearance similar to normal hepatocytes. During the process of dedifferentiation, there is progressive loss of organization of intracellular organelles. The cell cohesion is lost, intercellular gaps with microvilli appear, the sinusoids become capillarized, and reparative changes are seen in the spaces of Disse. A variety of inclusions, such as Mallory bodies, granular material, secondary lysosomes, and Dubin-Johnson pigment, have been described. Fibrolamellar carcinoma has a characteristic histological picture and ultrastructurally oncocytic features. Neuroendocrine granules and combination of HCC with bile duct carcinoma are seen by electron microscopy.
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PMID:Hepatocellular carcinoma: an update. 1178 14

A patient was first found to have Dubin-Johnson syndrome and chronic hepatitis at the age of 25 years. Two years later, he underwent gastrectomy because of massive bleeding from duodenal ulcer, followed by posttransfusion self-limited biochemical liver damage. Twenty-five years later, his jaundice worsened to a serum bilirubin level of 10 mg/dl. The test for circulating hepatitis C virus RNA was highly positive, and liver histology showed cirrhosis with brown pigment granules in small numbers of hepatocytes. Some pigment granules were positive for histochemical iron stain. Ultrastructural study on the liver showed (1) the presence of iron-specific X-ray-positive pigment granules, and (2) large numbers of myelin-like bodies throughout the hepatocyte cytoplasm. Histologically advanced hepatic lesions of hepatitis C virus infection and posttransfu-sion iron overload may exacerbate bilirubin transport dysfunction of the syndrome.
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PMID:Electron microscopic findings of the liver of a patient with Dubin-Johnson syndrome complicated by chronic hepatitis C and iron overload. 1181 Apr 46

A 72-year-old woman with hepatocellular carcinoma and HCV cirrhosis combined with Dubin-Johnson syndrome was successfully treated by a central bilateral segmentectomy. While the preoperative serum bilirubin level is one of the established criteria for determining the indications for a hepatic resection, it is not effective for HCV cirrhosis cases associated with Dubin-Johnson syndrome. Postoperative hyperbilirubinemia may be cured without special treatment such as bilirubin absorption or plasma exchange, but such patients must be carefully observed to ensure that liver failure does not occur.
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PMID:Hepatocellular carcinoma in a case of Dubin-Johnson syndrome treated successfully with a central bilateral segmentectomy. 1514 28

Liver dysfunction can appear at any point of pregnancy and causes great anxiety to the patient, her family and sometimes her medical attendants. This review concentrates on conditions specific to pregnancy (hyperemesis gravidarum, intrahepatic cholestasis of pregnancy, toxemia of pregnancy, HELLP syndrome) and provides a guide in diagnosis and management of hepatobiliary conditions that are probably related to pregnancy (e.g., gallstones, Budd-Chiari syndrome) or that are not specific to pregnancy (e.g., acute viral hepatitis), and also the situations in which pregnancy occurs during pre-existing liver disease (e.g., chronic active hepatitis, cirrhosis, Dubin-Johnson syndrome, Wilson's disease).
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PMID:Pregnancy and liver disease. 1780 41

Serum bilirubin measurements are commonly obtained for the evaluation of ill patients and to screen for liver disease in routine physical exams. An enormous research effort has identified the multiple mechanisms involved in the production and metabolism of conjugated (CB) and unconjugated bilirubin (UB). While the qualitative effects of these mechanisms are well understood, their expected quantitative influence on serum bilirubin homeostasis has received less attention. In this review, each of the steps involved in bilirubin production, metabolism, hepatic cell uptake, and excretion is quantitatively examined. We then attempt to predict the expected effect of normal and defective function on serum UB and CB levels in health and disease states including hemolysis, extra- and intrahepatic cholestasis, hepatocellular diseases (eg, cirrhosis, hepatitis), and various congenital defects in bilirubin conjugation and secretion (eg, Gilbert's, Dubin-Johnson, Crigler-Najjar, Rotor syndromes). Novel aspects of this review include: 1) quantitative estimates of the free and total UB and CB in the plasma, hepatocyte, and bile; 2) detailed discussion of the important implications of the recently recognized role of the hepatic OATP transporters in the maintenance of CB homeostasis; 3) discussion of the differences between the standard diazo assay versus chromatographic measurement of CB and UB; 4) pharmacokinetic implications of the extremely high-affinity albumin binding of UB; 5) role of the enterohepatic circulation in physiologic jaundice of newborn and fasting hyperbilirubinemia; and 6) insights concerning the clinical interpretation of bilirubin measurements.
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PMID:Quantitative assessment of the multiple processes responsible for bilirubin homeostasis in health and disease. 2521


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