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Biomedical subjects

Full-Young Chang

Publications and source records attributed to Full-Young Chang.

At least 55 records · Page 3Linked to original sources
PubMed2005

Smoking and hyperpepsinogenemia are associated with increased risk for duodenal ulcer in Helicobacter pylori-infected patients.

BACKGROUND: Although Helicobacter pylori has been established as a major etiologic factor of chronic gastritis and makes an important contribution to peptic ulceration, the reason why H. pylori causes different gastroduodenal diseases in different people is at present not clear. GOALS: The aim of this study is to identify risk factors associated with duodenal ulcers in H. pylori-infected patients in a multivariate context. STUDY: Demographic data, personal habits, stressful life events, psychologic distress, severity of histology of antral mucosa, and serum pepsinogen I concentrations were studied in 54 consecutive dyspeptic patients with duodenal ulcers and 40 patients with functional dyspepsia. RESULTS: As compared with functional dyspepsia patients, duodenal ulcer patients had more smokers (53.7% vs. 12.5%, P=0.000), higher pepsinogen I levels (median 96.0 vs. 74.5 ng/mL; P=0.002), more males (74.1% vs. 42.5%, P=0.004), more single (22.6% vs. 7.5%, P<0.05), and less in religion belief (44% vs. 70%, P<0.05). Only smoking remained significant on multivariate analysis (odds ratio=10.86, 95% CI=2.92-40.41, P<0.001). Among nonsmokers, only serum pepsinogen I level was found higher in duodenal ulcer patients as compared with functional dyspepsia patients (88 vs. 71, P<0.05). CONCLUSIONS: Smoking and hyperpepsinogenemia are associated with increased risk for duodenal ulcer in H. pylori-infected patients.

Biopsy↗
PubMed2005

Rapid urinary trypsinogen-2 test strip in the diagnosis of acute pancreatitis.

OBJECTIVES: Early diagnosis of acute pancreatitis remains a challenge. A rapid dipstick screening test for acute pancreatitis has been developed. This prospective study was designed to evaluate the diagnostic value and time course of the rapid urinary trypsinogen-2 test strip in acute pancreatitis, with comparisons with serum amylase and serum lipase. METHODS: A total of 165 patients with acute abdominal pain (67 with acute pancreatitis and 98 with other acute abdominal diseases) attending our emergency unit were included. All patients were tested with the urinary trypsinogen-2 test strip, and serum amylase and serum lipase concentrations were determined simultaneously. To measure the time course of the urinary trypsinogen-2 test, 32 patients with acute pancreatitis were tested with a urinary trypsinogen-2 test strip on days 1, 2, 3, and 4 after admission. RESULTS: Using a cutoff level of 50 microg/L for urinary trypsinogen-2, the sensitivity, specificity, and accuracy of the urinary trypsinogen-2 test strip for recognition of acute pancreatitis were 89.6%, 85.7%, and 87.3%, respectively. The diagnostic accuracy rates of serum amylase and serum lipase were 88.5% and 93.3%, using cutoff values of 3 times the upper normal limits for serum amylase and serum lipase, respectively. All but one of the 17 patients with severe acute pancreatitis was detected by the test strip (sensitivity, 94.1%). The time-course study of the urinary trypsinogen-2 test strip revealed that the sensitivity on days 1, 2, 3, and 4 was 90.6%, 81.2%, 59.4%, and 50%, respectively. There was no significant difference in the sensitivity between urinary trypsinogen-2 and serum lipase; however, the sensitivity values of serum lipase were significantly higher than those of serum amylase from days 1 to 4. CONCLUSION: The rapid urinary trypsinogen-2 test is a reliable and simple method for the early diagnosis of acute pancreatitis. A positive test identifies patients in need of further diagnostic measures. The urinary trypsinogen-2 test can be performed in health care units where laboratory testing facilities are not immediately available.

Abdominal Pain↗
PubMed2005

Evidence against a role for endotoxin in the hepatic encephalopathy of rats with thioacetamide-induced fulminant hepatic failure.

BACKGROUND AND AIMS: Endotoxin has been proposed to participate in the development of hepatic encephalopathy. However, there is no published data concerning the effects of endotoxin neutralization on the degree of hepatic encephalopathy. The present study investigated the effect of chronic intraperitoneal injection of polymyxin B, a neutralizing antagonist of endotoxin, on hepatic encephalopathy in rats with thioacetamide (TAA)-induced fulminant hepatic failure. METHODS: Male Sprague-Dawley rats weighing 300-350 g were used. Fulminant hepatic failure was induced by intraperitoneal injection of TAA (350 mg/kg/day) for 3 days. Two series of rats were designed to compare the effects of low dose (0.1 mg) or high dose (0.2 mg) intraperitoneal polymyxin B administration versus normal saline (NS) on hepatic encephalopathy. The injection was twice daily started from 2 days prior to TAA administration and lasted for 5 days. Severity of encephalopathy was assessed by the counts of motor activity in an Opto-Varimex animal activity meter. Plasma levels of endotoxin and tumor necrosis factor-alpha (an index of liver injury) were measured by Limulus assay and the ELISA method, respectively. RESULTS: Neutralization of endotoxin by either low dose or high dose polymyxin B administration did not significantly alleviate the degree of hepatic encephalopathy, as represented by the counts of motor activities (P > 0.05). Plasma levels of endotoxin and tumor necrosis factor-alpha were comparable between rats treated with polymyxin B or NS (P > 0.05). CONCLUSION: Our findings do not support the notion that endotoxin plays a major role in the pathogenesis of hepatic encephalopathy in rats with TAA-induced fulminant hepatic failure.

Animals↗
PubMed2005

Electrogastrography: basic knowledge, recording, processing and its clinical applications.

The slow wave (SW) of the gastrointestinal (GI) tract mainly functions to trigger the onset of spike to elicit smooth muscle contraction, which provides the essential power of motility. Smooth muscle myogenic control activity or SW is believed to originate in the interstitial cells of Cajal (ICC). The electrical coupling promotes interaction between muscle cells, and ICC additionally contribute to SW rhythmicity. Stomach SW originates in the proximal body showing the continuous rhythmic change in the membrane potential and propagates normally to the distal antrum with a regular rhythm of approximately 3 c.p.m. A technique using electrodes positioned on the abdominal skin to pick up stomach rhythmic SW refers to electrogastrography (EGG). The stomach SW amplitude is very weak, while many visceral organs also produce rhythmic electricities, for example heartbeat, respiration, other organs of the GI tract and even body movements. Thus noise other than SW should be filtered out during the recording, while motion artifacts are visually examined and deleted. Finally, the best signal among all recordings is selected to compute EGG parameters based on spectral analysis. The latter is done not only to tranform frequency domain to time domain but also to provide information of time variability in frequency. Obtained EGG parameters include dominant frequency/power, % normal rhythm, % bradygastria, % tachygastria, instability coefficient and power ratio. Clinical experience in EGG has been markedly accumulated since its rapid evolution. In contrast, lack of standardized methodology in terms of electrode positions, recording periods, test meals, analytic software and normal reference values makes the significance of EGG recording controversial. Unlike imaging or manometrical studies, stomach motility disorders are not diagnosed based only on abnormal EGG parameters. Limitations of EGG recording, processing, computation, acceptable normal parameters, technique and reading should be known to conduct subjective assessments when EGG is used to resolve stomach dysfunction. Understanding basic SW physiology, recording methodology and indications may open EGG as a new domain to approach the stomach motor dysfunction.

Action Potentials↗
PubMed2005

Effects of norepinephrine and acetylcholine on portal-systemic collaterals of common bile duct-ligated cirrhotic rat.

BACKGROUND: Catecholamine exerts profound vascular effects on vascular smooth muscle, and serum norepinephrine (Nepi) and sympathetic nervous activity are increased in cirrhosis. The vascular response of Nepi and acetylcholine (Ach) in portal-systemic collaterals of cirrhotic rats is unknown. The purpose of the present study was to investigate the effects of Nepi and Ach on portal-systemic collaterals of common bile duct-ligated (BDL) cirrhotic rats. METHODS: Perfusion studies were performed 6 weeks after BDL when hepatic cirrhosis was induced. Three series of experiments were performed in BDL rats: (i) the Nepi (10(-10) mol/L-10(-5) mol/L) vasoconstrictory responses with (n = 6) and without (n = 5) alpha1- (phentolamine, 5 x 10(-6) mol/L) or beta- (propranolol, 10(-5) mol/L) receptor antagonist (n = 6 and 5, respectively); (ii) the Ach (10(-8) mol/L-10(-5) mol/L) vasodilatory responses in Nepi- preconstricted portal-systemic collaterals in the absence (n = 7) or presence (n = 8) of N(pi)- L-nitro-arginine (NNA, 10(-4) mol/L); and (iii) the effect of indomethacin (10(-5) mol/L; n = 6) on Nepi responses. The collateral vascular responses were evaluated by the in situ collateral perfusion. RESULTS: Norepinephrine significantly increased the perfusion pressure and was inhibited by phentolamine (P < 0.05). The constrictive responses of Nepi were not significantly modified in the presence of propranolol (P > 0.05). Acetylcholine produced >50% relaxation of the Nepi-preconstricted collateral vessels and was inhibited by NNA (P < 0.05). In addition, indomethacin significantly enhanced the constrictive response of Nepi (P < 0.05). CONCLUSION: Norepinephrine has a vasoconstrictive effect on the portal-systemic collaterals of cirrhotic rats and this effect was mediated by alpha1-receptor. Both nitric oxide and prostaglandin are endogenous modulators in the collateral circulation of cirrhotic rats.

Acetylcholine↗
PubMed2005

Comparison of recurrence after hepatic resection in patients with hepatitis B vs. hepatitis C-related small hepatocellular carcinoma in hepatitis B virus endemic area.

PURPOSE: Hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are two important factors in the development of hepatocellular carcinoma (HCC). The carcinogenic mechanism of HBV and HCV is considered to be different. It is interesting to compare the recurrence after hepatic resection in patients with small HCC who were infected with HBV or HCV. METHODS: From 1991 to 1995, 145 patients who were positive for hepatitis B surface antigen (HBsAg) or antibody to HCV (anti-HCV) and diagnosed as small HCC (< or =3 cm) in three medical centers in Taiwan were evaluated in this study. All patients underwent hepatic resection. Among them, 83 (57.2%) were infected by HBV, 51 (35.2%) were infected by HCV, and 11 (7.6%) had dual HBV and HCV infection. RESULTS: Anti-HCV+ HCCs were associated with older age, lower serum albumin, higher alanine transaminase (ALT) level and multi-nodular tumors during diagnosis. During the follow-up, 92 (63.4%) patients developed tumor recurrence. Anti-HCV + HCC had a higher cumulated recurrence rate than HBsAg+ HCC (72.4% vs 53.6 % at 5 year, P = 0.032). In multivariate analysis, the presence of vascular invasion and lower serum albumin levels (<3.9 g/dl) were the determinants for tumor recurrence. CONCLUSIONS: HCV infection, as compared with HBV infection, had a higher cumulated recurrence after hepatic resection in patients with small HCC. Low serum albumin level was significantly associated with recurrence among these patients.

Adult↗
PubMed2005

Intracisternal des-acyl ghrelin inhibits food intake and non-nutrient gastric emptying in conscious rats.

Although des-acyl ghrelin is thought of as a non-functional peptide, studies show that it decreases food intake and gastric emptying in mice. However, no studies have examined the effects of centrally administered des-acyl ghrelin on food intake and gastrointestinal transit in rats. We investigated the effects of intracisternal (IC) administration of des-acyl ghrelin on food intake in free-feeding and food-deprived rats, as well as on the gastrointestinal transit in conscious rats. IC injection of des-acyl ghrelin dose-dependently (0.1 and 1.0 nmol/rat) decreased 20-min, 1-h and 2-h cumulative food intake in 16-h food-deprived, but not free-feeding rats, while IC administration of O-n-octanoylated (acylated) ghrelin (1 nmol/rat) increased food intake in both fed and fasted rats. IC-administered des-acyl ghrelin dose-dependently inhibited charcoal semi-liquid gastric emptying (0.01, 0.1, 0.3 and 1.0 nmol/rat) compared to saline-injected controls, but did not affect the geometric center and running percentage of small intestinal transit. However, IC acylated ghrelin enhanced gastric emptying and geometric center of small intestinal transit, but did not change running percentage of small intestinal transit. The studies suggest that IC des-acyl ghrelin decreases food intake in food-deprived rats and inhibits gastric emptying without altering small intestinal transit. These results establish the role of des-acyl ghrelin in regulating food intake as well as gastric emptying.

Acylation↗
PubMed2004

Pentagastrin-induced gastric acid secretion in the diabetic rats: role of insulin.

Streptozotocin-induced diabetic rats have excessively pentagastrin-simulated acid output in which insulin seems to attenuate rather than further stimulate acid output. The aim of this study was to determine the insulin impact on pentagastrin-stimulated acid output of diabetic and non-diabetic rats to resolve whether an attenuated effect does exist. Diabetic rats were induced by the streptozotocin i.v. injection four days before acid study. Some streptozotocin-treated rats additionally received daily insulin (2.4 IU/kg) injection. Using an autotitrator, acid output was measured every five minutes by the titration of gastric perfusate. Basal output was collected for 45 min before the 90-min pentagastrin infusion (0.89 microg/kg/min). Plasma gastric inhibitory polypeptide (GIP) levels were measured. Both doses (0.067 and 0.133 IU/kg/min) of insulin infusion resulted in stimulated acid output in normal rats. The subsequent insulin infusion (0.133 IU/kg/min) for non-diabetic rats undergoing pentagastrin-treatment suppressed their stimulated acid output almost down to the basal level. Pentagastrin-stimulation led to the excessively increased acid output of diabetic rats throughout the whole infusion period (P < 0.01). Correction of hyperglycemia with insulin for diabetic rats normalized the stimulated acid output. Measured basal and stimulated plasma GIP levels of those diabetic rats during acid stimulation remained higher, regardless of insulin treatment (P < 0.05). Our results suggest that insulin has the ability to attenuate pentagastrin-stimulated acid output in rats, whereas GIP is not involved in this attenuation. This effect appears to be responsible for the excessive acid output of diabetic rats undergoing pentagastrin stimulation.

Animals↗
PubMed2004

Advantages of assaying telomerase activity in ascites for diagnosis of digestive tract malignancies.

AIM: To evaluate the diagnostic value of assaying telomerase activity in ascites cells for the differential diagnosis of malignant and non-malignant ascites. METHODS: Ascites from 40 patients with hepatocellular carcinoma (HCC), 31 with non-HCC gastrointestinal carcinoma (CA), and 24 with liver cirrhosis (LC) were analyzed for telomerase activity. The telomerase activities in cell pellets from ascites were measured according to the Telomeric Repeat Amplification Protocol (TRAP) and quantified with a densitometer. RESULTS: Positive telomerase activity was detected in 16 of 31 (52%) CA patients, 10 of 40 (25%) HCC patients, and 1 of 24 (4%) LC patients (P<0.001). The telomerase activity was higher in the ascites of CA patients than in the ascites of HCC or LC patients (CA: 22.9 +/- 5.8, HCC: 6.7 +/- 2.5, LC: 1.3 +/- 1.3, P = 0.001). Cytology was positive in 18 CA patients (58%) and 1 HCC patient (2.5%), respectively. The positive telomerase activity was not related to patients' age, gender, and ascitic protein concentration, but to white blood count (r = 0.31, P = 0.002), neutrophil count (r = 0.29, P = 0.005), and the C-reactive protein level (r = 0.29, P = 0.018). When the results of both cytological examination and telomerase assay were considered together, the sensitivity increased to 77% for CA patients, 25% for HCC patients, and 48% for all 71 gastrointestinal cancer patients. CONCLUSION: Combining cytological examination of ascites with telomerase activity assay significantly improves the differential diagnosis between malignant and non-malignant ascites.

Aged↗
PubMed2004

Thrombocytosis: a paraneoplastic syndrome in patients with hepatocellular carcinoma.

AIM: Hepatocellular carcinoma (HCC) patients manifest a variety of paraneoplastic syndromes. Thrombocytosis was reported in children with hepatoblastoma. The aims of this study were to evaluate the prevalence and clinical significance of thrombocytosis in HCC patients and its relationships with serum thrombopoietin (TPO). METHODS: We retrospectively reviewed clinical, biochemical and image data of 1,154 HCC patients. In addition, we measured platelet count and serum TPO in HCC patients with and without thrombocytosis, in patients with cirrhosis, chronic hepatitis and healthy subjects in a cross-sectional study. RESULTS: Thirty-one (2.7%) of 1,154 HCC patients had thrombocytosis (platelet count > or = 400 K/mm3). HCC patients with thrombocytosis were significantly younger, had a higher serum alpha-fetoprotein, higher rate of main portal vein thrombosis, larger tumor volume, shorter survival, and were less likely to receive therapy than HCC patients without thrombocytosis. Multivariate logistic regression analyses showed that tumor volumes > or = 30% and serum alpha-fetoprotein > or = 140,000 ng/mL could significantly predict thrombocytosis. HCC patients with thrombocytosis had a significantly higher mean serum TPO than those without, as well as patients with cirrhosis, chronic hepatitis and healthy subjects. Platelet count and serum TPO dropped significantly after tumor resection in HCC patients with thrombocytosis and re-elevated after tumor recurred. Furthermore, the expression of TPO mRNA was found to be more in tumor tissues than in non-tumor tissues of liver in an HCC patient with thrombocytosis. CONCLUSION: Thrombocytosis is a paraneoplastic syndrome of HCC patients due to the overproduction of TPO by HCC. It is frequently associated with a large tumor volume and high serum alpha-fetoprotein.

Adolescent↗
PubMed2004

Hepatitis C virus infection is a risk factor for tumor recurrence after resection of small hepatocellular carcinomas.

Hepatocellular carcinoma (HCC) is closely associated with chronic hepatitis B or C virus (HBV, HCV) infection. Tumor recurrence frequently occurs after surgical resection and may adversely affect the outcome. This study aimed to investigate the effect of viral hepatitis in association with HCC recurrence after resection. A total of 248 patients [HBV in 165, HCV in 44, dual HBV+HCV in 15, and non-B non-C (NBNC) in 24] who underwent curative resection for HCC were included. The cumulative recurrence rate was compared according to the etiology of the underlying hepatitis and was stratified by tumor size and other clinicopathologic parameters. Altogether, 116 patients (47%) had a tumor recurrence within 17 +/- 11 months after resection. No significant difference in recurrence was noted among the four groups of patients (HBV, HCV, HBV+HCV, NBNC) ( p = 0.248). Persistent hepatitis was more common in the HCV group ( p < 0.001) after resection. Among the 157 patients with a small (= 5 cm) tumor, the recurrence rate was significantly higher in the HCV group than in the HBV, HBV+HCV, and NBNC groups ( p = 0.036). Cox multivariate analysis showed that HCV infection [relative risk (RR) 4.4, 95% confidence interval (CI) 1.3-14.8, p = 0.018] and vascular invasion (RR 3.2, 95% CI 1.2-8.9, p = 0.044) were independent predictors of tumor recurrence. Stratified analysis in other parameters did not show significant differences in terms of tumor recurrence among the four virologic groups ( p > 0.1 for all parameters). In conclusion, patients with small HCCs and concurrent HCV infection are at a high risk of tumor recurrence after resection.

Adult↗
PubMed2004

Benign nontraumatic inflammatory stricture of mid portion of common bile duct mimicking malignant tumor: Report of two cases.

Benign nontraumatic inflammatory stricture of the common bile duct (CBD) may result in obstructive jaundice, which can be misdiagnosed as a malignant tumor of the CBD preoperatively. Two cases with strictures of the mid portion of the common bile duct presenting with obstructive jaundice are reported herein. Preoperative radiological studies prompted us to confidently make the diagnosis of cholangiocarcinoma. However, the postoperative diagnosis on histological examination of the resected lesions was chronic inflammation and fibrosis. The complications of chronic duodenal ulcer are considered as the etiology of these two disorders.

Aged↗
PubMed2004

Deterioration of hepatic functional reserve in patients with hepatocellular carcinoma after resection: incidence, risk factors, and association with intrahepatic tumor recurrence.

Hepatocellular carcinoma (HCC) is frequently associated with liver cirrhosis. Patients with HCCs undergoing surgical resection may have declining hepatic functional reserve over time. However, the incidence and risk factors of hepatic decompensation, and its relation to postoperative tumor recurrence are unknown. This study investigated 241 HCC patients (208 male; age 61 +/- 13 years) undergoing resection with a long-term follow-up. The Child-Pugh scoring system was used to evaluate the postoperative deterioration of liver reserve, defined as a sustained increment in the Child-Pugh score by 2 or more. The 1-, 3-, and 5-year cumulative probabilities of postoperative decompensation were 14%, 32%, and 56%, respectively, during a follow-up period of 27 +/- 18 months (range 3-75 months). The average increment in Child-Pugh score was 1.4 +/- 1.1 in 2.3 +/- 1.5 years, or 0.6 point per year. Altogether, 74 (31%) patients developed postoperative hepatic decompensation during the follow-up period, 43 (58%) of whom had decompensation within 2 years of resection. Large (> 3 cm) tumor size was the only independent predictor associated with hepatic decompensation (relative risk 1.7, 95% confidence interval 1.1-2.8, p = 0.041) and was a significant risk factor for intrahepatic tumor recurrence ( p = 0.018). Patients with tumor recurrence more frequently (40% of 109 patients vs. 23% of 132 patients, p = 0.005) and more rapidly (0.8 vs. 0.4 point per year) developed hepatic decompensation than those without recurrence. In conclusion, large HCCs are closely associated with hepatic decompensation in patients after resection. Tumor recurrence may predispose to the development of hepatic decompensation in these patients.

Age Distribution↗
PubMed2004

Antibiotic prophylaxis after endoscopic therapy prevents rebleeding in acute variceal hemorrhage: a randomized trial.

Bacterial infection may adversely affect the hemostasis of patients with gastroesophageal variceal bleeding (GEVB). Antibiotic prophylaxis can prevent bacterial infection in such patients, but its role in preventing rebleeding is unclear. Over a 25-month period, patients with acute GEVB but without evidence of bacterial infection were randomized to receive prophylactic antibiotics (ofloxacin 200 mg i.v. q12h for 2 days followed by oral ofloxacin 200 mg q12h for 5 days) or receive antibiotics only when infection became evident (on-demand group). Endoscopic therapy for the GEVB was performed immediately after infection work-up and randomization. Fifty-nine patients in the prophylactic group and 61 patients in the on-demand group were analyzed. Clinical and endoscopic characteristics of the gastroesophageal varices, time to endoscopic treatment, and period of follow-up were not different between the two groups. Antibiotic prophylaxis decreased infections (2/59 vs. 16/61; P <.002). The actuarial probability of rebleeding was higher in patients without prophylactic antibiotics (P =.0029). The difference of rebleeding was mostly due to early rebleeding within 7 days (4/12 vs. 21/27, P =.0221). The relative hazard of rebleeding within 7 days was 5.078 (95% CI: 1.854-13.908, P <.0001). The multivariate Cox regression indicated bacterial infection (relative hazard: 3.85, 95% CI: 1.85-13.90) and association with hepatocellular carcinoma (relative hazard: 2.46, 95% CI: 1.30-4.63) as independent factors predictive of rebleeding. Blood transfusion for rebleeding was also reduced in the prophylactic group (1.40 +/- 0.89 vs. 2.81 +/- 2.29 units, P <.05). There was no difference in survival between the two groups. In conclusion, antibiotic prophylaxis can prevent infection and rebleeding as well as decrease the amount of blood transfused for patients with acute GEVB following endoscopic treatment.

Adult↗
PubMed2004

Changing seroepidemiology of hepatitis B, C, and D virus infections in high-risk populations.

Needle-sharing and sexual contact are important transmission routes of hepatitis B, C, and D virus (HBV, HCV, HDV) infection. This study aimed to investigate the current status of these viral infections among high-risk populations including prostitutes and intravenous (i.v.) drug users, compared with the prevalence rate reported previously to examine the changing seroepidemiology. Of the 916 female prostitutes, 79 (9%) were positive for antibody to HCV (anti-HCV), 111 (12%) were positive for HBV surface antigen (HBsAg), and 5 (5%) had antibody to HDV (anti-HDV). The prevalence rate was significantly lower compared to that in 1989-1991 (12%, P = 0.037) for HCV infection, and to that in 1988 (59%) and 1996 (40%) (P < 0.0001) for HDV infection. Of the 494 i.v. drug users, 87 (18%) patients were HBsAg carriers and 12 (14%) were anti-HDV-positive. The prevalence rate of HDV infection was significantly lower than that reported in 1985 (79%, P < 0.0001). Among the 443 tested i.v. drug users, 182 (41%) were anti-HCV-positive, significantly lower than that in 1985 (53%, P = 0.026). Of the 263 male prostitutes, 11 (4%) were anti-HCV-positive, 45 (17%) were HBsAg-positive, and 7 (16%) were anti-HDV-positive. Of the 129 illegal immigrant prostitutes, 7 (5%) were anti-HCV-positive, 15 (12%) were HBsAg-positive and none were positive for anti-HDV. In conclusion, the findings indicate a declining prevalence of HCV and HDV infections among drug users and prostitutes over the past 16 years. Male prostitutes and immigrant prostitutes are new "high-risk" populations and may become a reservoir for disease transmission.

Adolescent↗
PubMed2004

Determination of the optimal model for end-stage liver disease score in patients with small hepatocellular carcinoma undergoing loco-regional therapy.

The model for end-stage liver disease (MELD) has been a prevailing system to prioritize cirrhotic patients awaiting liver transplantation. An "exceptional" MELD score of 20 and 24 points is assigned for stage T1 and T2 patients with small hepatocellular carcinoma (HCC), respectively. However, this strategy is based on scarce data and the optimal score for these patients remains uncertain. We investigated 238 patients with small HCC who were candidates for liver transplantation and underwent arterial chemoembolization or percutaneous injection therapy using acetic acid or ethanol. Tumor stage (P = .001) and Child-Turcotte-Pugh (CTP) class (P < .001) were independent risk factors predicting tumor progression or death in survival analysis. The risk of disease progression in HCC patients stratified by tumor stage was mapped and equated with the risk of mortality of 456 cirrhotic patients without HCC. The 6- and 12-month rates of disease progression were 4% and 6%, respectively, for stage T1 HCC patients (n = 50; mean MELD: 9.5). These rates were close to and no higher than the mortality rate in MELD category 8-12 at the corresponding time period (7.1% and 11.3%, respectively; n = 141). For stage T2 patients (n = 188; mean MELD: 9.3), the corresponding rates were 5.3% and 13.8%, respectively, which were close to and no higher than the mortality rate in MELD category 10-14 (9.0% and 13.9%, respectively, n = 166). In conclusion, the risk of disease progression is quite low for selected HCC patients undergoing loco-regional therapy. A lower MELD score may be suggested to be equivalent to the risk of short- and mid-term mortality in the cirrhosis group.

Acetic Acid↗
PubMed2004

Chronic inhibition of nitric oxide increases the collateral vascular responsiveness to vasopressin in portal hypertensive rats.

BACKGROUND/AIMS: Nitric oxide (NO), a potent vasodilator, plays a significant role in the vascular hyposensitivity to vasoconstrictors related to portal hypertension. Chronic NO inhibition ameliorates portal-systemic collaterals in portal hypertensive rats. This study investigated whether chronic NO inhibition by NG-nitro-L-arginine methyl ester (L-NAME) improves the portal-systemic collateral vascular responsiveness to arginine vasopressin (AVP) in portal hypertensive rats. METHODS: Partially portal vein-ligated (PVL) rats received L-NAME in tap water (approximately 25 mg/kg per day) or tap water only (control) since 2 days prior to until 7 days after PVL. Mean arterial pressure was measured on the 8th day. By in situ perfusion model, different concentrations of AVP (10(-10)-10(-7) M) with a constant flow rate (20 ml/min) were applied to assess the perfusion pressure of collateral vessels. In another series, perfusion with different flow rates (5-30 ml/min) was used to obtain flow-pressure curves: the slopes represent collateral vascular resistances and higher resistances indicate less collaterals. RESULTS: Mean arterial pressure was higher in the L-NAME-treated group than that of the control group (P<0.05). As compared with the controls, L-NAME-treated rats achieved significantly higher perfusion pressures in response to AVP. In addition, chronic L-NAME treatment also induced an increase of collateral vascular resistance, suggesting the attenuation of portal-systemic shunting. CONCLUSIONS: Chronic NO inhibition ameliorates portal-systemic shunting and improves the collateral vascular responsiveness to AVP in portal hypertensive rats.

Animals↗