AB-Yogurt helps!! ....Treatment Options - H.Pylori eradication

Helicobacter pylori eradication protocols is a standard name for all treatment protocols for peptic ulcers and gastritis; the primary goal is not only temporary relief of symptoms, but total elimination of Helicobacter pylori infection.

Definition

A good, clinically useful H. pylori eradication protocol is a treatment protocol, which ensures at least 80% H. pylori eradication rate, is not longer than 14 days (preferably 7 or 10 days) and is not too toxic (side effects should occur in not more than 10–15% patients receiving treatment by this protocol, and should not be so severe to warrant treatment discontinuation).

The treatment regimen should also be easy to follow by the patient, both human and canine, to improve or maintain high rate of treatment compliance.

During last decades, several new eradication protocols have been developed. This allowed clinicians to target several goals:

• improved treatment compliance;
• sharpened dietary component
• no need to strictly follow a diet, due to new proton pump inhibitor efficacy;
• decreased duration of therapy: from 14 to 7–10 days;
• decreased number of different tablets to ingest, due to combined standard preparations;
• decreased number of daily tablets from 4 times a day to twice-daily schemes;
• lessened toxicity and probability of side effects;
• improved clinical efficacy in terms of H. pylori eradication ratios;
• overcoming the problem of antibiotic resistance;
• satisfied the need for alternative protocols for those patients who are allergic to one of the standard antibiotics used in standard protocols.

Molecular model of H. pylori urease enzyme 

The standard first-line therapy is a one week "triple therapy" consisting of proton pump inhibitors such as omeprazole,lansoprazole and the antibiotics clarithromycin and amoxicillin. 

Variations of the triple therapy have been developed over the years, such as using a different proton pump inhibitor, as with pantoprazole or rabeprazole, or replacing amoxicillin with metronidazole for people who are allergic to penicillin. 

Such a therapy has revolutionized the treatment of peptic ulcers, and has made a cure to the disease possible; previously, the only option was symptom control using antacids, H₂-antagonists or proton pump inhibitors alone.

An increasing number of infected individuals are found to harbour antibiotic-resistant bacteria. This results in initial treatment failure and requires additional rounds of antibiotic therapy or alternative strategies, such as a quadruple therapy, which adds a bismuth colloid, such as bismuth subsalicylate.

 For the treatment of clarithromycin-resistant strains of H. pylori, the use of levofloxacin as part of the therapy has been suggested

An article in the American Journal of Clinical Nutrition found evidence that "ingesting lactic acid bacteria exerts a suppressive effect on Helicobacter pylori infection in both animals and humans," noting that "supplementing with Lactobacillus- and Bifidobacterium-containing yogurt (AB-yogurt) was shown to improve the rates of eradication of H. pylori in humans

This bacteria that causes ulcers may also play a role in the development of diabetes

Immunohistochemical staining of H. pylori from a gastric biopsy 

Helicobacter pylori (English pronunciation: /ˌhɛlɨkɵˈbæktər paɪˈlɔraɪ/; H. pylori),  is a Gram-negative, found in the stomach. It was identified in 1982  present in patients with chronic gastritis and gastric ulcers, conditions that were not previously believed to have a microbial cause. 

It is also linked to the development of duodenal ulcers and stomach cancer. However, over 80 percent of individuals infected with the bacterium are asymptomatic and it has been postulated that it may play an important role in the natural stomach ecology.

More than 50% of the world's population harbor H. pylori in their upper gastrointestinal tract. Infection is more prevalent in developing countries, and incidence is decreasing in Western countries. H. pylori's helix shape (from which the generic name is derived) is thought to have evolved to penetrate the mucoid lining of the stomach.

Doctors Yu Chen, PhD, and Martin Blaser, MD, in two large cohorts, Helicobacter pyloricolonization was positively associated with levels of glycosylated hemoglobin (HbA1c) 

The combination of H. pylori colonization and elevated body mass index was associated with higher HbA1c levels than either factor alone.

The findings come from a cross-sectional analysis of two cohorts from the National Health and Nutrition Examination Surveys -- NHANES III, conducted from 1988 to 1994, and NHANES 1999-2000.

The surveys are the only two of the NHANES series in which lab data on H. pylori status were collected, the researchers noted. NHANES III also collected data on the presence or absence of the H. pylori virulence factor cytotoxin-associated gene A (cagA).

For this analysis, Chen and Blaser studied 7,417 participants in NHANES III (18 and older) and 6,072 in NHANES 1999-2000 (3 and older) who had data available on H. pylori, HbA1c, and sociodemographic and lifestyle variables.

The researchers found no association between H. pylori and history of self-reported diabetes.

However, after excluding people with a history of diabetes and controlling for potential confounders, colonization with H. pylori -- and especially a strain with the cagA gene -- was associated with HbA1c levels.

Specifically:

1. In NHANES 1990-2000, the 2,403 participants who were H. pylori-positive had a mean HbA1c level of 5.49%, compared with 5.40% among the 3,669 who were not colonized.
2. The difference was significant at P=0.02 and remained significant after self-reported diabetics and insulin users were excluded.
3. The association was significant among those 18 and older (at P<0.01) but lost significance among those under 18.
4. In NHANES III, the overall difference in HbA1c levels was non-significant, but became significant (at P<0.01) when diabetics and insulin users were excluded.
5. In both cohorts, there was also an interaction between H. pylori and body mass index of 25 or higher -- increased HbA1c associated with having both H. pylori and higher BMI was greater than the sum of their individual effects.
6. The interaction was significant at P=0.04 in NHANES III and P<0.01 in NHANES 1999-2000.

In NHANES IIII, which assessed levels ofcagA, there was a progressive increase in average HbA1c levels when participants without H. pylori were compared with those with the bacterium but not cagA and those with both, the researchers said.

The trend overall was significant at P=0.02 and at P<0.01 when diabetics and insulin users were excluded.

The researchers cautioned that the study is cross-sectional and therefore can't say anything about causality. But reverse causation is unlikely, they said, simply because H. pylori is usually acquired in childhood.

In an accompanying editorial they stated that, people with H. pylori colonization and a higher body mass index -- even if they have no symptoms -- may need treatment to prevent or control diabetes.

But, they cautioned, the findings need to be confirmed and more study is needed -- especially in the form of randomized trials -- to tease out the effect of H. pylori treatment on diabetes and HbA1c levels.

We will talk about treatment of Helicobacter pylori soon