Maxillofacial morphological characteristics in growing orthodontic patients with non-syndromic oligodontia.

OBJECTIVE: Patients with oligodontia frequently show different types of malocclusions. However, how oligodontia affects the maxillofacial growth remains uncertain. This study aimed to investigate the maxillofacial morphological characteristics in growing patients with oligodontia. SETTING AND SAMPLE POPULATION: The study subjects included 33 Japanese children with non-syndromic oligodontia (14 boys and 19 girls; mean age: 10.2 years) who visited the orthodontic clinic of Fukuoka Dental College Medical and Dental Hospital from 1999 to 2019. MATERIALS AND METHODS: Cephalometric analyses were performed, and the variables measured in each subject were converted into Z scores in relation to the mean and standard deviation of the Japanese norms matched for growth stage. The one-sample t-test or Wilcoxon signed-rank test was performed to compare the mean scores in the patients with oligodontia with those of the Japanese norms. RESULTS: Compared with the Japanese norms, patients with oligodontia showed a smaller convexity and larger A-B plane and SNB angles. The Frankfort-mandibular plane and gonial angles were smaller, whereas the height of the ramus was larger. The vertical height of the alveolar bone in the maxillary and mandibular incisors and molar areas was smaller in patients with oligodontia. CONCLUSIONS: Patients with oligodontia showed Class III skeletal tendency with mandibular prognathism and flattened mandibular plane with a smaller gonial angle. These maxillofacial morphological features can be induced by a deficiency in the vertical growth of the alveolar bone in the maxillary and mandibular molar areas due to the lack of tooth germs.

The promotion of nephropathy by Porphyromonas gingivalis lipopolysaccharide via toll-like receptors.

BACKGROUND: Recently, we reported that toll-like receptor (TLR)2 and TLR4 localized on the glomerular endothelium in the glomeruli of streptozotocin (STZ)-induced type 1 diabetic mice and high fat diet feed-induced type 2 diabetic mice, and that periodontal pathogen Porphyromonas gingivalis LPS (Pg-LPS) administration lowered the survival rate of diabetic mice. The present study aims to examine the effect of TLR4 blocking on the suppression of Pg-LPS-induced diabetic nephropathy. METHODS: The survival rate and morphological/biochemical features for streptozotocin-induced diabetic mice with Pg-LPS and TLR4 blocker eritoran administration were investigated by reporter gene assay, urine and blood analysis, immunohistochemistry, and real time-PCR. RESULTS AND CONCLUSIONS: All of the diabetic mice administered Pg-LPS were euthanized within the survival period of almost all of the diabetic mice. The blood urea nitrogen and creatinine, expression of TLR2 and TGF-b, and type 1 collagen accumulation, in the diabetic mice increased significantly with the Pg-LPS administration. In spite of the limited TLR4 activation with Pg-LPS, the TLR4 blocker eritoran decreased blood urea nitrogen and creatinine, and raised the survival rate of the Pg-LPS-administered diabetic mice slightly. The high expression levels of TLR2, TGF-b, and type 1 collagen in Pg-LPS-administered diabetic mice decreased with eritoran. Nuclear STAT3 which enhances TLR2 expression was detected in the TLR2-expressing glomeruli of diabetic mice. The TLR2 and STAT3 gene expression increased by the Pg-LPS administration but decreased with eritoran. These may suggest that Pg-LPS-induced diabetic nephropathy is mainly dependent on TLR2 signaling on glomerular endothelial cells, and that TLR4 blocker eritoran may play a role to slow the progress of diabetic nephropathy.

Expression of toll-like receptor 2 in glomerular endothelial cells and promotion of diabetic nephropathy by Porphyromonas gingivalis lipopolysaccharide.

The toll-like receptor (TLR) has been suggested as a candidate cause for diabetic nephropathy. Recently, we have reported the TLR4 expression in diabetic mouse glomerular endothelium. The study here investigates the effects of the periodontal pathogen Porphyromonas gingivalis lipopolysaccharide (LPS) which is a ligand for TLR2 and TLR4 in diabetic nephropathy. In laser-scanning microscopy of glomeruli of streptozotocin- and a high fat diet feed-induced type I and type II diabetic mice, TLR2 localized on the glomerular endothelium and proximal tubule epithelium. The TLR2 mRNA was detected in diabetic mouse glomeruli by in situ hybridization and in real-time PCR of the renal cortex, the TLR2 mRNA amounts were larger in diabetic mice than in non-diabetic mice. All diabetic mice subjected to repeated LPS administrations died within the survival period of all of the diabetic mice not administered LPS and of all of the non-diabetic LPS-administered mice. The LPS administration promoted the production of urinary protein, the accumulation of type I collagen in the glomeruli, and the increases in IL-6, TNF-α, and TGF-ß in the renal cortex of the glomeruli of the diabetic mice. It is thought that blood TLR ligands like Porphyromonas gingivalis LPS induce the glomerular endothelium to produce cytokines which aid glomerulosclerosis. Periodontitis may promote diabetic nephropathy.

[A case report of hepatocellular carcinoma with metastases to the lip, stomach, and colorectum].

A 79-year-old man was diagnosed with hepatocellular carcinoma in 2000 and treated with partial hepatectomy. Intrahepatic carcinoma recurred with lung metastases 7 years later. Several transcatheter arterial chemoembolizations were performed to treat the recurrence, and a right lower lobectomy was performed for lung metastasis. Twelve years after the original carcinoma diagnosis, lip and lung metastases were detected, and he was hospitalized for radiotherapy of the lung metastasis; an oral molecular-targeting drug was initiated. During the therapy, hematochezia was observed, and a colonoscopy was performed. A submucosal lesion with a blood clot measuring approximately 4mm in diameter was found in the sigmoid colon, and endoscopic mucosal resection was performed. Furthermore, an elevated lesion with a 5-mm diameter recess was observed on upper gastrointestinal endoscopy. Both lesions were diagnosed histopathologically as hepatocellular carcinoma metastases.

Altered dynamics in the renal lymphatic circulation of type 1 and type 2 diabetic mice.

The dynamics of the renal lymphatic circulation in diabetic nephropathy is not fully elucidated. The present study evaluated the effect of diabetic nephropathy on the renal lymphatic circulation in streptozotocin (STZ)-induced type 1 diabetic mice (ICR-STZ) and in type 2 diabetic KK/Ta mice which were fed a high fat diet (KK/Ta-HF). The diabetic mouse kidneys developed edema because of the nephropathy. In control mice renal lymphatic vessels distributed in the cortex but rarely in the medulla while in ICR-STZ and KK/Ta-HF mice, there were many lymphatic vessels with small lumen in both cortex and medulla. Total numbers and areas of renal blood vessels in the diabetic mice were similar to those in the controls while the total numbers and areas of renal lymphatic vessels were larger in diabetic mice than in the controls. There were statistically significant differences in the numbers of lymphatic vessels with diameters of 50-100 µm between the ICR-STZ and the control ICR mice, and in the numbers of lymphatic capillaries with diameters smaller than 50 µm between the KK/Ta-HF and the control KK/Ta mice. The diabetic nephropathy may induce the lymphangiogenesis or result in at least the renal lymphatic vessel expansion.

Expression of Toll-Like Receptor 4 in Glomerular Endothelial Cells under Diabetic Conditions.

Diabetic conditions promote glomerulosclerosis by mesangial cells but the mechanisms are not fully elucidated. The present study evaluated the expression of toll-like receptor 4 in glomerular endothelial cells in the streptozotocin (STZ)-induced type 1 diabetic mouse (ICR-STZ) and the type 2 diabetic KK/TaJcl mouse which were fed a high fat diet feed (KK/Ta-HF). In the ICR-STZ and KK/Ta-HF almost glomeruli were immunostained with anti-TLR4 but there was no glomerulus immunostained by ani-TLR4 in the control ICR and KK/Ta. Laser-scanning confocal microscopy showed that the TLR4-positive region did not coincide with the podoplanin-positive region but coincide with the PECAM-1- and VE-cadherin-positive regions in the glomeruli of the ICR-STZ and KK/Ta-HF. The in situ hybridization showed that almost signals for TLR4 mRNA were present in the glomerulus of the ICR-STZ and KK/Ta-HF to a stronger extent than in the control ICR and KK/Ta. These suggest that glomerular endothelial cells usually express the TLR4 gene and hyperglycemia in the diabetic condition induces the TLR4 protein expression in the glomerular capillary endothelial cells. Cytokine productions through the TLR signaling pathway in glomerular endothelial cells may allow mesangial cells to produce extracellular matrix proteins in the diabetic milieu.

Gastric cancer development after Helicobacter pylori eradication therapy: a new form of gastric neoplasia.

BACKGROUND AND AIM: Along with the widespread use of eradication for Helicobacter pylori (H. pylori), the incidence of gastric cancer after eradication has also been increasing. There is a need for clarification of the clinical and biological characteristics of these neoplasms. PATIENTS AND METHODS: We studied 27 cases of gastric cancer that developed after eradication (group AE). Out of the 27, we selected 26 with early-stage gastric cancer and compared them with 78 age-matched gastric cancer patients with H. pylori infection (group Pos) and 20 patients without H. pylori (group Neg). The patient with autoimmune gastritis was not included. Clinicopathological features, mucus patterns and Wnt5a expressions were compared among these groups. RESULTS: Among group AE patients, there were more males than females, and the tumor histology was mainly intestinal type, a significant difference from group Neg. In contrast, macroscopically, the tumors were predominantly of the flat-depressed type, a feature similar to that of group Neg but significantly different from that of group Pos. MUC2 and Wnt5a expression was significantly lower in group AE than in group Pos. CONCLUSION: Gastric cancer development after eradication may have a carcinogenic pathway similar to that in cancer with H. pylori infection, though macroscopic/biological features may be modified by eradication therapy.

Serum screening for detection of high-risk group for early-stage diffuse type gastric cancer in Japanese.

BACKGROUND AND AIM: Serum screening systems are beneficial for gastric cancer mass surveys; however, the marker for diffuse type gastric cancer (DGC) is not defined. We attempted to define the high-risk group for DGC by using serum markers of anti-Helicobacter pylori antibody and pepsinogens (PG). METHODS: Forty-two patients in the early stage of DGC and 511 controls were enrolled. Fasting serum samples were collected, and anti-H. pylori antibody and PG were evaluated. The risk for DGC was calculated. RESULTS: The prevalence of DGC was higher in H. pylori-positive patients (odds ratio [OR] = 4.3 in men, 9.6 in women). DGC prevalence was significantly higher in the PG1+ group in women (OR = 10.7); however, it was lower in the PG3+ group in both men and women. Patients with PG II ≥ 30 revealed a significantly higher risk for DGC. By combining factors, higher OR (OR = 12.5 in men, 42.7 in women) were obtained when we defined the risk group as H. pylori-positive, PG-negative, and having PG II ≥ 30. CONCLUSION: The risk group for DGC can be defined by evaluating ordinary serum gastritis markers.

Low prevalence of Helicobacter pylori-negative gastric cancer among Japanese.

BACKGROUND AND AIMS: The true prevalence of Helicobacter pylori-negative gastric cancer (HpNGC) is unknown. We attempt to clarify the prevalence and clinicopathologic features of HpNGC in Japanese. METHODS: Helicobacter pylori infection was detected by antibody titer and microscopic observation. In addition, we confirmed the lack of endoscopic atrophy and histologic gastritis. In these cases, we added urea breath test or rapid urease test to confirm the absence of H. pylori. The mucus phenotype of gastric cancer tissue was also evaluated by immunohistochemistry. RESULTS: We screened 3161 gastric cancer cases from 1996 to 2010, and 21 cases were regarded as H. pylori negative. Clinically, patients with HpNGC were younger than patients with H. pylori-positive gastric cancer (controls), and revealed a lack of male dominancy. Histologically, diffuse type was frequently found. All patients examined were pepsinogen negative. Among HpNGC cases with endoscopic resection, the depressed macroscopic appearance was dominant. The prevalence of HpNGC was calculated as 0.66% (95% confidence interval = 0.41-1.01). The mucus phenotype of HpNGC was similar to that of the controls. CONCLUSION: The prevalence of HpNGC is very low and its pathological characteristics are different from common gastric cancer.

Helicobacter pylori cagA polymorphism and gastric inflammation: an international comparison between Japanese and Brazilian patients.

OBJECTIVE: Gastritis induced by Helicobacter pylori can cause the onset of gastric cancer, and H. pylori cytotoxin associated gene A (cagA) is considered to be an important factor for its development. We investigated the relationship between the grades of gastritis and cagA phenotype in Japanese and Brazilian patients. MATERIAL AND METHODS: We studied 47 Brazilian and 47 age-, gender-matched Japanese patients. Status of H. pylori infection, the degree of histologic gastritis, and the levels of serum pepsinogen levels were evaluated. DNA was extracted from paraffin-embedded sections and a portion of the cagA gene was amplified using the polymerase chain reaction, followed by direct sequencing of the fragment. We investigated the cagA subtype using a newly developed restriction fragment length polymorphism (RFLP) system. RESULTS: In H. pylori-positive patients, the grades of histological and serological gastritis were more prominent in the Japanese subjects than their Brazilian counterparts, although no difference was detected in the H. pylori-negative subjects. According to cagA phenotype analysis, our RFLP system was helpful for evaluating cagA phenotype, and we found that the prevalence of the East Asia subtype was significantly higher in the Japanese subjects than in the Brazilian. CONCLUSION: Infection with H. pylori possessing the East Asian cagA gene contributes to the progression of gastritis.

Plaunotol induces a comparative increase of acidic mucin fraction in gastric juice.

BACKGROUND/AIMS: Gastric mucus protects the gastric mucosa. Plaunotol, a gastroprotective agent, has been shown to increase mucus production in animal models. However, it is unclear whether plaunotol benefits human gastric mucus secretion. METHODOLOGY: Twenty-five patients with atrophic gastritis were studied. All patients underwent gastroendoscopy and gastric juice was collected before and after plaunotol treatment for 3 months. Gastric juice mucin was examined by gel filtration as well as anion-exchange chromatography. The identification of each fraction was examined by enzyme-linked immunosorbent assay (ELISA) with the use of HGM75 and HIK1083, antibodies against mucin from surface mucus cells and from gastric glandular mucus cells, respectively. RESULTS: Plaunotol significantly increased the total gastric juice volume (7.8mL before vs. 10.7mL, after administration; p=0.03). By anion exchange chromatography, we detected three mucin fractions (Fr I-III). Fr I strongly reacted with HGM75 but did not react with HIK1083. The other fractions (Fr II, III) reacted with HIK1083 but weakly reacted with HGM75. After administration of plaunotol, a significant increase in Fr III (acidic mucin) was observed (p=0.02). CONCLUSIONS: Long-term administration of plaunotol changes the composition of gastric juice mucin, including a significant increase in the proportion of acidic mucin fraction.

Relationship between Helicobacter pylori tyrosine-phosphorylated CagA-related markers and the development of diffuse-type gastric cancers: a case-control study.

BACKGROUND/AIMS: Tyrosine phosphorylation of the EPIYA motif in Helicobacter pylori CagA (CagA-P) plays an important role in toxic reaction. Diffuse-type gastric cancer (DGC) has a poor prognosis. We tried to clarify the expression level of CagA-P in DGC patients. METHODS: We enrolled 42 early-stage DGC patients (DGC group; 20 males, 22 females, mean age 58.2 years) and 42 age- and gender-matched atrophic gastritis (AG) patients (AG group) as controls. We evaluated histological and serological gastritis and examined two markers; the serum titer of anti-CagA-P antibody and CagA-P expression in gastric mucosa. RESULTS: In the DGC group, we found significantly higher corpus histological gastritis scores for activity, atrophy, and intestinal metaplasia. The titer of anti-CagA-P antibody and CagA-P expression in the corpus were significantly higher in the DGC group, especially in females (p < 0.05). Sixteen patients (38.1%) in the DGC group showed both positive markers, and the odds ratio for DGC occurrence was 4.00 (95% CI = 1.07-14.91), while that for females was 9.00 (95% CI = 1.29-62.97). CONCLUSIONS: CagA-P plays a role in active corpus gastritis, which may link to DGC carcinogenesis. Clinical quantification of CagA-P-related markers may be useful for the evaluation of DGC risk, especially in females.

Little necessity of acid inhibition against proton pump inhibitor rebound effects and prior helicobacter pylori eradication therapy in gastric ulcer patients: a randomized prospective study.

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) eradication therapy increases acid secretion and promotes the development of gastroesophageal reflux disease (GERD) and reflux esophagitis (RE). Rebound acid hypersecretion develops after the use of proton pump inhibitors (PPI). We examined the clinical necessity of acid inhibitors to prevent GERD or RE caused by PPI rebound phenomenon and prior H. pylori eradication therapy. METHODOLOGY: We enrolled 39 patients who underwent successful H. pylori eradication therapy prior to endoscopic mucosal resection of gastric cancer. After 8-week rabeprazole treatment for iatrogenic ulcer, they were randomly divided into two groups (who took nizatidine (group N) and sofalcone (group S)), and took each for 16 weeks, we compared RE/GERD symptoms with the baseline by endoscopy and QUEST score. RESULTS: All patients had corpus atrophy in which there was no difference between the two groups. Only 1 patient in group S (5.9%) developed symptomatic GERD, and 1 patient in group N (4.5%) developed RE. CONCLUSIONS: In severe atrophic gastritis patients, there is little clinical necessity of acid inhibitors to prevent GERD/RE caused by PPI rebound and prior H. pylori eradication therapy.

Clinical prevention of gastric cancer by Helicobacter pylori eradication therapy: a systematic review.

Helicobacter pylori (H. pylori) infection plays an important role in gastric carcinogenesis. We conducted a systematic review concerning gastric cancer development after H. pylori eradication therapy. In total 15 papers matched our criteria, the results were reviewed. The H. pylori eradication therapy statistically diminished the prevalence of clinical gastric cancer by approximately one-third. The studies from Japan supported this conclusion; however, studies from overseas reported conflicting results. The differences in these conclusions lie in the diagnostic ability of endoscopic examination, since the clinical stage was quite different between these studies. Gastric cancer that developed after eradication revealed a mainly intestinal type histology and depressed-type appearance. The following are possible reasons for reduced gastric cancer: (1) eradication therapy inhibits the new occurrence of gastric cancer, (2) eradication regresses or inhibits the growth of gastric cancer, and (3) eradication interferes with the discovery of gastric cancer. Considering the biological nature of cancer cell proliferation, a sufficiently long-term follow-up may clarify the effect of eradication therapy on inhibition of the development (not discovery) of gastric cancer and reduction of gastric cancer-related mortality.

Pathogenetic role of the tyrosine-phosphorylated CagA EPIYA sequence of Helicobacter pylori in histological gastritis in Japanese patients.

BACKGROUND: Helicobacter pylori (H. pylori) CagA protein plays an important role in the clinical outcome of gastritis treatment. Tyrosine phosphorylated Glu-Pro-Ile-Tyr-Ala motif in CagA (CagA-P) plays a critical role in the morphological transformation of cells. AIM: We examine the relationship between serum titer of anti-CagA-P antibody and gastric inflammation as well as the status of the CagA-P expression in gastric mucosa. METHODS: Fasting sera from 127 dyspeptic patients were collected, and anti-CagA-P antibody was evaluated. Gastric biopsy specimens were collected and histological gastritis was evaluated. We investigate the expression of CagA-P in human gastric mucosa by Western blotting and immunohistochemistry. RESULTS: The titers of anti-CagA-P antibodies in the sera of H. pylori (+) patients were significantly higher than those of H. pylori (-) patients (P < 0.001). In 107 H. pylori (+) patients, anti-CagA-P titer was statistically higher in patients with high gastritis scores in the corpus than in those with low scores (P < 0.05). CagA-P expression was detected in the foveolar epithelium of the H. pylori infected gastric mucosa. CONCLUSION: CagA-P is an antigen-peptide against the host, and serum titer of anti-CagA-P antibody may be a new marker for gastritis in the corpus.

Role of Helicobacter pylori infection and chronic inflammation in gastric cancer in the cardia.

BACKGROUND: Helicobacter pylori-induced gastritis is an important factor for gastric carcinogenesis. However, it is still controversial whether it is also applicable for cardiac cancer development. Recently, we reported that H. pylori is an important factor for the induction of cardiac inflammation. We examined the status of H. pylori-induced gastritis in patients with cardiac cancer. METHODS: Seventy-five Japanese patients (58 men; mean age, 64.2 years) with cardiac cancer were studied. Cardiac cancer was defined as that mainly located within 2 cm from the squamo-columnar junction (SCJ). Histological gastritis including the cardiac region was evaluated using the biopsy or surgically resected sections. Cardiac inflammation was evaluated at 1 cm distal from SCJ in lesser curvature. Sera were collected and several markers were evaluated. The status of H. pylori infection was evaluated by histology and serum antibodies. Expressions of cytokeratins were examined by immunohistochemical analysis. RESULTS: Out of 75 patients with cardiac cancer, H. pylori was positive in 71 (95%) patients. The cardiac inflammation was examined in 30 patients (26 with H. pylori and four without H. pylori infection) and we found cardiac inflammation was present in all cases with H. pylori infection. Histologically, H. pylori-related gastritis was also found in the gastric corpus and antrum. Serological data were consistent with the presence of chronic atrophic gastritis. Intestinal metaplasia was found in 18 cases in the cardiac mucosa, and their cytokeratin 7/20 pattern was judged as a gastric pattern in all cases. CONCLUSION: H. pylori infection is closely associated with cardiac cancer.

Host factors contributing to the discovery of gastric cancer after successful eradication therapy of Helicobacter pylori: preliminary report.

BACKGROUND AND AIM: Clinical features of patients who develop gastric cancer after successful eradication of Helicobacter pylori are still unclear. We attempted to identify host factors associated with the discovery of gastric cancer, including changes in the background gastric mucosa in patients with atrophic gastritis. METHODS: We enrolled 101 patients (59 men, 42 women; mean age 56.0 years) who underwent successful eradication therapy. All patients had no neoplastic lesion in the stomach and were diagnosed with corpus atrophic gastritis histologically before the eradication therapy. After successful eradication, these patients were followed up by an annual endoscopic examination (mean follow-up time 63.2 months; range 12-157 months). Fasting sera were obtained before and after eradication therapy and the serum levels of gastrin/pepsinogens were evaluated. RESULTS: Gastric cancer occurred during follow-up in eight of the 101 patients (7.9%). We compared the host features between the cancer-discovered group (n = 8) and the non-discovered group (n = 93). We found no difference in gender, history of previous treatment of gastric cancer, and serum pepsinogen/gastrin levels at entry between them. The trends in alterations of serum markers did not differ between the two groups. However, gastric cancer was more frequently found in older patients (>54 years at eradication) than in others (P < 0.05). CONCLUSION: Improvement of gastric inflammation did not correlate with the discovery of gastric cancer after eradication; however, age at the time of eradication seemed to be important. Strict follow-up after eradication is needed in older patients with atrophic gastritis.

The effect of Helicobacter pylori eradication therapy on gastric ulcer healing after endoscopic mucosal resection.

BACKGROUND AND AIM: It remains unclear whether Helicobacter pylori eradication therapy accelerates the healing of acute gastric ulcer after endoscopic mucosal resection (EMR) of gastric tumor. We examined the effect of H. pylori eradication therapy on ulcer healing after EMR. METHODS: Twenty-six patients who underwent successful H. pylori eradication therapy before EMR were followed prospectively. Patients underwent endoscopic examination 1 or 2 months after EMR, during which the ulcer status and reduction rate were assessed. The effect of H. pylori eradication on the quality of ulcer healing was also evaluated. Six patients in whom eradication therapy failed and 26 patients who underwent EMR without eradication therapy served as control subjects. RESULTS: Endoscopically, 18 (75%) of 24 ulcers in the eradication group were at the healing stage 1 month after EMR. The ulcer reduction rates were 85.0 +/- 2.6% and 96. 9 +/- 1.1% at 1 and 2 months after EMR, respectively. Ulcer stage and reduction rate did not differ significantly between the eradication group and control group. However, we frequently observed a better quality of ulcer healing in the eradication group than in the control groups (P < 0.01). CONCLUSION: H. pylori eradication therapy does not accelerate ulcer healing after EMR but may improve the quality of ulcer healing of gastric ulcer after EMR.

A combination of the Helicobacter pylori stool antigen test and urea breath test is useful for clinical evaluation of eradication therapy: a multicenter study.

BACKGROUND: Helicobacter pylori stool antigen (HpSA) test is a new tool for evaluating the H. pylori infection. The present study was carried out to investigate the clinical usefulness of the HpSA test in the evaluation of eradication therapy by comparing it with the (13)C-urea breath test (UBT). METHODS: One hundred and five patients received eradication therapy for H. pylori. After more than 8 weeks, the success of the therapy was evaluated by the HpSA test and the UBT. Concordant results were regarded as a final diagnosis, but when the results were discordant, histological examination was carried out. RESULTS: Of the 105 patients receiving eradication therapy for H. pylori, 25 patients were regarded as H. pylori positive by the UBT and and 20 patients were regarded as H. pylori positive by the the HpSA test. Nine patients (8.6%) showed discordant results (seven cases with UBT(+) and HpSA(-), and two with UBT(-) and HpSA(+)). Five cases out of nine were ultimately judged as having a false-positive result of the UBT, and in these cases the UBT values were relatively low (below 10 per thousand). The final diagnostic accuracies of the UBT and the HpSA test were 94.3% (88.0-97.9%; 95% CI) and 97.1% (91.9-99.4%), respectively. When we used the HpSA test in cases with weakly positive UBT values, we were able to diagnose the correct status of H. pylori infection after eradication in 99% of all patients (94.8-100.0%). CONCLUSION: The HpSA test is a useful tool for the evaluation of eradication therapy and a combination of the HpSA test and UBT is clinically recommended.