Ulcer pills linked to B12 deficiency



Medication used to treat stomach ulcers may cause potentially harmful vitamin B12 deficiency, say experts.

A US study of 200,000 people in the Journal of the American Medical Association found the link.

People who took tablets known as proton pump inhibitors (PPIs) or histamine antagonists (H2RAs) were more likely to lack enough vitamin B12 for good health.

Left untreated, B12 deficiency can lead to dementia and neurological problems.

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Only a minority of patients on long term proton pump inhibitors showed evidence of vitamin B12 deficiency”

Prof Mark Pritchard of the British Society of Gastroenterology

The study authors say doctors should still prescribe these medicines, but that they should weigh possible harms against any benefits in patients who need the drugs for prolonged periods of time.

More investigations are needed to fully evaluate the risk which appears to be in people who take these medications for two or more years, they say.

Link not proof

The Kaiser Permanente researchers found that the link with B12 deficiency increased with dose and was stronger in women and younger age groups.

But the overall risk was still low.

PPIs and H2RAs are commonly prescribed for patients with symptoms of stomach ulcers such as heartburn and indigestion.

The tablets are also widely available to buy without a prescription, ‘over-the-counter’ at pharmacies.

They work by reducing the amount of acid made by your stomach.

Stomach acid is needed for us to absorb vitamin B12 from our food, such as meat, fish and dairy.

If identified, most cases of B12 deficiency can be easily treated by giving supplements or an injection of vitamin B12.

But symptoms, such as lethargy, can be vague and overlooked.

Prof Mark Pritchard of the British Society of Gastroenterology said people should not be concerned by the findings.

“Only patients who had taken these tablets for more than two years were at risk and only a minority of patients on long-term proton pump inhibitors showed evidence of vitamin B12 deficiency.”

He said people taking ulcer medications could ask their GP for a simple blood test to measure vitamin B12 levels if they are worried.

H. Pylori Eradication Might Reduce Recurrent Gastric Cancer After Surgery.


Thirty-six months after subtotal gastrectomy for gastric cancer, patients who were H. pylori-free had less glandular atrophy and intestinal metaplasia than infected patients.

Intestinal metaplasia (IM) and glandular atrophy (GA) have been identified as preneoplastic conditions in patients infected with Helicobacter pylori. The role of H. pylori eradication in improving these conditions after subtotal gastrectomy for gastric cancer is unclear.

To investigate this issue, researchers in Korea randomized 190 patients with gastric cancer and H. pylori infection to receive 7 days of proton-pump inhibitor–based triple therapy or placebo prior to surgery. The greater and lesser gastric curvatures were biopsied prior to surgery and at 12 and 36 months after surgery and evaluated according to the updated Sydney criteria. H. pylori infection was determined by both a rapid urease test and histologic examination of endoscopic biopsies. Histological findings of GA and IM were scored to indicate presence and severity (absent, 0; mild, 1; moderate, 2; severe, 3).

At 36 months, 75% of patients in the treatment group were free of H. pylori compared with 41% of the placebo group. The mean GA and IM scores did not differ between the two groups. However, compared with H. pylori-infected patients, those without H. pylori had less atrophy (P=0.005) and IM (P=0.03).


The lack of difference in glandular atrophy or intestinal metaplasia between study groups at 36 months might be explained by a type II error. Histological scores for both were lower in the treatment group, but these differences did not reach statistical significance, possibly because of the low eradication rate in the treatment group, the high spontaneous remission rate in the placebo group, or the relatively large number of patients lost before the final analysis. As the authors concluded, the findings suggest that successful H. pylori eradication might reduce the preneoplastic changes in the gastric remnant after gastric surgery, but the clinical significance of the histologic changes remains to be determined.

Source: NEJM

An Aspirin Every Other Day May Help Ward Off Colorectal Cancer in Women.

Low-dose aspirin taken every other day lowers the risk for colorectal cancer in middle-aged women, according to an Annals of Internal Medicine study.

Nearly 40,000 women aged 45 and older were randomized to take low-dose aspirin (100 mg) or placebo every other day for roughly 10 years; 84% were followed for an additional 7 years after treatment ended.

During the total follow-up, colorectal cancer risk was lower in the aspirin group (hazard ratio, 0.80), mostly owing to a reduction in proximal colon cancer, which emerged after 10 years. The incidence of total, lung, or breast cancer did not differ between the groups. Gastrointestinal bleeding and peptic ulcers occurred more often with aspirin.

An editorialist says that while aspirin may have a chemopreventive role in high-risk patients, the increase in bleeding and lack of effect on total cancer or all-cause mortality “should temper any recommendations for widespread use … in healthy middle-aged women.”

Health Benefits Of Turmeric

Turmeric is a wonderful superfood that is a must have!

(it’s so good at helping skin problems we accidentally wrote it twice!)

The health benefits of turmeric include:

  • Helps prevent gas
  • Helps prevent cancer
  • Natural Antibiotic
  • Aids in weight management
  • Natural antiseptic
  • Reduces the side effects of chemo
  • Natural analgesic
  • Improves skin conditions
  • Speeds up wound healing
  • Anti-arthritic
  • Lowers cholesterol
  • Improves asthma
  • Heals stomach ulcers
  • Helps coughs
  • Blood Purifier

No Evidence of Cancer Risk from Long-Term PPI Therapy.

Hormonal and histologic changes observed with long-term use of proton-pump inhibitors do not seem to translate into an elevated risk for mucosal gland atrophy or cancer.

Prolonged use of proton-pump inhibitors (PPIs) has been associated with an increase in serum gastrin levels, which could drive proliferation of enterochromaffin-like (ECL) cells in the gastric mucosa and contribute to mucosal gland atrophy in the presence of Helicobacter pylori infection. Two recent studies evaluated the long-term effects of PPI use on gastric mucosa.

In a multicenter study, Fiocca and colleagues randomized 554 patients with chronic gastroesophageal reflux to receive 20 mg of esomeprazole daily or undergo laparoscopic antireflux surgery. Gastric biopsies and serum samples for gastrin and chromogranin A were taken at baseline and at 1, 3, and 5 years. Biopsies from each time point were available for 338 participants. In the esomeprazole arm, ECL cell hyperplasia increased between time points, mucosal inflammation decreased (only in those with H. pylori infection), and serum gastrin and chromogranin A levels increased moderately. No atrophy or intestinal metaplasia occurred. The authors concluded that despite moderate increases in gastrin and chromogranin A levels, 5 years of esomeprazole therapy did not cause dysplastic or neoplastic changes and decreased inflammation in patients with H. pylori infection.

Brunner and colleagues report the longest follow-up results to date of efficacy, safety, and tolerability in 142 patients who received pantoprazole for a mean of 9.2 years to treat peptic ulcers or reflux esophagitis. Gastric biopsies and serum gastrin levels were obtained at baseline, during healing (until week 12), every 6 months during the first 5 years, and annually during the subsequent 10 years. The ECL cell density increased moderately during the first 3 years and then stabilized. Investigators observed no clinically relevant changes in the gastric mucosa or increase in intestinal metaplasia. Serum gastrin levels rose to moderate levels and subsequently remained constant but showed high variability between patients. In patients with H. pylori infection, antral gastritis regressed after eradication of the infection. The authors concluded that maintenance therapy with pantoprazole for up to 15 years is well tolerated, with no evidence of increased risk for gastric cancer.

Comment: Both studies confirm that long-term PPI treatment increases serum gastrin levels and is associated with an increase in ECL cells. Serum gastrin levels rose to a moderate level early in treatment and then remained constant for the duration of follow-up. The absence of histologic evidence of intestinal metaplasia or other precancerous mucosal changes suggests that the risk for gastric cancer is probably not increased by PPI therapy. However, both of these prospective studies were small and underpowered to detect a small increase in risk.

Source: Journal Watch Gastroenterology


Is Helicobacter pylori Eradication Sufficient for Bleeding Ulcers?

A prospective study suggests that peptic ulcer rebleeding is very unusual after H. pylori eradication and that maintenance antiulcer therapy may not be needed.

Helicobacter pylori infection is associated with peptic ulcer disease, and eradication of the infection reduces ulcer recurrence. The need for maintenance acid-reduction therapy in this setting is controversial.

To explore this issue, investigators at 10 university hospitals in Spain prospectively studied 1000 patients with endoscopically documented bleeding peptic ulcers and H. pylori infection. Participants were treated until eradication of the infection was confirmed by breath test. Thereafter, they received no acid-reduction therapy and were told not to take aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). They returned at 1-year intervals for a clinical examination and a breath test for H. pylori. If signs or symptoms of upper gastrointestinal bleeding occurred, urgent endoscopy was performed.

All participants were followed for at least 12 months (total, 3253 patient-years of follow-up). Recurrence of peptic ulcer bleeding was rare, occurring in three participants during year 1 and two during year 2. All five cases of rebleeding involved either H. pylori reinfection or NSAID use. The cumulative incidence of rebleeding was 0.5% (95% confidence interval, 0.16%–1.16%) overall and 0.15% (95% CI, 0.05%–0.36%) per patient-year of follow-up.

Comment: These findings provide excellent evidence that H. pylori eradication is sufficient therapy for peptic ulcer patients — even if they had bleeding — in the absence of other causes for ulcers. Forty-one percent of the patients in this study had previously used NSAIDs or aspirin. Without a control group in which NSAIDs are continued, we cannot assess the effect of H. pylori eradication alone, but if such agents are avoided, H. pylori eradication appears to be definitive ulcer therapy. The real clinical challenge is to keep these patients from taking NSAIDs and identify those at high risk for H. pylori reinfection to determine who should be considered for continued antiulcer therapy.

Source: Journal Watch Gastroenterology