primidone in serum/plasma
Indications
Reference interval
Principle
The unique reagents in the methodology are the matched lots of antiprimidone antibody & the primidone-glucose-6-phosphate dehydrogenase conjugate. The reaction sequence, in two steps, is as shown:
- Ab + Prim -----------> Ab-Prim + Prim-G6PD (active)
Prim-G6PD + Ab ------> Ab-Prim-G6PD (inhibited)
- Glucose-6-phosphate 6-phosphogluconolactone
Prim-G6PD
+ ------------> +
NAD NADH (absorbs at 340 nm)
Where: Ab = Antiprimidone antibody
Prim = Primidone
Prim-G6PD = Primidone-glucose-6-phosphate dehydrogenase conjugate
The concentration of primidone determines the amount of primidone glucose-6-phosphate dehydrogenase conjugate that is bound to antiprimidone antibody. The unbound conjugate catalyzes the oxidation of glucose-6-phosphate with the simultaneous reduction of NAD+ to NADH more rapidly than does the bound conjugate. The rate of increase of absorbance at 340 nm due to the increase in NADH is related to the primidone concentration by means of a standard curve
Clinical significance
Primidone is effective in the treatment of tonic-clonic & complex-partial seizures. The action of this drug is due partically to the accumulation of its major metabolite, phenobarbital. A second metabolite of primidone, phenylethyl malonamide (PEMA), also has some antiepileptic activity. Primidone is rapidly & completely absorbed after oral administration. Disposition of the drug is not known to be significantly altered by other disease states or other drugs.
Since phenobarbital is an active metabolite of primidone, concurrent analysis of phenobarbital is required for complete interpretation of results. Toxicity due to accumulation of primidone is usually associated with symptoms of sedation, nausea, vomiting, diplopia, ataxia, & a PHNO level >40 ug/mL.
Coadministration of acetazolamide with primidone will result in decreased gastrointestinal absorption of primidone & subsequent diminished plasma concentrations. Primidone administered in association with phenytoin (PTN) will produce a modest elevation of the PHNO/PRIM ratio since PTN competes with the hepatic hydroxylating enzymes associated with phenobarbital's metabolism.
Specimen
Patient Preparation: No special patient preparation is required.
- Serum is the specimen of choice. Serum is collected in a red top vacutainer by venipuncture. Serum samples can be stored at room temperature for several hours. If frozen at -20 C, serum is stable for at least one year.
- Plasma samples are to be collected in a green top vacutainer containing heparin by venipuncture. Plasma separated from erythrocytes can be stored at room temperature for several hours & frozen at -20 C for one year.
Minimum sample size is 0.6 mL: With an optimum size of 1.5 mL or larger.
More general terms
More specific terms
Additional terms
References
- ↑ Kaplan, L., & Pesce, A., Clinical Chemistry:theory, analysis, & correlation, C. V. Mosby Co., St. Louis, MO., 1984, pp. 1336.
- ↑ Tietz, N., Fundamentals of Clinical Chemistry, 3rd edition W. B. Saunders Co., Philadelphia, 1987, pp. 854.
- ↑ Tietz, N., Textbook of Clinical Chemistry, W. B. Saunders Co., Philadelphia, 1986, pp. 1634.
- ↑ ACA IV Discrete Clinical Analyzer Instrument Manual, Volume 1:Operation, DuPont Company, Wilmington, Delaware, 1984.
- ↑ ACA IV Discrete Clinical Analyzer Instrument Manual, Volume 3:Chemistry, DuPont Company, Wilmington, Del, 1984.
- ↑ Mini Panel of 2 tests: Phenobarbital . Primidone (Mysoline) Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0090202.jsp