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At least 145 records · Page 8Linked to original sources
PubMed1991

Hepatic histological findings after transplantation for chronic hepatitis B virus infection, including a unique pattern of fibrosing cholestatic hepatitis.

Long-term follow-up of 27 patients with hepatitis B virus-related chronic liver disease treated by transplantation showed that 23 had hepatitis B virus recurrence. In 13 patients late changes in the grafts were similar to those described in other series: minor abnormalities in five cases, chronic active hepatitis in five cases and non-hepatitis B virus-related graft dysfunction in three cases. Three patients had incomplete histological follow-up. Analysis of the histological changes and viral antigen expression in six cases revealed a distinct and novel pattern termed fibrosing cholestatic hepatitis. Development of fibrosing cholestatic hepatitis was associated with rapidly progressive graft dysfunction. It is postulated that this pattern of fibrosing cholestatic hepatitis develops because of a high cytoplasmic expression of viral antigens, including HBsAg. The remaining case had some features of fibrosing cholestatic hepatitis. The main histological features of this unique syndrome include thin, perisinusoidal bands of fibrosis extending from portal tracts to surround plates of ductular-type epithelium; prominent cholestasis; ground-glass transformation; and ballooning of hepatocytes with cell loss and mild mixed inflammatory reaction.

Adult↗
PubMedDate not supplied

The comparative effect of administration of substances via the hepatic artery or portal vein on hepatic arterial resistance, liver blood volume and hepatic extraction in cats.

Compounds reaching the liver do so via either the hepatic artery or the portal vein. This paper reports on the effectiveness of administration of compounds into these alternate routes for their effects on the hepatic parenchymal cells, the hepatic arterial resistance vessels (blood flow) and hepatic capacitance (blood volume responses). All tests were done on cats under pentobarbital anesthesia. Perfusion of the parenchymal cell mass was assessed by comparing the hepatic elimination of indocyanine green (ICG) administered via the two vascular routes. The ICG uptake was assessed by measuring relative areas under the hepatic venous outflow curve obtained following bolus injections of ICG into the artery and portal vein. In a separate series, using different methods, the hepatic venous levels reached early (2 min) and later (5 min) during a constant infusion were compared during administration via the two routes and found to be equal. Parenchymal cell functions (ICG extraction, bile salt stimulation of bile flow) indicate that blood from the artery and portal vein supplies the hepatic parenchymal cells equally well. This suggests a well-mixed blood supply prior to exposure of either blood stream to parenchymal cells. Substances being processed by the liver are thus equally well handled if reaching the liver via either the arterial or portal blood stream. This has significance in validating the use of some isolated liver perfusion methods that perfuse only via the portal vein. Access of vasoactive compounds in the two blood streams to hepatic arterial resistance vessels was assessed using electromagnetic flow probes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1997

Hepatic expression of inducible nitric oxide synthase transcripts in chronic hepatitis C virus infection: relation to hepatic viral load and liver injury.

Hepatitis C virus (HCV) causes acute and often also chronic liver disease. Hepatocellular injury might result from both a host response directed to inhibit viral spread and from processes initiated by the virus itself. To study mechanisms involved in hepatocellular injury, liver tissue from chronically HCV-infected patients was analyzed for the expression of the inducible isoform of nitric oxide synthase (iNOS) and for interferon gamma (IFN-gamma) by a quantitative, competitive reverse-transcription-polymerase chain reaction (RT-PCR) technique. Moreover, hepatic viral load was determined by two independent techniques, and liver tissue was evaluated histopathologically in detail. Liver tissue from HCV-infected patients was shown to express elevated levels of iNOS transcripts compared with non-HCV-infected patients. Increased iNOS transcript expression, however, was not accompanied by significantly elevated serum nitrite plus nitrate (NOx) concentration, although some of the chronic HCV-infected patients reached markedly higher serum NOx levels than the control group or healthy individuals, respectively. Hepatic iNOS expression was found to be positively correlated to hepatic HCV-RNA content on the one hand, and weakly to hepatic IFN-gamma expression, previously shown to be solely associated with hepatic necro-inflammatory activity among the histopathological parameters studied, on the other hand. In contrast to IFN-gamma transcript expression, neither hepatic iNOS expression nor hepatic HCV-RNA content were related to hepatic inflammatory activity. The presented data are compatible with the assumption that HCV might be able to stimulate iNOS expression both directly and indirectly via its capacity to induce IFN-gamma.

Adult↗
PubMed1998

Hepatic microcirculation during transient hepatic venous occlusion--intravital microscopic observation using hepatic vein clamp model in the mouse.

The purpose of this experiment was to evaluate the etiology of hepatic dysfunction in patients difficult to wean from cardiopulmonary bypass. We hypothesized that increased central venous pressure and subsequent hepatic congestion during weaning from cardiopulmonary bypass would lead to hepatic dysfunction. To induce hepatic congestion in mice, we clamped the hepatic vein for fifteen min, and observed the microcirculation of the liver using an intravital microscope during clamping and the following 30 min of reperfusion. During reperfusion, non-reflow phenomenon, leukocytes adhesion to the wall of sinusoids, erythrocytes sludging, acute swelling of hepatic cells and narrowing of sinusoids were observed. These phenomena were indicative of warm ischemia-reperfusion injury of the liver itself. Based on these findings we concluded that, after repeated episodes of warm ischemia and reperfusion of the liver, hepatic cells would be damaged, and finally hepatic dysfunction was induced. To prevent hepatic dysfunction, repeated attempts to wean the patient from cardiopulmonary bypass should be avoided and increases central venous pressure should be prevented by early use of cardiopulmonary support.

Animals↗
PubMedDate not supplied

Changes of serum hepatitis B virus DNA in two types of clinical events preceding spontaneous hepatitis B e antigen seroconversion in chronic type B hepatitis.

Two types of clinical events, acute exacerbation and uneventful course, precede spontaneous HBeAg seroconversion to its antibody (anti-HBe) in chronic type B hepatitis. To examine the possible mechanism responsible for these two types of clinical events, serial serum specimens from 75 patients who underwent spontaneous HBeAg seroconversion were assayed for hepatitis B virus DNA by slot blot hybridization with 32P-labeled cloned hepatitis B virus DNA as probe. Of these 75 patients, 47 (62.7%) had episodes of acute exacerbation (ALT greater than 300 IU per liter) within 3 months prior to HBeAg seroconversion. All of these 47 patients had high hepatitis B virus DNA levels (greater than 1,000 pg per ml) at the onset of acute exacerbation. Their serum hepatitis B virus DNA disappears shortly before or simultaneously with the HBeAg clearance in 27 patients (57.4%) and persisted but with decreasing levels for 2 to 40 months in 20 patients. Most of these patients had high alpha-fetoprotein levels or evidence of bridging hepatic necrosis. In contrast, the serum hepatitis B virus DNA was undetectable for a minimum of 3 (3-17) months in the 28 patients who had an uneventful course before HBeAg seroconversion. Twenty of these 28 patients had well-documented episodes of acute exacerbation with high hepatitis B virus DNA levels, but with normal alpha-fetoprotein and little evidence of extensive necrosis as far back as 6 to 27 months before HBeAg seroconversion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2005

Transplantation of hepatitis B surface antigen-positive livers into hepatitis B virus-positive recipients and the role of hepatitis delta coinfection.

The scarcity of liver donors requires consideration of grafts from sources not previously used. Allografts from hepatitis B surface antigen (HBsAg)-carriers without a significant liver disease have been proposed for liver transplant recipients with hepatitis B virus (HBV)-related cirrhosis and hepatocellular carcinoma (HCC). Combination prophylaxis schemes against HBV post-liver transplantation (LT) recurrence are currently available; the efficacy of those schemes in HBV-related cirrhosis and HCC must be assessed. This report describes the allocation of HBsAg-positive grafts in three HBsAg-positive recipients, with HBV-related cirrhosis and evolving HCC lesions, two of them with hepatitis Delta virus (HDV) coinfection. Patients were administered anti-hepatitis B immunoglobulins (HBIGs) and lamivudine in order to prevent HBV recurrence. In spite of anti-HBV prophylaxis, HBV infection did persist after LT in all patients (no serum clearance of HBsAg). HBV replication assessed by serum HBV deoxyribonucleic acid (DNA) presence was detected in the first month after LT in the 3 recipients. A prompt HDV reinfection with a clinical and histological pattern of hepatitis was observed in the 2 HBV / HDV coinfected recipients. In 1 of them, an evolving chronic hepatitis required a second LT. The non-HDV-infected patient showed an uneventful follow-up, but the lack of the neutralizing effect of HBIGs and the high risk of escape mutants forced the addition of adefovir-dipivoxil to lamivudine, in order to prevent viral variants and hepatitis recurrence. In conclusion, allografts from HBsAg-positive donors in HBsAg-positive recipients are associated with the persistence of the HBsAg after LT due to the failure of HBIG prophylaxis, even if lamivudine does inhibit virion production. This condition favors HDV replication and HDV hepatitis recurrence in coinfected patients. The allocation of HBsAg-positive grafts in HBsAg-positive recipients could be justified only in recipients without HDV coinfection and a combined prophylaxis with lamivudine and adefovir-dipivoxil is currently the best way to manage escape mutants in these recipients.

Adult↗
PubMedDate not supplied

Current tests for antibody to hepatitis b core antigen used to screen donors for non-A, non-B hepatitis are comparable to the original radioimmunoassay for hepatitis B core antigen.

Prospective studies have shown a relationship between the transfusion of donor blood which is positive for antibodies to hepatitis B core antigen (anti-HBc) and an increased incidence of non-A, non-B hepatitis. The anti-HBc test was selected on the assumption that epidemiologic circumstances predisposing donors to hepatitis B infection also might favor exposure to non-A, non-B hepatitis. Current radioimmunoassays (RIA) and enzyme-linked immunoassays (EIA) for anti-HBc utilize hepatitis B core antigen (HBcAg) prepared by recombinant DNA technology, whereas the original RIA anti-HBc assay used HBcAg derived from hepatitis B virions. In the current study, 1329 sera were evaluated of which 23.3 percent were anti-HBc positive. The results indicate that sensitivity, specificity, and positive and negative predictive values of the current EIA and RIA tests for anti-HBc (Abbott Diagnostic Laboratories) are virtually identical to the original RIA test kit. In addition, all donor samples (128 specimens) administered to 57 cases of non-A, non-B hepatitis that were prospectively followed at Baylor College of Medicine for the Transfusion-Transmitted Viruses (TTV) Study group were retested with the EIA-recombinant anti-HBc assay. All 21 samples which were reactive in the original RIA anti-HBc test also were positive by the current EIA procedure. One sample was EIA positive/RIA negative, and 106 other samples were negative by both assays. Thus, commercial anti-HBc kits based on HBcAg derived by recombinant DNA technology, should retain their predictive value for reducing the incidence of non-A, non-B hepatitis as described in the prospective studies.

Antibodies, Viral↗
PubMed1996

Hepatic expression of hepatitis B virus genome in chronic hepatitis B virus infection.

The expression of hepatitis B virus (HBV) DNA in the liver was studied by nonisotopic in situ hybridization and correlated with liver histology, different phases in the natural evolution of chronic hepatitis B, and hepatic expression of HBV antigens in 251 Chinese patients with chronic HBV infection. A good correlation was found between the detection of HBV-DNA by in situ hybridization and serum HBV-DNA (P < .01). Chronic active hepatitis had the highest HBV-DNA detected in cytoplasm and nuclei, compared with livers showing minimal change, chronic persistent hepatitis, cirrhosis, and hepatocellular carcinoma. HBV-DNA in cytoplasm exceeded HBV-DNA in nucleus in all patients except in livers with hepatocellular carcinoma. Hepatic HBV-DNA correlated with disease activity (P < .02) and the correlation was highly significant with intralobular activity (P < .001). Patients in the early viral replicative phase of infection had higher levels of cytoplasmic and nuclear HBV-DNA compared with the late viral nonreplicative phase. Cytoplasmic and nuclear HBV-DNA correlated with hepatic expression of HBcAg and HBsAg (P < .05 in both cases), but not with HBeAg. These data indicate that hepatic expression of HBV-DNA follows the natural history of chronic HBV infection and is associated with active liver disease.

Adolescent↗
PubMed2003

Significance of hepatitis B viremia levels determined by a quantitative polymerase chain reaction assay in patients with hepatitis B e antigen-negative chronic hepatitis B virus infection.

OBJECTIVES: In hepatitis B e antigen (HBeAg)-negative chronic hepatitis B virus (HBV) infection, the clinical relevance of low viremia levels remains unclear. We evaluated the clinical significance of a single baseline serum HBV DNA measurement by a quantitative polymerase chain reaction (PCR) assay in this setting. METHODS: In total, 196 patients with HBeAg-negative chronic HBV infection (62 inactive carriers, 134 with chronic hepatitis B) were studied. ALT activity was normal at baseline in 25/134 HBeAg-negative chronic hepatitis B patients (18.7%), whereas it remained normal throughout follow-up in all inactive carriers. RESULTS: HBV DNA was <30,000 copies/ml in 14 (10.5%) and <100,000 copies/ml in 17 (12.9%) HBeAg-negative chronic hepatitis B patients, whereas it was <30,000 copies/ml in all inactive carriers (undetectable in 14). In particular, HBV DNA levels were <100,000 copies/ml in eight (32%) and <30,000 copies/ml in five (20%) of the 25 patients with HBeAg-negative chronic hepatitis B and normal baseline ALT values. HBV DNA levels with a cut-off at 30,000 or 100,000 copies/ml could correctly classify 92.9% or 91.3% of patients with HBeAg-negative chronic HBV infection, whereas ALT or IgM anti-HBc (IgM class antibody to HBV core antigen) index > 0.200 could correctly classify only 87.2% and 82.1% of patients, respectively. A combined HBV DNA and IgM anti-HBc index performed better by correctly classifying 94.4% of cases. CONCLUSIONS: Serum HBV DNA levels evaluated by sensitive quantitative PCR assays can be used for differentiation between HBeAg-negative chronic hepatitis B and inactive hepatitis B surface antigen carrier state, but the cut-off level should be set at approximately 30,000 copies/ml and certainly lower than the recently suggested level of 100,000 copies/ml.

Adolescent↗
PubMed1997

A randomized, controlled trial of a 24-month course of interferon alfa 2b in patients with chronic hepatitis B who had hepatitis B virus DNA without hepatitis B e antigen in serum.

Short-term interferon treatment of serum hepatitis B e antigen (HBeAg)-negative carriers with serum hepatitis B virus (HBV) DNA and histological features of chronic hepatitis B has been largely unsuccessful. In a pilot study of long-term treatment, 42 such patients were randomly assigned to 6 million units of interferon alfa 2b (IFN-alpha2b) three times per week for 24 consecutive months (n = 21, 4 with cirrhosis) or to no therapy (n = 21, 3 with cirrhosis). Five patients (24%) discontinued therapy because of treatment-related adverse reactions. Serum levels of alanine transaminase (ALT) became persistently normal and HBV DNA undetectable by dot-blot assay in 8 patients receiving interferon and in 2 untreated controls (38% vs. 10%; P = .03). Hepatitis flare-ups disappeared in 17 patients during therapy compared with 6 controls (81% vs. 29%; P < .001). During a median period of 22 months after interferon was stopped, 2 treated patients (10%) lost serum hepatitis B surface antigen (HBsAg) and seroconverted to antibodies to hepatitis B surface antigen (anti-HBs). Serum ALT remained persistently normal and HBV DNA undetectable by dot-blot assay in 6 initial responders and 1 initial nonresponder, compared with none of the 21 untreated controls (sustained response: 33% vs. 0; P < .001). Comparative analysis of pre- and posttreatment liver biopsies showed that mean Knodell scores dropped in the treated group (10.3 to 5.3; P = .01), but not in the untreated group (9.3 to 9.8; not significant). In conclusion, a 24-month course of treatment with 6 MU IFN-alpha2b was well tolerated by most patients, led to sustained suppression of HBV in one third, and attenuated hepatitis in 81% of patients.

Adult↗
PubMed1980

IgM responses to hepatitis-A virus and hepatitis-B core antigen in acute and chronic liver disease in Malawi; possible role of non-A, non-B, hepatitis.

Of 33 patients with acute hepatitis in Malawi, 21 had infection by hepatitis-B virus (HBV), five by hepatitis-A virus (HAV) and seven, who had no markers of current HBV or HAV infections, were probably infected by the agent(s) of non-A, non-B, hepatitis. 87 of 88 sera from persons without liver disease contained antibody to HAV and 49 antibody to hepatitis-B surface antigen (anti-HBs) (six were positive for hepatitis-B surface antigen). The diagnosis of recent infection by HAV was made by detecting HAV-specific IGM in single serum samples and, although such tests showed that HAV caused acute hepatitis, its absence in patients with chronic liver disease suggests that, unlike HBV, infection by HAV does not play a role in chronic liver disease in Malawi. Anti-hepatis-B core antigen (anti-HBc)-specific IgM was detected in 19 of 21 patients with acute HBV infection, in three of five HbsAg-positive patients with cirrhosis, but in none of five HbsAg-positive patients with hepatoma.

Adolescent↗
PubMed1995

Induction of T-helper cell response to hepatitis B core antigen in chronic hepatitis B: a major factor in activation of the host immune response to the hepatitis B virus.

The T helper (Th) cell response to hepatitis B core antigen (HBcAg) was analyzed in 76 chronic hepatitis B virus (HBV) carriers with varying degrees of hepatic inflammation and HBV replication. Fifty-five patients had active viral replication, 28 with minimal histological changes and normal alanine transaminase (ALT) and 27 with active hepatic inflammation and elevated ALT. The remaining 21 chronic hepatitis B surface antigen (HBsAg) carriers had undetectable HBV replication, minimal histological activity, and normal ALT. In addition, 34 chronic HBV carriers were studied prospectively during treatment with alpha-interferon. The HBcAg-specific Th cell response was evaluated by a proliferative assay using 3H-thymidine uptake and gamma-interferon production by peripheral blood mononuclear cells. The proliferative response and gamma-interferon production of patients with active hepatic inflammation were significantly higher than in patients with minimal histological changes and in controls. In the longitudinal analysis during alpha-interferon treatment, 22 of 34 patients sustained an ALT flare accompanied by a parallel, significant Th cell response, which preceded or coincided with the ALT flare. The elevation in the Th cell response and the ALT flare were followed by a significant rise in the serum immunoglobulin (Ig) M anti-HBc index. Ten of twenty-two patients with an enhanced Th cell response and an ALT flare seroconverted after alpha-interferon treatment. The Th cell activity in the 10 responders rapidly subsided after hepatitis B e antigen (HBeAg) to anti-HBe seroconversion, whereas in the 12 nonresponders it remained elevated.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗
PubMed1987

[Hepatitis non-A, non-B: epidemiological significance in acute viral hepatitis and chronic active hepatitis of hepatological consultation].

157 acute viral hepatitis and 60 chronic active ones have been analyzed focusing on NANB etiology. HAV was implicated in 36.3% of the hole acute viral hepatitis sample, HBV in 29.3%, and HNANBV was presumed as etiology in 31.2%, 5 patients (3.2%) had acute infection by HAV, on previous one by HBV, except for Epstein-Barr virus, no other test for viruses were determined (CMV, HSV, etc.). Male/female ratio was 1.4:1, 1.9:1, and 1.4:1 for HAV, HBV and HNANBV acute hepatitis respectively; HAV was the main etiology in the 0-9 age group (72.2%) although it only represents 11.5% of the sample; small occurrence of HAV hepatitis were found in patients over 40 (8.8%); HBV was clearly prevalent in patients over 50 (65.2%); the highest concentration of NANB etiology was found between 20-39 years old, but it was represented in all age-groups. Out of 49 NANB acute hepatitis, 12.2% had related transfusional antecedents, 12.2% belonged to health care worker group, and 4.1% had a close family NANB hepatitis contact; 71.5% had no reported antecedent. Viral source was presumably implicated in 75.0% of chronic active hepatitis, 25.0% attributable to HNANBV. Results seem not feasible to transfer to general population due to the facts that most patients were of specialized consult, and pediatric assistance is unusual to the authors practice.

Argentina↗
PubMed2002

Prevalence and significance of hepatitis GB virus-c/hepatitis G virus viremia in a large cohort of patients with chronic hepatitis B infection, with chronic hepatitis C infection, and on renal replacement therapy in Hong Kong.

A total of 455 patients were recruited to study the prevalence of hepatitis GB virus-C/hepatitis G virus viremia in Hong Kong. There was no significant increase in the prevalence of hepatitis GB virus-C viremia in asymptomatic hepatitis B virus- and hepatitis C virus-infected patients compared to that of controls (1.56% and 7.14%, respectively, vs 3.85%, both P = NS). Renal patients as a whole had a significantly higher prevalence of hepatitis GB virus-C viremia compared to that of controls (13.95% vs 3.85%, P = 0.0271). The duration of the replacement therapy, especially for patients with peritoneal dialysis was associated with a higher chance of hepatitis GB virus-C viremia. Among renal patients, renal transplanted patients had the highest prevalence of hepatitis GB virus-C viraemia (19.1%) probably because of a higher susceptibility as a result of immunosuppression. However, hepatitis GB virus-C viraemia did not cause liver biochemistry derangement in renal transplanted patients.

Adult↗
PubMed2000

Fulminant hepatitis associated with hepatitis A virus superinfection in patients with chronic hepatitis C.

There have been conflicting reports of the clinical outcome of acute hepatitis A virus (HAV) infection in patients with chronic hepatitis C virus (HCV) infection. A prospective study evaluated 432 patients with chronic hepatitis C (183 with cirrhosis) over a 7-year period. Of the 17 patients with concurrent HAV infection, seven developed fulminant hepatitis and six died. None of these patients had cirrhosis; however, the HLA phenotype (A1; B8:DR3) appeared to be a significant factor in the development of fulminant hepatitis. Patients with this phenotype had high titres of antinuclear antibodies, antismooth muscle antibodies and antiasialoglycoprotein-receptor antibodies, possibly reflecting the induction of autoimmune hepatitis in this group. The high frequency of fulminant hepatitis in patients with HAV/HCV coinfection contrasts with other surveys, although a large Centers for Disease Control and Prevention (CDC) survey demonstrated that HAV infection in patients with pre-existing chronic liver disease (CLD) is associated with increased mortality. It is likely that CLD has some importance as an underlying factor in the development of fulminant hepatitis following HAV infection. Further prospective studies are needed to clarify this issue.

Comorbidity↗
PubMed2002

Association between severity of type A hepatitis and nucleotide variations in the 5' non-translated region of hepatitis A virus RNA: strains from fulminant hepatitis have fewer nucleotide substitutions.

BACKGROUND: Type A hepatitis is still a considerable problem in both underdeveloped and developed countries. Why some patients progress to fulminant type A hepatitis and others do not is unclear. AIMS: To determine if nucleotide differences in the genome of hepatitis A virus (HAV) are responsible for the range of clinical severities, we analysed the 5' non-translated region (5'NTR) of the HAV genome, which has an internal ribosomal entry site and is important for cap independent translation of the viral message. METHODS: Serum samples from 84 Japanese patients with sporadic type A hepatitis from five distant regions of Japan, comprising 12 patients with fulminant hepatitis (FH), 13 with severe acute hepatitis (AHs), and 59 with acute hepatitis (AH), were examined for HAV RNA. The fragment between nucleotides 75 and 638 of the 5'NTR was amplified by reverse transcription-polymerase chain reaction, and the nucleotide sequence was determined by direct sequencing. RESULTS: Comparison of sequences of the 5'NTR revealed relatively fewer nucleotide substitutions in FH and AHs patients compared with the considerable sequence variations found in strains of AH. This tendency was most prominent between nucleotides 200 and 500. Strains from FH and AHs cases had fewer nucleotide substitutions (p<0.001) in this region. CONCLUSIONS: Nucleotide variations in the central portion of the 5'NTR of HAV may influence the severity of type A hepatitis.

5' Untranslated Regions↗
PubMed1994

Obstructive jaundice due to compression of the common hepatic duct by right hepatic artery--a case associated with the absence of the lateral segment of the left hepatic lobe.

Various benign and malignant conditions can cause biliary obstruction. We present a rare case of obstructive jaundice due to the compression of the common hepatic duct by the anteriorly overriding right hepatic artery. This case was also associated with the absence of the lateral segment of the left hepatic lobe. The patient was a 39 year-old housewife with a 4-day history of jaundice and occasional febrile sensation. An abdominal computed tomography showed absence of the lateral segment of the left hepatic lobe and a percutaneous transhepatic cholangiography showed a band-like filling defect of 2 mm width at the level of the upper common hepatic duct. The anteriorly overriding right hepatic artery compressing the common hepatic duct and the absence of the lateral segment of the left hepatic lobe were confirmed by operation.

Adult↗
PubMed1993

[Comparison of hepatic tissue extraction rates of cytotoxic anticancer drugs during hepatic arterial chemotherapy--evaluation using direct hemoperfusion under hepatic venous isolation].

Hepatic extraction rates (ER) of anticancer drugs during hepatic arterial infusion were investigated with the aid of direct hemoperfusion (DHP) under hepatic venous isolation (HVI). Using mongrel dogs (n = 6), adriamycin (ADR), mitomycin C (MMC) and cisplatin (CDDP) were simultaneously administered to the hepatic artery at each dosage of 1 mg/kg in 10 minutes under HVI.DHP. Hepatic venous flow and plasma concentrations of each drug at the carotid artery, the inlet and outlet sides of DHP were periodically determined during HVI.DHP. Based on these data, drug adsorption and removal rates were estimated. In addition, hepatic tissue uptakes of each drug were calculated from the amounts of drug administered and leaked in the hepatic effluent. Subsequently, the percentage of tissue uptake of each drug to the amount of drug administered was determined as ER of each drug. Drug adsorption rates during the first 10 minutes after infusion showed no significant difference among three drugs. Drug removal rate of CDDP tended to be higher than those of other two drugs. ER of CDDP (54.8 +/- 18.3%) were significantly lower (p < 0.01) as compared to ADR (84.4 +/- 16.2%) and MMC (83.1 +/- 15.7%). These results indicate that ER of each drug should be taken into consideration to determine appropriate drug for hepatic arterial chemotherapy.

Adsorption↗