Search PubMed⌕ Search

Biomedical subjects

H Kumada

Publications and source records attributed to H Kumada.

At least 37 records · Page 2Linked to original sources
PubMed2001

Evaluation of quantitative measurements of hepatitis C virus RNA to predict sustained response to interferon by genotype.

Hepatitis C virus (HCV) virus load is one of the most important predictive factors for the outcome of interferon (IFN) therapy. Recent technological advances have allowed a more precise measurement of HCV load. However, the exact cutoff values that could be used to predict the outcome of IFN have not been established for each assay. Five recent quantitative assays were evaluated for the measurement of HCV (Amplicor monitor ver 1.0, Amplicor monitor ver 2.0 (GT), Amplicor monitor ver 2.0 (Cobas), Quantiplex branched DNA amplification (bDNA) ver 2.0 and HCV core protein level by enzyme immunosorbent assay) in 209 consecutive patients with chronic hepatitis C, who received IFN therapy. The results of the two second generation Amplicor monitor tests (GT and Cobas) showed the best correlation (r = 0.930), but the other tests also showed relatively good correlations (r = 0.646-0.925). Each method predicted the effect of IFN with comparable predictive efficacy, ranging from 77.0 to 80.8%. Receiver operating characteristic (ROC) curve analysis showed that Amplicor monitor ver 2.0 and bDNA ver 2.0 are superior in predicting the response in genotype 2a. The best cutoff value for predicting the response to IFN was different by genotype, which should be considered in selecting candidates for IFN treatment.

Adult↗
PubMed2001

Randomized controlled clinical trial of lymphoblastoid interferon-alpha for chronic hepatitis C.

Objective: Most of chronic hepatitis C patients with HCV-genotype 1 and a high virus load fail to eradicate the HCV-RNA by the interferon (IFN) or IFN/ribavirin therapy. But in these patients, IFN is often effective with regard to normalization of alanine aminotransferase (ALT). We had therefore the following two randomized controlled clinical trials to evaluate the effect of IFN which reduce ALT and maintain normalization of ALT. One approach (study 1) was to compare the efficacy of a 6 month course of three different dosages of recombinant IFN-alpha-2a in patients with chronic hepatitis C associated with HCV-genotype 1b and a high serum HCV-RNA level of more than 1 Meq/ml. Another approach (study 2) was to make clear the significance of an additional 6 month course of IFN in patients who had biochemical response during the first 6 month course of IFN (study 1). Methods: (1) Study 1; 45 patients with HCV-genotype 1b and a high serum HCV-RNA level of more than 1 Meq/ml were randomly assigned into three equal groups; group 1 was treated with 3 million units (MU), group 2 with 6 MU and group 3 with 9 MU. They were treated with IFN 3 times weekly for 6 months. Biochemical response was defined as normalization of ALT at the 6 month after initiation of IFN; (2) Study 2; Subsequently, of 23 patients with biochemical response by the first study, 22 were randomly assigned to two groups; patients in group A were continued to receive 3 MU of IFN-alpha-2a three times a week for an additional 6 months and patients in group B were discontinued IFN therapy. Results: (1) Study 1; One patient in group 1, three in group 2 and five in group 3 withdrew from IFN therapy because of IFN-related side-effects. Biochemical response was 10 (66.7%) patients of group 1,8 (53.3%) of group 2 and 5 (33%) of group 3 by the intention-to-treat (ITT) analysis. The biochemical response rate in group 1 was slightly higher than that in other two groups by the Cochran Armitage two-tailed test (P=0.066). With respect to serum HCV-RNA level, one patient in group 1, six patients in group 2 and four patients in group 3 became negative for HCV-RNA by reversed transcription nested-polymerase chain reaction (RT nested-PCR) at the end point of first 6 month course of IFN; (2) Study 2; The maintenance rate of ALT normalization was 88.9% (9/11) in group A and 11.1% (2/11) in group B. The maintenance rate of ALT normalization in group A was significantly higher than that in group B by the Fisher exact's test (P=0.0089). With respect to serum HCV-RNA level by RT nested-PCR, four patients in group A had negative HCV-RNA at the end of an additional IFN therapy. On the other hand, all the patients in group B had positive HCV-RNA at the same time. Conclusion: Our data suggested that a prolonged IFN therapy using a dose of 3 MU of IFN-alpha-2a is safe strategy to reduce ALT and to maintain ALT normalization in patients with HCV-genotype 1b and a high serum HCV-RNA level of more than 1 Meq/ml.

Journal Article↗
PubMed2001

Rapid decrease of plasma HCV RNA in early phase of twice daily administration of 3 MU doses interferon-beta in patients with genotype 1b hepatitis C infection: a multicenter randomized study.

Virological response to interferon (IFN) is poor in patients with plasma levels of HCV RNA higher than 1 Meq/ml and genotype 1b hepatitis C viral infection. In 60 patients, a randomized control study was conducted to compare 3 MU of IFN-beta twice daily for four weeks (group A) and 6 MU once a day for four weeks (group B) followed by a four-week administration of 6 MU once a day. The plasma levels of HCV RNA, determined by an amplicore-monitor method, for patients in group A were significantly lower than those for group B at the fourth and eighth day of IFN administration, and complete virological responses were noted in two patients from group A but none in group B. It is concluded that twice daily administration of 3 MU IFN-beta is more effective than once a day 6 MU in the early phase of IFN therapy.

Female↗
PubMed2001

Role of protein kinase C in the reduction of infarct size by N-methyl-1-deoxynojirimycin, an alpha-1,6-glucosidase inhibitor.

Preischaemic treatment with N-methyl-1-deoxynojirimycin (MOR-14), an alpha-1,6-glucosidase inhibitor, attenuates glycogenolysis and lactate accumulation during ischaemia and markedly reduces infarct size in rabbit hearts. In the present study, we have investigated whether protein kinase C (PKC), a principal mediator of ischaemic preconditioning, is also involved in the cardioprotective effect of MOR-14. To assess the effect of PKC inhibition on infarct size in MOR-14-treated hearts, 38 rabbits were subjected to 30 min of ischaemia followed by 48 h of reperfusion. Infarct size, as a per cent of area at risk, was significantly smaller in rabbits administered 100 mg kg(-1) of MOR-14 10 min before ischaemia (17+/-2%, n=10), than in a control group (46+/-5%, n=10). This beneficial effect of MOR-14 was abolished when 5 mg kg(-1) of chelerythrine, a PKC inhibitor, was given 10 min prior to MOR-14 injection (39+/-4%, n=10), although chelerythrine alone did not alter infarct size (43+/-4%, n=8). Further, chelerythrine had no effect on MOR-14-induced attenuation of glycogen breakdown and lactate accumulation in hearts excised at 30 min of ischaemia. Immunoblot analysis of PKC in homogenates of Langendorff-perfused rabbit hearts revealed that MOR-14 significantly increased levels of PKC-epsilon in the particulate fraction at 20 and 30 min of ischaemia and in the cytosolic fraction at 30 min of ischaemia. Taken as a whole, our data suggest that PKC acts downstream of the inhibition of glycogenolysis by MOR-14 to reduce infarct size. Thus, activation of PKC is a more direct mediator of the cardioprotection afforded by MOR-14 than is inhibition of glycogenolysis.

1-Deoxynojirimycin↗
PubMed2001

Long-term interferon therapy for 1 year or longer reduces the hepatocellular carcinogenesis rate in patients with liver cirrhosis caused by hepatitis C virus: a pilot study.

BACKGROUND AND METHODS: In order to elucidate the influence of a long-term administration of interferon on the appearance rates of hepatocellular carcinoma (HCC) in hepatitis C virus (HCV)-related cirrhosis, we retrospectively analyzed 694 patients with cirrhosis. A total of 113 patients underwent interferon therapy, including 25 patients with a long-term administration of interferon for 1 year or more, and the other 581 patients received no antiviral drugs. RESULTS: Crude cumulative appearance rates of HCC in the interferon and the untreated groups were 14.1, and 28.4% at the end of the 5th year, and 36.7 and 52.5% at the end of the 10th year, respectively (P = 0.0028). As there was a waiting time between diagnosis and treatment (median 2.0 months, average 21.3 months) in the treated group, Cox proportional hazard analysis using a time-dependent covariate was introduced to evaluate the anticarcinogenic effect of interferon. Although male sex, higher alpha-fetoprotein, older age, lower albumin concentration, and lower platelet count significantly increased the carcinogenesis rate, interferon was not a significant contributing factor to the carcinogenesis rate as a whole (hazard ratio = 0.83, P= 0.32). When the patients with interferon were divided into two groups according to therapy duration, long-term interferon therapy significantly decreased the hepatocellular carcinogenesis rate after an adjustment by significant covariates (hazard ratio = 0.28, P= 0.0048). CONCLUSION: When interferon is administered for 12 months or longer, effective cancer prevention will be achieved, even in patients with HCV-related cirrhosis.

Adult↗
PubMed2001

Muscle weakness in a Japanese family of Arg1239His mutation hypokalemic periodic paralysis.

Familial hypokalemic periodic paralysis is an autosomal dominant disorder. Recently, three predominant mutations were found in the muscle dihydropyridine-sensitive calcium channel alpha 1-subunit gene. We present a Japanese family that displays one of these, the Arg1239His mutation. All the affected individuals of this family displayed this mutation. Two cases had a history of recurrent episodes of muscle weakness and difficulty in running before their first paralytic attack. It is suggested that there are no racial differences with this mutation, and that mild muscle weakness occurs not only after but also preceding the first attack.

Adult↗
PubMed2001

Lamivudine therapy for spontaneously occurring severe acute exacerbation in chronic hepatitis B virus infection: a preliminary study.

OBJECTIVE: The nucleoside analogue lamivudine, a potent inhibitor of hepatitis B virus replication, has shown notable results in treating chronic hepatitis B. However, lamivudine has not been specifically tested for effectiveness against spontaneously occurring severe acute exacerbations of hepatitis in patients chronically infected with this virus. We addressed this issue in a pilot study. METHODS: Ten patients with chronic hepatitis B developed severe acute exacerbation spontaneously during follow-up; 3 of them developed hepatic failure shortly before entering the trial. Lamivudine was administered long-term to the 10 patients at a daily oral dose of 100 or 300 mg. RESULTS: All 3 patients with hepatic failure at initiation of treatment recovered dramatically. Of the remaining 7 patients, 5 recovered rapidly with lamivudine, but 2 progressed quickly to hepatic failure despite treatment. One died of sepsis and the other of multiorgan failure. In the 8 survivors, serum alanine transaminase activity decreased rapidly to normal with lamivudine therapy, and serum hepatitis B virus DNA level declined rapidly to undetectable levels. Serum total bilirubin concentrations normalized somewhat later. Prothrombin time improved steadily and gradually. Hepatitis B e antigen elimination or seroconversion was achieved in 3 survivors. No adverse effects were noted in any patient. All survivors had good quality of life with long-term lamivudine monotherapy. CONCLUSIONS: Lamivudine is effective, safe, and well tolerated by patients with spontaneous, severe, acute exacerbation complicating chronic hepatitis B virus infection, even in the presence of hepatic failure. Lamivudine appears to be an attractive therapeutic option and may represent the best choice.

Acute Disease↗
PubMed2001

Pathogenic significance and organic virus levels in patients infected with TT virus.

Previous reports documented the recovery of a DNA virus from a patient with posttransfusion non-A-G hepatitis and named TT virus (TTV). Although the virus was initially detected as a causative agent of hepatitis, there is doubt about its pathogenicity. The aim of this study was to clarify the relationship between TTV and liver diseases. Histopathological examination of liver biopsies from 14 patients with TTV genotype 1 positive non-B, non-C and non-G chronic hepatitis showed mild fibrosis and periportal/piecemeal necrosis. Using the real-time detection (RTD)-PCR method, we found that TTV DNA levels of genotype 1 in liver samples from 3 such patients were 100- to 1,000-fold higher than those in the paired serum samples. Further investigation using various tissues from 2 autopsies of patients with hepatitis C with hepatocellular carcinoma revealed that the concentrations of TTV DNA in the liver were also higher than in serum samples. However, the highest TTV DNA concentrations in these 2 autopsies were found in the lung and bone marrow, respectively. Our results suggest that TTV may replicate in various tissues including the liver and may cause only mild liver damage.

Adult↗
PubMed2001

[A trial of new interferon therapy for the patients with chronic hepatitis C resistant to interferon therapy].

HCV-RNA clearance rates are reported to be about 30-40% of the patients treated with IFN for less than 6 months. But IFN therapy is ineffective for chronic hepatitis C patients with HCV-genotype 1b and a high virus load. We evaluated the efficacy of different IFN therapy compared with standard IFN therapy for chronic hepatitis C patients resistant to interferon therapy. That is, we assessed the following therapy; 1) prolonged IFN therapy, 2) IFN-beta therapy of twice a day, 3) IFN-beta therapy daily for 24 weeks, 4) combination therapy of IFN-alpha and IFN-beta. In some cases, these IFN therapies were effective than a standard IFN therapy.

Adult↗
PubMed2001

[Hepatocellular carcinogenesis and prognosis of elderly patients with chronic hepatitis type C].

Among 457 elderly patients of 65 years or older with chronic hepatitis or cirrhosis caused by hepatitis C virus, 117 patients underwent interferon therapy for the elimination of hepatitis C virus. A total of 87 patients could be analyzed for the interferon effect, since the remaining 20 patients had still been receiving or just finished the therapy. Thirty-six patients(41.4%) achieved complete elimination of HCV-RNA with interferon therapy. Although those patients with a milder hepatitis stage and better virological condition(low viral concentration or group 2 subtype) were preferentially enrolled in the therapy, 13 patients(11.1%) discontinued the administration with varied side effects: severe general malaise in 6 patients, depression in 3, pneumonia/pneumonitis in 2, and retinopathy in 2. Crude hepatocellular carcinogenesis rates in the subgroup of F1 + F2 and the subgroup of F3 + F4 were 1.8%, 21.2% at the end of 5th year, and 14.3% and 53.7% at the tenth year, respectively.

Aged↗
PubMed2000

Molecular structures and magnetic properties of the mixed-ligand complexes of bis(hexafluoroacetylacetonato)manganese(II), -copper(II), and -zinc(II) with 4,4'-bis(N-tert-butyl-N-oxylamino)-2,2'-bipyridine. Isosceles triangular hetero-three-spin systems consisting of aminoxyls and metal ions.

4,4'-Bis(N-tert-butyloxylamino)-2,2'-bipyridine (4) and its 1:1 complexes with bis(hexafluoroacetylacetonato)manganese(II), -copper(II), and -zinc(II) were prepared. An X-ray structure analysis of free ligand 4 reveals that the molecule has a trans conformation with Ci symmetry and the aminoxyl radical center has a short contact of 2.36 A with one of the neighboring molecules. The three 1:1 complexes have mutually similar molecular structures in which the 2,2'-bipyridine moiety has a cis conformation and serves as a bidentate ligand and coordination geometry around the metal atom is a distorted octahedron. The EPR experiments for free ligand 4 and [Zn(hfac)2.4] in frozen solution suggested that the exchange couplings between the two aminoxyls (R) through the 2,2'-bipyridine rings are antiferromagnetic with JR-R/kB = -19.3 +/- 0.5 and -24.3 +/- 0.4 K, respectively. Isosceles triangular three-spin models were applied to the 1:1 magnetic metal complexes to give JR-M/kB = -19.1 +/- 0.2 K and JR-R/kB = -32.9 +/- 0.3 K for [Mn(hfac)2.4] and JR-M/kB = +73 +/- 18 K and JR-R/kB = -24.5 +/- 6.5 K for [Cu(hfac)2.4].

Journal Article↗
PubMed2000

Incidence of primary cholangiocellular carcinoma of the liver in japanese patients with hepatitis C virus-related cirrhosis.

BACKGROUND: Hepatitis C virus (HCV) infection is a major risk factor for the development of hepatocellular carcinoma. However, the risk factors for primary cholangiocellular carcinoma of the liver (PCC-L) have not been fully investigated. The authors determined the incidence of PCC-L in patients with HCV-related cirrhosis. METHODS: Between 1980 and 1997, the authors prospectively studied 600 consecutive patients for the appearance of PCC-L; these patients were positive for HCV and later developed cirrhosis. The follow-up period ranged from 0 to 18.5 years (median, 7.2 years). RESULTS: During the observation period, PCC-L developed in 14 patients (2.3%). Among these, 11 (1.8%) had cholangiocellular carcinomas and the other 3 (0.5%) had a combined type of hepatocellular and cholangiocellular carcinoma. Within the same period, hepatocellular carcinoma (HCC) developed in 206 patients (34.3%). The cumulative rates of newly diagnosed PCC-L were 1.6% at 5 years and 3.5% at 10 years, which was about 1000 times higher than the estimated incidence of PCC-L in the general population of Japan. PCC-L was treated by surgical resection in 3 patients who survived for > 3 years. However, the other 11 patients received palliative therapy or chemotherapy. The survival rates among PCC-L patients were 39.3%, 23. 6%, and 16.5% at the end of 1, 3, and 5 years, respectively, and were significantly lower than those of HCC (P = 0.0001). CONCLUSIONS: The results of this study show a relatively high incidence of PCC-L in patients with HCV-related cirrhosis, and also show that this type of liver cancer is associated with a relatively poor prognosis. These results indicate that HCV-related cirrhosis is a major risk factor for PCC-L in Japanese patients.

Adult↗
PubMed2000

Fluctuation patterns of HCV-RNA serum level in patients with chronic hepatitis C.

The serum level of hepatitis C virus (HCV)-RNA is clinically important as a predictor of the response to interferon (IFN) therapy in patients with chronic hepatitis C. If serum HCV-RNA levels fluctuate during follow-up, and IFN therapy is begun at the time of a low HCV-RNA level, the IFN therapy may be more effective. We evaluated the fluctuation of HCV-RNA serum levels for 2 years in 212 patients with chronic hepatitis C, untreated with IFN who had HCV genotype 1b and an HCV-RNA level of 10 Meq/ml or more at first consultation. The HCV-RNA level was measured monthly for 2 years with an HCV branched DNA probe assay (b DNA probe assay). We classified HCV-RNA patterns into three types by the ratio of maximum HCV-RNA level (a) to minimum HCV-RNA level (b). In pattern 1 (constant type, 151 patients; 71.2%) the a/ b ratio was 1-5. In pattern 2 (slight fluctuation type, 46 patients; 21.7%) the a/b ratio was 5-10. In pattern 3 (severe fluctuation type, 15 patients; 7.1%), the a/b ratio was 10 or more. Next, we evaluated the factors associated with the three patterns. Acute exacerbation of chronic hepatitis was regarded as an increase in serum alanine aminotransferase (ALT) level to more than 250 IU/l. The incidence of acute exacerbation for a 2-year follow-up was 13.9% (21/151) in pattern 1, 19.6% (9/46) in pattern 2, and 53.3% (8/15) in pattern 3. Multivariate analysis showed that acute exacerbation was the most important factor in the manifestation pattern 3. In conclusion, we found that: (1) about 70% of patients had a constant HCV-RNA levels for 2 years. (2) A few patients had severe fluctuation of serum HCV-RNA level after acute exacerbation of chronic hepatitis.

Adult↗
PubMed2000

Hepatic vascular side effects of styrene maleic acid neocarzinostatin in the treatment of hepatocellular carcinoma.

Styrene-maleic acid neocarzinostatin (SMANCS) sometimes causes hepatic vascular side effects, including arterial stricture, obstruction, and arterio-portal shunt. A total of 128 intra-arterial SMANCS injection treatments, performed for 89 patients with hepatocellular carcinoma, were analyzed to determine the relationship between angiographic findings and subsequent hepatic vascular injuries. After SMANCS therapy, hepatic arterial stricture or obstruction occurred in 5 patients (5/128; 3.9%), arterio-portal shunting in 12 (12/128; 9.4%), liver shrinkage in 4 (4/128; 3.1%), and cholangitis or biloma in 2 (2/128; 1.6%). Among 23 patients whose plain abdominal X-ray films just after SMANCS injection showed Lipiodol retention in the hepatic artery, 5 patients developed arterial obstruction, 10 developed arterio-portal shunt, and 2, cholangitis or biloma. Among 26 patients with Lipiodol retention in the portal vein, 4 developed hepatic lobe atrophy with aggravation of liver function. Among 3 patients with Lipiodol retention in both the hepatic artery and the portal vein, 1 developed arterio-portal shunt. In 76 treatments without excessive Lipiodol retention, only 1 of the patients developed arterio-portal shunt. Excessive retention of Lipiodol in hepatic vascular beds just after SMANCS therapy was significantly associated with future vascular side effects (22/52 vs 1/76; P < 0.0001). Lipiodol retention in arteries just after SMANCS injection was closely associated with subsequent arterial obstruction or arterio-portal shunt, and Lipiodol retention in the portal vein was related to subsequent hepatic lobe atrophy.

Adult↗
PubMed2000

Progressive and sufficient decrease of hepatitis B core antibody can predict the disappearance of hepatitis B virus DNA in Japanese patients with hepatitis B surface antigen clearance.

The aim of this study was to elucidate the relationships among serum levels of hepatitis B virus (HBV) DNA, periods after hepatitis B surface (HBs) antigen clearance, and the titer of hepatitis B core (HBc) antibody in 200-fold diluted serum. Twelve patients who had clearance of HBs antigen from serum were studied. Five patients had not received any treatment (group A), and seven had received prednisolone withdrawal therapy. The patients in groups A and B were followed up for 86 months and 108 months (median), respectively. Serum HBV was measured by the nested polymerase chain reaction method. In both groups, serum HBV tended to become gradually undetectable after HBs antigen clearance. The positive rate of HBV in the sera 5 years or more after HBs antigen clearance was significantly lower than that in the sera at less than 5 years, both in group A (P = 0.004) and group B (P = 0.010). In both groups, the titer of HBs tended to decline every year after HBs antigen clearance. HBV was still detectable in the sera of some patients for a long period of time after they showed seroconversion to HBs antibody. The results suggest that detection of HBV was difficult in sera with an HBc titer of 30% or lower and at more than 5 years after HBs antigen clearance in both groups. It is important to note that HBV DNA rarely exists in the serum, even when HBs antigen and HBc are both negative.

Adolescent↗
PubMed2000

Increased response rate to interferon therapy after a second course in hepatitis C patients who show relapse after the initial course.

Some patients with chronic hepatitis C become HCV-RNA seronegative during interferon (IFN) therapy. However, about one-half of these patients show a relapse, evident by high serum alanine aminotransferase (ALT) level. In some patients with biochemical relapse, the serum HCV-RNA level becomes low immediately after the ALT relapse. Here, we assessed the changes in serum HCV-RNA level in patients with ALT relapse after IFN therapy, and evaluated the efficacy of a second course of IFN, started at the recovery stage after ALT relapse. Two hundred and seventy-seven patients who showed HCV-RNA seronegativity by reverse transcription nested-polymerase chain reaction (RT nested-PCR) and normalization of ALT during the initial IFN therapy, and had positive HCV-RNA with ALT relapse (> 100 IU/l) within 3 months after completion of the initial IFN course were enrolled in this retrospective study. Two hundred and sixty patients were followed-up without further IFN retreatment after the ALT relapse (group 1), and 17 patients received another 6-month course of IFN after the ALT relapse (group 2). The median level of serum HCV-RNA, determined with a branched DNA probe assay (version 1; Chiron-Dai-ichi Kagaku Tokyo, Japan), in group 1 was 3.1 Meq/ml before IFN therapy, 1.3 Meq/ml at the time point of the ALT peak after the completion of IFN therapy, and 0.7 and 2.6 Meq/ml at 2-4 and 6-8 weeks after the ALT peak, respectively. The serum HCV-RNA level at 2-4 weeks after the ALT peak was lower than that before IFN therapy. The eradication rate of HCV-RNA (complete response; CR) in group 2 (47.1%; 8/17) was significantly higher than that in group 1 (1.5%; 4/260; P < 0.001). In conclusion, our data suggested that: (1) patients who showed biochemical relapse after initial IFN therapy had a significantly lower serum HCV-RNA level at recovery after ALT relapse compared with that before initial IFN therapy. (2) A high response rate was noted after a second course of IFN administered at the recovery stage of the ALT relapse, compared with patients without IFN retreatment.

Adult↗
PubMed2000

Distinction between chronic hepatitis and liver cirrhosis in patients with hepatitis C virus infection. Practical discriminant function using common laboratory data.

In order to distinguish patients with cirrhosis from those with chronic hepatitis, multivariate discriminant analysis was performed using common laboratory data. A total of 205 consecutive patients were diagnosed by peritoneoscopy and biopsy as having chronic liver disease caused by hepatitis C virus (HCV), 168 with chronic hepatitis and 37 with cirrhosis. Twenty variables and their natural logarithmic transformation were employed in the multivariate analysis. After stepwise variable selection, the following function was finally obtained to discriminate the disease severity, z=0.120xgamma-globulin (%)+0.423xln (hyaluronate) (µg l(-1))-0.059xplatelet (x10(4) counts per mm(3))-0.364xsex (male, 1; female, 2)-3.953. Since the function contained an expression of logarithm and was slightly troublesome to apply, we prepared another discriminant function composed of usual figures without logarithmic transformation, z=0.124x(gamma-globulin (%))+0.001x(hyaluronate) (µg l(-1))-0.075x(platelet (x10(4) counts per mm(3)))-0.413xgender (male, 1; female, 2)-2.005. When a positive result is calculated in the latter equation, the diagnosis of the liver disease indicates cirrhosis, and negative result chronic hepatitis. Accuracy of the two discriminant functions was 90.3 and 91.2%, respectively. A concise linear discriminant function could successfully differentiate liver cirrhosis from chronic hepatitis with an accuracy of 91.2%.

Journal Article↗