The serum transaminase test in various diseases; its diagnostic value in liver disease.
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Hematologic Tests↗
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Adult polycystic liver disease presenting in a patient with metastatic adenocarcinoma. Cytologic and histologic findings.
The clinical, cytologic, and histologic features are presented in a case of polycystic disease of the liver. The patient was a 65-year-old female who presented with clinical and radiologic findings suggestive of metastatic adenocarcinoma to the pleural cavity and liver. Cytologic and histologic examination yielded an unsuspected diagnosis of polycystic liver disease. Metastatic adenocarcinoma to the pleura was subsequently identified on open biopsy.
Adenocarcinoma↗
Nonalcoholic Fatty Liver Disease (NAFLD): Approach in the Adolescent Patient.
Nonalcoholic fatty liver disease (NAFLD) is a spectrum of liver disease whose hallmark is the accumulation of large-droplet fat in hepatocytes. This metabolic disorder occurs mainly in overweight or obese individuals. The disease mechanism involves hyperinsulinemia and hepatic insulin resistance, not ethanol abuse. NAFLD may be the hepatic manifestation of the "metabolic syndrome" classically associated with type 2 diabetes mellitus and cardiovascular disease. NAFLD ranges from simple steatosis, which is the least rapidly progressing disorder, to nonalcoholic steatohepatitis to cirrhosis, which can evolve to chronic liver failure. The high prevalence of NAFLD in children has been recognized only in the past 5 to 10 years, as rates of childhood obesity have soared. Accordingly, the best strategies for diagnosis and treatment of childhood NAFLD are a work in progress and remain controversial. Weight reduction through a healthy diet and regular medium-intensity exercise is the mainstay of current treatment. Few research data are available to guide pharmacologic therapy. Certain points regarding management of childhood NAFLD require emphasis: It is a serious liver disease that requires detailed clinical investigation. Other liver diseases causing fatty liver and/or abnormal liver tests, notably Wilson disease and chronic viral hepatitis, need to be excluded. Liver biopsy can provide critical diagnostic and staging information. Associated genetic or endocrine disorders need to be identified. Treatment should begin with a low-glycemic index diet that provides adequate nutrients but is low in harmful fats and eliminates foods causing postprandial hyperglycemia. Initially, this can target two to three problem foods so that it is easy for the adolescent to follow. Regular exercise suited to the capabilities and interests of the teenager should be added to the daily routine. Where possible, a team approach, including a dietician and psychologist, should be utilized, as adolescents do better in a supportive atmosphere. Optimal drug treatment requires further research: current front-runners are vitamin E and metformin. The roles of drugs that alter appetite and bariatric surgery for adolescents with NAFLD have not been determined.
Journal Article↗
Health Locus of Control in problem drinkers with and without liver disease.
The purpose of this study was to investigate whether patients who developed alcoholic liver disease have more awareness of the link between their behaviour and subsequent health than patients with non-alcoholic liver disease and people with drink problems with no liver disease. This study included three groups of patients, alcoholic liver disease (ALD) (n=57), non-alcoholic liver disease (n=77), and problem drinkers with no liver disease attending a London community day treatment centre (ACCEPT) (n=115). Health locus of control differentiates people into two groups, health externals who are individuals who maintain that their health is largely determined by external factors, as opposed to health internals, who believe that their behaviour plays a major role in determining their subsequent health or illness. The results of the Health Locus of Control (HLC) scale administered to the above subjects suggested that the ALD group had limited insight into the relationship between their drinking and subsequent liver disease, compared to the ACCEPT group. It is suggested that alcoholic liver disease patients receive counselling as part of their total management.
Adolescent↗
Treatment of alcoholic liver disease.
The treatment of alcoholic liver disease at present consists of abstinence from alcohol, bed rest, and dietary intake or administration of adequate amounts of calories and protein. Besides corticosteroids, which have been shown to improve hospital survival in severely ill patients with alcoholic hepatitis and liver transplantation in advanced cirrhosis, no successful specific therapy is available for alcoholic liver disease. Potential new therapeutic approaches include: (1) Treatment with specific dietary supplements such as polyunsaturated lecithin, which in baboons prevented the progression of the early stages of pericentral and interstitial fibrosis to septal fibrosis and cirrhosis; (2) antagonists to cytokines or antibodies to cytokine receptors for cytokines that have been shown to enhance hepatocellular necrosis or fibrosis; (3) substances that block pathways of oxygen radical formation or increase their metabolism or binding to form nonharmful compounds; (4) inhibition of collagen synthesis by proline analogues that increase intracellular collagen degradation or increase in collagen degradation by stimulation of collagenase or by insertion of exogenous DNA encoding amino or carboxyterminal peptides of procollagen into hepatocytes; and (5) stimulation of hepatic regeneration and recovery from alcohol-inducer liver injury.
Adrenal Cortex Hormones↗
High expression of CD34-positive sinusoidal endothelial cells is a risk factor for hepatocellular carcinoma in patients with HCV-associated chronic liver diseases.
CD34 has been widely used for the assessment of sinusoid-like neoangiogenesis in hepatocellular carcinoma (HCC). Recently, it was demonstrated that CD34-positive cells isolated from human peripheral blood differentiate into endothelial cells and contribute to neoangiogenesis in adults. We investigated the localization and the substantial role of CD34-positive endothelial cells in the liver with hepatitis C virus (HCV)--associated chronic liver diseases. Liver tissue sections obtained by biopsy from 56 patients with HCV-associated chronic liver diseases by were examined immunohistochemically using anti-CD34, anti-von Willebrand factor (vWF), and anti-vascular endothelial growth factor (VEGF) antibodies. CD34 was stained in the sinusoid, showing dotty, linear, semicircular, or circular patterns. However, sinusoidal expression of vWF was not substantially identified in the same specimens, indicating the existence of sinusoidal CD34-positive but vWF-negative endothelial cells. We classified these cells as CD34 LI and found that CD34 LI was correlated with the expression of VEGF. Among 34 patients with advanced-stage disease, the cumulative incidence of HCC was significantly higher in patients with CD34 LI >or= 12 (n = 16) than in those with CD34 LI < 12 (n = 18; P = .009). Moreover, among several clinicopathologic risk factors, CD34 LI could be recognized as an independently significant factor for development of HCC (relative risk, 7.36; P = .019). We conclude that CD34-positive endothelial cells are regulated by several factors, such as VEGF, and might play a substantial role in hepatocarcinogenesis. Furthermore, high expression of CD34-positive sinusoidal endothelial cells is a risk factor for HCC in patients with HCV-associated chronic liver diseases.
Adult↗
Type IV collagen and laminin contents of livers from patients with alcoholic liver disease.
Characteristic histological features of alcoholic liver disease (ALD) are pericellular and perivenular fibrosis. It has been emphasized from immunohistochemical studies that pericellular and perivenular fibrosis may be caused by the increase of type IV collagen (IV-C) and/or laminin (LM). However, quantitative changes of hepatic IV-C and LM contents in ALD are not well known. Recently, we have developed assay systems for IV-C and LM contents in liver biopsy specimens. In the present study, hepatic IV-C and LM contents in ALD and non-ALD patients were measured. Liver biopsy specimens were obtained from 36 patients with ALD, 24 patients with non-ALD and five patients without liver disease. IV-C and LM contents in liver biopsy specimens were measured using the one-step sandwich enzyme immunoassay system for human serum IV-C and LM levels. Total collagen (T-C) content was also measured by the method of Leon and Rojkind. Hepatic IV-C, LM and T-C contents were significantly higher in all types of liver disease than in controls, and tended to increase with the progression of fibrosis. Especially in ALD, both IV-C and LM contents increased from the early stage, and the values in each type of ALD were significantly higher than those in the corresponding type of non-ALD. The ratio of IV-C or LM to T-C was also significantly higher in ALD than in the corresponding non-ALD. The prominent increases of IV-C and LM at the early stage of fibrosis may be one of the characteristics of collagen metabolism in ALD.(ABSTRACT TRUNCATED AT 250 WORDS)
Biomarkers↗
Systemic haemodynamic changes in patients with cystic fibrosis with and without chronic liver disease.
BACKGROUND/AIMS: There are well-documented systemic haemodynamic changes associated with chronic liver disease. Patients with cystic fibrosis may develop chronic liver disease, but it is not known whether these systemic haemodynamic changes develop and, if they do, whether they are influenced by the associated chronic lung disease. We therefore undertook a study to document the circulatory status of cystic fibrosis patients with and without chronic liver disease. METHODS: Fifty-six subjects with cystic fibrosis were studied. Systemic haemodynamic and pulmonary parameters, in sub-groups both with (LD) and without (NLD) liver disease, were measured at rest and during measured exertion. Cystic fibrosis-related chronic liver disease was diagnosed using previously validated ultrasound criteria. Patients underwent assessment at rest and in the fourth minute of seated bicycle exercise at 25W. Heart rate (ECG), blood pressure (semiautomated sphygmomanometer), aortic blood velocity (pulsed Doppler suprasternal probe), arterial oxygen saturation (pulse oximeter) and respiratory variables (pneumotachometer with expired gas analysis by an automatic system) were measured. RESULTS: A complete data set was available for 45 patients (22 LD) at rest and 40 patients (19 LD) on exercise. The patients were well matched for age, sex, height, weight, and pulmonary function. Patients with chronic liver disease had a hyperkinetic circulation while ventilatory variables before and during exercise were similar for the two groups. There was evidence that the circulatory changes were exacerbated by both deteriorating hepatic and pulmonary function. CONCLUSIONS: Cystic fibrosis patients with chronic liver disease have a hyperdynamic circulation similar to that documented in other forms of chronic liver disease. These circulatory changes are exacerbated by deteriorating hepatic and pulmonary function.
Adult↗
Sublobular differences in hepatic microtubular changes of alcoholic liver disease: morphometrical analysis.
To clarify the cause of predominant hepatocytic changes in the centrolobular area of livers with alcoholic liver injuries, changes in hepatic microtubules at different sublobular areas of liver with alcoholic liver disease were analyzed by ultrastructural morphometry. Hepatocytic volumes in both the centrolobular and periportal areas of livers with alcoholic liver disease were significantly larger than those in the corresponding areas of livers with non-alcoholic liver disease, respectively. The volume of hepatocytes was significantly larger in the centrolobular area than in the periportal area in both alcoholic and non-alcoholic liver diseases. However, the degree of hepatocytic enlargement in the centrolobular area was more prominent for alcoholic liver disease than for non-alcoholic liver disease. The mean volumes of microtubules, expressed per single hepatocyte, in both areas of alcoholic liver disease were significantly lower than those in the corresponding areas of non-alcoholic liver disease, respectively. In alcoholic liver disease, the microtubular volume was significantly lower in the centrolobular area than in the periportal area. However, no such difference was observed in non-alcoholic liver disease. These results indicated that a decrease in microtubules of the centrolobular area might play an important role in the development of hepatocytic changes in the centrolobular area of livers with an alcoholic liver disease.
Hepatitis, Alcoholic↗
Influence of hepatitis B virus genotypes on the development of preS deletions and advanced liver disease.
Hepatitis B virus (HBV) mutants with deletions in the preS region have not been evaluated for association with viral genotypes. In a case-control study, HBV DNA samples collected from 80 each of carriers infected with HBV genotype B or C were examined for preS deletions. PreS deletion mutants were found in a total of 37 of 160 (23%) HBV carriers. Carriers with preS deletion mutants were older (56.0 +/- 12.7 vs 49.3 +/- 16.9 years, P < 0.05), were infected more frequently with HBV genotype C (84% vs 40%, P < 0.05), and had more advanced disease, such as liver cirrhosis and hepatocellular carcinoma (54% vs 31%; P < 0.05), than did those without such mutants. In a multivariate analysis, genotype C (odds ratio [OR] = 9.3, P < 0.001) and advanced liver disease (OR = 3.1, P < 0.01) were the most significant variables in association with preS deletions. A direct repeat sequence (TCAGG) was found at the start or at the end of preS1 deletions in 6 of the 20 (30%) cases examined, and preS2 deletions in these cases were clustered over the 5'-terminal half of this region. These results indicate that the development of preS deletion mutants depends on HBV genotypes and that it may be associated with progressive liver disease.
Adult↗
Review article: thrombocytopenia in chronic liver disease and pharmacologic treatment options.
In patients with liver disease, thrombocytopenia is a clinical feature that may represent an obstacle to invasive diagnostic or therapeutic procedures, chemotherapy, and anti-viral treatment. Stimulation of the bone marrow is the most promising therapeutic intervention for thrombocytopenia in patients with chronic liver disease. The description of thrombopoietin and its (de)regulation in patients with chronic liver disease have disclosed new treatment opportunities. Indeed, pharmacologic treatment options for thrombocytopenia can be divided into treatments targeted at the thrombopoietin receptor (synthetic thrombopoietins and thrombopoietin-mimetic agents), and use of cytokines with general thrombopoietic potential. Unfortunately, use of synthetic thrombopoietin was hampered by the development of neutralizing antibodies, and thrombopoietin mimetic agents have not yet entered clinical studies. Interleukin-11 proved to be useful in increasing platelet count in patients with chronic liver disease, although its use is limited by side-effects. Erythropoietin has shown promising results in improving thrombocytopenia in cirrhotic patients. In patients with chronic liver disease, safe and well-tolerated treatments aimed at improving thrombocytopenia are still lacking. Larger studies are needed to evaluate and better characterize the thrombopoietic potential of erythropoietin. Human studies with thrombopoietin-mimetic agents are eagerly awaited in order to assess both effectiveness and safety of these drugs.
Chronic Disease↗
Liver diseases unique to pregnancy.
Severe liver diseases occur in less than 0.1% of pregnancies. Accurate diagnosis and appropriate therapy are essential to the health and survival of both the mother and fetus. Because of their low incidence and the fact that most pregnant women are cared for primarily by their obstetricians, gastroenterologists only infrequently encounter these diseases. This review is intended to update the practicing gastroenterologist on the complex spectrum of liver diseases unique to pregnancy.
Female↗
Cryptogenic chronic liver disease and hepatitis C virus infection in children.
The clinical features of 'cryptogenic' chronic liver disease and the prevalence of antibody to hepatitis C virus (HCV) in serum have been investigated in 33 Italian children (mean age 5 years). The diagnosis was based on the persistence of increased alanineaminotransferase values for longer than 6 months after the exclusion of biliary diseases, of extra-hepatic causes of hypertransaminasemia, of infection with known hepatotropic viruses and of autoimmune or metabolic disorders. Five patients had been transfused early in life, three had undergone surgery and one girl's mother had had acute non-A, non-B hepatitis during pregnancy. The remaining patients had no history of overt parenteral exposure. At presentation only 11 patients were symptomatic, the others had been referred after a check-up for intercurrent diseases. Liver histology performed in 21 cases showed persistent or mild active hepatitis in 18 cases and severe hepatitis or cirrhosis in three cases. Anti-HCV antibodies were found in 48% of the cases, including 88% with obvious exposure and 33% of the remaining cases. During a mean follow-up period of 5 years (range 1-14 years) only 11% of the cases achieved sustained biochemical remission, although none developed signs of liver failure. There was no significant difference in the clinical features and outcome of the disease between anti-HCV-positive and -negative patients. The results of this study suggest that HCV is implicated in most cases of 'cryptogenic' chronic liver disease observed in Italian children with a history of parenteral exposure and in at least one-third of the cases without overt exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
Alanine Transaminase↗
Urinary kininogen: a possible regulator of kinin formation in normal individuals and subjects with essential hypertension, end-stage renal and liver disease.
Most previous studies have not significantly correlated urinary kallikrein to urinary kinins. We investigated whether urinary kininogen might influence kinin formation within the urine. On an ad-lib diet the 24 hour excretion of total and intact kininogen, kinins and kallikrein was determined in 24 control subjects, 20 untreated essential hypertensives, 12 with end-stage renal disease and 8 subjects with liver disease. Kallikrein and kinins were measured by a direct radioimmunoassay. Total kininogen was determined from the sum of preformed kinins and kinins generated after trypsin (intact kininogen). Cross reactivity between purified human low molecular weight kininogen and bradykinin antiserum was 3%. Total and intact kininogen were significantly correlated with kinins in controls, essential hypertension and liver disease. In essential hypertension, end-stage renal and liver diseases kinins were significantly decreased. This was associated with a reduction in kininogen but not kallikrein in essential hypertension and liver disease, and a reduction in kallikrein but not kininogen in end-stage renal disease. Thus, renal kinin generation in various states may be affected by either or both kininogen and kallikrein.
Humans↗
Management of liver disease in dogs and cats.
Liver disease may cause a variety of clinical signs, including depression, anorexia, weakness, weight loss, vomiting, diarrhea, fever, abdominal pain, jaundice, ascites and CNS signs. Treatment is aimed at eliminating the cause, providing supportive care, and preventing secondary complications. Rest facilitates liver regeneration. Hypokalemia, respiratory alkalosis and hypoglycemia may complicate liver disease. Fluids should be given IV rather than SC to severely dehydrated animals. Preferred solutions include Ringer's and half-strength saline with 2.5% dextrose. Solutions containing lactate should not be used. Dietary management includes feeding adequate amounts of protein of high biologic value, carbohydrates, fat, vitamins and minerals.
Acid-Base Imbalance↗
Biliary excretion of aluminum in aluminum osteodystrophy with liver disease.
Two patients with chronic liver disease developed elevated serum aluminum concentrations and biopsy-proven osteodystrophy. Neither patient had chronic renal failure but both had received aluminum-containing antacids for long periods. We measured biliary and urinary aluminum excretion during antacid loading in patients with normal liver function. Our studies show that biliary excretion is an important route of elimination of orally absorbed aluminum, and we suggest that long-term antacid therapy in patients with severe liver disease be monitored with periodic serum and urinary aluminum determinations to avoid aluminum osteodystrophy.
Adult↗
Metabolic liver disease in the pediatric patient.
Most metabolic liver diseases that affect pediatric patients present in the neonatal period with either cholestasis or acute liver failure. Metabolic liver disease in the older child has considerable overlap with adult patients. New diagnostic methods and therapy, including liver transplantation, has radically changed the outcome of many metabolic liver diseases.
Alagille Syndrome↗
The diagnostic value of the ratio of serum gamma-glutamyl transpeptidase to alkaline phosphatase in alcoholic liver disease.
A prospective study of the initial liver laboratory tests was carried out in the following patients: 55 patients with alcoholic liver disease, 53 with cholangitis, 41 with hepatocellular carcinoma, 65 with acute viral hepatitis, and 49 with hepatitis-B surface antigen-positive chronic active hepatitis. There was considerable overlap in the levels of the serum gamma-glutamyl transpeptidase (GT) and alkaline phosphatase (AP) among the five groups. However, the ratio of GT to AP was significantly higher in the group with alcoholic liver disease than in any of the other four groups. When the ratio was higher than 1.4, the diagnostic efficiency for distinguishing the alcohol group from the other four groups was 78% (the normal upper limit for GT and AP being 35 and 115 U/1, respectively). A possible explanation for this higher ratio in alcoholic liver disease is suggested. We conclude that when the GT and AP is greater than 1.4, it is of greater diagnostic value than either variable alone in differentiating alcoholic from other liver diseases.
Alkaline Phosphatase↗