Lithium Pharmacokinetics, Duration of Therapy, and the
Adenylate Cyclase System

Goodnick, Paul J.; Fieve, Ronald R.; Meltzer, Herbert L.; Dünner, David L.

doi:10.1159/000468560

Cited by 11 publications

(1 citation statement)

References 13 publications

(19 reference statements)

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“…Similar patterns following lithium withdrawal can be found in platelet serotonin content (1 8), clonidine-induced hypotension (17), and red blood cell kinetics (19). Since half-life of elimination of lithium varies only from 1 to slightly over 2 days (20), these results occur gradually despite the absence of lithium. Thus, some patients may relapse during re-institution of biochemical vulnerability state secondary to removal of lithium-induced receptor changes.…”

Section: Symptoms and Moodmentioning

confidence: 62%

Clinical and laboratory effects of discontinuation of lithium prophylaxis

Goodnick

1985

Acta Psychiatr Scand

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Twelve patients who met Research Diagnostic Criteria for a history of bipolar affective disorder gave informed consent for open discontinuation of lithium therapy for 3 weeks. There was no significant change after lithium discontinuation in the number of depressive or manic symptoms, in mood score, in total Zung Depression score, or in any of the 20 items found in the Zung Depression scale. There were significant reductions in total severity of side effects, and improvement in the three side effects reflecting renal function: polydipsia, polyuria, and nocturia. These changes were reflected in the significant increase in urine specific gravity. Significant changes in side effects did not take place until at least 2 weeks after lithium was discontinued. Other significant relationships were found between increases in serum thyroid hormone levels and in urine specific gravity, and decreases in Vmax of platelet serotonin uptake and increases in degree of clonidine-induced hypotension.

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Section: Symptoms and Moodmentioning

confidence: 62%

Clinical and laboratory effects of discontinuation of lithium prophylaxis

Goodnick

1985

Acta Psychiatr Scand

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GABAergic mechanism of interaction of lithium and valproate in discrete rat brain regions following their combind treatment and subsequent withdrawal

Shukla¹

1987

Drug Development Research

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Shukla, G.S.:GABAergic mechanism of interaction of lithium and valproate in discrete rat brain regions following their combined treatment and subsequent withdrawal. Drug Dev. Res. 11:209-218. 1987.Rats administered intraperitoneally with 1 mmol lithium carbonatelkglday, 300 mg valproic acidlkglday, and their combination for 12 days lithium treatment were found to increase the levels of r-aminobutyric acid (GABA) and its synthesizing enzymes, glutamic acid decarboxylase (GAD), in corpus striatum and midbrain regions. However, these elevated levels returned to normal after withdrawal of the treatment for 2 days. Valproic acid treatment alone increased GABA and GAD in the cerebral cortex and hippocampus regions. In addition, an increased cerebellar GABA concentration was observed. The combined treatment of lithium and valproic acid enhanced GABA and GAD levels in all brain regions, except for GABA in the pons-medulla. A statistically significant synergistic effect of the two drugs was noticed in elevating GABA and GAD levels in the corpus striatum, cerebral cortex, and midbrain regions. Furthermore, the elevated levels remained stable even 2 days after cessation of the combined therapy. The observed stable and synergistic increase in the regional GABA and GAD suggested a possible role of facilitated GABAergic transmission in the mechanism of therapeutic action of lithium and valproic acid combination in the treatment of mania.

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On the elimination half‐life of lithium in long‐term treatment of patients with affective disorders

Nilsson¹,

Axelsson²

1989

Human Psychopharmacology

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The elimination half‐life of lithium was investigated in 55 patients on long‐term treatment in 1980, when their mean treatment time was 7·5 years. Twenty‐seven of the patients were reinvestigated 7 years later, at which point their mean treatment time was 15 years. An approximate method for determining the elimination half‐life of lithium was used, and this variable was tested in eight chronic psychotic patients on lithium treatment, in whom the elimination half‐life was also determined by a conventional technique. The elimination half‐life was 32 h in 1980 and varied between 15 and 128 h. The elimination half‐life was significantly increased 7 years later, with a median increase of 8 h. The elimination half‐life of lithium was closely correlated to age and to daily weight‐related dose of lithium when the patients entered the study in 1980, but this was not seen at the time of the reinvestigation in 1987. The elimination half‐life did not vary with serum creatinine, maximal urine osmolality, or with the concomitant neuroleptic medication. Further studies are needed to clarify the clinical significance of the prolonged elimination half‐life with time.

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Lithium Pharmacokinetics, Duration of Therapy, and the Adenylate Cyclase System

Cited by 11 publications

References 13 publications

Clinical and laboratory effects of discontinuation of lithium prophylaxis

Clinical and laboratory effects of discontinuation of lithium prophylaxis

GABAergic mechanism of interaction of lithium and valproate in discrete rat brain regions following their combind treatment and subsequent withdrawal

On the elimination half‐life of lithium in long‐term treatment of patients with affective disorders

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