In clinical reports, it has been noted that serum lithium may rise an average of 0.2 - 0.4 mmol/L after intake of 300 mg and 0.3 -0.6 mmol/L after intake of 600 mg of lithium carbonate. However, renal lithium excretion may vary greatly between individuals and lithium dosage must, therefore, be adjusted individually. The dose necessary to maintain a given concentration of serum lithium depends on the ability of the kidney to excrete lithium. Renal lithium clearance is, under ordinary circumstances, remarkably constant in the same individual but decreases with age and falls when sodium intake in lowered. A low salt intake resulting in low tubular concentration of sodium will increase lithium reabsorption and might result in retention or intoxication. The half-life of elimination of lithium is approximately 24 hours. The renal clearance of lithium is proportional to its plasma concentration. Lithium is filtered by the glomeruli and 4/5 (80%) of the filtered lithium is reabsorbed in the tubules, probably by the same mechanism responsible for sodium reabsorption. Lithium is excreted primarily in urine with less than 1% being eliminated with the feces. The distribution of lithium in the body approximates that of total body water, but its passage across the blood-brain barrier is slow and at equilibration the CSF lithium level reaches only approximately half the plasma concentration. Peak plasma lithium concentrations are reached 2-4 hours after LITHANE administration. Lithium ions are rapidly absorbed from the gastrointestinal (GI) tract following oral administration of LITHANE (lithium carbonate). It does not appear to protect against the action of stimulant and convulsive drugs and produces only slight potentiation of CNS depressants.ĮCG changes with lithium have been reported in both animals and man.
Lithium is inactive in most screening psychopharmacological tests but it produces marked potentiation of amphetamine hyperactivity in animals. However, the specific biochemical mechanism of action of lithium in mania is still largely unknown. Lithium alters sodium transport in nerve and muscle cells, affects a shift toward intraneuronal metabolism of catecholamines and has an inhibitory action on the intracellular formation of cyclic AMP.
Although lithium is useful for its antimanic effect and in preventing relapses in patients with a clearcut diagnosis of bipolar affective disorder, it has very little, if any, direct effect on moods, normal or abnormal.
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