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Biomedical subjects

J C Wu

Publications and source records attributed to J C Wu.

At least 109 records · Page 6Linked to original sources
PubMed1999

Characteristics and risk factors of acetaminophen-induced hepatitis in Taiwan.

BACKGROUND: Overdose of acetaminophen may cause hepatic injury and fatal fulminant hepatic failure. Acetaminophen is the most common form of drug-induced hepatic injury in Western countries. However, there is no formal report of this important issue in Taiwan. To assess the clinical characteristics and risk factors of acetaminophen-induced hepatitis in Taiwan, we conducted this study. METHODS: A total of 71 patients who were intoxicated or overdosed with acetaminophen at Veterans General Hospital-Taipei between February, 1991 and June, 1997 were enrolled in this study. Acetaminophen-induced hepatitis was defined according to the Paris international consensus criteria. RESULTS: Suicide attempt was the major cause (67/71) of acetaminophen overdose. Sixty-two of the patients were female. The mean patient age was 24.5 +/- 9.7 years (+/- standard deviation, SD). Nineteen of 71 patients had acetaminophen-induced hepatitis. The peak serum alanine aminotransferase, aspartate aminotransferase and total bilirubin concentrations were 4,181.0 +/- 931.4 IU/l (mean +/- SD), 4,148.0 +/- 1,147.5 IU/l and 2.6 +/- 0.4 mg/dl, respectively. The hepatitis group had higher ingested acetaminophen doses and serum peak acetaminophen levels than did those of the nonhepatitis group (24.9 g vs 12.9 g, p = 0.004; 132.0 mg/l vs 61.7 mg/l, p = 0.013). A higher percentage of alcohol consumption was also noted in the hepatitis group than in the nonhepatitis group (32% vs 12%, p = 0.05). After logistic regression for multivariate analysis, alcohol consumption was the most important risk factor for acetaminophen-induced hepatitis (odds ratio = 8.14, p = 0.018), followed by ingested acetaminophen dose (odds ratio = 1.21, p = 0.001). Most patients received acetylcysteine treatment in time. Two of the 19 patients with hepatitis died. CONCLUSIONS: The majority of acetaminophen-induced hepatitis in Taiwan occurs in young females who attempt suicide. Alcohol consumption and the dose of acetaminophen ingested were the significant risk factors for acetaminophen-induced hepatitis. Alcohol should not be concomitantly used with acetaminophen. Early diagnosis and administration of the antidote are crucial to decrease mortality.

Acetaminophen↗
PubMed1999

Hemostatic changes in patients with liver cirrhosis.

BACKGROUND: Hemostatic changes in liver disease are complicated. An overall evaluation of the main hemostatic parameters in patients with different degrees of cirrhosis of the liver has not been reported in Taiwan. METHODS: A series of hemostatic tests and parameters including activated partial thromboplastin time, prothrombin time, thrombin time, bleeding time, factor VIII assay, antithrombin activity, fibrinogen, plasminogen, protamine sulfate test, fibrin(ogen) degradation products, D-dimer, thrombin-antithrombin complex (measured by modified antithrombin), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1, euglobulin lysis test and venous occlusion test were performed in 51 patients with cirrhosis of the liver and 33 healthy controls. Among the cirrhotics, 18 were classified as Child-Pugh group A, 16 were B and 17 were C. RESULTS: Plasminogen, antithrombin and platelet count decreased progressively, starting with group A, then B and then C, relative to the controls. Factor VIII, activated partial thromboplastin time, prothrombin time, bleeding time, D-dimer and fibrin(ogen) degradation products increased progressively starting with group A, to B and then C, relative to controls. Severity of cirrhosis correlated with hemostatic changes. No significant change in the fibrinolytic response after challenge with the venous occlusion test was found in either Child-Pugh groups A, B, C or the controls, though progressive increases in tPA were found starting with group A, to B and then C, relative to controls. CONCLUSIONS: Our study proved a close relationship between the severity of cirrhosis and hemostatic changes. Activated partial thromboplastin time was better than bleeding time or thrombin time to demonstrate the severity of liver damage and hemostatic change in cirrhosis. Because the deterioration of coagulation function and increased fibrinolytic activity paralleled the severity of liver cirrhosis, adequate treatment for cirrhotic bleeding should not only correct the coagulation defects, but should also lower the increasing fibrinolytic activity.

Adult↗
PubMed1999

Interleukin-8 and alcoholic liver disease.

Interleukin-8 (IL-8), a cytokine produced by a host of cells including monocytes, macrophages, Kupffer cells and hepatocytes, can activate neutrophils. Peripheral neutrophilia and liver neutrophil infiltration are frequently noted in patients with alcoholic liver disease (ALD). Serum IL-8 levels are markedly elevated in patients with alcoholic hepatitis compared with those in patients with alcoholic cirrhosis, alcoholic fatty liver and non-alcoholic liver disease. The levels are also elevated in patients who die of hepatic failure and correlate with biochemical and histologic parameters and severity of liver injury. Patients with high serum IL-8 had a higher mortality rate than those with lower levels. In liver tissue from patients with ALD, local IL-8 levels also correlated with the degree of neutrophil infiltration. Serum IL-8 levels decreased gradually with abstinence from alcohol. Ethanol can increase plasma endotoxin, a potent inducer of tumor necrosis factor (TNF)-alpha and IL-1. Subsequently, TNF-alpha and IL-1, together with endotoxin, stimulate circulating and local IL-8 in ALD. Activated IL-8 then mediates neutrophil infiltration, a pivotal process in the pathogenesis of ALD. IL-8 levels might reflect the stage and severity of ALD and might serve as a predictor of survival in patients with alcoholic hepatitis. The development of agents with an anti-IL-8 effect is promising for the therapy of ALD.

Humans↗
PubMed1999

Circulating intercellular adhesion molecule-1 in chronic liver disease and hepatocellular carcinoma.

BACKGROUND: Intercellular adhesion molecule-1 (ICAM-1) is important in the migration and adhesion of immune cells from the circulation to their targets. A circulating form of ICAM-1 (cICAM-1) is elevated in the serum of patients with hepatitis and various cancers. Our aim was to determine the clinical significance of cICAM-1 in chronic liver diseases and hepatocellular carcinoma (HCC). METHODS: We measured the serum cICAM-1 levels in 91 patients with HCC, 47 with liver cirrhosis, 41 with chronic viral hepatitis and 32 healthy controls using an enzyme-linked immunosorbent assay. Ninety-eight patients had serial follow-up. RESULTS: The cICAM-1 levels in patients with HCC (737 +/- 212 ng/ml) and liver cirrhosis (593 +/- 145 ng/ml) were significantly higher than those in patients with chronic viral hepatitis (488 +/- 127 ng/ml) and controls (318 +/- 64 ng/ml). HCC patients had higher cICAM-1 levels than all the other groups. cICAM-1 levels in patients with chronic viral hepatitis correlated with serum alanine aminotransferase, prothrombin time and indocyanine green retention ratio. In HCC patients, alpha-fetoprotein levels and tumor size paralleled cICAM-1 concentrations. Furthermore, HCC patients with distant metastases had higher cICAM-1 levels than those without distant metastases, and levels of cICAM-1 in patients with stage IV HCC were higher than those in HCC patients with stages I, II or III disease. During a seven-year follow-up, 14 patients with chronic hepatitis developed liver cirrhosis when their cICAM-1 levels increased significantly. In 47 HCC patients, cICAM-1 levels decreased after tumor resection or transcatheter arterial embolization, and increased when the tumor recurred. cICAM-1 levels increased gradually in 14 patients with advanced HCC without specific therapy. CONCLUSIONS: CICAM-1 levels are increased in patients with chronic hepatitis, liver cirrhosis and HCC. This reflects the severity and progression of chronic liver disease and HCC. Sequential measurements of cICAM-1 seem more valuable than a single-point assessment in evaluating the progress of liver disease.

Adult↗
PubMed1999

Multiple myeloma presenting with a paraspinal tumor and malignant effusion: case report.

We describe a patient with multiple myeloma which presented as a thoracic paraspinal tumor and myelomatous pleural effusion. He had manifested a gradual onset of upper back pain with radiation to the left chest wall for 3 months. A radiographic examination showed left pleural effusion and a paraspinal tumor with rib destruction at the--left T5-6 level. Laboratory data showed anemia and a reversed serum albumin to globulin ratio. Protein electrophoresis and immunoelectrophoresis showed a monoclonal IgG-lambda chain component in the serum, urine, and pleural effusion fluid. Ultrasound-guided transthoracic mass biopsy and thoracentesis were performed for diagnosis. Biopsy of the thoracic tumor showed a solid mass composed of immature plasma cells. The pleural effusion fluid contained numerous immature plasma cells. An immunophenotype study of the pleural effusion fluid revealed monoclonal plasma cells, compatible with malignant pleural effusion. A specimen of bone marrow was interpreted as typical for plasma cell myeloma. Local radiotherapy and chemotherapy with melphalan and prednisolone resulted in good partial remission with a stable condition. Later, however, the disease flared up and hyperviscosity syndrome developed with epistaxis and retinal hemorrhage. He died of sepsis about 15 months after the initial diagnosis.

Aged↗
PubMed1999

Chronic hepatitis B exacerbated by Guillain-Barré syndrome: a report of two cases.

Several neurologic complications involving both the central and peripheral nervous systems due to acute viral hepatitis have been described, but Guillain-Barré (G-B) syndrome occurring as a complication of chronic viral hepatitis is extremely rare. Although it is generally agreed that G-B syndrome develops as an immune-mediated reaction, its exact pathogenesis remains obscure. We report the cases of two patients with chronic hepatitis B virus (HBV) infection acutely exacerbated by the development of G-B syndrome. G-B syndrome was diagnosed by nerve conduction velocity studies, electromyographic studies and a rise in acellular total protein in the cerebrospinal fluid (albumino-cytologic dissociation). In these two patients, we were able to accurately define the relationship between the onset of acute exacerbation of chronic HBV infection and G-B syndrome. The neurologic symptoms of G-B syndrome resolved with the return of liver enzymes to normal. Interferon therapy may be beneficial in relieving neurologic symptoms in patients with HB infection-related G-B syndrome.

Adult↗
PubMed1999

E-, P-, and N-cadherin are co-expressed in the nasopharyngeal carcinoma cell line TW-039.

The cadherin/catenin complex plays a key role in the initiation of cell-cell recognition, and adhesion, and the elaboration of structural and functional organization in multicellular tissues and organs. It is associated with tumor metastasis and also acts as an "invasion suppressor" of cancer cells. Nasopharyngeal carcinoma (NPC) is notorious for its highly metastatic nature. The expression of the E-cadherin/catenin complex is down-regulated in NPC tumor specimens. To obtain better insight into the intercellular adhesive property of NPC cells, we used immunofluorescence microscopy, immunoprecipitation, and immunoblot analysis to examine the expression of the classical cadherins and beta-catenin in a NPC cell line, TW-039. The results demonstrate a change in the distribution of E-cadherin from cytosolic flakes to cell-cell contacts with increasing time in culture. Between days 1 and 5 after plating, the detergent-insoluble fraction of E-cadherin increased from 20% to 37% of total E-cadherin, and that for P-cadherin increased from 33% to 40%. By contrast, the values for beta-catenin remained unchanged (26% and 25%). Both immunofluorescence and immunoblot studies suggested that P-cadherin may be involved in pioneer contact adhesion of TW-039 cells. Interestingly, E-, P-, and N-cadherin are co-expressed in this cell line. Immunoprecipitation studies also showed that other members of the cadherin family may be involved in the contact adhesion of TW-039 cells.

Blotting, Western↗
PubMed1999

Mixed genotypes infection with hepatitis D virus.

Heterogeneity of hepatitis C viral (HCV) genomes results in escape from immune clearance. Super-infection or mixed infection of different genotypes of HCV are seen commonly in humans. Hepatitis D virus (HDV) is classified into 3 genotypes. This study was planned to investigate if mixed genotypes infection of HDV occurs in humans. HDV genotyping based on restriction fragment length polymorphism (RFLP) was used to screen 60-99 HDV clones from each case of 7 prostitutes and 11 patients. Mixed infections were diagnosed by the finding of two or more different RFLP patterns in a case and were confirmed by sequencing. Five prostitutes had mixed infections of genotypes IIa and IIb HDV, while only 2 patients had mixed infections of genotypes I and II HDV (P< 0.05). The heterogeneity in nucleotide sequence was generally below 2% among HDV quasi-species from the same subject, while the heterogeneity was 27.7% between genotypes I and II HDV, and 22.8% between genotypes IIa and IIb HDV from a subject with mixed infection. Multiple HDV clones from the spouses of the 2 index cases were also analyzed. One spouse had mixed infection and the other did not, corresponding to the index cases. In cases with mixed genotypes infections, the prevalence of the minor strain was less than 10% of the total colony population analyzed.

Adult↗
PubMed1998

Distribution of the cadherin-catenin complex in normal human thyroid epithelium and a thyroid carcinoma cell line.

E-cadherin is the major cell-cell adhesion molecule expressed by epithelial cells. Cadherins form a complex with three cytoplasmic proteins, alpha-, beta-, and gamma-catenin, and the interaction between them is crucial for anchoring the actin cytoskeleton to the intercellular adherens junctions. The invasive behavior of cancer cells has been attributed to a dysfunction of these molecules. In this study, we examined the distribution of the cadherin-catenin complex in a Chinese human thyroid cancer cell line, CGTH W-2, compared with that in normal human thyroid epithelial cells. In the normal cells, using immunofluorescence staining, E-cadherin and alpha-, beta-, and gammm-catenin were found to be localized at the intercellular junction and appeared as 135, 102, 90, and 80 kD proteins on Western blots. In CGTH W-2 cells, no E-cadherin and gamma-catenin immunoreactivity was detected by immunofluorescence or Western blotting; alpha- and beta-catenin were detected as 102 and 90 kD proteins on blots but gave a diffuse cytoplasmic immunofluorescence staining pattern in most cells, while beta-catenin was also distributed throughout the cytoplasm in most cells but was found at the cell junction in some, where it colocalized with alpha-actinin. The present data indicate that the loss of cell adhesiveness in these cancer cells may be due to incomplete assembly of the cadherin-catenin complex at the cell junction. However, this defect did not affect the linkage of actin bundles to vinculin-enriched intercellular junctions.

Actinin↗
PubMed1998

Bcl-xL functions downstream of caspase-8 to inhibit Fas- and tumor necrosis factor receptor 1-induced apoptosis of MCF7 breast carcinoma cells.

Stimulation of the Fas or tumor necrosis factor receptor 1 (TNFR1) cell surface receptors leads to the activation of the death effector protease, caspase-8, and subsequent apoptosis. In some cells, Bcl-xL overexpression can inhibit anti-Fas- and tumor necrosis factor (TNF)-alpha-induced apoptosis. To address the effect of Bcl-xL on caspase-8 processing, Fas- and TNFR1-mediated apoptosis were studied in the MCF7 breast carcinoma cell line stably transfected with human Fas cDNA (MCF7/F) or double transfected with Fas and human Bcl-xL cDNAs (MCF7/FB). Bcl-xL strongly inhibited apoptosis induced by either anti-Fas or TNF-alpha. In addition, Bcl-xL prevented the change in cytochrome c immunolocalization induced by anti-Fas or TNF-alpha treatment. Using antibodies that recognize the p20 and p10 subunits of active caspase-8, proteolytic processing of caspase-8 was detected in MCF7/F cells following anti-Fas or TNF-alpha, but not during UV-induced apoptosis. In MCF7/FB cells, caspase-8 was processed normally while processing of the downstream caspase-7 was markedly attenuated. Moreover, apoptosis induced by direct microinjection of recombinant, active caspase-8 was completely inhibited by Bcl-xL. These data demonstrate that Bcl-xL can exert an anti-apoptotic function in cells in which caspase-8 is activated. Thus, at least in some cells, caspase-8 signaling in response to Fas or TNFR1 stimulation is regulated by a Bcl-xL-inhibitable step.

Apoptosis↗
PubMed1998

Prevalence, implication, and viral nucleotide sequence analysis of GB virus-C/hepatitis G virus infection in acute fulminant and nonfulminant hepatitis.

The clinical impact of GB virus-C (GBV-C)/hepatitis G virus (HGV) infection on various causes of acute hepatitis and fulminant hepatitis is controversial. In this study, serum samples from 164 patients with acute hepatitis of various causes, 34 asymptomatic hepatitis B virus (HBV) carriers, and 34 healthy adults were tested for GBV-C/HGV RNA by reverse transcription-nested polymerase chain reaction using primers based on the 5'-untranslated region. Nucleotide sequences of GBV-C/HGV RNA from various groups were compared. The prevalence of GBV-C/HGV RNA was significantly higher in patients with acute hepatitis D virus (HDV) superinfection than in HBV carriers or healthy controls (10/37 vs. 2/34, P < 0.02; 10/37 vs. 1/34, P < 0.005). GBV-C/HGV RNA was detected in 11.1% of acute hepatitis A patients, 9.5% of acute hepatitis B patients, 15.8% of acute hepatitis C patients, 12.5% of acute hepatitis E patients, 11.8% of chronic hepatitis B patients with acute exacerbation, and 11.1% in patients with non-A to -E hepatitis; each was not significantly higher than that in HBV carriers or healthy adults. There were no significant differences in gender, age, serum albumin, bilirubin, and alanine aminotransferase levels nor in the occurrence of fulminant hepatitis (6/28 vs. 36/136) between patients with or without GBV-C/HGV RNA. All six patients with fulminant hepatitis who had GBV-C/HGV RNA were complicated by infection with hepatitis B, C, or D. The GBV-C/HGV clones from 21 patients with or without fulminant hepatitis belonged to group 3. No particular strain of GBV-C/HGV was associated with fulminant hepatitis.

5' Untranslated Regions↗
PubMed1998

Well-differentiated thyroid carcinomas: p53 mutation status and microvessel density.

BACKGROUND: Risk-stratification schemes exist for well-differentiated thyroid carcinoma and include prognostic factors such as age, sex, extent of tumor, size of tumor, and presence of metastasis. Controversy continues, however, over the aggressiveness of initial surgical intervention because of anecdotal experiences of poor clinical outcomes in low-risk patients. Our objective is to determine the prognostic significance of two biologic tumor markers, the p53 gene mutation and CD34 microvessel density (MVD) count, in well-differentiated tumors of thyroid gland. METHODS: We selected 38 patients with well-differentiated thyroid carcinomas from the University of Illinois Tumor Registry. Patients had an average clinical follow-up of 10 years. Paraffin-embedded tumor specimens were available for all patients. Immunohistochemistry was performed to identify mutations of the p53 gene (Ab 1801) and to determine the MVD count (CD34). RESULTS: There were significant increases in MVD counts within thyroid tumor tissue, when compared with surrounding, normal thyroid tissue. There was no significant correlation noted, however, between increased MVD and histology or recurrence rates. There was a trend toward higher MVD counts in tumor specimens of patients initially seen with metastatic lymphadenopathy. The incidence of p53 mutation expression was 28%, and there was no correlation between p53 status and histology, sex, recurrence rate, or survival. CONCLUSIONS: This study supports the concept of tumor neovascularization but fails to correlate MVD with clinical behavior or pathologic features in well-differentiated thyroid carcinoma. Furthermore, we found that the p53 mutation status was not an independent prognosticator of tumor behavior in these lesions.

Adenocarcinoma, Follicular↗
PubMed1998

The impact of traveling to endemic areas on the spread of hepatitis E virus infection: epidemiological and molecular analyses.

Traveling to endemic areas carries a risk of hepatitis E virus (HEV) infection, but no molecular analysis to document sources of infection is available. Eighteen (38%) of 47 patients with acute non-A, non-B, non-C hepatitis were positive for antibody to HEV (anti-HEV), and 9 (50%) of these were also positive for serum HEV RNA by polymerase chain reaction following reverse transcription. Only 1 (5%) of the 21 patients with acute hepatitis A was positive for HEV RNA. Travel to endemic areas (mostly to China; odds ratio, 22.2; 95% confidence interval, 4.7-105.8) and deeper jaundice (odds ratio, 5.2; 95% confidence interval, 1.01-27.2) were the only factors associated with HEV infection in multivariate analysis. The two HEV isolates from two patients who had traveled to China and the HEV isolate from a patient whose travel history was obscure formed a monophyletic group with the isolates from Guangzhou. The HEV isolates from our patients show a homology of 72% to 78% in nucleotide sequence with the Burma, Beijing, India, Pakistan, and Xiangjiang strains; a homology of 81% to 91% with the Guangzhou strains; and a homology of 76% with the Mexico strain. The close relationship between the Taiwan isolates and the Guangzhou strains was further supported by the short Kimura's two-parameter distances among them. In summary, HEV infection does occur in this area. Epidemiological and molecular analyses strongly indicate that most cases of HEV infection originated from travel to HEV-endemic areas.

Adult↗
PubMed1998

Sero-clearance of hepatitis B surface antigen in chronic carriers does not necessarily imply a good prognosis.

The incidence of delayed hepatitis B surface antigen (HBsAg) clearance in the natural history of chronic hepatitis B virus (HBV)-infected patients was low. Previous studies regarding the prognosis in such patients were controversial. Among 1,355 chronic carriers from 1985 to 1997, spontaneous HBsAg clearance was observed in 55 patients. During a mean follow-up period of 23 months, 18 (32.7%; all were male subjects) developed serious complications, including 11 with hepatocellular carcinoma (HCC) (9 of them underwent surgical resection), 6 with cirrhosis, and 1 with subfulminant liver failure. The overall cumulative probability of complications was 29.8% at 4 years, and it was higher in males (P = .044) and patients aged 45 years or more (P = .006); the latter carried an 8.6-fold increased risk (95% CI: 1.2-64.6; P = .037) of adverse events. Histories of acute or chronic infection by hepatitis A virus, C virus (HCV), or D virus (HDV) were present in 42% of patients. Patients seropositive for antibodies against HCV (anti-HCV) or HDV (anti-HDV) had higher alanine transaminase (ALT) levels (>40 U/L; P = .008) after sero-clearance. HBV DNA was detectable in 31% of 51 subjects, in 20% of 20 with antibodies against HBsAg, in 40% of 20 with anti-HCV or anti-HDV, and also in an HCC patient's serum and tumor. Staining of liver HBsAg was positive in 30% of 10 HCC patients. In conclusion, our results demonstrated that hepatitis B viremia may persist, and adverse complications were not rare in HBsAg-clearance patients. All such patients should be closely monitored, which may allow for earlier detection of HCC.

Adult↗
PubMed1998

Detection of serum hepatitis B, C, and D viral nucleic acids and its implications in hepatocellular carcinoma patients.

The association of viremia, elevated serum alanine aminotransferase (ALT) levels, and hepatocyte inflammatory activity in hepatocellular carcinoma (HCC) patients was studied. Serum samples from 114 HCC patients undergoing surgery were assayed for hepatitis B, C, and D viral nucleic acids by polymerase chain reaction (PCR) prior to surgery. Of these patients, 65 had HBV infection alone, 15 had HCV infection alone, 4 had HDV infection, 20 had HBV and HCV superinfection, 1 had triple viral infection, and 9 were negative for HBV and HCV infections. The prevalence of active viral replication was significantly higher in HCV than in HBV (92% versus 70%; P = 0.006) patients, and significantly higher mean serum ALT levels were also noted in the HCV group than in the HBV group (P = 0.02). The incidence of marked ALT elevation (>200 U/l) was highest in the HCV (27%) and the HDV (25%) groups. Patients in the HCV group were 10 years older than those in the HBV group. Viral superinfection did not accelerate the development of HCC. Viral replication persisted in a significant portion of HCC patients and a higher prevalence of hepatic inflammation was noted in patients with HCV- and, possibly, HDV-related HCC.

Adult↗
PubMed1998

Does eradication of Helicobacter pylori impair healing of nonsteroidal anti-inflammatory drug associated bleeding peptic ulcers? A prospective randomized study.

BACKGROUND: Despite the widely accepted view that Helicobacter pylori is the most important cause of peptic ulcer disease, recent studies have suggested that the microbe protects against nonsteroidal anti-inflammatory drug (NSAID)-associated gastroduodenal lesions and promotes ulcer healing. We investigated the effects of H. pylori eradication on the healing of NSAID-associated bleeding peptic ulcers. METHODS: Chronic NSAID users presenting with peptic ulcer haemorrhage underwent endoscopy to secure haemostasis and to document H. pylori infection by rapid urease test and culture. They were prospectively randomized to receive either omeprazole (20 mg once daily) for 8 weeks or a 1-week course of triple therapy (bismuth subcitrate 120 mg, tetracycline 500 mg, metronidazole 400 mg, all given four times daily) plus omeprazole (20 mg once daily) for 8 weeks. Endoscopy was repeated after 8 weeks. Final H. pylori status was determined by a 13C-urea breath test that was performed at least 4 weeks after discontinuation of omeprazole. RESULTS: 195 H. pylori-infected NSAID users, complicated by bleeding ulcers, were randomized to receive omeprazole alone (102) or triple therapy plus omeprazole (93). 174 patients returned for second endoscopy at 8 weeks (91 in the omeprazole group, 83 in the triple therapy group). Urea breath test was negative in 14% in the omeprazole group vs. 92% in the triple therapy group (P < 0.001). Complete ulcer healing was achieved in 88 (97%) patients in the omeprazole group and 77 (93%) in the triple therapy group (P=0. 31). On intention-to-treat analysis, ulcers were healed in 86% of the omeprazole group and 83% of the triple therapy group (P=0.50). There was no significant difference in the healing rates of gastric or duodenal ulcers between the two groups. CONCLUSION: Eradication of H. pylori did not impair the healing of NSAID-associated bleeding peptic ulcers.

Adult↗
PubMed1998

Characterization and phylogenetic analysis of a novel hepatitis D virus strain discovered by restriction fragment length polymorphism analysis.

The hepatitis D virus (HDV) genotypes in 46 HDV-infected patients and 12 prostitutes were screened with Xhol restriction fragment length polymorphism (RFLP) analysis of reverse transcription PCR products of viral genomes and verified by phylogenetic analysis. The amplificates of three (6.5%) patients and two (17%) prostitutes showed a novel RFLP pattern different from those of the three known genotypes. Complete HDV genomic sequence identities between isolates with a novel RFLP and the HDV genotypes I, II and III were 72.3, 77.2 and 63.0%, respectively. Importantly, divergence was mostly seen in various regions related to replication or packaging. The novel isolates formed a monophyletic group (P < 0.05) and were most closely related to genotype II.

Amino Acid Sequence↗