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PubMed1987

The potential use of lithium as a marker for the assessment of the sources of dietary salt: cooking studies and physiological experiments in men.

Lithium was investigated for its possible use as a marker for identifying the various sources of NaCl in the diet. Micromolar concentrations of lithium can be detected in various vegetables, tap water and also in urine specimens of adult volunteers. The lithium content of vegetables varied from 6.1 to 24.5 mumol of lithium/kg dry weight, with the exception of spinach and aubergines which had much higher concentrations. The excretion of the element in 24 h urine specimens ranged from 2 to 4 mumol of lithium/day. Experiments were performed to assess whether both lithium and sodium would penetrate foods at the same rate during cooking. The rates of penetration into food for both elements were proportional to their concentration in the cooking water despite a sodium/lithium ratio of 50:1. Physiological experiments were conducted to investigate the handling of small doses of lithium by the body. A dose of 250 mumol of lithium was chosen as optimal and given orally to healthy volunteers in either single or continuous aqueous doses of lithium carbonate. The recoveries of oral lithium in urine were 92 +/- 5% (SD) and 97 +/- 4 (SD) (n = 5) for single and continuous doses respectively. The daily addition of 100 mmol of oral NaCl to the diet of volunteers receiving a standard dose of lithium did not affect urinary lithium excretion rates nor the final recovery of the administered lithium. These studies suggest that lithium carbonate may be a useful marker for the uptake of NaCl into cooked food; after eating lithium-enriched food the monitoring of urinary lithium output may then be used to quantify the amount of sodium derived from the specific foods.

Cooking↗
PubMed2003

Lithium-induced nephropathy: Rate of progression and prognostic factors.

BACKGROUND: Long-term lithium administration in humans may lead to chronic tubulointerstitial nephritis, which develops very slowly. Its progression to end-stage renal disease (ESRD) has been rarely reported. The aim of this study is to document the rate of progression of lithium-induced nephropathy and its prognostic factors, and to provide an estimation of the percentage of lithium-induced ESRD in France. METHODS: Two groups have been studied: 54 patients with lithium-induced renal failure, nine of whom underwent renal biopsy; and 20 patients who were referred for systematic renal biopsy, 14 of whom were subsequently followed up. In addition, a survey of lithium-induced ESRD was conducted in French dialysis centers. RESULTS: The mean annual loss of creatinine clearance in patients with lithium-induced nephropathy was 2.29 mL/min. Among 74 patients, 12 reached ESRD at a mean age of 65 years. Creatinine clearance at referral and at last follow-up was inversely related to the duration of lithium therapy in both univariate and multivariate analyses adjusting for age, gender, hypertension, and proteinuria. The degree of interstitial fibrosis on renal biopsy was also related to the lithium duration and cumulative dose. It was predictive of the final creatinine clearance. About 35% of the patients tested had moderate hypercalcemia, due to hyperparathyroidism. The prevalence of lithium-related ESRD in France was estimated as two per 1000 dialysis patients. The average latency between onset of lithium therapy and ESRD was 20 years. CONCLUSION: Lithium-induced chronic renal disease is slowly progressive. Its rate of progression is related to the duration of lithium administration. Lithium-related ESRD represents 0.22% of all causes of ESRD in France. Regular monitoring of estimated creatinine clearance is mandatory in long-term lithium-treated patients.

Adult↗
PubMed2005

Drug-drug interactions as a determinant of elevated lithium serum levels in daily clinical practice.

OBJECTIVE: Lithium is a drug with a narrow therapeutic window. Concomitantly used medication is a potentially influencing factor of lithium serum concentrations. We conducted a multicentre retrospective case-control study with the aim of investigating lithium-related drug interactions as determinants of elevated lithium serum levels in daily clinical practice. METHODS: Cases were patients with an increase of at least 50% in lithium serum concentrations resulting in an elevated lithium serum level of at least 1.3 mmol/L, and who were not suspected of a suicide attempt. Controls were patients who showed stable lithium serum levels within the therapeutic range. Use and start of non-steroidal anti-inflammatory drugs, diuretics, renin-angiotensin inhibitors, theophyllin and antibiotics were investigated as potential determinants of the elevated lithium serum levels. Irregularity in lithium dispensing pattern, change in lithium dosing regimen, age, gender, prescribing physician and laboratory parameters were investigated as potential confounders. RESULTS: We included 51 cases and 51 controls in our study. Five (9.8%) controls and 15 (29.4%) cases used potentially interacting co-medication [OR of 3.83 (95%CI 1.28-11.48)]. Start of potentially interacting co-medication was observed in eight (15.7%) cases and in zero (0%) controls resulting in an OR of 20.13 (95% CI 1.13-359). After adjustment for co-medication, irregularity in lithium dispensing pattern, change in lithium dosing regimen, and age, the statistically significant association was lost. We report an OR of 2.70 (95% CI 0.78-9.31) for use of concomitant medication, with a large contribution of antibiotic agents, and an OR of 3.14 (95% CI 1.15-8.61) for irregularity in lithium dispensing pattern. CONCLUSION: Use of co-medication, especially antibiotics, tends to be associated with elevated lithium serum levels.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1976

Lithium RBC/plasma ratio in subgroups of patients with affective disorders.

The lithium RBC/plasma ratio was determined in 59 patients during prophylactic lithium therapy -- 10 cycloid psychotics, 28 unipolars and 21 bipolars -- as well as in 20 patients during lithium therapy in phase of illness -- 8 cycloid psychotics, 5 unipolars and 7 bipolars. The lithium ratio was found to be normally distributed both among patients in phase of remission and those in phase of illness. No differences in lithium ratio were found between patients in phase of remission and phase of illness, respectively. During prophylactic lithium therapy, no differences were found in the lithium ratio between patients in different diagnostic subgroups. In a correlation matrix, the lithium ratio was found to correlate to lithium in RBC but not to age, sex, type of illness, weight, lithium dosage, duration of treatment or level of lithium in plasma. The lithium level in RBC was determined only by the lithium level in plasma. Thus, the lithium RBC/plasma ratio does not seem to be of diagnostic value in affective disorders.

Adult↗
PubMed1991

Effect of lithium on function and growth of thyroid cells in vitro.

Lithium has been reported to alter thyroid function and cause goiter in some patients. To explain the mechanism of lithium action in the thyroid gland, we studied the effect of lithium on thyroid function and cell growth in FRTL-5 rat thyroid cells and on de novo thyroid hormone formation in primary cultures of porcine thyroid follicles. TSH-induced iodide uptake was suppressed at 2 mM lithium in both FRTL-5 cells and porcine follicles. In porcine thyroid follicles, iodide uptake stimulated by 8-bromo-cAMP, iodine organification, and de novo thyroid hormone formation were also reduced by lithium; however, 2 mM lithium did not inhibit TSH-induced cAMP production. In FRTL-5 cells, lithium also inhibited forskolin-stimulated iodide uptake. These results suggested that lithium exerts its effect at a step involving cAMP signal transduction rather than inhibiting cAMP production. In both FRTL-5 thyroid cells and porcine follicles, lithium enhanced cell growth in basal states (lacking TSH) and with TSH treatment. In porcine thyroid cells, the protein kinase C activator, tetradecanoyl phorbol-13-acetate, increased cell growth, and lithium had an additive effect with tetradecanoyl phorbol-13-acetate on cell growth. To examine the possibility that the action of lithium was mediated by the protein kinase C pathway, porcine cells were incubated with lithium and H7, a selective protein kinase C inhibitor. Lithium-induced cell growth was suppressed to the basal level by H7. These results suggest that lithium exerts its growth-promoting effect through the protein kinase C system.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2003

Lithium interaction with the cyclooxygenase 2 inhibitors rofecoxib and celecoxib and other nonsteroidal anti-inflammatory drugs.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) have been reported to increase serum lithium concentrations. We sought to determine whether NSAIDs that selectively inhibit cyclooxygenase (COX) 2 also elevate serum lithium concentrations. METHOD: The U.S. Food and Drug Administration's Adverse Event Reporting System (AERS) database was searched in January 2003 for reports of interactions between lithium and rofecoxib or celecoxib, the selective COX-2 inhibitors marketed in the United States. Additionally, a literature search was performed using PubMed with the MeSH terms anti-inflammatory agents, nonsteroidal and lithium. Reports of interactions between NSAIDs and lithium were selected for review based on titles of retrieved citations. RESULTS: Eighteen cases of increased serum lithium concentrations after the addition of one of the COX-2 inhibitors to stable lithium therapy were retrieved from AERS, 13 with rofecoxib and 5 with celecoxib. Serum lithium concentration increases of up to 99% and 448% with concomitant celecoxib and rofecoxib use, respectively, were reported. Thirty-six English-language literature articles report interactions between lithium and various NSAIDs. Although some articles report no effect or decreased serum lithium concentrations with concomitant aspirin or sulindac, increased serum lithium concentration reports exist for aspirin, sulindac, and 14 other NSAIDs, including celecoxib and rofecoxib. CONCLUSION: Clinicians should consider NSAID use in the differential diagnosis of lithium toxicity, monitor patients' serum lithium concentrations during the initiation or discontinuation of NSAID therapy, and be aware that the selective COX-2 inhibitors can increase serum lithium concentrations leading to toxicity.

Adult↗
PubMed1991

Population pharmacokinetics of lithium.

The population pharmacokinetics of lithium was determined. Psychiatric inpatients who were at least 18 years old, had normal renal function, and were receiving lithium two or three times daily were the subjects of the study; 79 patients met the criteria. Serum lithium concentrations were measured by flame photometry 12 hours after the evening dose. Other data collected included age, gender, race, height, weight, serum creatinine and sodium concentrations, diet, and concurrent drug use. The nonlinear mixed-effects model (NONMEM) program was used to estimate lithium clearance, lithium volume of distribution, and error variability and to determine the influence of patient characteristics on lithium clearance. With the initial model, the mean lithium volume of distribution was 32.8 L and mean lithium clearance was 1.36 L/hr. With an intermediate model, lithium clearance estimates improved on the basis of patient size (weight and body surface area), daily lithium dosage, age, gender, and race. When only the most significant variables--lean body weight and creatinine clearance--were retained, a final model was obtained that yielded a coefficient of variation for lithium clearance of about 24% and gave fairly accurate predictions of steady-state lithium concentrations (coefficient of variation, about 16%). Analysis of lithium pharmacokinetics with the NONMEM program suggested that lean body weight and creatinine clearance are important predictors of lithium clearance.

Adolescent↗
PubMed1982

Structural and functional effects of long-term lithium therapy.

To determine the effects of long-term lithium therapy, we have studied the renal histology and the renal function of 47 patients with affective disorders who were either currently receiving or had previously received maintenance lithium therapy (lithium patients), and we have compared the results with those of 32 other psychiatric patients with similar affective illnesses who had never taken lithium (prelithium patients). The renal biopsy samples, analyzed by a point-counting technique for interstitial fibrosis, were not different in degree between the lithium and the prelithium patients. Interstitial fibrosis was also not different between prelithium patients and age-matched transplant donor kidney controls, but it was greater in lithium patients when compared with the donor kidney controls (P less than 0.01). The specific distal tubular lesion associated with lithium therapy was present in all the biopsy samples of the patients who were currently receiving lithium therapy. Marked distal nephron dysfunction, as measured by urinary concentrating ability (P less than 0.0001) and urinary acidification (P less than 0.0001), was evident in lithium patients compared with the prelithium patients. These defects were correlated with the duration of lithium therapy. Serum creatinine estimations (P less than 0.01), serum beta-2 microglobulins (P less than 0.01), and 51Cr-EDTA clearances (P less than 0.01) suggested some impairment of GFR in lithium patients compared with prelithium patients. These defects did not correlate with the duration of lithium therapy. From these studies we concluded that the marked distal nephron dysfunction induced by lithium might produce prerenal impairment of GFR because the renal function abnormalities have no structural basis when the degree of interstitial fibrosis of other psychiatric patients is used as a control. Prospective studies are needed to answer the controversial question of whether stable maintenance lithium therapy produces chronic nephrotoxicity.

Adult↗
PubMed1989

Effects of GTP on hormone-stimulated adenylate cyclase activity in cerebral cortex, striatum, and hippocampus from rats treated chronically with lithium.

The effects of lithium on guanosine triphosphate (GTP) stimulated adenylate cyclase activity and hormone-induced GTP activation of the enzyme have been studied in three regions of the rat brain. Chronic treatment with lithium, giving a serum lithium level of 0.71 +/- 24 mmol/L, reduced isoprenaline-induced GTP stimulation of adenylate cyclase activity in cortical membranes at concentrations of GTP up to 2 microM. No effect of lithium was observed at higher concentrations of GTP. The enzyme activity stimulated by GTP alone was unaltered by lithium ex vivo. In striatal membranes, lithium ex vivo decreased both dopamine-induced GTP activation of adenylate cyclase and GTP-stimulated adenylate cyclase activity at concentrations of GTP below 2 microM. No effects of lithium ex vivo were found in striatum at 2 microM GTP and above. In hippocampal membranes, lithium ex vivo did not influence either serotonin-induced GTP stimulation of the adenylate cyclase or GTP-stimulated enzyme activity at low levels of GTP. However, at 50 microM GTP, lithium ex vivo enhanced serotonin-stimulated enzyme activity. The present results suggest that lithium ex vivo decreases neurotransmitter activation of the cortical beta-adrenergic adenylate cyclase by influencing the mechanisms by which receptor agonists enhance the GTP stimulation of the adenylate cyclase. Furthermore, lithium ex vivo exerts a region-specific action on the brain adenylate cyclases, but in the brain regions studied, an effect of lithium on N-protein level might be of significance for the action of lithium ex vivo on neurotransmitter activation.

Adenylyl Cyclase Inhibitors↗
PubMed1992

Inositol trisphosphate, cyclic AMP, and cyclic GMP in rat brain regions after lithium and seizures.

The mechanism of action of lithium, the primary treatment for bipolar affective disorder, is unknown but may involve inhibition of second messenger production in the brain. Therefore, the concentrations of three second messengers, inositol 1,4,5 trisphosphate (Ins 1,4,5P3), cyclic adenosine monophosphate (AMP), and cyclic guanosine monophosphate (GMP), were measured in rat cerebral cortex and hippocampus after acute or chronic lithium administration, as well as after treatment with the cholinergic agonist pilocarpine alone or in combination with lithium at a dose that induces seizures only in lithium pretreated rats. Neither acute nor chronic lithium treatment altered the hippocampal or cortical concentration of Ins 1,4,5P3, cyclic AMP, or cyclic GMP. Pilocarpine administered alone increased Ins 1,4,5P3 in both regions, did not alter cyclic AMP, and slightly increased cyclic GMP in the cortex. Coadministration of lithium plus pilocarpine caused large increases in the concentrations of all three second messengers and the production of each of them was uniquely attenuated: lithium reduced pilocarpine-induced increases of Ins 1,4,5P3 in the cortex at 60 min; chronic lithium administration reduced stimulated cyclic AMP production in the hippocampus; and chronic lithium treatment impaired stimulated cyclic GMP production in both regions. In summary, chronic lithium treatment appeared only to reduce Ins 1,4,5P3 and cyclic AMP concentrations after a long period of stimulation whereas cyclic GMP production was reduced by chronic lithium administration after both short and long periods of stimulation. Thus cyclic GMP was most sensitive to lithium and lithium attenuation of second messenger formation may be most important in excessively activated pathways.

Animals↗
PubMed2003

Atomic resolution of lithium ions in LiCoO2.

LiCoO2 is the most common lithium storage material for lithium rechargeable batteries, used widely to power portable electronic devices such as laptop computers. Operation of lithium rechargeable batteries is dependent on reversible lithium insertion and extraction processes into and from the host materials of lithium storage. Ordering of lithium and vacancies has a profound effect on the physical properties of the host materials and the electrochemical performance of lithium batteries. However, probing lithium ions has been difficult when using traditional X-ray and neutron powder diffraction techniques due to lithium's relatively low scattering power when compared with those of oxygen and transition metals. In the work presented here, we have succeeded in simultaneously resolving columns of cobalt, oxygen and lithium atoms in layered LiCoO2 battery material, using experimental focal series of LiCoO2 images obtained at sub-ångstrom resolution in a mid-voltage transmission electron microscope. Lithium atoms are the smallest and lightest metal atoms, and scatter electrons only very weakly. We believe our observations of lithium to be the first by electron microscopy, and that they show promise for direct visualization of the ordering of lithium and vacancies in transition metal oxides.

Lithium↗
PubMed1990

Evaluation of the interaction of lithium and alprazolam.

A potential pharmacokinetic interaction between lithium and alprazolam was studied in 10 normal subjects. Pharmacokinetic parameters were determined from the following regimens: single-dose alprazolam, multiple-dose lithium, and multiple-dose alprazolam with lithium. Steady-state alprazolam clearance during multiple dosing with lithium was not different from that with the single dose of alprazolam. Lithium renal clearance decreased when it was coadministered with alprazolam (31.2 vs. 22.4 ml/minute, p less than 0.05). There was a small but significant increase in the steady-state area under the curve for lithium in the presence of alprazolam (10.3 vs. 11.1 mEq/hour/liter). The small increase in the serum lithium concentrations and decrease in lithium renal clearance was probably the result of lower urine flow rates (1.46 vs. 0.98 ml/minute, p less than 0.05) with the combination of the drugs. This is supported by a weak but significant linear relationship between urine flow rates and lithium renal clearance (N = 57, r = 0.353, p = 0.007). The percent of daily lithium dose recovered at steady-state from the 24-hour urine collection decreased significantly from 93.6% to 78.2% in the presence of alprazolam. This suggests that alprazolam may decrease lithium absorption. The results of this study do not support a definitive interaction of lithium and alprazolam and there is little clinical significance to the small rise in serum lithium concentrations.

Adult↗
PubMed2005

Suicide risk in patients treated with lithium.

CONTEXT: Prior observational studies suggest that treatment with lithium may be associated with reduced risk of suicide in bipolar disorder. However, these studies are biased toward patients with the most severe disorders, and the relation to sex and age has seldom been investigated. OBJECTIVE: To investigate whether treatment with lithium reduces the risk of suicide in a nationwide study. DESIGN: An observational cohort study with linkage of registers of all prescribed lithium and recorded suicides in Denmark during a period from January 1, 1995, to December 31, 1999. SETTING: All patients treated with lithium in Denmark, ie, within community psychiatry, private specialist practice settings, and general practice. PARTICIPANTS: A total of 13 186 patients who purchased at least 1 prescription of lithium and 1.2 million subjects from the general population. MAIN OUTCOME MEASURE: All suicides identified on the basis of death certificates completed by doctors at the time of death. RESULTS: Patients who purchased lithium had a higher rate of suicide than persons who did not purchase lithium. Purchasing lithium at least twice was associated with a 0.44 reduced rate of suicide (95% confidence interval, 0.28-0.70) compared with the rate when purchasing lithium only once. Further, the rate of suicide decreased with the number of prescriptions of lithium. There was no significant interaction between continued lithium treatment and sex and age regarding the suicide rate. CONCLUSION: In a nationwide study including all patients treated with lithium, it was found that continued lithium treatment was associated with reduced suicide risk regardless of sex and age.

Adult↗
PubMed2001

Lithium treatment inhibits protein kinase C translocation in rat brain cortex.

RATIONALE: Lithium, an effective psychotropic agent, affects membrane phospholipid metabolism, interferes with phosphoinositide signal transduction, and antagonizes the biological activity of calcium, all major factors of protein kinase C (PKC) activation. Consequently, lithium may interfere with cellular functions requiring PKC. Supporting this hypothesis, lithium was found to inhibit increased neurotransmitter release upon PKC activation and to prevent phorbol ester-mediated PKC translocation. OBJECTIVES: The present study was undertaken to determine whether the frontal cortex of rats treated with lithium exhibits altered PKC activity and translocation in response to phorbol ester, K+, or serotonin (5-HT) receptor stimulation and to determine whether specific PKC isozymes are disproportionately affected. METHODS: Rats were fed either a normal diet or one enriched with LiCl. In cerebrocortical slices or synaptosomes, cytosolic and membranous PKC activity and translocation in response to stimuli were determined after partial purification with anion exchange chromatography. RESULTS: In brain slices, lithium treatment inhibited phorbol 12-myristate, 13-acetate (PMA)-, 5-HT-, or K+-induced PKC translocation from cytosol to membrane without affecting basal membrane or cytosolic PKC activity. In synaptosomes, lithium also attenuated PMA- or K+-evoked translocation of PKC. Immunoblotting with isozyme-specific PKC antibodies revealed that chronic lithium treatment reduced basal cytosolic alphaPKC and deltaPKC but increased membrane-associated zetaPKC immunoreactivities. Stimulation with PMA, 5-HT or K+ elicited translocation of alpha, beta and gammaPKC isozymes and PMA induced translocation of delta and epsilonPKC isozymes. Stimulus-mediated translocation of PKC isozymes was attenuated in cortical tissue obtained from animals that received lithium for 6 weeks. In synaptosomes, PMA- or K+-induced PKC translocation was attenuated by in vitro lithium or chronic lithium treatment. Neither rubidium nor cesium affected PKC activities or PMA-induced translocation. Suppression of PMA-elicited translocation by lithium was partially antagonized by Ca2+. CONCLUSIONS: Lithium treatment reduces PKC translocation induced by either stimulation of a cell surface receptor or by direct enzyme stimulation with phorbol ester. This effect leads to reduced PKC-mediated phosphorylation of cellular proteins and may be responsible for the pharmacotherapeutic action of lithium.

Administration, Oral↗
PubMed2004

Prevention of MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) dopaminergic neurotoxicity in mice by chronic lithium: involvements of Bcl-2 and Bax.

Lithium has been reported to exert neuroprotective activity in several neuronal cell cultures and in vivo models against glutamate toxicity. Since this action was reported to be associated with alterations in the antiapoptotic Bcl-2 family proteins, the effect of chronic lithium diet on the ability of the parkinsonism neurotoxin, N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to deplete striatal dopamine in mice was determined. Mice were fed for with a diet containing 1.1, 2.2, 3.3, and 4.4 g/kg lithium chloride (LiCl) for 4 weeks, during which time serum levels of lithium were monitored. The 3.3 g/kg lithium diet gave serum level value very similar to what is observed in lithium therapy in man and the 4.4 g/kg well above this. At the end of this period the mice received 24 mg/kg MPTP i.p. once daily for 3 days. A direct relation was established with the increase in serum lithium and its ability to prevent MPTP induced depletion of striatal dopamine (DA) and its metabolites DPOAC and HVA. With the diet containing the highest lithium concentration there was an almost complete prevention of striatal dopamine depletion and the reduction in tyrosine hydroxylase activity and protein and it prevented the increase in dopamine turnover (DOPAC + HVA/DA) normally observed in MPTP treatment. Lithium did not interfere with the metabolism of MPTP, or with its brain uptake, since, the level of its monoamine oxidase (MAO) B derived metabolite, MPP+, in the striata of lithium and non-lithium treated mice were almost identical. Striatal Bcl-2 was significantly decreased, while Bax was increased in MPTP treated mice. Lithium treatment not only increased striatal Bcl-2 in control mice, but also prevented its reduction as induced by MPTP, and an opposing effect was seen with Bax. The neuroprotective action of lithium in this model of Parkinson's disease has been attributed to its antiapoptotic activity which among other factors includes induction of Bcl-2 and reduction of Bax.

Animals↗
PubMed2004

[Lithium].

The mode of action of the cation lithium is not well known. It is at present used as a topical drug in dermatology. Lithium inhibits many enzymes: Na/K ATPase, adenylcyclase, enzymes of the prostaglandines E1 synthesis, inositol-1-phosphatase. It is active on neutrophils et T lymphocytes, explaining in part its anti-inflammatory activity. It has a dose-dependent action on levures. It has possibly a direct inhibitory activity on DNA synthesis of herpes viruses. Lithium has a good local safety. Percutaneous penetration is weak and plasma concentrations are very much lower than that observed after oral intake. Lithium has been studied in seborrhoeic dermatitis. Its efficacy was primarily observed in psychotic patients. An assay with oral lithium did not confirmed the first observations. Topical lithium was found more efficient. Topical lithium succinate associated with zinc sulfate and lithium gluconate had a greater efficacy than placebo. Comparison with topical ketoconazole showed a non inferiority of lithium gluconate. Oral lithium also showed a reduction of symptoms' duration of herpes simplex. Cutaneous side-effects of oral lithium are frequent and numerous. Some of them may be explained by a lithium pharmacological cell activity (such as psoriasis). Teratogenicity is observed in mice and rats. Drug interactions are not expected after topical application. Irritants side effects are mainly observed after topical application; they are moderate and transitory. Lithium gluconate treatment of seborrhoeic dermatitis is a bid application during at least 8 weeks. It may be used in renal insufficiency. It is not recommended in the first trimester of pregnancy.

Administration, Oral↗
PubMed2000

A double-blind, placebo-controlled study of the effects of lithium on cognition in healthy subjects: mild and selective effects on learning.

BACKGROUND: Several studies have shown cognitive impairment in short-term memory, long-term memory and psychomotor speed in bipolar patients taking lithium. The aim of the study was to look at the effect of lithium in normal subjects (N=30) taking lithium for 3 weeks. A comprehensive battery was used to assess attention and memory. METHODS: Subjects were randomized to double-blind treatment with either lithium (N=15) or placebo (N=15) for a 3-week period. Thirteen participants in the lithium group and 15 in the placebo group completed the study. The lithium and placebo were administered twice daily in doses varying from 1050 to 1950 mg (mean=1569 mg). The initial daily dose was calculated according to the Pepin formula to achieve a blood serum lithium level of about 0.8 mmol/l. Cognitive performance (attention, memory) was assessed in each subjects during three periods, i.e. at baseline, after 3 weeks of lithium or placebo, and 2 weeks after discontinuation of study medication. RESULTS: In short-term memory tasks, the performance of subjects in the lithium group was worst 3 weeks after lithium treatment compared to 2 weeks after discontinuation. In long-term memory, a significantly higher number of words was recalled by the placebo group but not the lithium group. CONCLUSIONS: Lithium may have an effect on learning when long-term explicit memory test are administered repeatedly. It means that the practice effect when a subject performs the same task several times is less in the lithium-treated group than in the placebo group. This practice effect is related to the learning of a task.

Adolescent↗
PubMed1998

Lithium and psychosis revisited.

1. Using differential response to medications may help in resolving the central problem of heterogeneity of the psychoses, 2. A distinct subgroup of patients with a lithium responsive, nonaffective psychosis has been shown to have their core psychotic (nonaffective) symptoms respond to lithium alone. 3. The family histories of patients with lithium responsive, nonaffective psychoses suggests that there is less genetic loading for this subgroup of patients. 4. Research on the prodromal adjustment of lithium responsive, nonaffective psychosis patients has not been reported. 5. Lithium responsive patients showed significantly fewer negative symptoms than did those patients with a nonaffective psychosis who did not respond to lithium. 6. Patients with lithium responsive, nonaffective psychoses showed more extreme in vitro lithium ratios in the red blood cells and significantly less of all types of phospholipid methylation. 7. Patients with lithium responsive, nonaffective psychoses showed significantly greater reduction in symptoms during a physostigmine challenge test, but results from apomorphine challenge tests could not be replicated. 8. Aside from differential response to lithium, research on difference in treatment response and outcome for this group has not been reported. 9. Preliminary evidence may suggest that lithium responsive, nonaffective psychosis is a phenocopy of other psychotic disorders that is not associated with ventriculomegaly but is associated with stimulant abuse. 10. Lithium's effects on acetylcholine as well as effects on dopamine and serotonin may explain its efficacy with this subgroup of patients. 11. This review supports the existence of a distinct subgroup of patients with nonaffective psychoses who may have a separate disorder, but further research is necessary. 12. Lithium responsive nonaffective psychosis appears to be a separate, distinct psychotic phenocopy.

Antipsychotic Agents↗