Chronic diphenylhydantoin therapy does not reduce plasma 25-hydroxy-vitamin D

Area of Science:

• Pharmacology
• Endocrinology
• Clinical Medicine

Background:

• Diphenylhydantoin (DPH) is an anticonvulsant medication.
• Potential effects of DPH on vitamin D metabolism are a concern.
• Understanding DPH's impact on 25-hydroxyvitamin D (25-OHD) is crucial for patient management.

Purpose of the Study:

• To investigate the long-term effect of diphenylhydantoin (DPH) therapy on plasma 25-hydroxyvitamin D (25-OHD) levels.
• To assess whether DPH treatment leads to a clinically significant decrease in 25-OHD.
• To evaluate the persistence of any DPH-induced changes in 25-OHD after drug cessation.

Main Methods:

• A randomized controlled study design.
• Involved 18 non-epileptic subjects receiving monitored diphenylhydantoin (DPH) therapy for 2 years.
• Included a control group of 18 subjects for comparison of plasma 25-OHD and serum alkaline phosphatase (SAP) levels.

Main Results:

• Mean plasma 25-OHD levels at 2 years were not significantly different between DPH-treated and control groups (59 +/- 8 nmol/l vs. 54 +/- 8 nmol/l).
• Plasma 25-OHD levels showed no significant change one month after discontinuing DPH therapy.
• The DPH-treated group exhibited higher mean serum alkaline phosphatase (SAP) levels, consistent with hepatic enzyme induction.

Conclusions:

• Therapeutic doses of diphenylhydantoin (DPH), when used without other anticonvulsants, do not appear to cause a clinically significant reduction in plasma 25-hydroxyvitamin D (25-OHD).
• The observed increase in serum alkaline phosphatase (SAP) is likely due to hepatic enzyme induction by DPH.
• DPH therapy does not necessitate routine vitamin D supplementation in non-epileptic individuals based on these findings.