[Rapid reversal of cirrhosis after excision of the cirrhotic portion of the liver; effect of liver diet; laws governing liver regeneration].
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Animals↗
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Carcinoembryonic antigen(s) in liver disease. II. Isolation from human cirrhotic liver and serum and from normal liver.
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Adenocarcinoma↗
[Determination of the biological value of liver-protective agents with special reference to liver preparations. 8. Description of the method for the biological evaluation of preventive and therapeutic liver-protective agents].
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Alcohols↗
[Histological follow-up of latent chronic liver diseases in an area with endemic liver cancer and liver cirrhosis (Tomie-Cho, Goto Island, Nagasaki Prefecture].
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Adolescent↗
Auxiliary liver transplantation for acute liver failure.
In summary, the following principles are worth reiterating: 1. In the treatment of acute liver failure, protection of the native liver in anticipation that it will recover, but positioning of the allograft in a manner that optimizes its function for both the short and long term (in the event that the native liver does not recover) are important goals. Therefore, orthotopic positioning offers advantages over the heterotopic position in most cases. Development of better techniques for predicting native liver recovery might remove any of these advantages of the orthotopic position. 2. Other than the presence of fibrosis, the performance of a native liver biopsy does not appear to predict native liver recovery. The decision of whether to attempt auxiliary grafting must be based on an understanding of the natural history of the disease causing the acute liver failure. 3. The heterotopic position has the advantage of not requiring partial native hepatectomy in order to accommodate the allograft. However, except for the recent experience of Terpstra et al, this technique has carried a higher risk of venous outflow obstruction. It also requires additional space within the abdomen, usually mandating the use of prosthetic abdominal wall closures and the construction of venous conduits for portal venous inflow to the liver. There is the additional theoretical concern about competition for portal venous flow leading to eventual atrophy of the allograft liver. 4. Common events that follow liver transplantation result in changes in portal venous resistance within the liver, events that therefore alter the relative distribution of portal venous inflow between native and auxiliary livers. These events include reperfusion injury, allograft rejection, allograft viral infection (e.g., cytomegalovirus, Epstein-Barr virus, recurrent viral hepatitis), and native liver regeneration. Attempts to control portal venous flow to favor one liver over the other must account for the effect of these factors. 5. In general terms, auxiliary transplantation is not indicated for diseases in which the residual native liver either represents an ongoing threat to the recipient or is incapable of supporting life alone. This may be the case in both metabolic disorders and in cirrhosis. Most of the alleged difficulties of native hepatectomy are no longer relevant. Therefore, auxiliary transplantation is rarely if ever indicated for chronic liver disease and may not be of any additional benefit over total transplantation in the treatment of many metabolic disorders. 6. In the treatment of acute liver failure, the value of an auxiliary transplant over total transplant is obtained when the native liver recovers and the patient is withdrawn from immunosuppression. If further experience shows the effectiveness of this option, total liver transplantation with the requirement for life-long immunosuppression will no longer be appropriate for the treatment of patients with acute liver disease.
Arteriovenous Shunt, Surgical↗
Hepatic stellate cells and liver retinoid content in alcoholic liver disease in humans.
Body retinoids are stored in the lipid droplets of hepatic stellate (Ito) cells. In chronic liver disease, the stellate cells differentiate into myofibroblast-like cells, a process whereby they lose their retinoid-containing lipid droplets. We studied the relation between liver retinoid content, the number of lipid droplets per stellate cell, and the number of stellate cells per mm2 in human alcoholic liver disease. Semithin sections of liver biopsies from normal subjects and patients with early (steatosis, inflammation, and mild fibrosis) and late (cirrhosis and cirrhosis with acute alcoholic hepatitis) alcoholic liver disease were morphometrically evaluated. Liver retinoid content was determined by HPLC. In normal patients, liver retinoid content was 901 +/- 213 IU/g of liver (mean +/- SEM). There was a decrease in liver retinoid content in early alcoholic liver disease (409 +/- 50 IU/g) and a further reduction in cirrhosis (153 +/- 50 IU/g). In patients with acute alcoholic hepatitis, retinoid content was strikingly low (5.2 +/- 1.8 IU/g). There was a progressive decrease in the number of stellate cells per mm2 associated with progressive liver damage. We found a fair correlation between the number of stellate cells per mm2 and liver retinoid content in all patient groups (overall correlation: 0.71). In normal subjects, the mean number of lipid droplets per stellate cell was 7.4 +/- 0.7. In patients with early alcoholic liver disease and in patients with alcoholic cirrhosis, this value was increased to 13.6 +/- 0.8 and 10.4 +/- 2.0, respectively. In patients with acute alcoholic hepatitis, only a few lipid droplets were present (4.2 +/- 0.5). There was a good correlation between liver retinoid content and mean number of lipid droplets in normal patients (r = 0.58). In alcoholic cirrhosis, however, correlation was poor (r = 0.34). In early alcoholic liver disease, the correlation was absent (r = 0.004). In conclusion, the major finding of our study is that the correlation between the mean number of lipid droplets per stellate cell and liver retinoid content varies according to the hepatic pathology considered. Marked lipid droplet accumulation occurs in stellate cells in early alcoholic liver disease and, to a lesser extent, in alcoholic cirrhosis, but there is no correlation between the mean number of lipid droplets per stellate cell and liver retinoid content. Therefore, not retinoids but probably lipids are responsible for the accumulation of lipid droplets. We also find that there is a fair correlation between the number of stellate cells per mm2 and liver retinoid content in all patient groups. Finally, we confirm the decrease in hepatic retinoid content that occurs in alcoholic liver disease in humans, even at the early stages of the disease.
Biopsy↗
Auxiliary partial orthotopic liver transplantation for acute liver failure in two children.
Acute liver failure in children and adults is associated with a high mortality rate. At present the treatment of choice is orthotopic whole-liver transplantation. However, allogeneic liver transplantation necessitates lifelong immunosuppressive therapy, which is associated with substantial risks to the patient. Temporary auxiliary partial orthotopic liver transplantation has been developed recently as an alternative, enabling the native liver to regenerate while avoiding the risks of long-term immunosuppressive treatment. Here we describe two cases of partial orthotopic liver transplantation in children. Auxiliary partial orthotopic liver transplantation was performed in two boys (5 and 6 years old) suffering from acute liver failure of unknown origin. The native left lateral liver lobes (segment II and II) were removed and replaced by left lateral liver grafts from young blood-group-compatible adults. In the first child the native liver, which was 80% necrotic at time of transplantation, showed regeneration within two weeks and the partially necrotic graft could be surgically removed on day 15 after auxiliary transplantation. Four years after transplantation, the child is in excellent condition with normal liver function and does not require any treatment. In the second case the native liver (90% necrotic at time of transplantation) regenerated within 6 weeks of transplantation, at which time the transplanted liver was removed. The patient developed aplastic anemia and died 2 months after transplantation from candida sepsis. The conclusion was that auxiliary partial liver transplantation in childhood provides a valuable option to maintain liver function in acute liver failure until functional recovery of the native liver. The main advantage over whole-liver transplantation is the chance to avoid lifelong immunosuppression. However, there is a higher surgical risk. Therefore, auxiliary transplantation should be considered carefully in every case of acute liver failure in children.
Adult↗
Role of fatty liver, dietary fatty acid supplements, and obesity in the progression of alcoholic liver disease: introduction and summary of the symposium.
Alcoholic liver disease is a major cause of illness and death in the United States. In the initial stages of the disease, fat accumulation in hepatocytes leads to the development of fatty liver (steatosis), which is a reversible condition. If alcohol consumption is continued, steatosis may progress to hepatitis and fibrosis, which may lead to liver cirrhosis. Alcoholic fatty liver has long been considered benign; however, increasing evidence supports the idea that it is a pathologic condition. Blunting of the accumulation of fat within the liver during alcohol consumption may block or delay the progression of fatty liver to hepatitis and fibrosis. To achieve this goal, it is important to understand the underlying biochemical and molecular mechanisms by which chronic alcohol consumption leads to fat accumulation in the liver and fatty liver progresses to hepatitis and fibrosis. In addition to alcohol consumption, dietary fatty acids and obesity have been shown to affect the degree of fat accumulation within the liver. Again, it is important to know how these factors modulate the progression of alcoholic liver disease. The National Institute on Alcohol Abuse and Alcoholism and the Office of Dietary Supplements, National Institutes of Health, sponsored a symposium on "Role of Fatty Liver, Dietary Fatty Acid Supplements, and Obesity in the Progression of Alcoholic Liver Disease" in Bethesda, Maryland, USA, October 2003. The following is a summary of the symposium. Alcoholic fatty liver is a pathologic condition that may predispose the liver to further injury (hepatitis and fibrosis) by cytochrome P450 2E1 induction, free radical generation, lipid peroxidation, nuclear factor-kappa B activation, and increased transcription of proinflammatory mediators, including tumor necrosis factor-alpha. Increased acetaldehyde production and lipopolysaccharide-induced Kupffer cell activation may further exacerbate liver injury. Acetaldehyde may promote hepatic fat accumulation by impairing the ability of peroxisome proliferator-activated receptor alpha to bind DNA, and by increasing the synthesis of sterol regulatory binding protein-1. Unsaturated fatty acids (corn oil, fish oil) exacerbate alcoholic liver injury by accentuating oxidative stress, whereas saturated fatty acids are protective. Polyenylphosphatidylcholine may prevent liver injury by down-regulating cytochrome P450 2E1 activity, attenuating oxidative stress, reducing the number of activated hepatic stellate cells, and up-regulating collagenase activity. Nonalcoholic steatohepatitis may develop through several mechanisms, such as oxidative stress, mitochondrial dysfunction and associated impaired fat metabolism, dysregulated cytokine metabolism, insulin resistance, and altered methionine/S-adenosylmethionine/homocysteine metabolism. Obesity (adipose tissue) may contribute to the development of alcoholic liver disease by generating free radicals, increasing tumor necrosis factor-alpha production, inducing insulin resistance, and producing fibrogenic agents, such as angiotensin II, norepinephrine, neuropeptide Y, and leptin. Finally, alcoholic fatty liver transplant failure may be linked to oxidative stress. In vitro treatment of fatty livers with interleukin-6 may render allografts safer for clinical transplantation.
Animals↗
Evaluation of the effect of age on functioning hepatocyte mass and liver blood flow using liver scintigraphy in preoperative estimations for surgical patients: comparison with CT volumetry.
BACKGROUND: The effect of age on functioning hepatocyte mass and liver blood flow was examined using (99m)Tc-galactosyl-human serum albumin (GSA) liver scintigraphy in patients with liver tumors awaiting surgery. MATERIALS AND METHODS: Seventy-two patients with liver tumors, but normal liver parenchyma, were included in this study; patients with compromised hepatic blood flow as a result of vascular invasion or thrombus were excluded. The liver volume, calculated liver volume, and liver blood flow index (K value) were preoperatively determined by liver scintigraphy using GSA. These three parameters and liver volume measured by computed tomography volumetry (CT-LV) and the standard liver volume (ST-LV), calculated from the patient's body surface area, were examined for correlations with the patient's age. The K value was compared with the indocyanine green dye retention rate, and both sets of results were examined for correlation with the patient's age. RESULTS: Both the CT-LV and the ST-LV decreased with age, resulting in an unchanged CT-LV/ST-LV ratio with aging. The liver volume and calculated liver volume measured by scintigraphy both decreased with age, even when body size was taken into account. Therefore, in elderly patients, the liver was not morphologically smaller, but the hepatocyte mass in the liver decreased. Furthermore, liver blood flow per unit of functional liver volume determined from the blood flow index did not change with age. CONCLUSIONS: These results, suggesting a discrepancy between liver volume estimated by CT and actual functioning hepatocyte volume in the elderly, may have a critical impact on preoperative liver functional reserve evaluation prior to hepatic resection in elderly patients.
Adult↗
Rejection of pig liver xenografts in patients with liver failure: implications for xenotransplantation.
The pathophysiological state of rejection in liver xenotransplantation is poorly understood. Data from clinical pig liver perfusion suggest that pig livers might be rejected less vigorously than pig hearts or kidneys. Pig livers used in clinical xenoperfusions were exposed to blood from patients with liver failure. We have shown in an animal model that transplant recipients with liver failure are less capable of initiating hyperacute rejection of a xenografted liver than a healthy transplant recipient. The goal of this report is to examine the pathological characteristics of pig livers used in 2 clinical pig liver perfusions and combine this information with in vitro studies of pig-to-human liver xenotransplantation to determine whether the findings in the perfused pig livers could be explained in part by the diminished capacity of the patient with liver failure to respond to xenogeneic tissue. Pathological analysis of the perfused pig livers showed immunoglobulin M deposition in the sinusoids with little evidence of complement activation. Our in vitro studies showed that serum from patients with liver failure caused less injury to pig liver endothelium than serum from healthy subjects. Serum from patients with liver failure had similar levels of xenoreactive antibodies as serum from healthy humans. Incubation of serum from patients with liver failure with pig hepatic endothelial cells generated less iC3b, Bb fragment, and C5b-9 than serum from healthy subjects. We conclude that the altered injury in the perfused pig livers can be attributed to the relative complement deficiency that accompanies liver failure.
Animals↗
Etiology of human liver cancer: controlled prospective study in liver cirrhosis.
The incidence of primary liver cell carcinoma was investigated in a prospective study over 6 yr and 5 mo in 403 clinically unselected patients derived from a homogeneous population by means of serial determination of alpha 1-fetoprotein (AFP) by radioimmunoassay. The diagnosis of liver cirrhosis was proved in 90% by laparoscopy and/or histology and/or autopsy. The incidence of primary liver cell carcinoma in liver cirrhosis in the clinically studied patients was 4.47%, significantly lower than in the autopsy material (11.03%; p less than or equal to 0.025). In the follow-up study, all patients with increasing AFP concentrations exhibited a primary liver cell carcinoma. A transitory rise of AFP (higher than 50 ng/ml) was observed in 15.1% of patients with liver cirrhosis without primary liver cell cancer. In contrast to the results of animal experiments, this transitory rise of AFP was not followed by malignant transformation of the cirrhotic tissue. Posthepatitic liver cirrhosis was observed in 21.57%, postalcoholic liver cirrhosis in 42.93%, and cryptogenic liver cirrhosis in 27.30%. Liver cirrhosis of other etiology occurred in 8.19%. The incidences of primary liver cell cancer in these 4 groups were 4.94, 4.62, 5.45, and 0%, respectively. These differences are not statistically significant, although in absolute figures postalcoholic liver cirrhosis is the main cause of primary liver cell carcinoma in this sample from West Germany. HBs antigen-positive liver cirrhosis was more often associated with primary liver cell cancer than HBs antigen-negative liver cirrhosis (6.58 versus 3.96%); this difference also is not statistically significant. Observations of larger groups of patients may show a higher risk of developing primary liver cell carcinoma in those with a combination of alcohol abuse and HBs antigenemia and/or acute hepatitis in the history. Patients without these 2 risk factors had an incidence of primary liver cell carcinoma of 2.61%; those with 1 risk factor, 5.77%; and those with both risk factors, 10.71%.
Carcinoma, Hepatocellular↗
New management options for end-stage chronic liver disease and acute liver failure: potential for pediatric patients.
The management of children with end-stage chronic liver disease and acute liver failure mandates a multidisciplinary approach and intense monitoring. In recent years, considerable progress has been made in developing specific and supportive medical measures, but studies and publications have mainly concerned adult patients. Therapeutic approaches to complications of end-stage chronic liver disease and acute liver failure (e.g. refractory ascites, hepatorenal syndrome, encephalopathy, and cerebral edema) that may be applied to children are reviewed in this article.Mild-to-moderate ascites should be managed by modest salt restriction and oral diuretic therapy in the first instance. Large volume paracentesis associated with colloid volume expansion and diuretic therapy may be effective for acute relief. Treatment of hepatorenal syndrome type 1 with vasopressin analogs (terlipressin) is recommended prior to liver transplantation in order to improve renal function. Prevention and treatment of chronic hepatic encephalopathy are directed primarily at controlling the events that may precipitate hepatic encephalopathy and at reducing ammonia generation and increasing its detoxification or removal. In addition to reduction of gut ammonia production using non-absorbable disaccharides such as lactulose and/or antibacterials such as neomycin, sodium benzoate may be used on a long-term basis to prevent, stabilize, or improve hepatic encephalopathy. The management of hepatic encephalopathy in acute liver failure is considerably more unsatisfactory; treatment is aimed at preventing brain edema and intracranial hypertension. Extracorporeal liver support devices are now used commonly in critically ill children with acute renal failure, advanced hepatic encephalopathy, cerebral edema, intracranial hypertension, and severe coagulopathy. Continuous renal replacement therapy could potentially help support patients until liver transplantation is performed or liver regeneration occurs. The Molecular Adsorbent Recirculating System (MARS or albumin dialysis) is the liver support system most frequently used worldwide in adults and appears to offer distinct advantages over hepatocyte-based systems. There are no specific medical therapies or devices that can correct all of the functions of the liver. Apart from a few metabolic diseases presenting with severe liver dysfunction for which specific medical therapies may preclude the need for liver transplantation, liver transplantation still remains the only definitive therapy in most instances of end-stage chronic liver disease and acute liver failure. Future research should focus on gaining a better understanding of the mechanisms responsible for liver cell death and liver regeneration, as well as developments in hepatocyte transplantation and liver-directed gene therapy.
Ascites↗
[Therapy effects of fenofibrate on alcoholic fatty liver and drug-induced fatty liver in rats].
OBJECTIVE: To investigate the fat decreasing effects of fenofibrate on alcoholic fatty liver and drug-induced fatty liver in rats. METHODS: Alcoholic fatty liver and drug-induced fatty liver rats models were established. The two kinds of rats with fatty liver were seperatedly divided into fenofibrate treatment group (80 mg/kg daily) and control group without treatment. Rats were killed after four weeks, then the levels of serum triglycerides (TG), total cholesterol (TC), high density lipoprotein (HDL) and malondialdehyde (MDA), hepatic lipase (HL), lipoprotein lipase (LPL) both in serum and liver tissue were measured according to the Test Kits. Histopathological changes in liver was dyed with HE and observed under light microscope. RESULTS: After treatment by fenofibrate, in the serum of rats with alcoholic fatty liver, the level of TG decreased significantly (1.07 mmol/L 0.06 mmol/L vs 1.56 mmol/L 0.29 mmol/L, t=5.115, p<0.001), while the level of TC had no alteration. The levels of MDA both in serum and liver tissue decreased (1.10 nmol/L 0.22 nmol/L vs 1.26 nmol/L 0.21 nmol/L, t=0.592, p<0.05; 5.92 nmol/g 1.24 nmol/g vs 7.42 nmol/g 1.22 nmol/g, t=3.477, p<0.05, respectively), while the levels of HL, LPL in serum and liver tissue increased significantly (Serum: 0.053muEq/ml/h 0.006muEq/ml/h vs 0.037 muEq/ml/h 0.006muEq/ml/h, t=-5.086, p<0.001; 0.018 muEq/ml/h 0.004 muEq/ml/h vs 0.014muEq/ml/h 0.004muEq/ml/h, t=-2.485, p<0.05. Liver tissue: 0.075muEq/ml/h 0.010muEq/ml/h vs 0.065muEq/ml/h 0.007muEq/ml/h, t=-2.437, p<0.05; 0.022 muEq/ml/h 0.014 muEq/ml/h vs 0.008 muEq/ml/h 0.002 muEq/ml/h, t=-2.876, p<0.05). Fat content in liver decreased (26.01 mg/g 1.69 mg/g vs 71.45 mg/g 2.66 mg/g, t=-43.224, p<0.001). The pathological changes of liver in fenofibrate-treated rats with alcoholic fatty liver were improved. For the drug-induced fatty liver rats, fenofibrate treatment group had no difference from the untreated control group. CONCLUSION: Fenofibrate can significantly decrease the fat content in liver tissue of rats with alcoholic fatty liver, as well as ameliorating liver pathological changes. But fenofibrate has no effect on drug-induced fatty liver.
Animals↗
[Prospective study of liver parenchyma volume in hepatectomy of primary liver cancer].
OBJECTIVE: To explore the secure resection margin (RM) of hepatectomy for primary liver cancer (PLC) with the coexistence of cirrhosis or hepatitis by studying the correlations of the resected liver parenchyma volume with postoperative liver function, complication and RM clinically. METHODS: The volume of tumor and the surrounding liver in resected liver specimen was measured and calculated in continuous 76 PLC patients prospectively, and the total liver parenchyma volume was measured and calculated using computed tomography (CT) images in former 40 patients. Under ideal circumstances, the surrounding liver volume, which would be resected theoretically, was calculated according to various sizes of tumors and RMs. The correlations of the resected liver volume or hepatic parenchyma-resected rate (HPRR) with postoperative liver function, complication and RM were analysed. RESULTS: The RM was (5 +/- 7) mm in 76 patients. The volume of the tumors and the surrounding liver in the specimens were (107 +/- 203) cm(3) and (153 +/- 120) cm(3), respectively. In 40 patients, the total nontumorous liver volume using CT images was (1079 +/- 179) cm(3), and HPRR was (14 +/- 9)%. There were statistically significant differences in HPRR (P < 0.05) between three groups with complication score 0, 1-2 and 3-6 points, the value of the first group were lower than that of the third group at the level P < 0.05. The significant factors affecting liver function and complication are HPRR, the size of operation, the time of hepatic portal occlusion and the resected liver volume (P < 0.05) apart from preoperative liver function. CONCLUSIONS: When hepatectomy was performed in PLC patients with preoperative liver function of Child A grade and the coexistence of cirrhosis or hepatitis, 30% HPRR was a lower limit for greatly increasing the chance of developing serious postoperative complications, while 20% HPRR was a safe upper limit for achieves quick postoperative recovery or developing only a few mild complications. When PLC patients without macroscopic tumor thrombi or macrosatellites undergo hepatectomy, 10 mm RM is enough to ensure sufficient liver function residue and achieve complete micrometastasis clearance in liver parenchyma surrounding the lesion if the diameter of a tumor is less than 10 cm and 6 mm RM is enough to ensure sufficient liver function residue and obtain 99% micrometastasis clearance if the diameter of a tumor is greater than 10 cm, while with macroscopic tumor thrombi or macrosatellites, 20 mm RM is enough to ensure sufficient liver function residue and achieve 99% micrometastasis clearance if the diameter of a tumor is less than 6 cm.
Adult↗
A clinicopathologic study of adenomatous hyperplasia of the liver in 209 consecutive cirrhotic livers examined by autopsy.
BACKGROUND: Adenomatous hyperplasia (AH), also called macroregenerative nodule, of the cirrhotic liver is currently considered to be a preneoplastic or early neoplastic lesion in human hepatocellular carcinogenesis. METHODS: The authors surveyed 209 consecutive cirrhotic livers from patients who had undergone autopsy at our laboratory during the last 18 years (1974-1991), and examined the prevalence and clinicopathologic characteristics of cirrhotic livers with AH. AH was classified into two types: ordinary and atypical. Ordinary AH (OAH) is devoid of hepatocellular atypia, whereas atypical AH (AAH) consists of atypical hepatocytes equivocal as to benignity and malignancy and occasionally contains overt malignant foci. RESULTS: A total of 123 AH were found in 45 (21.5%) of the 209 cirrhotic livers; 38 AAH were found in 12 cirrhotic livers (5.7%), and 85 OAH was found in 41 cirrhotic livers (19.6%). Nineteen AAH contained overt malignant hepatocellular foci. Comparing the first 9 years (1974-1982) with the latter 9 years (1983-1991), 4 (3.8%) of 104 cirrhotic livers harbored AAH in the first period, and 8 (7.4%) of 105 cirrhotic livers contained AAH in the latter period. Sixteen (15.4%) of 104 cirrhotic livers harbored OAH in the first period, and 25 (23.8%) of 105 cirrhotic livers contained OAH in the latter period. Etiology of the 12 cirrhotic livers with AAH was as follows: 1 was hepatitis B virus, 10 were non-A non-B hepatitis virus, and 1 was primary biliary cirrhosis. Etiology of 41 cirrhotic livers with OAH was as follows: 16 were hepatitis B virus, 18 were non-A non-B hepatitis virus, and 7 were other causes. AAH occurred commonly in mixed nodular cirrhosis, whereas OAH occurred usually in macronodular or mixed nodular cirrhosis. All 12 cirrhotic livers with AAH were associated with hepatocellular carcinoma (HCC), particularly HCC of nodular type, whereas 17 cirrhotic livers with OAH were associated with HCC and the remaining 24 cirrhotic livers with OAH were not associated with HCC. CONCLUSIONS: These results suggest that the number of cirrhotic livers with AH is increasing gradually, and that cirrhotic livers with AAH are characterized by the association with non-A non-B hepatitis virus as well as simultaneous occurrence of HCC. Thus, AAH may be an important preneoplastic lesion in cirrhotic livers associated with non-A non-B hepatitis virus (probably hepatitis C virus).
Adolescent↗
Definition of liver tumors in the presence of diffuse liver disease: comparison of findings at MR imaging with positive and negative contrast agents.
PURPOSE: The potential to define liver tumors at magnetic resonance (MR) imaging was compared with a positive and a negative contrast agent (gadoxetic acid disodium, or gadolinium EOB-DTPA [a hepatocyte-directed agent], and ferumoxides, or superpara-magnetic iron oxide particles [a Kupffer cell-directed agent], respectively) in normal rats and in rats with induced acute hepatitis, fatty liver, or cirrhosis. MATERIALS AND METHODS: Rats with implanted liver adenocarcinomas were divided into four groups: no diffuse liver disease ("normal" [n = 6]) and diffuse liver diseases (induced acute hepatitis [n = 6], fatty liver [n = 6], or cirrhosis [n = 6]). Rats first received gadoxetic acid disodium (50 mumol/kg) and then, 45 minutes later, ferumoxides (10 mumol/kg). Liver signal intensity enhancement and tumor-to-liver contrast-to-noise ratio (C/N) were measured in each group. RESULTS: Mean liver signal intensity enhancement values with gadoxetic acid disodium and ferumoxides were excellent in the normal liver model (176% and -62%, respectively; P < .01) but were significantly reduced in the acute hepatitis model (82% and -36%, respectively). In the fatty livers compared with the normal livers, enhancement with gadoxetic acid disodium was reduced (57%) but with ferumoxides was excellent (-55%). In the cirrhotic livers compared with the normal livers, enhancement with gadoxetic acid disodium (174%) was virtually the same but was impaired with ferumoxides (-43%). CONCLUSION: Hepatic enhancement and tumor-to-liver C/N with either positive or negative liver-enhancing agents can be impaired by the presence of underlying liver disease. Prior knowledge of the type of diffuse liver disease may influence the choice of contrast agent for tumor detection.
Acute Disease↗
Phenotypic and functional characteristics of lymphocytes isolated from liver biopsy specimens from patients with active liver disease.
Liver-derived lymphocytes were isolated from 73 liver biopsy specimens obtained from patients with chronic active liver disease and from six samples of normal liver. Mean absolute numbers (+/- S.E.M) of liver-derived lymphocytes recovered from needle biopsy specimens by mild enzymatic digestion of the liver tissue varied from 0.7 +/- 0.3 x 10(3)/mm3 in allografts being rejected to 8.9 +/- 0.9 X 10(3)/mm3 in chronic non-A, non-B hepatitis. By two-color flow cytometry, T lymphocytes (CD3+) were the major liver-derived lymphocyte population in all biopsy specimens. The mean CD4/CD8 ratio (0.6 +/- 0.2) was similar for liver-derived lymphocytes obtained from samples of normal or diseased liver. However, activated (human leukocyte antigen DR+) T cells were significantly (p less than 0.05) increased in liver-derived lymphocytes obtained from liver disease specimens than they were in samples from normal livers. Natural killer cells were less numerous than T cells in specimens obtained from diseased livers, with the mean natural killer/T cell ratio ranging from a low of 0.1 in allograft rejection to a high of 0.8 +/- 0.3 in primary sclerosing cholangitis. Liver-derived lymphocytes isolated from diseased liver contained significantly fewer (p less than 0.05) CD3-CD56+ or CD56+CD16-natural killer cells than did those obtained from normal liver samples. Natural killer activity was consistently detectable in liver-derived lymphocytes obtained from specimens of normal or diseased livers. Moreover, natural killer activity in the liver did not differ significantly from that in either normal or patient peripheral blood.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Signal changes in liver and spleen after Endorem administration in patients with and without liver cirrhosis.
The goal of this study was compare the effect of Endorem on the signal intensity of the spleen in patients with normal liver tissue and in patients with liver cirrhosis. Thirty patients with normal liver tissue and 47 with liver cirrhosis were examined before and after i.v. Endorem administration. The patients were examined with a 1.5-T magnet system (Magnetom Vision) using a semiflexible cp-array coil. Three different pulse sequences were used: a T1-weighted gradient-echo sequence, a T2-weighted fast spin-echo sequence with spectral fat suppression, and a T2*-weighted gradient-echo sequence. The signal-to-noise ratios (SNRs) of two areas of the liver and spleen were determined. The mean SNRs of the liver and spleen in patients with and without liver cirrhosis were compared. For assessment of statistical significance, the t-test at a level of P < 0.05 was applied. After i.v. administration of Endorem, no differences were seen with the T1-weighted gradient-echo sequence for the liver and spleen and, with the T2-weighted fast spin-echo sequence, no differences were found for the spleen. Significant differences between both groups were seen for the liver with the T2-weighted fast spin-echo sequence. The SNR in the noncirrhotic liver group was 57.4% lower than the SNR in the cirrhotic liver group. With the T2*-weighted gradient-echo sequence, the SNRs of the liver and spleen in the noncirrhotic liver group, compared with the cirrhotic liver group, were 126.8% and 45.6% less, respectively. The effect of Endorem on the liver in patients with Child C-stage liver cirrhosis was 32.1% less than in patients with Child B-stage liver cirrhosis. Likewise, the Endorem effect on the spleen was 27.1% less in patients with Child C-stage compared with Child B-stage liver cirrhosis. Hepatic and splenic uptake of Endorem is significantly decreased in patients with liver cirrhosis.
Adult↗