Hepaplastin Test Research Articles

多臓器不全を来したIII度熱中症の管理において持続脳波モニタリングが有用であった1例(Usefulness of continuous electroencephalography in severe heat stroke complicated with multi–organ failure: a case report)

要旨III度熱中症では，熱や循環障害などによる中枢神経障害や体腔臓器機能障害による代謝性脳症により意識障害を来す。しかし，いずれの病態により意識障害を呈しているかの判断は困難である。今回，持続脳波モニタリング（continuous electroencephalography: cEEG）を行い，三相波を認めたことから重症急性肝不全の診断に至り，人工肝補助療法を行い良好な転帰を得た症例を経験した。71歳の女性。意識障害のため搬送。III度熱中症と診断しICUに入室，cEEGを開始した。第2病日に肝機能障害を認め，第3病日に意識障害の増悪を認めた。第4病日にcEEGにて三相波を認め，急性肝不全による肝性脳症合併と判断し，人工肝補助療法を開始，その後意識障害の改善を認めた。熱中症においてcEEGは有用である。

Effects of cefotaxime on the coagulation system, especially their dependence on vitamin K-related factors

The authors administered cefotaxime to 20 children and studied laboratory parameters concerning peripheral blood: hemoglobin count, blood platelet count, red blood cell count, and hematocrit value, and the coagulation system: protein induced by vitamin K deficiency or by the presence of a vitamin K antagonist II (PIVKA II), hepaplastin test (HPT), prothrombin time (PT) and active partial thromboplastin time (APTT). The results obtained are summarized as follows: 1. Peripheral blood No abnormal values were observed. 2. Coagulation system (1) PIVKA II: In all cases, PIVKA II was negative. (2) HPT, PT and APTT: In all cases, no significant changes of these values which would suggest the tendency for prolonged bleeding were observed.

1,5-Anhydroglucitol levels are low irrespective of plasma glucose levels in patients with chronic liver disease

Serum 1,5-anhydroglucitol (1,5-AG) is a known marker reflecting recent glycaemic control. In this study, we examined serum 1,5-AG levels in chronic liver disease (CLD) patients with and without diabetes mellitus. Eighty patients with CLD were compared with 667 subjects without CLD. Glycaemic control of the CLD patients was evaluated by estimated glycated haemoglobin (HbA(1C)) calculated using the equation by Rohlfing et al. from mean plasma glucose because CLD patients have apparently low HbA(1C). When the study participants were divided into subgroups stratified by HbA(1C) levels, the CLD patients whose estimated HbA(1C) levels were less than 7.0% showed significantly lower 1,5-AG than their counterparts of the control subjects. Stepwise multivariable analysis revealed that estimated HbA(1C) was the significant explanatory variable for 1,5-AG in the CLD patients. However, in the CLD patients with estimated HbA(1C) less than 5.8%, only hepaplastin test was the significant explanatory variable for 1,5-AG. Serum 1,5-AG levels are low irrespective of plasma glucose levels in the CLD patients with and without diabetes. The CLD patients who had low serum 1,5-AG levels were associated with deteriorated liver function.

Association of serum glycated albumin to haemoglobin A1C ratio with hepatic function tests in patients with chronic liver disease

In patients with chronic liver disease (CLD), glycated haemoglobin (HbA(1C)) levels have been shown to be apparently lower than real values, whereas serum glycated albumin (GA) levels are apparently higher. The present study was aimed to examine whether both glycaemic indices are influenced by hepatic function. Subjects consisted of 82 patients with CLD. Various indicators for hepatic function as well as HbA(1C) and GA were also measured. Estimated HbA(1C) values were calculated from the mean plasma glucose levels. Two hundred and two type 2 diabetic patients without CLD were studied as controls. Although GA was strongly correlated with HbA(1C) in patients with CLD as well as diabetic patients, GA levels in patients with CLD were relatively higher than those in diabetic patients. In patients with estimated HbA(1C) < or = 5.8%, GA levels significantly increased but HbA(1C) levels decreased as a function of decreasing hepaplastin test (HPT). The ratio of GA/HbA(1C) (G/H ratio) increased as a function of decreasing HPT. In patients with estimated HbA(1C) > 5.8%, in contrast, GA levels were independent of HPT levels. In the patients with CLD, GA and HbA(1C) were associated with mean plasma glucose levels and some indicators for hepatic function. The multivariate analysis revealed a significant association of G/H ratio with HPT, cholinesterase and direct bilirubin. The G/H ratio was not associated with the mean plasma glucose but with HPT and cholinesterase levels. The G/H ratio correlates with hepatic function but not with plasma glucose levels. Therefore, CLD should be suspected for diabetic patients with an elevated G/H ratio.

Fibrinogen Storage Disease Caused by Aguadilla Mutation Presenting With Hypobeta‐lipoproteinemia and Considerable Liver Disease

Fibrinogen Storage Disease Caused by Aguadilla Mutation Presenting With Hypobeta‐lipoproteinemia and Considerable Liver Disease

Assessment of liver function for successful hepatectomy in patients with hepatocellular carcinoma with impaired hepatic function

This study aimed to construct a formula for assessing liver function in order to prevent post-hepatectomy liver failure. A formula was constructed by analyzing data from 28 patients with hepatocellular carcinoma (HCC) with liver cirrhosis operated on between 1981 and 1984. Next, we evaluated the validity of this formula in 207 hepatectomy patients operated on from 1985 to 1999. For 145 hepatectomy patients operated on from 2000 to 2006, this formula was calculated before surgery in order to assess their risk of hepatectomy. The formula for liver functional evaluation, constructed from preoperative hepatic function parameters, was: liver failure score = 164.8 - 0.58 x Alb - 1.07 x HPT + 0.062 x GOT - 685 x K. ICG - 3.57 x OGTT. LI + 0.074 x RW, where Alb is albumin (g/dl); HPT, hepaplastin test (%); GOT, glutamate oxaloacetate transaminase (U/l); K. ICG, K value of indocyanine green clearance test; OGTT. LI, 60-min/120-min glucose level in 75-g oral glucose tolerance test. linearity index of OGTT; and RW, weight of resected liver (g). We decided that a score below 25 would be safe for hepatectomy. The mortality rate decreased from 3.9% in 1985--1999 to 1.3% in 2000--2006. This finding allows us to conclude that the formula is valid for assessing the risk of post-hepatectomy liver failure.

Advantage of Ischemic Preconditioning for Hepatic Resection in Pigs

Ischemic preconditioning (IP) and intermittent inflow occlusion (IO) have provided beneficial outcomes in hepatic resection. However, comparison of these two procedures against warm hepatic ischemia-reperfusion injury has not been studied enough. Pigs that had undergone 65% hepatectomy were subjected to Control (120 min continuous ischemia, n = 6), IP (10 min ischemia and 10 min reperfusion, followed by 120 min continuous ischemia, n = 6), and IO (120 min ischemia in the form of eight successive periods of 15 min ischemia and 5 min reperfusion, n = 6). We evaluated hepatocyte injury by aspartate aminotransferase, lactate dehydrogenase and hepaplastin test, hepatic microcirculation by hepatic tissue blood flow (HTBF) and endothelin (ET)-1, inflammatory response by tumor necrosis factor-alpha (TNF-alpha), and histopathology after reperfusion. IP prevented hepatocyte injury, HTBF disturbance, and hepatocyte necrosis in histopathology as well as IO. These two groups showed significantly better outcomes than Control. IP produced significantly less ET-1 and TNF-alpha than IO. IP ameliorated hepatic warm ischemia-reperfusion injury. Furthermore, IP gained more advantages in preventing chemokine production such as ET-1 and inflammatory response over IO. IP could take the place of IO for hepatectomy.

A Case of Neonatal Hemochromatosis‐Like Liver Failure with Spontaneous Remission

A Case of Neonatal Hemochromatosis‐Like Liver Failure with Spontaneous Remission

Local recurrence is an important prognostic factor of hepatocellular carcinoma

To clarify the importance of complete treatment by PEIT. A total of 140 previously untreated cases of HCC were enrolled in this study from 1988 to 2002. The inclusion criteria were: a solitary tumor less than 4 cm in diameter or multiple tumors, fewer than four in number and less than 3 cm in diameter, without extrahepatic metastasis or vessel invasion. As general principles for the treatment of HCC, the patients underwent transcatheter arterial chemoembolization (TACE) prior to PEIT. After the initial treatment of the patients, ultrasonography and computed tomography were performed, and measurement of serum levels of alpha-fetoprotein (AFP) was determined. When tumor recurrences were detected, PEIT and/or TACE were repeated whenever the hepatic functional reserve of the patient permitted. We then analyzed the variables that could influence prognosis, including tumor size and number, the serum levels of AFP, the parameters of hepatic function (albumin, bilirubin, ALT, hepaplastin test, platelet number, and indocyanine green retention at 15 min (ICG-R15)), combined therapy with TACE, distant recurrence, and local recurrence. Univariate analysis identified the ICG test, serum levels of AFP and albumin, tumor size and number, and local recurrence, but not distant recurrence, as significant prognostic variables. In multivariate analysis using those five parameters, the ICG test, tumor size, tumor number, and local recurrence were identified as significant prognostic factors. In both univariate and multivariate analyses, the relative risk for the ICG test was the highest, followed by local recurrence. We found that local recurrence is an independent prognostic factor of HCC, indicating that achieving complete treatment for HCC on first treatment is important for improving the prognosis of patients with HCC.

Effect of Hypothermia on Serum Electrolyte, Inflammation, Coagulation, and Nutritional Parameters in Patients With Severe Traumatic Brain Injury

We evaluated the effect of induced hypothermia on biochemical parameters in patients with severe traumatic brain injury. We obtained hemoglobin, hematocrit, white blood count, lymphocyte count, platelet count, and serum concentrations of sodium, potassium, glucose, albumin, and C-reactive protein, and prothrombin time, hepaplastin test, activated partial thromboplastin time, antithrombin-III, alpha2PI, and nitrogen excretion on the day of admission, and on days 1, 3, 5, 7, 14, and 21 after the injury in 31 patients with severe head injury who were treated with hypothermia of 33 degrees ranging from 48 to 72 hours. We selected 33 normothermic patients as a control group; these patients were selected from patients who had been treated before hypothermia was used as a treatment modality, by the same criteria for hypothermia therapy. We compared the biochemical markers and rectal temperature and intracranial pressure in the hypothermia group with those in the normothermia group. Outcome was assessed using the Glasgow Outcome Scale at 6 months after injury. The demographic characteristics, severity, and outcome were similar in the hypothermia and normothermia group. Intracranial pressure was significantly decreased by hypothermia. Serum potassium concentration decreased significantly during hypothermia. White blood cell counts and C-reactive protein levels were higher after rewarming in the hypothermia group, and these were also higher in the patients with infectious complications, although the incidence of infectious complications did not differ between the hypothermia and normothermia groups. There were no statistically significant prolongations of activated partial thromboplastin time and no decline in prothrombin time with hypothermia. Platelet count, antithrombin-III, and alpha2PI did not differ significantly between the two groups. Hypothermia of 33 degrees for 48-72 hours does not appear to increase the risk for coagulopathy and infections, although hypothermic patients exhibited significant increments in inflammatory markers such as C-reactive protein and white blood counts after rewarming.

Maternal total parenteral nutrition and fetal subdural hematoma

background Fetal subdural hematoma is rare, and no case resulting from vitamin K deficiency secondary to maternal total parenteral nutrition has been reported. Case A 28-year-old woman was managed with total parenteral nutrition from 28 weeks’ gestation because of continuous vomiting due to esophageal hiatal hernia. A sinusoidal pattern by cardiotocogram was observed at 31 weeks’ gestation. Serial sonograms showed a fetal subdural hematoma, and cesarean delivery was performed. Although the maternal hepaplastin test result was normal and the maternal PIVKA-II concentration was only slightly elevated, the neonate was severely anemic and had severe vitamin K deficiency. Conclusion Severe fetal vitamin K deficiency can develop even when the maternal deficiency is mild. When maternal total parenteral nutrition is necessary, supplemental vitamin K should be administered.

Shift of Serum Osteocalcin Components between Cord Blood and Blood at Day 5 of Life

Vitamin K deficiency is a relatively common condition in neonates. However, the role of vitamin K in neonatal bone metabolism remains to be determined. Osteocalcin (OC) is the most abundant noncollagenous protein in bone, and is regulated to be gamma-carboxylated by vitamin K. In this study, we measured gamma-carboxylated osteocalcin (Gla-OC) and non- or undercarboxylated osteocalcin (Glu-OC) separately, and examined the effects of vitamin K on osteocalcin metabolism. Eighteen full-term healthy neonates were enrolled in this study. In the cord and d-5 blood samples, the OC levels were determined by three different methods to examine the intact OC by immunoradiometric assay (IRMA), Gla-OC, and Glu-OC. Serum vitamin K fractions, hepaplastin test, and type 1 procollagen carboxyl extension peptide were also determined. Urine samples were also collected from the first voiding and on d 5 to determine urinary pyridinoline, deoxypyridinoline, and gamma-carboxylated glutamic acid. Serum levels of phylloquinone (PK) and menaquinone (MK)-4 increased on d 5 following vitamin K administration and increased intake in breast milk and/or formula. The OC levels determined by IRMA did not change between cord and d-5 blood samples, but the Gla-OC level increased remarkably and Glu-OC reduced to a negligible level. OC in cord blood is mainly Glu-OC, and Glu-OC is replaced with Gla-OC within 5 d of life after vitamin K supplement. The IRMA assay fails to distinguish Gla-OC from Glu-OC and caution is needed to estimate bone turnover with this method in the perinatal period.

Shift of Serum Osteocalcin Components between Cord Blood and Blood at Day 5 of Life

Vitamin K deficiency is a relatively common condition in neonates. However, the role of vitamin K in neonatal bone metabolism remains to be determined. Osteocalcin (OC) is the most abundant noncollagenous protein in bone, and is regulated to be γ-carboxylated by vitamin K. In this study, we measured γ-carboxylated osteocalcin (Gla-OC) and non- or undercarboxylated osteocalcin (Glu-OC) separately, and examined the effects of vitamin K on osteocalcin metabolism. Eighteen full-term healthy neonates were enrolled in this study. In the cord and d-5 blood samples, the OC levels were determined by three different methods to examine the intact OC by immunoradiometric assay (IRMA), Gla-OC, and Glu-OC. Serum vitamin K fractions, hepaplastin test, and type 1 procollagen carboxyl extension peptide were also determined. Urine samples were also collected from the first voiding and on d 5 to determine urinary pyridinoline, deoxypyridinoline, and γ-carboxylated glutamic acid. Serum levels of phylloquinone (PK) and menaquinone (MK)-4 increased on d 5 following vitamin K administration and increased intake in breast milk and/or formula. The OC levels determined by IRMA did not change between cord and d-5 blood samples, but the Gla-OC level increased remarkably and Glu-OC reduced to a negligible level. OC in cord blood is mainly Glu-OC, and Glu-OC is replaced with Gla-OC within 5 d of life after vitamin K supplement. The IRMA assay fails to distinguish Gla-OC from Glu-OC and caution is needed to estimate bone turnover with this method in the perinatal period.

Plasma and urine levels of urinary trypsin inhibitor in patients with acute and fulminant hepatitis.

Urinary trypsin inhibitor (UTI) is synthesized by hepatocytes and excreted into urine. Plasma and urine UTI levels have been measured to evaluate whether these levels may be useful markers in various pathological conditions. However, there has been no study on plasma and urine UTI levels in patients with acute liver diseases. The aim of the present study was to evaluate plasma and urine UTI levels and their relationship with the severity of hepatic damage in patients with acute liver diseases. Plasma and urine UTI levels were measured by newly developed enzyme-linked immunosorbent assay in 15 patients with acute hepatitis (AH), 12 patients with acute severe hepatitis (ASH) and 10 patients with fulminant hepatitis (FH), as assessed on admission. The serial changes in plasma and urine UTI were also observed in some patients with AH and ASH. Plasma UTI levels (U/mL, median [25-75th percentile]) were: 11.0, (9.5-16.1) in patients with AH; 7.8 (5.6-11.5) in those with ASH; 6.5 (4.0-9.5) in patients with FH; and 9.7 (7.3-11.0) in normal controls. Plasma UTI levels in patients with FH were significantly lower than in those with AH. Plasma UTI levels showed significant positive correlations with the levels of prothrombin time (PT), hepaplastin test, antithrombin III, alpha2-plasmin inhibitor, plasminogen (Plg) and fibrinogen. After the recovery of liver dysfunction, increased plasma UTI levels in patients with AH were decreased, whereas previously decreased plasma UTI levels in patients with ASH were increased. Urine UTI levels were significantly increased in patients with AH compared with those of normal controls. In patients with ASH and FH, urine UTI levels were increased but not significantly. Urine UTI levels significantly positively correlated with PT and Plg. After the recovery of liver dysfunction, previously increased urine UTI levels in patients with AH were decreased. The correlation between plasma UTI and urine UTI levels was not significant. The findings of the present study suggested that the levels of plasma and urine UTI changed in patients with AH and were closely related to the abnormalities of coagulo-fibrinolysis, including PT. Further studies are needed to clarify whether these levels may be useful markers to predict the prognosis of acute hepatitis.

Plasma endothelin-1 level as a marker reflecting the severity of portal hypertension in biliary atresia

Background/Purpose: The aim of this study was to examine if the plasma endothelin-1 (ET-1), a potent vasoconstrictor, level may reflect the severity of portal hypertension associated with liver cirrhosis in biliary atresia (BA). Methods: Forty-eight postoperative BA patients aged 6 months to 20 years were studied. Plasma ET-1 was measured by a sandwich method of enzyme immunoassay. ET-1 was compared with Child's score and laboratory data. ET-1 levels were compared among groups of patients with various degrees of histologic fibrosis and portal hypertension. Results: Plasma ET-1 was 5.3 ± 3.5 pg/mL in BA, higher than in controls (3.1 ± 0.8, n = 27; P < .05). ET-1 correlated with Child's score, serum total bilirubin, direct bilirubin, aspartate aminotransferase, albumin, prothrombin time, hepaplastin test, fibrinogen, cholinesterase, total cholesterol, Fischer's molar ratio, prealubumin, and hyaluronic acid, respectively (P < .05). ET-1 also correlated with the severity of histologic fibrosis, gastroesophageal varices, the presence of splenomegaly, ascites, venous dilatation on the abdominal wall, or pulmonary vascular abnormalities. In 4 patients undergoing liver transplantation (LTx), ET-1 after LTx was lower than that before LTx (P < .05). Conclusion: Plasma ET-1 level may be a useful index reflecting the severity of cirrhosis and portal hypertension in BA. J Pediatr Surg 36:1609-1612. Copyright © 2001 by W.B. Saunders Company.

Plasma Endotoxin and Serum Cytokine Levels in Patients With Alcoholic Hepatitis: Relation to Severity of Liver Disturbance

Endotoxin plays an important role in the initiation and aggravation of alcoholic liver disease. In this study, we evaluated plasma endotoxin levels and serum concentrations of cytokines and lipopolysaccharide binding protein (LBP) during the acute and recovery phase of patients with alcoholic hepatitis; we also explored the prognostic factors associated with a fatal outcome. Fourteen patients, consisting of eight patients with alcoholic hepatitis (AH), five cirrhotics with superimposed AH (LC+AH), and one patient with severe alcoholic hepatitis (SAH), were studied. Among these, two with LC+AH died of hepatic failure. Plasma endotoxin levels in the acute phase were higher in patients with AH (184.4 +/- 159.4 pg/ml) and LC+AH (206.9 +/- 174.9 pg/ml) than in healthy subjects (10.4 +/- 5.5 pg/ml, p < 0.001). In particular, in one patient with SAH and one of two nonsurvivors, plasma endotoxin levels were markedly high relative to the other cases. In most survivors, plasma endotoxin levels decreased in the recovery phase, whereas they further increased at the terminal stage in one of two nonsurvivors. Serum interleukin (IL)-6 and IL-8 levels in the acute phase were significantly higher in patients with AH and LC+AH as compared with healthy subjects. These levels were especially high in nonsurvivors and in one patient with SAH. IL-10 increased in two nonsurvivors, one patient with SAH, and one with LC+AH. In the recovery phase, these cytokine levels in survivors tended to decrease, but in nonsurvivors, IL-6 remained high, and IL-8 and IL-10 further increased. Tumor necrosis factor-alpha levels were below the detection limit throughout the course in all patients. Serum lipopolysaccharide binding protein (LBP) generally was elevated in the acute phase and decreased in the recovery phase in all survivors, but in one of the nonsurvivors, LBP was elevated markedly at the terminal stage. In the acute phase, plasma endotoxin levels were correlated positively with white blood cell counts, neutrophil counts, and serum IL-8. IL-8 was correlated positively with neutrophil counts and negatively with serum cholinesterase, hepaplastin test, and serum albumin levels. IL-6 was correlated positively with white blood cell and neutrophil counts, C-reactive protein, and serum total bilirubin and negatively with hepaplastin test and serum total protein levels. Serum LBP was correlated positively with white blood cell and neutrophil counts. Endotoxemia and related elevation of IL-8 may play an important role in the activation and migration of neutrophils in patients with alcoholic hepatitis. Marked elevation of inflammatory cytokines, IL-6 and IL-8, are related to severity and poor prognosis of alcoholic hepatitis. Serum LBP may serve as an index of inflammatory reaction in alcoholics.

Liver Function Assessed by Increased Rate of Portal Venous Blood Flow after Oral Intake of Glucose

To find out whether an increased rate of portal venous blood flow after oral intake of glucose could be used to estimate liver function. Prospective study. University hospital, Japan. Sixty patients, of whom 23 had hepatocellular carcinoma and liver cirrhosis, 21 had tumours metastatic to normal liver, and 16 had obstructive jaundice treated with percutaneous transhepatic biliary drainage (PTBD). Portal flow was measured after oral intake of glucose 75 g using pulsed-Doppler ultrasonography. The ratio of portal flow 30 minutes after glucose intake to that before intake (PVFR30) was significantly lower in cirrhotic patients than in those with metastases and a normal liver. A PVFR30 of less than 1.5 indicated impaired hepatic function assessed by the Child-Pugh scores, indocyanine green clearance test, prothrombin time, and hepaplastin test. It also indicated less reduction in total bilirubin concentrations in the first week after PTBD. Results suggest that PVFR30 can be used to estimate liver function and predict outcome after PTBD.

Prognostic factors in severe alcoholic liver injury. Nara Liver Study Group.

Severe alcoholic liver injury has been relatively rare, but is gradually increasing in Japan. The clinical features and prognostic factors in severe alcoholic liver injury were retrospectively investigated in 105 patients, consisting of 3 with severe alcoholic hepatitis (SAH), 43 with cirrhosis with superimposed alcoholic hepatitis [liver cirrhosis (LC)+alcoholic hepatitis (AH)], 38 with AH, and 21 with alcoholic cirrhosis. Seven of the 105 patients (6.7%, 2 with SAH and 5 with LC+AH) died of hepatic failure. Patients with SAH showed severe hyperbilirubinemia, reduced hepatic biosynthetic capacity, and marked acute inflammatory reactions, and developed multiple organ failure, such as disseminated intravascular coagulation (DIC), renal failure, acute pancreatitis, or pneumonia. Two SAH patients died within 1 month, whereas five with LC+AH died within 77 days during the second episode of AH. In these nonsurvivors, the serum total bilirubin (T.Bil) level was not normalized, and the hepaplastin test (HPT), serum albumin, cholesterol, and platelet count were not markedly improved after the first episode of AH. In the survivors, elevation of AST lasted longer, and the improvement of T.Bil, hepatic biosynthetic capacity, and the platelet count were much less in patients with LC+AH than in those with AH. Multivariate analysis using the Cox proportional hazards model showed serum C-reactive protein (CRP) and DIC as significant independent prognostic factors among SAH, LC+AH, and AH groups. When factors related to multiple organ failure, such as DIC and renal failure, were excluded, T.Bil and CRP were selected as independent prognostic factors. In patients with LC+AH and AH, CRP, and HPT were shown to be significant independent prognostic factors. These results suggest that SAH with multiple organ failure, and another episode of AH in advanced LC with hyperbilirubinemia and reduced hepatic biosynthetic capacity, are indicative of an extremely poor prognosis in chronic alcoholics.

TT virus (TTV) is not associated with acute sporadic hepatitis.

A novel virus, TT virus (TTV), recently discovered by Okamoto et al. in the serum of a patient with posttransfusion hepatitis, is thought to be one of the causative agents of blood-borne acute hepatitis. The association of this virus with acute sporadic hepatitis was evaluated. TTV DNA was detected in 4 (4.9%) of 81 cases of acute hepatitis A, in 5 (16.7%) of 30 cases of acute hepatitis B, in 1 (25.0%) of 4 cases of acute hepatitis C, in 1 (9.1%) of 9 cases of cytomegalovirus and Eppstein-Barr infection, and in 8 (13.6%) of 59 cases of acute hepatitis of unknown etiology. These positive rates of TTV in various etiologies did not differ significantly amongst each other, and were similar to those of healthy volunteers, i.e. 12.0% (12/100). The comparison of levels of alanine aminotransferase, aspartate aminotransferase, total bilirubin, hepaplastin test and prothrombin time between TT virus-positive and -negative patients did not show any differences. This indicates that TTV is neither a main causative agent of acute sporadic hepatitis of unknown etiology, nor does it affect the clinical features of acute hepatitis with already known etiology.

EFFECT OF INTRAOPERATIVE ADMINISTRATION OF PROSTAGLANDIN E1 (PGE1) ON LIVER FUNCTION IN PATIENTS WITH RESECTABLE HEPATOCELLULAR CARCINOMA

In spite of numerous reports on the cytoprotective effect of prostaglandin E1 (PGE1), its clinical usefulness is still controversial. We retrospectively studied the effect of the intraoperative administration of PGE1 (0.01_??_0.1μg/kg/min) on liver function in 77 patients with resectable hepatocellular carcinoma (HCC). The patients were divided into two groups, a PGE1 group (n=30) and control group (n=47). The liver function tests that were compared between the two groups on day 1, 3, 7, and 14 were: total bilirubin, glutamyl pyruvic transaminase (GPT), the hepaplastin test (HPT), and cholinesterase (ChE). We also compared the ratio of postoperative to preoperative level (Rpost/pre) to further evaluate sequential changes in liver function. The surgical factors, such as operation time, blood loss, and blood transfusion did not differ between the two groups. Postoperative decreases in HPT or ChE were ameliorated by the treatment with PGE1, and significant difference was observed in the Rpost/pre values of these two parameters (p<0.05). On the other hand, there were no significant differences in total bilirubin or GPT, either with actual values or Rpost/pre. These findings indicate that intraoperative administration of PGE1 enhanced hepatic synthesis of coagulation factors or ChE, and that its effect on ischemia-reperfusion injury was not significant in our clinical setting.