Dilatation of the cystic duct appears to be rare but was demonstrated in the patient illustrated below. A 36-year-old man was investigated because of upper abdominal symptoms including abdominal pain. Blood tests revealed a minor elevation of bilirubin (1.7 mg/dl, 29 μmol/l) and a mild elevation of alanine aminotransferase and gamma-glutamyl transpeptidase. An ultrasound study showed a dilated bile duct, mild dilatation of intrahepatic ducts and minor thickening of the wall of the gallbladder. MRCP revealed a dilated lower bile duct and marked dilatation of the portion of the cystic duct that entered the bile duct (Figure 1).

Other images showed that the junction of the cystic duct and bile duct was widely patent. Epigenetics inhibitor Figure 2 demonstrates a narrow distal bile duct (short arrow), the main pancreatic duct (long arrows) and a long common channel (thick arrow). As the cyst appeared to spare at least some of the common hepatic duct, it was classified as type IB with atypical involvement of a portion of the cystic Selumetinib duct. He was treated by cyst excision, cholecystectomy and Roux-en-Y hepaticojejunostomy to correct the extrahepatic obstruction and to minimize the risk of malignant change within the cyst wall. “
“A national viral hepatitis therapy program was launched in

Taiwan in October 2003. This study aimed to assess the impact of the program on reduction of end-stage liver disease burden. Profiles of national registries of households, cancers and death certificates were used to derive incidence and mortality Amine dehydrogenase of end-stage liver diseases from 2000 to 2011. The age-gender-adjusted incidence and mortality rates of hepatocellular carcinoma (HCC) and chronic liver diseases and cirrhosis of adults aged 30-69 years were compared before and after launching the program using Poisson regression models. A total of 157,570 and 61,823 patients (15-25% of the eligible for reimbursed treatment) received therapy for chronic hepatitis B and C, respectively,

by 2011. There were 42,526 chronic liver diseases and cirrhosis deaths, 47,392 HCC deaths, and 74,832 incident HCC cases occurred in 140,814,448 person-years from 2000 to 2011. Male gender and elder age were associated with a significantly increased risk of chronic liver diseases and cirrhosis and HCC. The mortality and incidence rates of the end-stage liver diseases decreased continuously from 2000-2003 (before therapy program) through 2004-2007 to 2008-2011 in all age and gender groups. The age-gender-adjusted rate ratio (95% confidence interval, p-value) in 2008-2011 was 0.78 (0.76-0.80, p<0.001) for chronic liver diseases and cirrhosis mortality, 0.76 (0.75-0.78, p<0.005) for HCC mortality, and 0.86 (0.85-0.88, p<0.

Neointimal hyperplasia can be reduced by intravenous transfusion of EPCs and analyzed on in vivo MR imaging after vascular injury. “
“To investigate the role of preoperative magnetic resonance tomographic angiography (MRTA) in predicting the clinical outcomes of trigeminal neuralgia (TN) patients following microvascular decompression (MVD). Preoperative MRTA imaging was performed on 167 consecutive patients with TN. The characteristics of offending vessels were determined by MRTA prior to MVD. The relationship

of neurovascular contact click here was classified into 3 types: positive, negative, and contralateral positive, which were compared with the surgical findings and clinical outcomes. MRTA showed obvious neurovascular learn more compression in accordance with surgical findings in 144 patients. Among the remaining 23 patients with negative finding

on preoperative MRTA images, neurovascular compression (vein alone or in combination with artery) were found in 16, no definite vascular compression in 7. The sensitivity of MRTA on the symptomatic side was therefore 90%, the specificity was 100% in our series. A correlation was found between clinical outcomes and preoperative findings on MRTA. In 144 MRTA-positive patients, 136 achieved “excellent” or “good” outcomes after MVD and were significantly better than the MRTA-negative group (P < .01). The outcomes of patients with a single artery compression were significantly better than those with venous compression, vein in combination with artery compression, or without obvious neurovascular contact (P < .01). Seven of 23 MRTA-negative patients obtained poor outcomes after operation, venous compression were identified intraoperatively in 4 of them, no definite offending vessel was found in 3 patients. This study suggests that the curative rate of TN following MVD is higher in the MRTA-positive group. Venous compression and no neurovascular contact that were negative on MRTA image are poor prognostic factors for surgical outcome of TN. Thus, preoperative MRTA

serves as a useful tool in patient selection and outcome prediction. “
“Fenestrations involving aneurysms have been well documented. Only sporadic papers have been reported on fenestrations associated with AVMs (arteriovenous malformations) with few cases. Our study is to determine the rate of co-occurrence (-)-p-Bromotetramisole Oxalate of fenestrations and AVMs and to analyze the possible relationship between them by CTA. Between January 2006 and February 2012, the CTA data of 5,657 consecutive patients were retrospectively reviewed. A total of 12 cases (.21%) of fenestrations associated with AVMs were found. Of these, single-fenestrations were identified in 9 cases, and multifenestrations were found in 3 cases. Among 349 fenestrations, there were 15 cases of multifenestrations. The frequency of multifenestrations among fenestrated patients without AVMs was 3.6%.

5 versus 33.9 years; P < 0.003). Males with a truncating variant were younger (31 ± 12 years) than those with missense variant (40 ± 13 years); likewise, females with a truncating variant were younger (26 ±6 years) than those with a missense variant (40 ± 13 years) (P < 0.001). There was no significant association between truncating sequence variations and severity of either acute or chronic biliary complications (severe biliary complications defined as

acute pancreatitis, recurrent cholangitis, segmental spindle-shape dilatation of the biliary tree filled with gallstones): odds ratio (OR) = 0.8 (95% confidence interval [CI] 0.3-3.7, P = 0.8). These complications were more frequent in men (71% versus 45%, P = 0.05, OR 2.9, 95% CI 1.0-9.6), that in women, independently of age at onset of symptoms and type of variant. About half of the women who had pregnancy experienced SCH772984 purchase ICP. The frequency and severity of ICP did not differ in patients with missense (44%) and truncating variant (69%) (P = 0.2). In patients without an

ABCB4 detectable variant the clinical characteristics BMN 673 in vitro were similar to those observed in patients with gene variation. Of note, in a subset of patients the phospholipid/bile acid ratio measured in hepatic bile (ratio of control gallbladder bile >25%) did not differ between the two groups: 11%, range 4%-16% (n = 7) versus 12%, range 1.4%-16% (n = 8) in patients with and without the ABCB4 variant, respectively. In the overall cohort, biliary cirrhosis was detected in only two patients. Both patients had a missense heterozygous variant (location selleckchem and nucleotide changes: c.523A>G and c.959C>T). Intrahepatic

cholangiocarcinoma leading to death was observed in a noncirrhosis female patient with a heterozygous splicing mutation (c.1005+5 G>A). All the patients received ursodeoxycholic acid (UDCA) (8-10 mg/kg/day) as the mainstay treatment after the diagnosis had been made. All the patients with severe chronic biliary complications had sphincterotomy. Patients with symptomatic intrahepatic bile duct dilatations filled with gallstones had repeated endoscopic procedures to remove the stones. All the patients with or without detectable variant and free of intrahepatic bile duct dilatations with gallstones became asymptomatic up to now. The only exception was a patient who did not tolerate UDCA because of bile acid-induced watery diarrhea. Among patients presenting with symptomatic cholelithiasis, three main features defined the syndromatic phenotype termed LPAC: recurrence of biliary symptoms after cholecystectomy, intrahepatic lithiasis, and age <40 years. The results of the present study may be summarized as follows: (1) half of the patients with the LPAC phenotype have detectable sequence variations of the ABCB4 gene, most of them being heterozygous missense.

Additionally for IBS, CFS, and FM a positive screen with the validated instrument was also considered selleck chemicals llc as presence of the condition. Validated questions

defined by the Rome II criteria (Rome Foundation, Inc., McLean, VA, USA) for the diagnosis of IBS were used.22,23 Criteria established by the U.S. Centers for Disease Control and Prevention (CDC, Atlanta, GA, USA) were used for a likely diagnosis of CFS. The American College of Rheumatology (ACR) criteria24 for the diagnosis of FM was used in this study, including a history of widespread pain plus pain at 11 of the 18 tender point sites as recorded by the examining physician at the end of the survey. In women, EM was based on self-reported physician diagnosis. For the purpose of final analyses respondents were classified as “cases with comorbidities” based on self-reported physician diagnoses, or validated criteria for the comorbidity, or both. Depression.— The Patient Health Questionnaire (PHQ-9) is a self-reported diagnostic

and severity measure GW-572016 molecular weight for current depression (in the prior 2 weeks) using criteria from the Diagnostic and Statistical Manual of Mental Disorders (DSM) IV.25 In this study, participants with PHQ-9 score >10 were considered positive for current depression. Anxiety.— The Beck Anxiety Inventory (BAI) was in this study to assess the severity of patient anxiety. The questionnaire consists of both physiological and cognitive components of anxiety addressed in the 21 items describing subjective, somatic, or panic-related symptoms.26 In this study, participants with BAI score

≥8 were considered positive for current anxiety. Statistical Analysis.— All statistical analyses in this study were performed using SAS version 9.1 (SAS Institute, Inc., Cary, NC, USA) and described in detail in Part I.17 An ordinal logistic regression models (CLOGIT) was used to examine mafosfamide the relationship between comorbid pain conditions and childhood abuse and neglect. In this model the dependent variable was number of comorbid conditions defined as 0, 1, 2, ≥3 conditions. In a separate model restricted to women, the dependent variable was defined as 0, 1, 2, 3, ≥4 conditions. Both models were adjusted for age, race, education, household income, and current depression and anxiety. Adjusted odds ratios (ORs) and 95% confidence intervals (CI) were used to measure the strength of the relationships, and the significance of the ORs was examined using Wald’s χ2 test statistic. A total of 1348 patients who received a diagnosis of migraine completed the surveys. The ICHD-2 diagnosis and characteristics of the study population are presented in Table 1. Additional characteristics of the study population are available in Table 1 of Part I and II of this study. In brief, a diagnosis of migraine with aura was recorded in 40% of the participants. The majority of the participants were women (88%) and the average age of the participants in this study was 41 years.

These analyses revealed only marginal Mcl-1 mRNA and protein expression compared to WT livers (Fig. 4E; data not shown). This strongly suggests that tumors did not originate from a conceivable subset of hepatocytes with a growth advantage due to leaky knockout of Mcl-1, but rather from Mcl-1–deficient hepatocytes. Finally, we set out to investigate whether HCC nodules of Mcl-1Δhep mice contain chromosomal aberrations. Five HCCs (ranging from 5-30 mm in diameter) GSK1120212 price derived from independent Mcl-1Δhep livers were analyzed by aCGH analysis. This revealed numerous,

chromosomal aberrations with amplifications and deletions on several chromosomal regions that were statistically significant (P < 0.05; Fig. 5). No clearly mutual pattern of chromosomal aberrations was detected in Mcl-1Δhep HCCs. These observations not only confirmed the neoplastic nature of the tumor nodules, but also indicated that HCCs contained different chromosomal aberrations. To further explore possible signaling mechanisms, which may contribute to hepatocarcinogenesis in the presented model, p53 expression was analyzed. No significantly buy FK228 different mRNA expression levels were detected when livers of Mcl-1Δhep mice were compared to WT and Mcl-1flox/wt mice. In addition, no p53 accumulation was detectable by immunostaining, in neither tumor nor nontumor tissues of Mcl-1Δhep mice (Supporting Fig. 1B). Based on these

findings, there was no evidence for p53 being a key factor for HCC formation in the presented model. Enhanced expression of the vascular endothelial growth factor-A (VEGF-A) has been discussed as being involved in hepatocarcinogenesis.23 Although a few tumors revealed a slightly enhanced VEGF-A expression by immunohistochemistry, this was not a constant finding (Supporting Fig. 1C).

HCC is Farnesyltransferase one of the most common cancers worldwide and frequently develops in the context of chronic liver disease and cirrhosis.24 However, the molecular mechanisms causing this sequence of events are still poorly understood. In this study, we describe HCC development in mice with hepatocyte-specific depletion of the antiapoptotic Bcl-2 family member Mcl-1. Apoptosis is generally considered a tumor-preventing mechanism, because it removes unwanted or dangerous cells, e.g., those with oncogenic alterations. Conversely, evasion of apoptotic cell death is considered a basic cellular feature contributing to cancer.25 We have recently shown that Mcl-1 is a crucial antiapoptotic factor in hepatocytes.10, 26 It is well known that liver cell death through apoptosis is a key pathogenic feature of acute and chronic liver diseases, including cholestasis, hepatitis C virus infection, as well as alcoholic and nonalcoholic steatohepatitis.27 Because mitochondrial activation is a central event in the induction of hepatocellular apoptosis, Bcl-2 family members play a pivotal role for the apoptosis regulation of hepatocytes.

It is known that RhoC protein plays an important role in controlling stress fiber and focal

adhesion contact formation.4 In another article from the same group, Yang et al. also observed that inhibition of RhoC in HCCLM3 (hepatocellular carcinoma lung metastasis 3rd selection) cells blocked autotoxin-induced stress fiber formation.2 ITF2357 So, is RhoC involved in the cytoskeletal change induced by Egfl7 protein? The authors interpreted this change due to FAK phosphorylation stimulated by Egfl7 protein, but we found some reports demonstrating that RhoC can activate FAK.5, 6 One group indicated that RhoC promotes tumor metastasis in prostate cancer by sequential activation of Pyk2 (Proline-rich tyrosine kinase 2), FAK, MAPK (mitogen-activated protein kinase), and Akt followed by the up-regulation of matrix metalloproteinase 2(MMP2) and MMP9, which results in the stimulation of invasiveness of tumor cells.5 So, can we hypothesize that Egfl7 activates FAK through RhoC protein in HCC cells? We also noticed one article from the same

group showing that overexpression of RhoC in HCC tissues was highly correlated with tumor invasion and poor prognosis,3 which is similar with the results of Egfl7.4 The HCC specimens used in the article regarding Egfl7 were from 112 patients with HCC in Xiangya Hospital of Central South University between 1998 and 2005,1 and specimens used in the RhoC article were collected from the same hospital between 1994 and 2002,3 so the period from 1998 to 2002 was overlapped. If the expression pattern of RhoC in these specimens is strongly correlated with that of Egfl7, FK506 research buy it will further confirm our hypothesis. Na Carnitine palmitoyltransferase II Liu*, Hongbo Zhang*, Kaichun

Wu*, Daiming Fan*, * State Key Laboratory of Cancer Biology and Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi’an, China. “
“See article in J. Gastroenterol. Hepatol. 2012; 27: 626–641. Functional dyspepsia is one of the commonest digestive disorders, which affects 10–20% of the adult population worldwide. Although it is not associated with excessive mortality, patients with functional dyspepsia often suffer from significant morbidity with functional impairment, loss of working days, and workload burden on the healthcare system. Despite the high prevalence and major impact in the community, the importance of functional dyspepsia has been relatively ignored in Asia. In the past two decades, there have been major breakthroughs in the diagnosis and treatment of Helicobacter pylori infection, peptic ulcer, gastric cancer and non-variceal upper gastrointestinal bleeding. On the other hand, there remain a lot of mysteries for functional dyspepsia. The etiology and mechanism of functional dyspepsia are heterogeneous and poorly understood. None of the reported pathophysiologic features are consistently observed in all patients and therefore there is no diagnostic biomarker.

The mechanism of what causes the development of BA remains unknown. However, BA patient livers show fibro-inflammatory blockage of bile ducts suggesting the involvement of inflammatory

and developmental pathways. Previous studies suggest that BA may result from overexpression of Hedgehog (Hh) signaling, potential autoimmunity, or possible epigenetic changes in gene expression. We previously reported that fish carrying a mutation in the S-adenylhomocysteine hydrolase gene (ahcy) reproduce important aspects of BA including increased immune expression and liver degeneration. Using the ahcy zebrafish model, we investigated the role Hh overexpression and inflammation has in liver development. Livers from ahcy larvae show increased expression see more of tumor necrosis factor alpha (TNFal-pha). Injection of TNFalpha into 2 days post fertilization fish causes liver abnormalities including duct defects and steatosis. TNFalpha injected larvae also show increased expression of the Hh pathway. Supporting a causative role for Hh overex-pression, inhibition of Hh signaling by cyclopamine treatment rescues liver morphology and function in ahcy larvae. Furthermore, we show that treatment of larvae with the Hh pathway agonist,

purmorphamine, not only produces biliary defects, but also causes increased expression of the inflammatory pathway. Our results CHIR-99021 suggest a potential crosstalk between Hh signaling and inflammatory pathways may result in defects observed in biliary atresia patients. Disclosures: The following people have nothing to disclose: Zenobia Cofer, Shuang Dichloromethane dehalogenase Cui, Valerie Sapp, Randolph P. Matthews Purpose/Background: The progression of alcoholic liver disease (ALD) is multifactorial, involving both

metabolic and immunological dysfunctions. MiR-122 has been shown to regulate essential functions in hepatic lipid metabolism, mitochondrial function, cell death pathways, fibrosis and carcinogenesis -major elements in ALD. While recent studies have demonstrated the therapeutic benefits of miR-122 inhibition in HCV infection, we have observed the reduction of miR-122 expression in the livers of alcohol-fed mice. Given the highly conserved role of this unique miRNA in hepatic homeostasis, we hypothesized that the loss of miR-122 contributes to ALD progression and may be a therapeutic target. In this study, our goals were twofold. First, we aimed to assess the effect of miR-122 inhibition on steatosis, inflammation, and fibrosis in ALD. Second, we sought to therapeutically restore miR-122 in the livers of alcohol-fed mice to alleviate liver injury. Methods: Wild-type 6-8 week old, female C57Bl/6 mice were injected intravenously with scAAV8 viral particles containing anti-miR-122 TuD (TuD), or scrambled vector (scr).

However, if the inflammatory response is severe and prolonged, hepatic necrosis may eventually lead to extensive loss of parenchyma and irreversible tissue fibrosis. Neutrophils are capable of migrating rapidly to foci of infection or inflammation. Infiltration and contact with inflammatory mediators can reprogram cells to alter effector responses. Chakravarti et al. 17 recently described a subset of human blood neutrophils that became long-lived, expressed human leukocyte antigen DR, CD80, and CD49d de novo, and alternatively produced leukotrienes, superoxide anions, and cytokines upon exposure MK0683 to granulocyte-macrophage colony-stimulating factor, tumor necrosis factor α, and

IL-4. Thus, the microenvironment can reprogram cells that traditionally have been thought to be terminally differentiated, and this can affect disease progression. Here, we show that IL-4 was necessary for the full development of hepatic necrosis in infected IL-10 KO mice, and CD4+ T cells, a proportion of which were activated within GALT, constituted a major source of IL-4 in the liver. Furthermore, our data Trametinib concentration indicated that neutrophils played a critical role in the progression from

hepatocellular injury to necrosis. The accumulation of neutrophils was inhibited in the absence of IL-4 concomitantly with altered expression of key activation molecules, highlighting a role for this cytokine in the management of neutrophil function. These data define a critical balance between IL-10 and IL-4 in the hepatic response to enteric infection and suggest a role for CD4+ T cells and IL-4 in regulation of neutrophil activity Branched chain aminotransferase during hepatic injury. Our results also demonstrated the utility of this in vivo system not only for the investigation of the specific roles of IL-10 and IL-4 in the hepatic response to infection with this parasite but also for broader

inquiry into the coordination of enteric and hepatic immune mechanisms. In several experimental models of liver injury, IL-4 has been shown alternatively to be protective or deleterious. For example, IL-4 protects mice from damage induced by ischemia/reperfusion, but it promotes hepatitis after concanavalin-A injection. 18, 19 Although IL-4 and neutrophils are known to participate in the pathogenesis of certain liver diseases, very little is established about how IL-4 directly or indirectly influences neutrophil activity. Interestingly, Huang et al. 20 recently reported that IL-4 stimulated the expression of chemokine (C-X-C motif) ligand 8, CD62E, vascular endothelial growth factor, and inducible nitric oxide synthase by equine pulmonary artery endothelial cells, resulting in neutrophil migration in vitro. In our studies, the capacity to produce IL-4 influenced expression of neutrophil adhesion molecules and sequestration in the liver.

Our results are of further relevance considering that most patients with HCC are diagnosed at an advanced stage and that this group included the majority of patients

who were candidates for sorafenib treatment. By contrast, BCLC B patients who failed or were not suitable for locoregional treatments are a heterogeneous group of patients, representing a small subgroup of HCC patients who are candidates for sorafenib treatment, and not fully representative of the entire BCLC B spectrum. The robustness of these results was confirmed selleck chemical in the probabilistic sensitivity analysis, showing that the probability of dose-adjusted sorafenib providing a cost-effective alternative to BSC was about 70% for advanced and 10% for intermediate HCC at a willingness-to-pay threshold of €38,000 per QALY.

The cost-effectiveness of dose-adjusted sorafenib in both advanced and intermediate HCC was sensitive to the BSC survival rate, sorafenib treatment duration, and the choice of parametric model used to predict survival gain. It is important to highlight that dose-adjusted sorafenib remains cost-effective in BCLC C HCC patients under a wide range of survival of untreated patients. This issue is very relevant, given the high heterogeneity and the unpredictability Akt inhibitor of clinical behavior of advanced HCC. 3 On the efficacy side of the cost equation, identification of robust predictive biomarkers would increase the overall efficacy of sorafenib for HCC by treating only those patients most likely to respond. This is not a trivial point, because sorafenib therapy is costly and still in search of optimization due to the lack of serum biomarkers of early response that are deemed necessary to generate Pyruvate dehydrogenase lipoamide kinase isozyme 1 response-guided therapeutic algorithms. Moreover, the identification of stopping rules based on predictors of mortality (such as early radiologic progression)

could assist the clinician in the cost-effective management of patients with HCC. Unfortunately, stopping sorafenib in patients with early radiologic progression only marginally improves the cost-effectiveness ratio. Therefore, the identification of the optimal sorafenib dose, effective but not toxic, remains to date the only strategy to substantially improve the ICER. Modeling the indication for treatment of advanced/intermediate HCC with dose-adjusted sorafenib clearly improves its cost effectiveness. In this line, the role of dose-adjusted sorafenib should be taken into account also for the future perspectives in the adjuvant setting after resection/ablation or after transarterial chemoembolization and for the design of future comparative trials versus novel targeted therapies. Although the proposed algorithms are useful tools for decision making, the treatment strategy should be carefully agreed upon with the patient, taking into account all the different factors, particularly the safety profile, that can interfere with treatment response.

00001 as shown in the Forrest Plot diagram. Conclusion: The metaanalysis results significantly favored the use of Omeprazole + Amoxicillin + Levofloxacin over the standard triple therapy of Omeprazole + Amoxicillin + Clarithromycin in eradicating H. Pylori infection. A triple drug regimen RG7420 price consisting of Omeprazole, Amoxicillin and Levofloxacin may be considered a better first-line treatment option for HP eradication in this country. Key Word(s): 1. Helicobacter Pylori; 2. Clarithromycin; 3. Levofloxacin; 4. Eradication; Presenting Author: VIDIORBA BUSRO Additional Authors: FUADORBA BUSRO, YUWONO BAKRY, AIDA FARIDA Corresponding Author: FUADORBA BUSRO,

YUWONO BAKRY, AIDA FARIDA Affiliations: dr. muhammad husin general hospital IDH inhibition Objective: Over 90% of chronic gastritis cases

are caused by Helicobacter pylori, and half of those patients show no clinical symptoms. Poor environmental sanitation, low socioeconomic status and malnutrion are playing important role of this infection. This study aim to assess the sensitivity and specificity value of saliva Helicobacter pylori examination in chronic gastritis patients. It was expected that the result of the study could be applied as basic scientific methods to develop a noninvasive detection to confirmed the existence of Helicobacter pylori infection in chronic gastritis besides urea breath test (UBT). Methods: The subjects of the study were adult male and female, in and out patients that have dyspepsia symptoms over 6 moths. There were 50 subjects (26 male and 24 female) followed this study from June 2010 until March 2011. The PCR methods applied in identifying the DNA sequences of Helicobacter pylori in chronic gastritis patients’ saliva is a modification of Hakayama’s methods. The result of bacteria DNA sequencing is 16 s RNA that is located in 100 bp. Results: The histopathology result in this study show that among the subjects who experiencing chronic dyspepsia there were 16 subjects (32%) positive for Protirelin Helicobacter pylori and 34 subjects (68%) negative for Helicobacter pylori. There were 27 subjects (44%) were chronic active gastritis with intestinal metaplasia,

15 subjects (30%) were chronic active gastritis- Helicobacter pylori positive with intestinal metaplasia, 7 subjects (14%) were chronic non-active gastritis with intestinal metaplasia and 1 subjects (2%) were chronic non-active gastritis-Helicobacter pylori positive with intestinal metaplasia and atrophic. The result of the DNA sequences of chronic gastritis patients’ saliva using PCR show 47 subjects (94%) had positive result for Helicobacter pylori DNA sequence that consist of 23 male (46%) and 24 female (48%) subjects, while 3 subjects (all male) had negative result for Helicobacter pylori DNA sequences. Sensitivity and specificity values of Helicobacter pylori DNA sequences in saliva examination was 93.75% and 5.8% respectively with positive prediction value 31.9% and negative prediction value 66.67%.