Changes in Antibiotic Susceptibility of Helicobacter pylori in the Course of Eight Years in the Zaanstreek Region in The Netherlands.

Background. Failure of anti-Helicobacter therapy is the result noncompliance and resistance to the prescribed antibiotics. Aim. Antibiotic susceptibility of H. pylori was determined in native Dutch patients and patients of Turkish descent. Methods. In a period of eight years a total of 925 strains of H. pylori were cultured. Bacterial susceptibility was successfully determined in 746 (80.6%) of these isolates. Three hundred and nine strains (33%) originated from patients of Turkish descent. Results. In total clarithromycin resistance was found in 146 (20.5%) strains, metronidazole resistance in 147 (19.9%) strains. Amoxicillin resistance was found to be present in five strains. There is a slight but nonsignificant decrease in the percentage of clarithromycin-resistant strains in the consecutive period of eight years from 20% to 18%. No changes were seen in the consecutive years in metronidazole resistance. The number of clarithromycin-resistant strains decreased in Turkish patients, not in native Dutch patients. Conclusion. Resistance did not change significantly in consecutive years. But clinicians should take not only the antibiotic history into account but also ethnicity before prescribing metronidazole or clarithromycin.

Functional dyspepsia is associated with cagA-positive Helicobacter pylori strains.

BACKGROUND: The antigen CagA can be used as a marker for virulence of Helicobacter pylori. It is tempting to assume that H. pylori strains positive for cytotoxin-associated gene A (cagA) could be responsible for functional dyspepsia. A cross-sectional study was performed in patients presenting with functional dyspepsia to correlate the clinical presentation with the presence of cagA-positive and -negative H. pylori strains. METHODS: Consecutive patients referred for endoscopy were studied. An inclusion criterion was the absence of any endoscopic abnormality. Biopsy specimens were obtained from the gastric antrum for HE and immunoperoxidase stain, rapid urease test, and culture. A serum sample was taken for detection of IgG antibodies against H. pylori as well as CagA. A validated questionnaire of 14 questions regarding the upper gastrointestinal tract was used for assessment of the clinical presentation. Nine questions were scored on a 5-point Likert scale. RESULTS: 422 patients were included, 222 were H. pylori-positive, the remaining 200 were H. pylori-negative. Mean symptom score in patients with cagA-positive strains was significantly higher than in patients with cagA-negative strains. No difference was present if cagA-negative patients were compared with H. pylori-negative dyspeptics. Four different complaints were more prevalent in the cagA-positive patients compared with cagA-negatives. When cagA-positive patients were compared with H. pylori-negative dyspeptics, seven complaints were significantly more prevalent in cagA-positives; when cagA-negatives were compared this number was only two. CONCLUSIONS: Functional dyspeptics with cagA-positive H. pylori strains have more dyspeptic symptoms and higher symptom scores than patients with cagA-negative H. pylori strains as well as H. pylori-negative functional dyspeptics.

Colonization with cagA-positive Helicobacter pylori strains inversely associated with reflux esophagitis and Barrett's esophagus.

AIM: The hypothesis that colonization with cagA(+) Helicobacter pylori strains protects against the development of gastroesophageal reflux disease (GERD) and its complications is tested. METHODS: Patients with reflux esophagitis and Barrett's esophagus were studied. Antral biopsy specimens were obtained for detection of H. pylori. A serum sample was obtained for determination of IgG antibodies to H. pylori and to the CagA protein. RESULTS: 736 patients were studied. 118 patients had reflux esophagitis, 36 had Barrett's esophagus, 108 had hiatal hernia without signs of inflammation (the reflux group), and 20 patients had esophageal or stomach cancer. The remaining 454 patients had no signs of GERD. The 262 patients with reflux disease had a significantly lower prevalence of H. pylori (34.9%) than the 454 controls (54.6%; p<0. 001). Among 310 H. pylori-positive patients from whom serum was available, colonization with cagA(+) strains was detected in 59% in the control group versus 35% in the reflux group (p<0.001). CONCLUSION: Patients with reflux esophagitis and Barrett's esophagus have a significantly lower prevalence of H. pylori colonization than controls, in particular of the cagA(+) type. These data suggest that colonization with cagA(+) H. pylori strains may be protective against the development of GERD

Clinical presentation of Helicobacter pylori-positive and -negative functional dyspepsia.

BACKGROUND: A questionnaire was used to record the clinical presentation of functional dyspepsia in relation to Helicobacter pylori infection in a consecutive series of patients sent for upper gastrointestinal endoscopy. Only patients without macroscopic abnormalities in their oesophagus, stomach and duodenum were included. METHODS: The study questionnaire included two questions related to daily life, and the calculation of a symptom score. Biopsy specimens were taken from all patients for histological and microbiological examination, and immunoglobulin G antibodies were also determined. RESULTS: Two hundred and twenty-two patients were H. pylori positive and 182 patients were H. pylori negative. Loss of weight was significantly more common in the H. pylori positive group (P<0.001). Patients with H. pylori infection had a significantly higher overall symptom score compared with H. pylori-negative subjects (P<0.05). In addition, the severity of epigastric and nocturnal pain, heartburn, retrosternal heartburn, and vomiting was significantly higher in H. pylori-positive functional dyspeptic patients, and the influence on daily life and activities was significantly worse. CONCLUSIONS: The combination of retrosternal pain, weight loss, food intolerance and the absence of halitosis signified a 64% accuracy in predicting H. pylori infection. It is not possible to differentiate between H. pylori-positive and H. pylori-negative functional dyspeptics on the basis of clinical presentation and the number of complaints. However, overall symptom score and severity of several symptoms was significantly higher in the H. pylori-positive group.

IgG antibody titer against Helicobacter pylori correlates with presence of cytotoxin associated gene A-positive H. pylori strains.

The level of the IgG antibody titer against Helicobacter pylori correlates with the severity of gastritis. H. pylori strains can harbor the so-called pathogenicity island, containing the cytotoxin associated gene (cagA). Since cagA-positive strains are more virulent it can be postulated that the gastritis will be more severe and hence the IgG antibody titer higher. In a cross-sectional study the correlation of IgG antibody titer and cagA status was studied from patients undergoing upper gastrointestinal endoscopy. Biopsy specimens were obtained to determine the H. pylori status. In addition a serum sample was taken for detection of IgG antibodies against H. pylori as well as CagA. A total of 290 patients positive for IgG antibodies against H. pylori were included. Of these 153 were cagA-positive and 137 were cagA-negative. The mean IgG antibody titer was significantly higher in cagA-positive patients compared to cagA-negatives, 0.75 (S.D. 0.22) versus 0.69 (S.D. 0.24) (P=0.033). It is concluded that the IgG antibody titer is significantly higher in patients harboring cagA-positive H. pylori strains. However, in daily practice the level in IgG antibody titer cannot predict whether or not an individual carries a cagA-positive H. pylori strain since major overlap in IgG antibody titer between cagA-positive and cagA-negative patients is present.

Functional dyspepsia has a good prognosis irrespective of H. pylori status. Long-term follow-up of symptoms after anti H. pylori treatment.

AIM: A prospective study with anti H. pylori therapy was done in patients with functional dyspepsia. METHODS: Inclusion criterion was the absence of any macroscopic abnormality in oesophagus, stomach, and duodenum, irrespective whether H. pylori was present or not. A questionnaire and a symptom score on a five-point Likert scale were used. Antral biopsy specimens were taken for detection of H. pylori. Treatment consisted of omeprazole 20 mg bid and amoxicilline 500 mg tid during 14 days. Patients were followed during 12 months. At follow-up the questionnaire and the symptom score were used. The main endpoint of the study was clinical remission after 1 year of follow-up. RESULTS: In 1 year 163 patients were included (85 men, 78 women, mean age 47 years, range 21-83 years). H. pylori was present in 91 patients. In the H. pylori positive group 38 patients showed a decrease in IgG antibody titre of more than 50% during follow-up of 3-12 months, 26 showed no change or increase following initial decrease. Overall there was no difference in presence or absence of specific complaints at inclusion and final follow-up. The symptom score decreased significantly in all groups (P < 0.001). CONCLUSION: The symptoms of functional dyspepsia improved to a similar extent in both H. pylori positive dyspeptics and the control group. This symptom improvement was irrespective of the change of IgG H. pylori antibodies after therapy.

Can screening for IgG antibodies against Helicobacter pylori be used in clinical practice? Omit endoscopy in seropositive or seronegative patients?

The objective of this study was to test the feasibility of a screening strategy for IgG antibodies against Helicobacter pylori in patients presenting with upper abdominal complaints. Biopsy specimens were taken for histological and microbiological investigations from consecutive patients undergoing upper gastrointestinal endoscopy. In addition, a serum sample was taken for detection of IgG antibodies against Helicobacter pylori, using an ELISA technique. Serum samples from 1294 consecutive patients were available. IgG antibodies against Helicobacter pylori were present in 622 patients (48%), the remaining 671 (52%) were negative. If endoscopy had been omitted in seronegative patients below the age of 45 years, this would have resulted in 234 patients not endoscoped. However, it can be assumed that 62 of these patients would undergo endoscopy because of recurrent complaints due to underlying disease or abnormality. Therefore 182 of 1294 (14%) of endoscopies would have been avoided. Application of this strategy on the total group of seronegatives would save 353 of 1294 (27.3%) endoscopies. If endoscopy had been omitted in seropositive cases below the age of 45 years, and these patients were treated with anti-Helicobacter therapy, an initial 145 endoscopies would have been avoided. However, 26 of these patients would undergo endoscopy because of persistent complaints due to underlying disease. Therefore 119 (9%) endoscopies would have been avoided. Applying this strategy in the total group of seropositives would have saved 434 of 1294 endoscopies (34%). Applying the IgG screening strategy in all patients would result in a significant number of endoscopies being avoided in the seropositive group, 434 versus 353 (P < 0.001). In conclusion, omitting endoscopy in seropositive cases, regardless of age, can reduce the workload more than omitting endoscopy in seronegative cases: 34% fewer endoscopies versus 27%.

Symptom clusters cannot be used in distinguishing Helicobacter pylori positive or negative patients with functional dyspepsia.

BACKGROUND: A retrospective study was done in consecutive patients in order to seek out whether dyspepsia subgroups (reflux-like, ulcer-like, and, dysmotility-like dyspepsia) can be useful in describing Helicobacter pylori positive and negative functional dyspepsia. METHODS: Consecutive patients who underwent upper gastrointestinal endoscopy were included if no macroscopic lesions in oesophagus, stomach or duodenum were seen. Antral biopsy specimens were taken for detection of H. pylori. A validated questionnaire was used. RESULTS: Six hundred patients fulfilled the inclusion criteria. Three hundred were positive for H. pylori. In the H. pylori positive (HP+) patients only 3 (1.2%) had 'pure' reflux-like dyspepsia, 17 (6.9%) had ulcer-like dyspepsia and 10 (4%) suffered from dysmotility-like dyspepsia. In the H. pylori negative (HP-) patients these figures were 6 (2.3%), 17 (6.6%) and 7 (2.7%), respectively (ns). The majority of patients had a combination of complaints belonging to the three subgroups. Reflux-like dyspepsia was present in 179 (73%) HP+ dyspeptics and 195 (76%) HP-'s (ns). Ulcer-like dyspepsia was present in 213 (88%) HP+ cases and 233 (92%) HP-'s (ns). Dysmotility-like dyspepsia was present in 197 (81%) HP+'s and 212 (82%) HP-'s (ns). CONCLUSIONS: It is concluded that it is not possible to identify patients suffering from H. pylori infection on basis of symptom clusters.

The clinical presentation of peptic ulcer disease.

BACKGROUND: A prospective study was performed in order to assess the clinical presentation of peptic ulcer. METHODS: Consecutive patients undergoing upper GI endoscopy (n = 1527) received a questionnaire consisting 23 questions related to the upper abdomen. Eleven questions were scored on a linear scale and a symptom score was calculated. Patients with a gastric (GU) or duodenal (DU) ulcer were included. As a reference group, patients in whom endoscopy did not reveal abnormalities were included. This group was subdivided depending on whether their history was positive (PPU+) or negative (PPU- ) for previous peptic ulcer. RESULTS: GU was diagnosed in 43 patients, DU in 60; PPU+ consisted of 94 patients and PPU- of 382 patients. Patients with GU were significantly older (P < 0.0001). The symptom score was 14 (SD 8.6) in GU, 16.6 (SD 8.5) in DU, 19.5 (SD 9.8) in PPU+, and 16.7 (SD 9.6) in PPU-. PPU+ had significantly higher symptom score than the other groups. If all ulcer patients (amalgamation of DU, GU and PPU+) were compared with PPU-, a prior history of peptic ulcer, pain waning after a meal, and smoking were the only features linked to peptic ulcer. On the other hand, postprandial pain, food intolerance, nausea, and alcohol use have a negative prediction. CONCLUSIONS: It can be concluded that the symptom score in peptic ulcer disease is low (the maximum possible score was 55). It is not possible to distinguish peptic ulcer patients from other dyspeptics on basis of the clinical presentation.

Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis.

In a prospective study of consecutive patients with reflux esophagitis and/or hiatal hernia and Barrett's esophagus, the prevalence of Helicobacter pylori was assessed. Antral biopsy specimens were studied and a serum sample for detection of IgG antibodies against Helicobacter pylori was taken. As a reference group patients presenting with a normal esophagus, stomach, and duodenum were taken. Reflux esophagitis was diagnosed in 118 patients, hiatal hernia without esophageal inflammation in 109, and Barrett's esophagus in 13. Helicobacter pylori was present in 74 (30%) of these patients and in 204 (51%) of the reference group. Prevalence of Helicobacter pylori was significantly lower in all groups compared with the reference group (P < 0.001). There was no difference when patients with esophagitis, Barrett's esophagus, or hiatal hernia were compared. Patients with esophagitis and Helicobacter pylori in their antrum are significantly older than esophagitis patients without concomitant Helicobacter infection, 61.5 (SD, 17) versus 53 (SD, 17) years (P < 0.001). It is concluded that the prevalence of Helicobacter pylori infection in patients with gastroesophageal reflux disease is significantly lower than in the reference group, irrespective of the severity of esophagitis. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis.

[A tropical ulcer; cutaneous diphtheria]. / Een ulcus uit de tropen; cutane difterie.

A 43-year-old woman, born in the Netherlands, developed ulcers on her left foot during a holiday in Gambia and Senegal. She had been bitten bij insects. The ulcers were caused by Corynebacterium diphtheriae. The patient was treated with antibiotics and recovered fully. A grey pseudomembrane covering the ulcer is a characteristic feature of cutaneous diphtheria. The treatment is with antibiotics and, after toxin tests have indicated that the bacterium is toxigenic, with antitoxin. In some cases screening of social contacts is advised.