Upper GI mucosal damage, H. pylori infection may increase risk for Parkinson’s disease
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Key takeaways:
- In a cohort of 9,350 patients, 2.2% with mucosal damage and 0.5% without developed Parkinson’s disease.
- Among those with mucosal damage, presence of H. pylori was linked to a higher probability of developing PD.
The presence of mucosal damage on upper gastrointestinal endoscopy was associated with a 76% greater risk for developing Parkinson’s disease, underscoring the need for “increased vigilance” among these patients, according to a cohort study.
“A recent nationwide study found no association between a history of inflammatory bowel disease and subsequent risk of [Parkinson’s disease (PD)], suggesting that mucosal damage (MD) in the distal GI tract where pelvic rather than vagal innervation is the hallmark may play a less important role in pathogenesis,” Jocelyn J. Chang, BS, of Tufts University School of Medicine, and colleagues wrote in JAMA Network Open. “Indeed, a significant gap remains in understanding the relationship between broader upper GI MD, such as peptic ulcer disease (PUD) and erosions, and the development of PD, as most studies to date have focused on correlational links to a history of H. pylori infection.”
To explore this gap, Chang and colleagues conducted a retrospective study of 9,350 patients (mean age, 52.3 years; 55.4% men; 73.7% white, 7.9% Black, 7.1% other and 2.9% Asian) who underwent upper endoscopy between January 2000 and December 2005. They matched patients with MD (n = 2,337) to those without (n = 7,013) in a 3:1 ratio based on age, sex and date of initial endoscopy and performed two nested case-control analyses to assess specific MD-related factors that may be associated with development of PD.
Covariates more common among patients with MD at baseline included a history of H. pylori infection, NSAID and proton-pump inhibitor use, GERD, smoking, constipation and dysphagia.
After a mean follow-up of 14.9 years, 2.2% of patients with MD and 0.5% without were diagnosed with PD, which corresponded with an incidence rate ratio of 4.15 (95% CI, 2.89-5.97) and overall incidence of 16 per 100,000 person-years. The risk associated with MD “remained pronounced” following covariate adjustment (HR = 1.76; 95% CI, 1.11-2.51), the researchers reported.
Results also showed that age (HR = 1.04; 95% CI, 1.02-1.05), a higher Charlson-Deyo Comorbidity Index (HR = 1.21; 95% CI, 1.09-1.35), constipation (HR = 2.65; 95% CI, 1.72-4.08) and dysphasia (HR = 2.33; 95% CI, 1.52-3.56) were associated with an increased risk for developing PD, while Asian, Black and other race were linked with a decreased risk (HR = 0.7; 95% CI, 0.54-0.89).
Further, results from the nested case-control analysis of patients with MD showed the presence of H. pylori on initial biopsy correlated with a “markedly higher probability” for PD (adjusted OR = 3.84; 95% CI, 1.22-12.13), with an increased risk also associated with GERD (aOR = 3.92; 95% CI, 1.04-14.76).
“A history of upper GI MD was associated with an increased risk of subsequently developing PD,” Chang and colleagues wrote. “These findings highlight the necessity for heightened monitoring of patients with MD given their increased clinical PD susceptibility and the importance of establishing gut biomarkers.”
They continued: “With PUD globally affecting upwards of 8.09 million people and H. pylori infection even more widespread, timely detection and treatment of H. pylori infection, along with MD management, may prove crucial to early recognition of risk of and potentially intervention against PD.”
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