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1.
Am J Gastroenterol ; 94(10): 2885-9, 1999 Oct.
Article in English | MEDLINE | ID: mdl-10520838

ABSTRACT

OBJECTIVE: Helicobacter pylori (H. pylori) infection has been linked to gastric cancer. The factors that promote carcinogenesis remain unknown. Epidermal growth factor (EGF) has been shown to be a potent epithelial mitogen and oncoprotein when sustained over expression occurs. Our aim was to compare gastric mucosal levels of EGF and its receptor (EGFR) among controls, H. pylori infected subjects, and subjects following H. pylori eradication using quantitative flow cytometric analysis. METHODS: Patients referred for evaluation of dyspepsia underwent EGD and six antral biopsies were performed (two each for rapid urease testing (RUT), histopathology, and flow cytometry). Controls were those found to be H. pylori negative while subjects had confirmed infection. The study patients were treated, then had repeat EGD with biopsies. RESULTS: There were 17 controls and 28 cases. Mean EGF and EGFR values were 2.69 and 2.46 for controls and 4.67 and 4.64 for subjects. Subjects' mean EGF was 73% higher (p = .035) and EGFR was 88% higher (p = 0.029) than controls. After treatment, the subjects' mean values declined 55% (p = 0.0001) for EGF and 40% (p = 0.002) for EGFR. Three subjects had persistent infection and showed no change in their EGF/EGFR levels. No difference was found among factor levels with respect to endoscopic findings. CONCLUSIONS: Both EGF and EGFR from gastric antral biopsies are increased nearly 2-fold in infection with H. pylori. Infection eradication reduces levels of both factors to those of controls. One major pathogenic mechanism for gastric mucosal hyperproliferation and possibly carcinogenesis related to H. pylori may be the over expression of EGF and increased receptor density of EGFR on gastric mucosal cells.


Subject(s)
Epidermal Growth Factor/metabolism , ErbB Receptors/metabolism , Gastric Mucosa/metabolism , Helicobacter Infections/drug therapy , Helicobacter pylori , Adult , Antacids/therapeutic use , Anti-Bacterial Agents , Anti-Ulcer Agents/therapeutic use , Biopsy , Bismuth/therapeutic use , Chronic Disease , Drug Therapy, Combination/therapeutic use , Female , Flow Cytometry , Gastric Mucosa/pathology , Gastritis/microbiology , Gastritis/pathology , Helicobacter Infections/metabolism , Helicobacter Infections/microbiology , Helicobacter pylori/isolation & purification , Humans , Male , Middle Aged , Omeprazole/therapeutic use , Organometallic Compounds/therapeutic use , Prospective Studies , Salicylates/therapeutic use
3.
South Med J ; 89(8): 775-8, 1996 Aug.
Article in English | MEDLINE | ID: mdl-8701375

ABSTRACT

In small preliminary trials, ciprofloxacin has failed to eradicate Helicobacter pylori. Since fluoroquinolones have a marked reduction in bactericidal activity at acidic pH, we altered the gastric pH using omeprazole and investigated the efficacy of ciprofloxacin in eradicating H pylori. Forty-four consecutive patients infected with H pylori were prospectively studied in a randomized, double-blind, controlled trial comparing ciprofloxacin with a placebo for 2 weeks. Both treatment groups received bismuth and omeprazole. In 36 patients, follow-up endoscopy was done 4 weeks after the cessation of all study drugs. The H pylori infection cleared in 13 of 17 patients (76%) in the ciprofloxacin group versus 5 of 19 (26%) in the placebo group. Concurrent administration of omeprazole with ciprofloxacin resulted in increased bactericidal activity against H pylori. Ciprofloxacin when combined with omeprazole and bismuth is efficacious for eradication of H pylori.


Subject(s)
Anti-Infective Agents/therapeutic use , Anti-Ulcer Agents/therapeutic use , Ciprofloxacin/therapeutic use , Duodenal Ulcer/drug therapy , Helicobacter Infections/drug therapy , Helicobacter pylori , Omeprazole/therapeutic use , Adult , Aged , Antacids/therapeutic use , Bismuth/therapeutic use , Double-Blind Method , Drug Therapy, Combination , Female , Gastroscopy , Humans , Male , Middle Aged , Prospective Studies
4.
Dig Dis Sci ; 40(9): 2081-3, 1995 Sep.
Article in English | MEDLINE | ID: mdl-7555468

ABSTRACT

Vagotomy is reported as a secondary cause of achalasia. Highly selective vagotomy, however, has rarely been reported to cause an achalasia-like syndrome. We suspect that periesophageal trauma accounted for the LES abnormalities seen at manometry in our patient but cannot explain the aperistalsis of the body of the esophagus. Pneumatic dilation improved his dysphagia only slightly but allowed him to maintain his nutrition with oral liquid enteral supplements. We recommend barium swallow, endoscopy, sounding the esophagus with a 50- to 60-French dilator, and manometry in evaluating patients with dysphagia after highly selective vagotomy. If an achalasia-like syndrome is demonstrated, then conservative management with observation and liquid nutritional supplements for four to eight weeks is appropriate. If this fails, pneumatic balloon dilation may be considered. Clearly, a preoperative history of dysphagia should prompt evaluation before highly selective vagotomy. This case represents a transient achalasia-like syndrome after highly selective vagotomy and signifies the importance of conservative management.


Subject(s)
Esophageal Achalasia/etiology , Vagotomy/adverse effects , Adult , Catheterization , Duodenal Ulcer/complications , Enteral Nutrition , Esophageal Achalasia/therapy , Humans , Male , Peptic Ulcer Hemorrhage/surgery
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