Monday, November 9, 2009

Antacid Abuse = Bad Breath, Gas, and Then What?

Dr. Harriott's Comment: Acid is not the ultimate enemy. Alkaline is not nervana. Balance is the objective. The body knows what to do, given the chance. If you get a symptom, and automatically think, "what medicine can I take to fix this?", please come talk to me.

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ACG: Chronic Acid Suppression Linked to Bacterial Overgrowth

By Charles Bankhead, Staff Writer, MedPage Today
Published: November 06, 2009

Action Points
Explain to patients that chronic use of acid-suppressing drugs might lead to abnormal bacterial growth in the small intestines.


The findings are based on a small number of patients from a retorspective review of data at a single institution.
SAN DIEGO -- Chronic acid suppression therapy may predispose otherwise healthy individuals to clinically significant small intestinal bacterial overgrowth (SIBO), according to data reported here.
Half of patients on chronic acid suppression had positive lactulose breath tests, compared with about 30% of a control group. Chronic acid suppression was associated with a significantly higher proportion of bacteria that produced mixed hydrogen-methane gas.

"If a patient has small-bowel bacterial overgrowth and has no other risk factors for it, physicians might consider stopping the patient's treatment with a proton pump inhibitor, if the patient can tolerate it, to prevent recurrence of the bacterial overgrowth," Walter Chan, MD, of Brigham and Women's Hospital in Boston, said during a presentation at the American College of Gastroenterology meeting.

"Particularly in patients who respond to treatment and then have recurrent symptoms, or who fail to respond to treatment-stopping PPI treatment might be considered as an adjunct to treatment of the small-bowel bacterial overgrowth."

Previous studies had suggested increased bacterial-colony formation in duodenal aspirates of asymptomatic patients on chronic acid suppression. However, no study had examined the effects of acid suppression on clinically significant SIBO, and the role of chronic acid suppression in symptomatic SIBO remained unclear.

To examine the association, Chan and colleagues retrospectively analyzed data on 108 adults who underwent lactulose breath test. The study population consisted of 43 patients who reported daily acid suppression therapy for at least two months and 65 patients who reported no acid suppression.

A positive breath test was defined as >20 ppm rise in breath hydrogen or methane within 60 minutes.

Baseline characteristics between the acid-suppression and control groups were similar, although women made up a higher proportion of the control group (86.1% versus 74.4%, P=0.06).

Among patients on chronic acid suppression, 49% had positive breath tests compared with 26% to 27% of the control group. The difference translated into more than a twofold greater likelihood of a positive test in the patients on chronic acid suppression (OR 2.311, P=0.019).

Gas-producing characteristics of the breath test showed that about 30% of the acid suppression group and about 20% of the control group generated hydrogen, and fewer than 10% of each group exhibited methane production.

About 10% of the acid-suppression group had mixed gas production, which was significantly different from the control group rate of about 1% (P=0.03). The finding indicated that chronic acid production might promote growth of a wider variety of bacterial species.

In light of findings, physicians might consider discontinuation of acid-suppressing drugs in patients with positive breath tests, particularly those who have recurrent symptoms of SIBO, the investigators concluded.