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-Glucosidase inhibitors ( -GI), such as acarbose and voglibose, are widely used in diabetic patients to suppress postprandial hyperglycemia by interfering with carbohydrate-digesting enzymes, thus delaying glucose absorption (1). Recently, acarbose and voglibose were reported to have different effects on the absorption of digoxin; acarbose has been shown to decrease the absorption of coadministered digoxin, whereas voglibose has been demonstrated to have no such effect (2–5). We describe here a diabetic patient with congestive heart failure whose serum digoxin concentration responded differently to acarbose and voglibose. An 82-year-old man with type 2 diabetes and congestive heart failure was treated with voglibose (0.9 mg/day) and digoxin. The serum level of digoxin remained within the therapeutic range (0.8–2.0 ng/ml). However, we decided to administer acarbose (300 mg/day) in place of voglibose because of high levels of HbA1c. The decision to switch from voglibose to acarbose was prompted by data from our earlier study, which demonstrated that acarbose (300 mg/day) has a stronger effect than voglibose (0.9 mg/day) on suppressing postprandial hyperglycemia (Y.N., T.H., unpublished data). Thereafter, the HbA1c level was improved by acarbose without flatulence and abdominal distention. However, subtherapeutic levels of digoxin (0.2–0.4 ng/ml) were found without changing the digoxin dosage. The patient showed no sign of worsening congestive heart failure. The patient asserted that he was taking the medications regularly according to the instructions, so compliance to the regimen did not appear to be the problem. We suspected the occurrence of a pharmacokinetic drug-drug interaction between acarbose and digoxin, a phenomenon previously described in earlier reports (2–4); therefore, we switched from acarbose back to voglibose (0.9 mg/day). Contrary to our expectations, the serum level of digoxin 1 month after voglibose readministration remained within the subtherapeutic range (0.3 ng/ml). Miura et al. (3) reported that administering acarbose reduces the absorption of digoxin. In a report on two patients who showed subtherapeutic levels of digoxin induced by acarbose, Ben-Ami et al. (4) proposed the following mechanisms to explain the phenomenon: 1) coadministration with acarbose increases gastrointestinal motility, leading to decreased absorption of digoxin, and 2) acarbose interferes with the hydrolysis of digoxin before its absorption, thereby altering the release of the corresponding genine and affecting the reliability of the digoxin laboratory test. However, another type of -GI voglibose was shown not to reduce the level of digoxin (5), casting doubt on the hypotheses from Ben-Ami et al. The most interesting finding in our case is that the level of digoxin was essentially unchanged after switching back from acarbose to voglibose. We have no knowledge of the mechanism behind this phenomenon; further studies are needed to clarify it. Although the precise mechanism of acarbose-induced reduction of digoxin levels remains unknown, voglibose should be recommended for diabetic patients with digoxin coadministration. If acarbose is needed, the dosage of digoxin and the timing of its administration should be considered.

Are there different effects of acarbose and voglibose on serum levels of digoxin in a diabetic patient with congestive heart failure?