H. pylori Does Not Cause Uterine Fibroids
There is no established causal relationship between Helicobacter pylori infection and uterine fibroids. H. pylori is a gastric pathogen with well-defined clinical manifestations limited to the gastrointestinal system and specific extragastric conditions, none of which include gynecologic disorders.
Established Clinical Manifestations of H. pylori
H. pylori infection causes a specific spectrum of diseases that are well-characterized in major international guidelines:
Primary gastrointestinal manifestations include:
- Chronic gastritis, peptic ulcer disease, gastric MALT lymphoma, and gastric adenocarcinoma 1, 2, 3
- H. pylori is responsible for 71-95% of all gastric cancers 1, 2
Recognized extragastric manifestations with evidence-based support:
- Iron-deficiency anemia (Evidence level 1a, Grade A recommendation) 3
- Idiopathic thrombocytopenic purpura (Evidence level 1b, Grade A recommendation) 3
- Vitamin B12 deficiency (Evidence level 3b, Grade B recommendation) 3
- Impaired bioavailability of thyroxine and L-dopa 3
Why Uterine Fibroids Are Not Related to H. pylori
The Maastricht IV/Florence Consensus Report explicitly states that there is no unequivocal causative association between H. pylori and extragastric disorders beyond those specifically mentioned (iron-deficiency anemia, idiopathic thrombocytopenic purpura, vitamin B12 deficiency) 3.
Uterine fibroids have distinct pathogenesis:
- Fibroids are benign uterine tumors characterized by proliferation of uterine smooth muscle cells embedded in abundant extracellular matrix 4
- Their prevalence exceeds 50% in women aged >45 years 4
- The pathogenesis involves hormonal factors, genetic mutations, and growth factors specific to uterine tissue 4
Common Pitfall to Avoid
Do not attribute unrelated conditions to H. pylori infection simply because the bacterium is highly prevalent. H. pylori infects more than half of the world's population 5, making it statistically likely that many patients with various unrelated conditions will coincidentally have H. pylori infection. The high seroprevalence in the general population and prevalent asymptomatic infection make it difficult to establish causality for conditions outside the established disease spectrum 6.
The evidence is clear that H. pylori's pathogenic mechanisms—including chronic inflammation, oxidative damage, and bacterial virulence factors (CagA, VacA)—operate specifically within the gastric mucosa and have defined systemic effects limited to hematologic and metabolic disorders 1, 5. There is no biological plausibility or clinical evidence linking these mechanisms to uterine fibroid development.