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Dipropylacetate and hyperglycinemia.

S Similä, L von Wendt, S L Linna

|May 1, 1979

Summary

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Dipropylacetate (DPA) treatment in epileptic patients caused significant hyperglycinemia, marked by increased glycine levels in plasma and cerebrospinal fluid, and a fourfold rise in urinary glycine excretion. This suggests DPA-induced hyperglycinemia may resemble secondary hyperglycinemia seen in organic acidurias.

Area of Science:

Biochemistry
Neurology
Clinical Pharmacology

Background:

Hyperglycinemia is a metabolic disorder characterized by elevated glycine levels.
Dipropylacetate (DPA) is an anticonvulsant drug with known metabolic effects.
Epileptic patients with neurological diseases may have complex metabolic profiles.

Purpose of the Study:

To investigate the effects of dipropylacetate (DPA) on glycine metabolism in epileptic patients.
To characterize the biochemical changes associated with DPA-induced hyperglycinemia.
To compare the DPA-induced condition with other forms of hyperglycinemia.

Main Methods:

Induction of hyperglycinemia using dipropylacetate (DPA) at doses of 14-41 mg/kg/day in 10 epileptic patients.
Measurement of glycine concentrations in plasma, cerebrospinal fluid (CSF), and urine.

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Comparison of glycine levels in treated patients with control groups (comparable non-treated patients and normal values).

Main Results:

DPA treatment led to significantly elevated plasma (475 +/- 76 mumol/l) and CSF (49 +/- 23 mumol/l) glycine concentrations.
A fourfold increase in urinary glycine excretion was observed in DPA-treated patients.
The plasma/CSF glycine ratio remained unaffected by DPA treatment.

Conclusions:

Dipropylacetate (DPA) induces hyperglycinemia in epileptic patients.
The pattern of glycine elevation suggests a mechanism similar to secondary hyperglycinemia in organic acidurias.
DPA's metabolic influence may mimic that of certain amino acid metabolites in organic acidemias.