Seroprevalence of Helicobacter pylori infection in patients with lymphoma

J Cuttner1, J L Werther, P McGlynn

  • 1Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.

Leukemia & Lymphoma
|June 28, 2001
PubMed

To determine the Helicobacter pylori (HP) seroprevalence in patients with non-Hodgkin's lymphoma (NHL) and other hematological conditions. Sera were collected from 444 patients with NHL, Hodgkin's disease (HD), lymphoproliferative disorders (LPD), myeloproliferative disorders (MPD), and other hematological conditions. HP seropositivity was determined by ELISA and the results were compared among diagnostic groups HP seropositivity was observed in 168/444 (38%) of the total population. Higher seropositivity rates were associated with increasing age (p=0.001), and country of birth outside the USA and Canada (p=0.0001). Among the diagnostic groups, patients with NHL demonstrated the highest frequency (43%) and those with HD, the lowest frequency (20%; p=.026) of HP seropositivity. The differences among diagnostic groups remained statistically significant after controlling for country of birth (p<0.05), but not after controlling for patient age at diagnosis. The HP seroprevalence of G1 NHL was 55% compared to 40% for non-G1 NHL (p=NS). The highest rate of HP seropositivity (67%) occurred in gastric MALT lymphoma patients, although this did not reach statistical significance compared to the non MALT group (50%) due to small sample size. In conclusion, the rate of HP seropositivity in patients with MALT lymphoma in the USA appears to be lower than in Europe. Helicobacter pylori does not appear to be an important factor in other types of NHL of the G1 tract or elsewhere. Studies of HP prevalence should be controlled for country of birth as well as for age.

Related Concept Videos

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies01:28

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies

Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...