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PubMed1991

Amenorrhoea in women with non-alcoholic chronic liver disease.

Amenorrhoea is common in women with non-alcoholic chronic liver disease, but little is known about its causes or consequences. We investigated 12 young women with non-alcoholic chronic liver disease and amenorrhoea and compared them with 11 healthy age matched controls studied in the follicular phase of the menstrual cycle. None of the patients had raised serum concentrations of follicle stimulating hormone suggesting primary gonadal failure, but the variance in serum concentrations of testosterone, oestradiol, prolactin, and luteinising hormone were significantly greater in chronic liver disease patients than control subjects (p less than 0.01). Seven of the 12 chronic liver disease patients had low serum luteinising hormone concentrations, and compared with controls these patients also had significantly reduced median values of oestradiol (64 pmol/l), testosterone (1.1 nmol/l), and follicle stimulating hormone, and were significantly underweight as assessed by skinfold thickness measurements (all comparisons p less than 0.025). In the group with chronic liver disease skinfold thickness was significantly correlated with serum luteinising hormone (p less than 0.02). The five patients with normal serum luteinising hormone had higher median values of both oestradiol (237 pmol/l) and testosterone (3.0 nmol/l) than the control subjects (oestradiol: 113 pmol/l, testosterone: 1.9 nmol/l) but were not more obese or hirsute. Amenorrhoea was unrelated to the duration or severity of liver disease. The metacarpal cortical bone area (an index of bone density) was inversely related to the duration of amenorrhoea (p less than 0.02). We conclude that amenorrhoea in women with non-alcoholic chronic liver disease arises from hypothalamic-pituitary dysfunction and can occur at any stage. The hormonal findings in amenorrhoeic chronic live disease patients are not uniform. In some, hypogonadotrophic hypogonadism is related to undernutrition whereas others have normal to high values of luteinising hormone and sex steroids. Prolonged oestrogen deficiency can be a risk factor for osteoporosis in women with chronic liver disease.

Adult↗
PubMed2004

Liver disease due to parenteral and enteral nutrition.

Liver disease due to parenteral and enteral nutrition is a well-recognized iatrogenic phenomenon, but its cause and pathogenesis have not been clearly elucidated. Various mechanisms have been postulated, but it is likely that the cause is multifactorial with significant interplay among several factors. A preventive approach to management is ideal but awaits a more complete understanding of the pathophysiology. A variety of management strategies has been proposed in small case series, but level 1 evidence-based guidelines have yet to be established. Although an abundance of both clinical and animal studies exist regarding liver disease associated with parenteral nutrition (PN), there is a paucity of data regarding enteral nutrition (EN)-associated hepatic disease. The latter probably reflects differences in the frequency and severity of PN- versus EN-associated liver disease. This article addresses the two routes of nutritional support individually, with the major focus on PN-associated liver disease.

Enteral Nutrition↗
PubMed1994

Increased serum iron and iron saturation without liver iron accumulation distinguish chronic hepatitis C from other chronic liver diseases.

One hundred twenty-three patients with chronic liver diseases of various etiologies were evaluated for their iron status. The patients were divided into four distinct groups: chronic hepatitis C (63), chronic hepatitis B (14), B + C (3) and nonviral chronic liver diseases (43). In 107 patients (87%) the chronic liver disease was confirmed by biopsy. Mean serum iron (+/- SD) levels in the above four groups were: 166 +/- 62, 103 +/- 52, 142 +/- 48, and 115 micrograms/dl; iron-binding capacity was 346 +/- 80, 325 +/- 72, 297 +/- 27, and 374 +/- 75 micrograms/dl, and iron saturation 50 +/- 18, 32 +/- 16, 48 +/- 16, and 28 +/- 10%, respectively. Serum ferritin, increased in all four groups, was highest in HCV; however, no evidence of hepatic iron accumulation could be found in any of the patients. There were no significant differences in liver function parameters measured in the four groups. We conclude that serum iron, iron saturation, and ferritin are increased in patients with hepatitis C in comparison to hepatitis B or other nonviral, nonhemochromatotic liver diseases. The increased iron status in hepatitis C patients is not manifested by increased liver iron. Awareness of these distinct features of chronic hepatitis C is essential in the diagnosis and treatment of chronic liver diseases.

Biopsy↗
PubMed1992

The spectrum of chronic liver disease in renal transplant recipients.

Chronic liver disease has been reported to be an important cause of late morbidity and mortality in renal transplant recipients. We have examined the prevalence and nature of chronic liver disease among 538 patients with functioning renal allografts managed at the Western Infirmary, Glasgow, between 1980 and 1989. Thirty-seven patients (7 per cent) satisfied biochemical criteria for chronic liver dysfunction. Liver biopsies were obtained from 24 of these, and autopsy tissue was available from three other patients. Chronic hepatitis of variable severity was present in 15 patients, haemosiderosis in 12 patients and nodular regenerative hyperplasia in five patients. Nineteen patients (51 per cent) had serological evidence of infection with the hepatitis C virus, and one of these developed chronic hepatitis B and D infection as well. Although a variety of chronic liver diseases occurred in our transplant population, the frequency of serious sequelae from liver dysfunction was much lower than that reported from transplant centres in other countries.

Chronic Disease↗
PubMed1979

Noninvasive kinetic approach to the estimation of total hepatic blood flow and shunting in chronic liver disease--a hypothesis.

The intact hepatocyte theory of chronic liver disease suggests a relationship between the degree of shunting of total liver blood flow around the functional liver cell mass and the fraction of functional liver cell mass. By defining this relationship we have developed pharmacokinetic equations to permit the estimation of both total hepatic blood flow and the extent to which this blood flow is shunted. The method requires the determination of the systemic (hepatic) clearances of a high (e.g., indocyanine green [ICG]) and a low (e.g., antipyrine [AP]) extraction ratio drug in the same patient. Applying these equations to literature data obtained from patients with moderate or severe chronic liver disease and from patients with a surgical portacaval shunt, we find: (1) a modest decrease in total hepatic blood flow (16%) and a significant degree of shunting (27%) in patients with moderate chronic liver disease; (2) a substantially reduced total hepatic blood (52%) and extensive shunting (72%) in patients with severe chronic liver disease, and (3) a degree of shunting comparable to that estimated in patients with moderate chronic liver disease but a seriously compromised total hepatic blood flow (a reduction of 55% compared to normal) in patients with surgical portacaval shunts.

Antipyrine↗
PubMed2006

[Epidemiology and natural history of primary nonalcoholic fatty liver disease].

The clinical impact of nonalcoholic fatty liver disease depends on its prevalence and natural history. The prevalence in the adult population is estimated to be about 23% and is on the increase. Thus, it has become the most common cause of persistent elevated liver enzymes, chronic liver disease, and cryptogenic cirrhosis in developed countries. The increasing prevalence of nonalcoholic fatty liver disease, which is approaching epidemic proportions, is parallel to that of other disorders associated with insulin resistance, especially obesity and type 2 diabetes mellitus. This entity occurs in men and women equally and in all age groups. The natural history is poorly defined mainly due to the scarcity of histologic follow-up studies. Although steatosis alone has a more benign clinical course, steatohepatitis is a progressive fibrotic disease, in which cirrhosis and liver-related death occur in a similar way to other causes of chronic liver diseases. Progression seems to be mainly dependent on the severity of histological damage at diagnosis, but age older than 40 years, obesity, and type 2 diabetes have also been associated with an increased risk of liver fibrosis and progression to cirrhosis.

Fatty Liver↗
PubMed2003

[Alcoholic liver disease].

Relations of alcohol and liver injury was noticed in 1793 by Matthew Baillie. Alcoholic liver disease occurs after prolonged consumption of large amounts of alcohol, at least 40-80 g/day. 15-20% alcoholics acquire liver cirrhosis. More severe liver injury were seen in women due to greater sensitivity for genetical and endocrinological reasons. In alcoholic liver disease, total abstinence is essential in treatment. Sufficient nutrition, vitamin diet especially B-complex diet also must be provided.

Humans↗
PubMed2006

A systematic review of the performance of the model for end-stage liver disease (MELD) in the setting of liver transplantation.

The Model for End-Stage Liver Disease (MELD) score is now used for allocation in liver transplantation (LT) waiting lists, replacing the Child-Turcotte-Pugh (CTP) score. However, there is debate as whether it is superior to CTP score to predict mortality in patients with cirrhosis on the LT waiting list and after LT. We reviewed studies comparing the accuracy of MELD vs. CTP score in transplantation settings. We found that in studies of the LT waiting list (12,532 patients with cirrhosis), only 4 of 11 showed MELD to be superior to CTP in predicting short-term (3-month) mortality. In addition, 2 of 3 studies (n = 1,679) evaluating the changes in MELD score (DeltaMELD) showed that DeltaMELD had better prediction for mortality than the baseline MELD score. The impact of MELD on post-LT mortality was assessed in 15 studies (20,456 patients); only 6 (9,522 patients) evaluated the discriminative ability of MELD score using the concordance (c) statistic (the MELD score had always a c-statistic < 0.70). In 11 studies (19,311 patients), high MELD score indicated poor post-LT mortality for cutoff values of 24-40 points. In re-LT patients, 2 of 4 studies evaluated the discriminative ability of MELD score on post-LT mortality. Finally, several studies have shown that the predictive ability of MELD score increases by adding clinical variables (hepatic encephalopathy, ascites) or laboratory (sodium) parameters. On the basis of the current literature, MELD score does not perform better than the CTP score for patients with cirrhosis on the waiting list and cannot predict post-LT mortality.

Follow-Up Studies↗
PubMed2003

[Anesthesia for living-donor liver transplantation in a patient with adult polycystic liver disease].

Anesthesia for living-donor liver transplantation (LDLT) was performed for two patients with adult polycystic liver disease (APLD). APLD is characterized by gradual cystic transformation of both lobes of the liver. Abdominal enlargement, poor appetite, abdominal pain, infection of liver cysts and portal hypertension are symptoms of this disease. Liver transplantation is indicated as the final therapy. Our two patients had very large livers (7400 g and 9500 g). The second patient had suffered renal failure due to a polycystic kidney so that continuous hemodiafiltration had to be performed after surgery. In both cases, sudden hypotension frequently occurred during manipulation of the enlarged liver. In the first case, sudden massive bleeding occurred as a result of laceration of the middle and left hepatic vein when the liver was dropped from the surgeon's hand. In both cases, the position of endotracheal tube became 2 cm shallower after surgery probably because of the shift in the position of the mediastinum after elimination of abdominal compression caused by the enlarged liver. One patient was discharged 39 days and the other 115 days after surgery. Anesthesiologists should pay special attention to the features reported here during LDLT for patients with APLD.

Anesthesia↗
PubMed1975

Althesin and pancuronium in chronic liver disease.

In 32 patients with chronic liver disease, undergoing major abdominal surgery, anaesthesia was induced with either Althesin (alphaxalone and alphadolone acetate) or thiopentone, and maintained with nitrous oxide, oxygen and increments of either pethidine or fentanyl. The patients were ventilated artificially to maintain PaCO, values in the normal range. Pancuronium bromide was used as the muscle relaxant. Liver function tests at 24 hr and 5 day after surgery showed only minor changes compared with findings before operation. There was no significant difference between the Althesin and thiopentone groups. In two patients with severe obstructive jaundice there was difficulty in reversing the effects of pancuronium, but "pancuronium resistance" was observed in all patients. It is concluded that the anaesthetic sequence described, with either Althesin or thiopentone induction, is satisfactory with respect to changes in liver function in patients with chronic liver disease undergoing major surgery.

Adolescent↗
PubMedDate not supplied

[Erythrocyte changes during alcoholism and chronic liver diseases].

50 patients with chronic liver disease and/or alcoholism were studied. 28 cases of anemia were found and macrocytes (and target m.), spurr-cells, spherocytes and stomatocytes observed. For each of these abnormalities the authors report the observed incidence and discuss the literature's data about the pathogenesis. A personal research on the influence of the liver's impaired capability of protein synthesis was also carried out. The usefulness of a careful examination of the blood film is finally stressed, in patients with liver disease and to discover alcoholic subjects still "healthy".

Adult↗
PubMed1993

Alterations in mitochondrial function and morphology in chronic liver disease: pathogenesis and potential for therapeutic intervention.

Studies assessing mitochondrial function and structure in livers from humans or experimental animals with chronic liver disease, including liver cirrhosis, revealed a variety of alterations in comparison with normal subjects or control animals. Depending on the etiology of chronic liver disease, the function of the electron transport chain and/or ATP synthesis was found to be impaired, leading to decreased oxidative metabolism of various substrates and to impaired recovery of the hepatic energy state after a metabolic insult. Changes in mitochondrial structure include megamitochondria with reduced cristae, dilatation of mitochondrial cristae and crystalloid inclusions in the mitochondrial matrix. The most important strategies to maintain an adequate mitochondrial function per liver are mitochondrial proliferation and increases in the activity of critical enzymes or in the content of cofactors per mitochondrion. Possibilities to assess hepatic mitochondrial function and to treat mitochondrial dysfunction in patients with chronic liver disease are discussed.

Animals↗
PubMed1997

Polymorphism in the cytochrome P450 2E1 gene and the risk of alcoholic liver disease.

BACKGROUND/AIMS: To study the genetic susceptibility to alcoholic liver disease, we investigated the association between genetic polymorphism in the cytochrome P450 2E1 gene and the occurrence of alcoholic liver disease. METHODS: Four previously described restriction fragment length polymorphisms (RFLPs) in the cytochrome P 450 2E1 gene were analyzed by restriction endonuclease (Dra I, Msp I, Pst I and Rsa I) digestion of polymerase chain reaction amplified DNA segments. Polymorphisms in these loci were compared to the occurrence of fatty liver, alcoholic hepatitis and liver fibrosis in 319 males comprising total abstainers, moderate alcohol consumers and chronic alcoholics. RESULTS: The allelic frequencies for each RFLP in this series were: 0.89 and 0.11 (Dra I), 0.98 and 0.02 (Msp I) and 0.99 and 0.01 (Pst I and Rsa I). The distribution of the alleles did not vary significantly between the different consumption groups. The allelic frequencies among patients with fatty liver, alcoholic hepatitis or liver fibrosis were not significantly different from the allelic frequencies among patients with normal liver histology. Comparison of different genotypes among moderate alcohol consumers (n = 43) or chronic alcoholics (n = 243) with or without liver disease showed no statistically significant associations. However, the rare polymorphic (d2) allele in the Dra I RFLP was found slightly more often among moderate consumers as well as alcoholics with alcoholic liver disease. CONCLUSIONS: These results indicate that the Msp I, Pst I and Rsa I RFLPs were very rare in the Finnish population, suggesting at most minor contribution to the inherited susceptibility to alcoholic liver disease. Polymorphism in the Dra I locus was more common in this study population, but showed no statistically significant association with alcoholic liver disease.

Adult↗
PubMed1999

A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women.

BACKGROUND: Acute fatty liver of pregnancy and the HELLP syndrome (hemolysis, elevated liver-enzyme levels, and a low platelet count) are serious hepatic disorders that may occur during pregnancy in women whose fetuses are later found to have a deficiency of long-chain 3-hydroxyacyl-coenzyme A (CoA) dehydrogenase. This enzyme resides in the mitochondrial trifunctional protein, which also contains the active site of long-chain 2,3-enoyl-CoA hydratase and long-chain 3-ketoacyl-CoA thiolase. We undertook this study to determine the relation between mutations in the trifunctional protein in infants with defects in fatty-acid oxidation and acute liver disease during pregnancy in their mothers. METHODS: In 24 children with 3-hydroxyacyl-CoA dehydrogenase deficiency, we used DNA amplification and nucleotide-sequence analyses to identify mutations in the alpha subunit of the trifunctional protein. We then correlated the results with the presence of liver disease during pregnancy in the mothers. RESULTS: Nineteen children had a deficiency only of long-chain 3-hydroxyacyl-CoA dehydrogenase and presented with hypoketotic hypoglycemia and fatty liver. In eight children, we identified a homozygous mutation in which glutamic acid at residue 474 was changed to glutamine. Eleven other children were compound heterozygotes, with this mutation in one allele of the alpha-subunit gene and a different mutation in the other allele. While carrying fetuses with the Glu474Gln mutation, 79 percent of the heterozygous mothers had fatty liver of pregnancy or the HELLP syndrome. Five other children, who presented with neonatal dilated cardiomyopathy or progressive neuromyopathy, had complete deficiency of the trifunctional protein (loss of activity of all three enzymes). None had the Glu474Gln mutation, and none of their mothers had liver disease during pregnancy. CONCLUSIONS: Women with acute liver disease during pregnancy may have a Glu474Gln mutation in long-chain hydroxyacyl-CoA dehydrogenase. Their infants are at risk for hypoketotic hypoglycemia and fatty liver.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMedDate not supplied

Serum thrombopoietin in chronic liver disease: relation to severity of the disease and spleen size.

BACKGROUND/AIMS: Thrombopoietin is a thrombopoietic factor mainly synthesized in the liver. Its production is regulated by the mass of megakaryocytes and platelets. Impaired production of thrombopoietin may be responsible for thrombocytopenia in chronic liver disease. METHODOLOGY: We studied thrombopoietin serum concentration in 68 patients with chronic liver disease of various degrees (39 with thrombocytopenia), in 5 patients with thrombocytopenia due to hematological disease, and in 27 healthy controls. RESULTS: Thrombopoietin concentration was higher in patients with liver disease than in controls. Patients with hematological disease had much higher thrombopoietin concentration than patients with liver disease. Among patients with liver disease and thrombocytopenia, thrombopoietin concentration was higher in cirrhosis than in chronic hepatitis. A negative correlation was found between platelet counts and spleen size and between thrombopoietin concentration and spleen size. No correlation was found between thrombopoietin concentration and liver disease severity. CONCLUSIONS: Patients with liver disease and thrombocytopenia have serum thrombopoietin concentration higher than normal controls. It seems therefore that the liver, even seriously diseased, maintains the ability to produce thrombopoietin. In the liver patients the number of circulating platelets and the serum levels of thrombopoietin are inversely correlated with the size of the spleen suggesting that thrombopoietin, although normally produced, might be turned over in platelets sequestrated in the spleen.

Aged↗
PubMed1990

Raised histamine concentrations in chronic cholestatic liver disease.

Pruritus is a frequent symptom in chronic cholestatic liver disease. To date, no single causative mechanism has been identified. We examined venous plasma concentrations of the known pruritogen, histamine, using a highly sensitive radioenzymatic assay in 42 patients with chronic cholestatic liver disease, and in normal controls. The mean plasma histamine level was significantly greater in chronic cholestatic liver disease patients (275 (117) pg/ml; X (SD) than in controls (140 (72) pg/ml, n = 20) (p less than 0.0001). No significant differences were found between histamine concentrations in the two chronic cholestatic liver disease subgroups: primary biliary cirrhosis and sclerosing cholangitis. Histamine concentrations were significantly greater (p less than 0.01) in the pruritic (319 (132) pg/ml) as compared with the non-pruritic (227 (75) pg/ml) chronic cholestatic liver disease patients. The histaminase activity was equivalent in patients and controls. The finding of raised histamine concentrations in chronic cholestatic liver disease suggests in vivo mast cell activation and a potential role for its mediators in the pruritus characteristic of these disorders.

Adult↗
PubMed2001

Autoantibodies in chronic liver diseases.

177 patients with chronic liver disease, among 115 with chronic hepatitis and 61 with liver cirrhosis were subjected to the autoantibodies examinations (ANA, AMA, ASMA, APCA, LKM, ATA) by means of immunofluorescent method (IFA). 25% of cases showed autoantibodies of autoimmunological disease index titre (1:80). Autoantibodies occurred more frequently in woman (75%), mainly in the age of 40-60. Patients with hepatic cirrhosis revealed autoantibodies as frequently as other patients. Among patients infected with hepatotropic viruses (HBV, HCV) with chronic liver diseases, autoantibodies were present in 23-28% of cases and in patients with chronic liver diseases of non-infectious etiology, autoantibodies were observed in 25% of cases.

Adolescent↗