An Investigation of the Association Between Helicobacter Pylori Infection and Abdominal Pain in Cystic Fibrosis Patients

Abdominal pain and Cystic Fibrosis Cystic fibrosis is the most common lethal autosomal recessive disease among Caucasians. CF is caused by a single gene mutation on chromosome 7, which encodes for a membrane protein, the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR channel dysfunction results in progressive pulmonary disease, which is the primary cause of the morbidity and mortality associated with the disease. Therapies directed to slow the progression of the lung disease have increased the USA median survival to 32.2 years.2 Abdominal complaints are very common among CF patients. Littlewood et al. reported that 31% of children had regular complaints of abdominal pain.3 Ravilly et al. performed a retrospective chart review on CF patients referred for treatment to the pain service and those that expired.4 They determined that pain was very common in CF and that 19% of the population had chronic complaints of abdominal pain, which was third behind chest pain and headaches.4 This study likely underestimated the prevalence of abdominal pain in CF, as it was evaluating an end stage lung disease group of patients that were frequently not eating and had severe pain from other disease processes (i.e. headaches from hypercarbia and/or hypoxia, and chest pain from rib fractures).

Known causes of CF related abdominal pain are: 1) malabsorption due to pancreatic steatorrhea, 2) gastroesophageal reflux, 3) esophagitis, 4) gastritis, 5) peptic ulcer disease, 6) pancreatitis, 7) Crohn's disease, 8) distal intestinal obstructive syndrome (DIOS), 9) biliary duct disease including cholocystitis and cholangitis, 10) intussception, 11) acute or chronic gastrointestinal infection, 12) acute appendicitis, and 13) constipation. Given this long list of potential causes, CF patients frequently undergo intensive examinations to determine the etiology of the abdominal pain.4 The testing unfortunately does not always reveal the etiology.

Helicobacter pylori World-wide, Helicobacter pylori (Hp) is increasingly being recognized as the etiology of peptic ulcer disease and other upper and lower gastrointestinal tract diseases.1 With the CF population, The role that Hp plays in abdominal pain has not been elucidated. Two studies have attempted to look at the epidemiology of Hp in CF; however, the approach utilized in those studies was determined to be inadequate. Johansen et al. and Israel et al. both attempted to utilize Hp serology to determine the prevalence in a CF population and determined that there was significant cross-reactivity between Hp and Pseudomonas aeruginosa antigens.10, 11. They concluded that different modes of testing are required if Hp is being evaluated in the CF population. To our knowledge, there have been no further evaluations of Hp in CF using the newer diagnostic tests available.

Testing for Helicobacter pylori Since the isolation of spiral urease-producing Helicobacter pylori bacteria (H. pylori) in 1983 by Drs. Marshall and Warren5, a significant body of evidence has accumulated indicating that the bacteria is an important pathogen in upper GI tract of humans 6,7. The causal relation ship between H.pylori and chronic active gastritis, duodenal ulcer, and gastric ulcer is well documented 8, 9. Methods available for detecting current infection of human stomach by Hp are generally divided into two general types: Invasive and Non-invasive.

Invasive methods include esophageogastroduodenoscopy (EGD) with collection of gastric biopsies. These biopsies are then examined by one or more detection methods: histological examination of stained tissue, microbiological culture of the organism, or direct detection of urease activity in the tissue (for example, the CLO test). Biopsy based methods are expensive, entail greater patient risk and discomfort than non-invasive tests, and may give false negative results due to sampling errors when colonization of the gastric mucosa is patchy 6.