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PubMed2003

Cryoprecipitate for the correction of coagulopathy associated with liver disease.

In patients with liver disease at risk of pulmonary oedema, cryoprecipitate (small volume) might be a viable alternative to fresh frozen plasma (FFP, large volume) in the correction of coagulopathy. However, the efficacy of cryoprecipitate in these patients has not been tested. We evaluated the role of cryoprecipitate in the correction of the coagulopathy of liver disease. To establish initial evidence of efficacy, six consecutive patients with hepatic failure and coagulopathy received five units of cryoprecipitate. Then, using a crossover design, 11 consecutive patients were randomized to receive either four units of FFP or five units of cryoprecipitate. Pre and post infusion International Normalized Ratio (INR), activated Partial Thromboplastin Time (aPTT), fibrinogen D-dimers, Factors V and IX, and reptilase time were measured. In the first six patients, cryoprecipitate improved the INR, aPTT and fibrinogen concentration (P = 0.03). In the crossover study, FFP administration produced a greater improvement in INR (P = 0.007) and aPTT (P = 0.005) than cryoprecipitate. However, there were no differences in any of the other measured variables. One patient developed acute pulmonary oedema while receiving FFP. Cryoprecipitate improves the coagulopathy of liver disease. Four units of FFP are more efficacious than five units of cryoprecipitate. Cryoprecipitate may have a role in correction of the coagulopathy associated with liver disease where concerns about pulmonary oedema exist.

Adult↗
PubMed1991

Sexual function and testosterone levels in men with nonalcoholic liver disease.

The effects of nonalcoholic liver disease on sexual desire, arousal, activity, orgasmic function and satisfaction and serum testosterone levels were studied in 75 men with nonalcoholic liver disease. Each man was interviewed about his sexual behavior and problems and was asked to comment on whether he felt liver disease affected his sexual function. The average age of the patients was 49 yr, and a wide variety of liver diseases was represented. Child-Pugh grading was A in 51 patients, B in 18 and C in 6; the mean duration of liver disease was 8 yr. Sexual desire, arousal and activity of patients with grade A disease were within the ranges observed in studies of healthy men of comparable age. Diminished sexual desire was reported by 2% of grade A patients and 35% of grade B and C patients (p less than 0.005). Arousal problems were noted by 16% of grade A patients, 60% of grade B patients and 67% of C patients (p less than 0.005). Loss of erection and inability to regain erection were noted by 7%, 40% and 67% of grade A, B and C patients, respectively (p less than 0.01). Premature and retarded ejaculation were more frequent in patients classed in Child-Pugh grades B and C. Frequency of coitus and orgasm were significantly higher in grade A patients than in grade B and C patients. Total and free testosterone levels were (in nanograms per milliliter) A, 677/1.78; B, 416/1.06; and C, 178/0.43 (p less than 0.002). We concluded that Child-Pugh grade A nonalcoholic liver disease in men does not affect sexual desire, function or performance. Men with disease grades B and C have significant sexual dysfunction and significant reduction of both total and free testosterone levels.

Adult↗
PubMed1996

IgA deposition in the skin of patients with alcoholic liver disease.

In patients with alcoholic liver disease, IgA deposits are often found in the liver, kidneys and skin. The present study was undertaken to determine the specificity, sensitivity and characteristics of IgA deposition in the skin of a group of alcoholic patients with or without overt liver disease, and compare these with findings in non-alcoholic cirrhotics. Twenty-six out of 28 patients with alcoholic cirrhosis had IgA deposition in the skin. In contrast, only 6 out of 11 patients who were alcoholic without any clinical liver disease and 3 out of 13 patients with non-alcoholic cirrhosis of the liver had IgA deposition. In the control group, only 1 out of 52 patients with various dermatoses (excluding IgA dermatoses) had this IgA deposition. Unlike other IgA dermatoses, such as Henoch-Schoenlein purpura or dermatitis herpetiformis, IgA deposition in alcoholic liver disease is characterized by its presence in the basement membrane of the eccrine secretory coils. This particular pattern of IgA deposition can be helpful in the diagnosis of alcoholic liver disease or alcoholism since the specificity is 100% with a sensitivity of 75%.

Adult↗
PubMed1988

Disposition of nitrendipine in patients with chronic liver diseases.

Metabolism of nitrendipine occurs principally in the liver. Therefore, an alteration of pharmacokinetics has to be discussed in patients with hepatic impairment. To evaluate steady-state plasma concentrations and pharmacokinetics, a low dose of nitrendipine (5 mg/day for 3 weeks) was administered orally to patients with different chronic liver diseases (fatty liver, n = 3; chronic hepatitis, n = 2; and cirrhosis of the liver, n = 5). Nitrendipine plasma concentrations were analyzed by using a gas-liquid chromatography procedure. Twenty-two days after beginning the study, steady-state plasma concentrations were lower than 1.0 microgram/L in one patient without liver disease and in seven patients with chronic liver diseases, in contrast to three patients with alcoholic cirrhosis (5.5, 1.3, and 2.9 micrograms/L). The maximum concentration (Cmax) was 2.3 micrograms/L in the patient without liver disease and 8.3 +/- 3.9 micrograms/L in the hepatic patients. The elimination half-life was prolonged in three of five patients with cirrhosis of the liver (35, 67, and 43 h), whereas in the other patients the half-life was in a normal range (4.2-21.3 h). The area under the concentration-time curve (AUC) was enhanced in three patients with liver cirrhosis (387, 69, and 126 h/micrograms/L); in the other seven hepatic patients, results were normal (35-49 h/micrograms/L). There were no alterations observed in any patient in blood pressure and laboratory data. Oral administration of a low dose of nitrendipine resulted in slightly enhanced steady state plasma concentrations only in patients with advanced cirrhosis of the liver. The half-life, AUC, and bioavailability also seem to be altered only in a more severe state of liver disease.

Adult↗
PubMed2005

Abnormal hepatic vein Doppler waveform in patients without liver disease.

In patients with liver cirrhosis Doppler ultrasound often detects absence of the retrograde (hepatopetal) flow phase in the hepatic vein, suggestive of an increased stiffness of the liver parenchyma around the vein. This is rarely or never reported in healthy control persons. We examined the frequency of absent retrograde flow in a consecutive series of 139 patients referred for abdominal ultrasound. We used state-of-the-art ultrasound scanners, and placed the Doppler gate so that in non-forced end-expiration it would sample the right hepatic vein 4-6 cm from the vena cava. There was no association between the hepatic vein flow pattern and age, sex or body mass index. 43 of 139 studied patients showed absent retrograde flow. Review of the case records revealed liver disease in 26 patients and no sign of liver disease in 17 patients. We suggest that absent retrograde flow in the hepatic veins may be seen not only in patients with overt liver disease but also in apparently liver-healthy patients.

Adult↗
PubMed1978

Liver disease and nutrition.

The liver plays a central role in the digestion, metabolism, and storage of nutrients. A deficiency of nutrients is often associated with liver disease and may be caused by decreased intake, decreased absorption, decreased storage, abnormalities in metabolism, or the increased requirements for nutrients. Alcoholism is a frequent cause of both malnutrition and liver disease, but nutritional deficiencies are also common in liver diseases not associated with alcoholism.

Alcoholism↗
PubMed2002

Early cell transplantation in LEC rats modeling Wilson's disease eliminates hepatic copper with reversal of liver disease.

BACKGROUND & AIMS: The Long-Evans Cinnamon (LEC) rat is an excellent model of Wilson's disease with impaired copper excretion, hypoceruloplasminemia, and copper toxicosis. We hypothesized that early hepatocyte transplantation would improve copper excretion and liver disease in Wilson's disease. METHODS: Normal syngeneic Long-Evans Agouti rat hepatocytes were transplanted intrasplenically into 2-week-old LEC rats. Untreated LEC pups were controls. Liver repopulation was shown by changes in serum ceruloplasmin, hepatic atp7b messenger RNA, and bile and liver copper levels. Histologic analysis of the liver was performed. RESULTS: Significant copper accumulation and liver disease were observed in 5-month-old LEC rats, with occasional treated rats showing increased bile copper excretion. The liver was repopulated extensively in 10 of 14 treated LEC rats (71%) 20 months after cell transplantation. In these 10 rats, hepatic copper content was virtually normal in 6 rats (53 +/- 12 microg/g liver) and substantially less in 4 others (270 +/- 35 microg/g) compared with elevated liver copper levels in untreated LEC rats (1090 +/- 253 microg/g) (P < 0.001). Changes in serum ceruloplasmin levels, bile copper excretion capacity, and liver histology were in concordance with decreases in liver copper levels. CONCLUSIONS: Transplanted cells proliferated subsequent to the onset of liver injury, and the liver was repopulated over an extended period. Cell transplantation eventually restored copper homeostasis and reversed liver disease without hepatic preconditioning in LEC rats.

Animals↗
PubMed1996

Liver transplantation for alcoholic liver disease.

UNLABELLED: Orthotopic liver transplantation (OLT) for individuals with alcoholic liver disease (ALD) remains controversial. This review was designed to evaluate the survival, recidivism, and rehabilitation of the alcoholic liver transplant recipient in a single transplant center. METHODS: Between 10/86 and 11/92 203 liver transplants were performed in 179 patients. In 42 patients (23%) the primary etiologic diagnosis was ALD (36 males, 6 females, median age 47 yr). All ALD patients were evaluated preoperatively by social service, psychiatry, and medical psychology, in addition to hepatology and transplant surgery. A minimum abstinence period of 3-6 months was encouraged, although exceptions were made for cases of extreme medical urgency in which a good prognosis for abstinence was predicted. RESULTS: In OLT recipients with ALD, actuarial survival at 1, 2, and 3 yr was 74%, 71%, and 71%, respectively, compared to 71%, 71%, and 69% for all OLT recipients. One- and two-year survival was 85% in the most recently transplanted 86 patients, 20 of whom (23%) had ALD with 1- and 2-yr survival of 84% (N.S.). Recidivism was monitored postoperatively by interviews with the patient and family, supplemented by random urine and serum toxicology. Of the 29 survivors, 2 (7%) returned temporarily to alcohol use but are presently abstinent. Although none of the ALD patients in this study was able to work prior to OLT, 76% of the survivors at least 4 months post-transplantation were employed. CONCLUSIONS: Although our experience is small, our results suggest that OLT is appropriate therapy for carefully selected patients with end-stage liver failure due to ALD. The multi-disciplinary approach to preoperative evaluation of the alcoholic liver transplant candidate is effective in determining those patients committed to abstinence after a successful transplant.

Actuarial Analysis↗
PubMed2005

Oxidative stress and antioxidant status in patients with alcoholic liver disease.

BACKGROUND: [corrected] Alcoholic liver diseases (ALD) are very common in lower socio-economical strata due to heavy drinking habits and multiple nutritional deficiencies. Ethanol causes liver damage by many mechanisms. The generation of lipid peroxidation by free radicals has been proposed as a mechanism for ethanol induced hepatotoxicity. These free radicals are destroyed by anti-oxidants. Many anti-oxidants are present in the diet, e.g., vitamin E, vitamin C etc. However, poor nutrition or malabsorption leads to deficiency of these vitamins. This may impair the anti-oxidative defense leading to ethanol induced oxidative stress and then to liver damage. METHODS: Oxidative stress and antioxidant defense were assessed in patients with alcoholic liver disease. Serum malondialdehyde (MDA) concentrations were measured as an index of lipid peroxidation, i.e., oxidative stress; and serum vitamins E and C concentrations were measured as an index of antioxidant status. RESULTS: Serum MDA concentrations were increased with the increase in severity of the disease. Concentrations of serum vitamins E and C were decreased in patients with alcoholic liver disease as compared to controls. CONCLUSIONS: Our observations may be due to increased demands of the same or increased utilization.

Adult↗
PubMed1989

Expression of cytokeratins in normal and diseased livers and in primary liver carcinomas.

Hepatocytes and bile duct epithelium express several types of cytokeratins, the characteristic intermediate-filament proteins of epithelial cells. The cytokeratin antigen expression was studied in normal and diseased livers, intrahepatic cholangiocarcinomas, and hepatocellular carcinomas by immunohistochemical methods using a panel of polyclonal and monoclonal antibodies to cytokeratins. Ten percent formaldehyde solution-fixed, paraffin-embedded sections obtained from ten patients without liver disease, 18 patients without liver disease, 18 patients with different stages of primary biliary cirrhosis, 14 patients with alcoholic hepatitis, ten patients with fatty liver hepatitis secondary to diabetes mellitus or morbid obesity, five patients with hepatocellular carcinomas, and five patients with cholangiocarcinomas were examined. The results suggested that hepatocytes and bile duct epithelium retain their distinct cytokeratin profiles in liver disease, including malignant transformation. Therefore, demonstration of cytokeratins in the liver is useful in establishing the cellular origin of neoplasms and understanding the pathogenesis of liver diseases.

Adenoma, Bile Duct↗
PubMed2000

Prognosis of alpha-1-antitrypsin deficiency-related liver disease in the era of paediatric liver transplantation.

BACKGROUND/AIM: Alpha-1-antitrypsin deficiency (alpha1ATD) is the commonest metabolic disease leading to liver transplantation (LT) in children. Approximately 10-15% of the PiZZ population develops liver disease. Five percent of them will require LT within the first 4 years of life. This study aimed to investigate the prognosis of the liver disease associated with PiZZ alpha1ATD in the era of liver transplantation and to determine predictors of outcome. METHODS: We reviewed retrospectively the clinical notes of 97 consecutive patients referred from January 1989, when LT became routinely available in our Unit, to July 1998. RESULTS: Of 26 (27%) patients who developed end-stage liver disease, 24 have been transplanted and two are waiting for LT. Twenty-one (81%) of these patients presented with neonatal hepatitis at a median age of 2.1 months. Of 71 (73%) children who have not required LT, 61 (86%) presented with neonatal hepatitis at a median age of 1.6 months. Among infants with neonatal hepatitis who required LT, 18 out of 21 (86%) had jaundice for more than 6 weeks compared with 34 of 61 (56%) who survived without LT (p<0.01). Children requiring LT had higher aspartate aminotransferase (AST) at presentation (p<0.0001) and both higher AST and gamma-glutamyl transferase (GGT) at 6 months (p<0.001), 1-year (p<0.0003) and 5-year (p<0.01) follow up when compared to those who are well without LT. Furthermore, children who developed end-stage liver disease more frequently had severe bile duct reduplication (p<0.01), severe fibrosis (p<0.03) with bridging septa (p<0.02) and established cirrhosis (p<0.04) in the initial liver biopsy. Ninety-five of the 97 children (98%) are currently alive; two died after LT. CONCLUSIONS: The advent of liver transplantation has significantly improved the prognosis of liver disease associated with PiZZ alpha1ATD. Duration of jaundice, severity of histological features and biochemical abnormalities predict outcome at an early stage of the disease.

Child↗
PubMed1996

Hepatic levels of bile acids in end-stage chronic cholestatic liver disease.

In chronic cholestatic liver disease hydrophobic and potentially cytotoxic bile acids are assumed to accumulate in the liver. To test this hypothesis we investigated bile acid levels and pattern in livers and serum of patients with, (A) end-stage chronic cholestatic liver disease, and with (B) end-stage cirrhosis of alcoholic/chronic hepatitic origin who underwent liver transplantation. Bile acids were also analyzed in (C) normal liver tissue. Levels of bile acids were 215 +/- 39.1 nmol/g liver (wet weight) in chronic cholestasis and 120 +/- 32.7 and 56.1 +/- 24.2 nmol/g liver in group B and group C (P < 0.01 and P < 0.005), respectively. Cholic acid was the prevailing bile acid in chronic cholestasis (51%) and was elevated eight-fold as compared to group C (P < 0.005). Chenodeoxycholic acid contributed 41% to total bile acids and was elevated four-fold (P < 0.005). Deoxycholic acid contributed only 1.5% to bile acids in chronic cholestasis as compared to 27% in group C (P < 0.01) and was absent in group B. Levels of lithocholic acid tended to be increased in chronic cholestasis as compared to group C and its sulfation was impaired (P < 0.05). The pattern of serum bile acids in chronic cholestasis agreed well with the bile acid pattern in the explanted livers. We conclude that hepatic accumulation of hydrophobic chenodeoxycholic acid and impaired sulfation of lithocholic acid might contribute to tissue degeneration in chronic cholestatic liver disease due to the detergent effects of these bile acids.

Aged↗
PubMed1997

Nutritional considerations and management of the child with liver disease.

Nutritional management of the infant and child with liver disease is highly dependent upon the type of liver disease. Acute liver disease, such as that secondary to viral hepatitis, requires no specific nutritional therapy with the exception that branched-chain amino acid supplements may be indicated in the management of hepatic encephalopathy. Nutritional management of the child with chronic liver disease depends upon whether or not cholestasis is present, since in that condition, large amounts of fat-soluble vitamin supplements and medium-chain triglycerides are usually required for optimum growth. However, anicteric cirrhotic liver disease also presents nutritional challenges because of hypermetabolism, enteropathy, and increased protein oxidation. Certain inborn errors of metabolism that result in liver disease (including galactosemia, hepatorenal tyrosinemia, hereditary fructose intolerance, and Wilson's disease) have specific nutritional requirements. And, finally, the advent of pediatric liver transplantation has placed new emphasis on the importance of optimum nutritional management of the child with chronic liver disease, since improvement of nutritional status in the pretransplant period maximizes success of the transplant. This review will focus on the pathogenesis of malnutrition in childhood liver disease and will provide recommendations for nutritional assessment and monitoring as well as nutritional management of cholestatic liver disease, anicteric cirrhotic liver disease, and the inborn errors of metabolism enumerated above. Specific recommendations for nutritional management of the child awaiting liver transplantation will be provided.

Child↗
PubMed1981

Chronic liver disease in transfusion-dependent thalassemia: liver iron quantitation and distribution.

The quantitative and/or qualitative distribution of liver iron was assessed in 81 transfusion-dependent thalassemia major patients with chronic liver disease (36 with chronic active hepatitis, 23 with chronic persistent hepatitis, 22 with siderosis). Viral marker studies showed only 3 cases with both HBsAg and anti-HBc positivity in the serum, while the others had anti-HBc and anti-HBs or only anti-HBs or no B viral markers. A significantly higher iron overload was found in chronic hepatitis, particularly chronic active hepatitis, than in siderosis. The increased iron overload may be due to less intensive chelation treatment, higher intestinal absorption secondary to lower mean Hb levels, and/or to liver inflammation-dependent iron deposition. The liver iron overload in turn amy facilitate the development or persistence of chronic progressive liver disease.

Adolescent↗
PubMed1996

Liver transplantation for adult polycystic liver disease.

Patients with adult polycystic liver disease and massive cystic replacement of the liver may present with severe debilitation and impairment of functional performance or, rarely, with signs of portal hypertension or hepatic dysfunction. In those patients incapacitated by severe hepatomegaly secondary to massive cystic replacement with predominantly small cysts (2 cm) without areas of parenchymal sparing, liver transplantation is a therapeutic option. Five patients with incapacitating symptoms from polycystic liver disease underwent liver transplantation as a final therapeutic procedure. Two patients had previous fenestration procedures without significant relief. All patients had radiographic evidence of concomitant polycystic kidney disease; two of these patients were dialysis-dependent at the time of liver transplantation. One patient underwent combined liver-kidney transplantation, whereas another received a six-antigen matched kidney transplant 64 months after liver transplantation. Four of five patients are alive 84, 39, 20, and 8 months after successful liver transplantation. All four have returned to normal functional status with complete resolution of symptoms. Liver transplantation is a suitable option for the patient with bilobar small cystic liver disease without areas of parenchymal sparing. However, only patients with severely compromised functional status should be offered this therapy. Concomitant renal evaluation is mandatory, and a knowledge of the natural history of this disease will aid in the decision of whether a combined liver-kidney transplantation is indicated.

Adult↗
PubMed1989

Sexual behavior in women with nonalcoholic liver disease.

Sexual behavior in women with liver disease was examined in 150 women to determine whether liver disease influenced sexual desire, frequency or performance. The average age of women studied was 53 years (range: 26 to 76 years), and a wide variety of liver diseases were represented. Sexual desire was reduced in 33%. Difficulty in becoming sexually aroused was noted by 18%. Orgasm during intercourse was not experienced by 25%. The frequency of sexual intercourse decreased since onset of disease in 27%. Dyspareunia was a complaint by 21%, most often attributed to decreased vaginal lubrication. Liver disease was considered a significant factor interfering with sexual function in 17%. No statistical difference was found between sexual desire or function in our study and in large studies of sexual behavior in women. Each category was subdivided by presence or absence of cirrhosis, pre- or postmenopausal state, laboratory values and duration of disease. Except for a greater number of postmenopausal women with complaints of painful intercourse, no statistical differences or trends were found. Nonalcoholic liver disease does not affect sexual desire, function or performance. Variables other than liver disease influence sexuality. Women with liver disease can thus be reassured that they can maintain normal sexual relations.

Adult↗
PubMed2006

Nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease is a common condition associated with metabolic syndrome. It is the most common cause of elevated liver enzymes in U.S. adults, and is diagnosed after ruling out other causes of steatosis (fatty infiltration of liver), particularly infectious hepatitis and alcohol abuse. Liver biopsy may be considered if greater diagnostic and prognostic certainty is desired, particularly in patients with diabetes, patients who are morbidly obese, and in patients with an aspartate transaminase to alanine transaminase ratio greater than one, because these patients are at risk of having more advanced disease. Weight loss is the primary treatment for obese patients with nonalcoholic fatty liver disease. Medications used to treat insulin resistance, hyperlipidemia, and obesity have been shown to improve transaminase levels, steatosis, and histologic findings. However, no treatments have been shown to affect patient-oriented outcomes.

Algorithms↗