Gastric and duodenal ulcers were long thought to be the cause of stress and spicy foods until Helicobacter pylori was discovered.
Before 1983, the major causes of peptic ulcer disease (PUD) were considered to be excess acid, diet, smoking, and stress, and most patients with recurrent peptic ulcer disease were treated with maintenance doses of acid-reducing medications.
In 1984, Marshall and Warren discovered a tiny curved or spiral-shaped gram-negative rod (bacilli) in the stomachs of persons with symptoms of peptic ulcers. The organism was named Campylobacter pylori but was later renamed Helicobacter pylori.
H. pylori is one of the most common, if not the most common chronic human infection. Approximately 10% of the population of the U.S. suffer from peptic ulcer disease (500,000-850,000 cases occur each year). Higher rates are seen in developing countries and lower socioeconomic groups. Up to 90% of some populations may be infected. In Columbia and China, H. pylori infects over half the population in early childhood.
Without treatment, H. pylori can colonize the stomach for many years with only low-grade inflammation of stomach mucosa; in most cases remaining asymptomatic. In others, symptoms of peptic ulcers (gastric and duodenal) are present. Long-term infection with H. pylori is associated with the development of stomach cancer, the second most common cancer worldwide.
H. pylori is not the only cause of peptic ulcers; another major cause is non-steroidal anti-inflammatory drugs (NSAIDS) such as aspirin, ibuprofen and naproxen. Another far less common cause is Zollinger-Ellison syndrome. Zollinger-Ellison involves overproduction of the hormone gastrin, which results production of large amounts of excess acid. The hyper-gastrin production is caused by tumors (usually malignant) on the pancreas or duodenum. The tumors must be removed to reduce acid production and relieve ulcer recurrence.
Peptic ulcers include both gastric (stomach) and duodenal (first part of the small intestine) ulcers. Therefore, stomach symptoms are often present.
H. pylori may also have associations with other diseases or conditions. H. pylori has recently (Felkner, 2007) been implicated in the cause of neural tube defects. Previous findings of the Texas Neural Tube Defects Projects suggested that bioavailability of nutrients is compromised during pregnancy for mothers of children affected with neural tube defects. Building on the Project findings, Felkner and his group hypothesized that H. pylori could be responsible for nutrient loss to the fetus. Although their study was somewhat inconclusive, data did suggest increased prevalence in certain populations. The study recommended further studies of populations with higher prevalence of H. pylori and low nutrient intake.
Read more about ulcers and H. pylori:
Helicobacter pylori: Its Role in Peptic Ulcer Disease
H. pylori: What Is It and How Do You Get It?
Sources:
Helicobacter pylori and Peptic Ulcer Disease: The Key to Cure (CDC)
Marshall, BJ and JR Warren. 1984. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet i:1311-1315.
Felkner M., L. Suarez, B. Liska, J.D. Brender, M. Canfield. Neural tube defects, micronutrient deficiencies, and Helicobacter pylori: A new hypothesis. Birth Defects Res A Clin Mol Teratol. 2007; July 11.
Jerris, R.C. Helicobacter in Manual of Clinical Microbiology, Sixth Edition. ASM Press. Washington. 1995. pp. 492-8.
