Saturday, 11 July 2015

Helicobacter and the cause of MS

Is Helicobacter a proxy for the hygiene hypothesis in MS? #MSResearch #MSBlog

"The small study below showing a higher seroprevalence, or seropositivity, rate of Helicobacter pylori in MSers compared to a control group of people with anaemia (low red cell or blood hemoglobin levels). Seropositivity simply means that you have been exposed to the bacterium the past and your immune system has made antibodies against the bacterium. 
Helicobacter is the bacterium that cause peptic ulcer disease (stomach and/or duodenal ulcers due to the effect of stomach acid). Based on  their own findings the authors jump to conclusions and start discussing causation. The science of causation is quite complex and we have discussed it many times on this blog in relation to EBV and CCSVI. The first criteria for causation is consistency of the findings; this is where things go wrong already as there are studies showing the exact opposite, i.e. lower rates of Helicobacter infection rates in MSers compared  to controls. Why study Helicobacter infection rates? Some claim it is a proxy for the hygiene hypothesis; the lower the background hygiene the more likely you are to be infected with Helicobacter the less likely you are to get MS. Clearly, this study contradicts this claim. My problems with this study is its size, its is simply too small, and the control group. I am not sure a group of people with anaemia are the most appropriate control group." 


"What next? I suggest someone with a large sibling / twin pair MS serum bank does a study to see if there are difference between MSers and their siblings in relation to Helicobacter seroprevalence rates. The use of sibling will partially control for the shared environment."

Gavalas et al. Relationship between Helicobacter pylori infection and multiple sclerosis. Ann Gastroenterol. 2015 Jul-Sep;28(3):351-354.

BACKGROUND: Recent data indicate the presence of immunomodulating properties of Helicobacter pylori (Hp) (Hp Sydney Strain-1 antigen) in an experimental model of multiple sclerosis (MS), and there are limited contradictory epidemiologic data regarding Hp serology in MS patients.

METHODS: The aim of this prospective, comparative study was to validate the incidence of active Hp infection by histology and the endoscopic abnormalities, in 44 patients with relapsing-remitting MS and 20 anemic controls.

RESULTS: The overall prevalence of histologically confirmed active Hp infection in 44 MS patients was 86.4% vs. 50% in 20 matched anemic control participants (P=0.002, odds ratio 6.33, 95%CI 1.85-21.64). Concomitant diseases of autoimmune origin including hypothyroidism and ulcerative colitis were exclusively present in MS patients. Moreover, a trend of increased presence of pathological endoscopic findings such as hiatus hernia, Barrett's esophagus and duodenal ulcer disease was observed in MS patients compared with controls; Barrett's esophagus and duodenal ulcers were exclusively observed in MS patients. Likewise, Hp (+) MS patients showed exclusive presence of hiatus hernia, esophagitis and duodenal ulcer disease compared with Hp (-) MS patients.

CONCLUSION: Hp infection appears to be more frequent in MS patients. If confirmed, this might indicate either a common factor that causes susceptibilities to both MS and Hp infection or that Hp might be a causal factor for developing MS. If a causal link between Hp infection and MS is confirmed in the future, this may have a major impact on the pathophysiology and management of MS.

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