Ranitidine and high concentrations of phenylpropanolamine cross react in the EMIT monoclonal amphetamine/methamphetamine assay.

Toxicity of heavy metals and the genetic porphyrias (most commonly acute intermittent porphyria, AlP) produce increased concentrations of &-aminolevulinic acid (SALA) or porphobilinogen in plasma and urine. The quantitative test for S-ALA or porphobilinogen in urine described by Mauzerall and Granick (1) involves column separation and is recommended (2). For monitoring patients more closely, it would be desirable to measure concentrations of S-ALA or porphobilinogen in blood. The only published method available for this requires synthesis of internal standards, multiple extractions, and gas chromatography with flame ionization (3). Because S-ALA is an amino acid, we evaluated its behavior in our system for assaying free amino acids in plasma (Pico-Tag method; Waters Chromatography, Milford, MA). This technique involves alkaline derivatization of ultraffitered serum with phenylisothiocyanate, gradient separation on a reversed-phase column, and detection at 254 nm. The S-ALA peak appeared at 6.5 mm (with a retention time ratio to alanine of 0.3 16), which, in our standard mixture, was in a “window” between a-aminoadipic acid (5.5 mm) and hydroxyproline (7.1 mm). Examination of computerstored amino acid chromatograms for normal subjects revealed the occasional presence of an unidentified peak at this time, corresponding to an S-ALA concentration of about 1 Mmol/L. [The reported normal value for S-ALA in plasma is <1 MmolJL (2, 3).] Our patient with an acute episode of AlP had three blood