A recent study in people with T2DM showed dramatic results: patients with T2DM who took a prescription drug called pantoprazole for 12 weeks had a decrease in their A1C levels -- from 7.6 to 6.8 (P < 0.001). That’s spectacular, and if these results can be proven to be reproducible in future larger studies, we may have another drug for the treatment of T2DM.
The study was appropriately double-blinded and randomized. But it was a very small study: only 16 patients got the active drug (and 15 got a placebo). Other results included a finding of “significantly increased” insulin levels and “improved β-cell function.” The abstract that’s available on-line doesn’t state what dose of pantoprazole was used, nor what drugs the T2DM patients were on, nor whether any hypoglycemia occurred in the study. I’ve asked for a copy of the full article, and upon receipt, will add an addendum to this blog.
Pantoprazole is a medication in a class called “proton pump inhibitors” that is approved for short-term treatment (8-16 weeks) of erosive esophagitis caused by gastroesophageal reflux disease (GERD). It also can be used as maintenance therapy after a satisfactory initial response is obtained. Pantoprazole is widely available worldwide, and is sold under a myriad of brand names.
I looked at the USPI for one brand of pantoprazole (Protonix), and it says nothing whatsoever about any effects on glucose control (no mention of adverse events of hypoglycemia, for instance), and says something that appears to contradict one of the recent study’s findings: “In a clinical pharmacology study, PROTONIX 40 mg given once daily for 2 weeks had no effect on the levels of the following hormones” then mentions insulin as one of the hormones studied. Of course, pantoprazole has its own collection of side effects; the ones I might worry most about most are those possibilities associated with the administration of the drug for an extended period of time: there’s an increased risk of fracture of the hip, wrist or spine with long-term use, and people who take pantoprazole for a long time may develop atrophic gastritis (weakening of the stomach lining), and rarely, low levels of magnesium in the blood.
One might also wonder whether other researchers are evaluating the use of pantoprazole in diabetes. According to the ClinicalTrials.gov website, there are only two studies that mention pantoprazole in the context of diabetes, and only one of general interest to T2DM (the other is studying its use in islet transplant recipients). The one study in ClinicalTrials.gov is another small study, in Mexico. (The present study, which was done in India, isn’t listed in ClinicalTrials.gov, so there might be other non-US studies evaluating pantoprazole in diabetes.) So as of now, it doesn’t appear that any of the manufacturers of pantoprazole have started gearing up to get a new indication for treatment of type 2 diabetes in the US – or there’d be more studies listed in ClinicalTrials.gov.
I look forward to more studies of the effects of pantoprazole in T2DM, and the possibility that someday we’ll have yet another drug for the treatment of T2DM. But I caution the eager reader that it’s way too soon to start begging your physician for a prescription for pantoprazole – let’s see what follow-up studies show.
Addendum August 31, 2012:
I have received a copy of the original report, Pantoprazole Improves Glycemic Control in Type 2 Diabetes: A Randomized, Double-Blind, Placebo-Controlled Trial and found some additional information.
1) Subjects were "Adult insulin-naive patients of either sex, having T2DM of less than 5-yr duration and HbA1c less than 8.5%... All of the patients were maintained on stable oral antidiabetic therapy with metformin and/or sulfonylurea for at least 1 month before enrollment in the study."
2) The dose of pantoprazole was 40 mg twice daily orally.
3) "None of the patients developed hypoglycemia, despite reduction in HbA1c and blood glucose." (I might add that this is difficult for me to believe, as some of the patients were on sulfonylureas -- which frequently provoke hypos, and addition of another glucose-lowering agent should have caused occasional hypos in these subjects.)
4) The mean fasting plasma glucose on pantoprazole dropped from 126.3 mg/dl to 109.2; on placebo, it went from 134.0 to 145.1.