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PubMed2005

Lrp5-independent activation of Wnt signaling by lithium chloride increases bone formation and bone mass in mice.

One of the well characterized cell biologic actions of lithium is the inhibition of glycogen synthase kinase-3beta and the consequent activation of canonical Wnt signaling. Because deficient Wnt signaling has been implicated in disorders of reduced bone mass, we tested whether lithium could improve bone mass in mice. We gavage-fed lithium chloride to 8-week-old mice from three different strains (Lrp5(-/-), SAMP6, and C57BL/6) and assessed the effect on bone metabolism after 4 weeks of therapy. Lrp5(-/-) mice lack the Wnt coreceptor low-density lipoprotein receptor-related protein 5 and have markedly reduced bone mass. Lithium, which is predicted to act downstream of this receptor, restored bone metabolism and bone mass to near wild-type levels in these mice. SAMP6 mice have accelerated osteoporosis due to inadequate osteoblast renewal. Lithium significantly improved bone mass in these mice and in wild-type C57BL/6 mice. We found that lithium activated canonical Wnt signaling in cultured calvarial osteoblasts from Lrp5(-/-) mice ex vivo and that lithium-treated mice had increased expression of Wnt-responsive genes in their bone marrow cells in vivo. These data lead us to conclude that lithium enhances bone formation and improves bone mass in mice and that it may do so via activation of the canonical Wnt pathway. Lithium has been used safely and effectively for over half a century in the treatment of bipolar illness. Prospective studies in patients receiving lithium should determine whether it also improves bone mass in humans.

Analysis of Variance↗
PubMed1985

Lithium induces corticotropin secretion and desensitization in cultured anterior pituitary cells.

Lithium stimulated corticotropin (ACTH) secretion by mouse pituitary tumor cells (AtT-20/D16-16) and by normal rat anterior pituitary cells in primary culture. Effects were observed at less than 2 mM LiCl. ACTH secretion was comparable in magnitude to that induced by other secretagogues, was calcium dependent, and was inhibited by somatostatin. Lithium also induced changes in [3H]inositide metabolism; these changes accompanied and were correlated with changes in ACTH secretion. The most prominent and reliable effect was to increase [3H]inositol monophosphate. Other secretagogues had no effect on [3H]inositides in the presence or absence of lithium. Pretreatment with lithium for 3 hr desensitized the cells to the effects of subsequent exposure to lithium. The cells were not desensitized to lithium by pretreatment with other secretagogues, nor were they desensitized by lithium to the effects of corticotropin-releasing factor, high potassium, or forskolin. However, pretreatment with lithium did desensitize the cells to stimulation by phorbol esters. The interaction between lithium and phorbol esters suggests the involvement of inositide metabolism and protein kinase C in the regulation of ACTH secretion and possibly of other hormones or neurotransmitters. It also suggests new avenues of research into the basis of lithium's psychopharmacological effects.

Adrenocorticotropic Hormone↗
PubMed2001

Phosphoglucomutase is an in vivo lithium target in yeast.

Lithium is a drug frequently used in the treatment of manic depressive disorder. We have observed that the yeast Saccharomyces cerevisiae is very sensitive to lithium when growing in galactose medium. In this work we show that lithium inhibits with high affinity yeast (IC50 approximately 0.2 mm) and human (IC50 approximately 1.5 mm) phosphoglucomutase, the enzyme that catalyzes the reversible conversion of glucose 1-phosphate to glucose 6-phosphate. Lithium inhibits the rate of fermentation when yeast are grown in galactose and induces accumulation of glucose 1-phosphate and galactose 1-phosphate. Accumulation of these metabolites was also observed when a strain deleted of the two isoforms of phosphoglucomutase was incubated in galactose medium. In glucose-grown cells lithium reduces the steady state levels of UDP-glucose, resulting in a defect on trehalose and glycogen biosynthesis. Lithium acts as a competitive inhibitor of yeast phosphoglucomutase activity by competing with magnesium, a cofactor of the enzyme. High magnesium concentrations revert lithium inhibition of growth and phosphoglucomutase activity. Lithium stress causes an increase of the phosphoglucomutase activity due to an induction of transcription of the PGM2 gene, and its overexpression confers lithium tolerance in galactose medium. These results show that phosphoglucomutase is an important in vivo lithium target.

Blotting, Northern↗
PubMed2003

Effect of an acute oral lithium intake on urinary Aquaporin-2 in healthy humans with and without simultaneous stimulation with hypertonic saline infusion.

OBJECTIVE: Animal experiments have shown that lithium interferes with the formation of Aquaporin-2 in the distal renal tubuli. The effect of lithium on formation of renal water channels has not been studied in healthy humans. The aim of this study was to test the hypotheses that a single oral dose of lithium will reduce the formation of water channels both with and without stimulation with hypertonic saline infusion, and that this effect can be detected by measurement of urinary excretion of Aquaporin-2 (u-AQP2). METHODS: In healthy subjects, Study 1 (n = 11) and Study 2 (n = 12), urine was collected in 6 and 7 periods between 08.00 and 14.00, respectively, and blood samples were drawn at 30- to 60-min intervals. The study medication was given at 09.00; u-AQP2 was determined by radioimmunoassay. RESULTS: In Study 1 neither u-AQP2 nor urinary output were significantly changed by lithium. In Study 2, u-AQP2 was increased by hypertonic saline infusion in parallel with an increase in arginine vasopressin. At the end of the study, u-AQP2 was increased by 30% with placebo but only by 13% with the 600 mg lithium dose, and urinary output was significantly higher after 600 mg lithium than after placebo and 300 mg lithium. CONCLUSIONS: U-AQP2 was not significantly changed after a single oral dose of lithium. The antidiuretic response to hypertonic saline infusion was reduced when lithium was given. It is suggested that lithium increases urinary output by inhibiting trafficking of renal water channels in healthy humans.

Administration, Oral↗
PubMed2004

Glycogen synthase kinase 3beta as a likely target for the action of lithium on circadian clocks.

Although lithium is one of the most commonly used drugs in the prophylaxis and treatment of bipolar disorder, the mechanisms underlying its therapeutic action are still unclear. Together with its mood-stabilizing effects, lithium is also known to influence the circadian clocks of several organisms including man. Circadian rhythms are altered in patients with bipolar disorder, and it is believed that these rhythms may play an important role in disease mechanisms. It is therefore possible that some of the therapeutic actions of lithium may be related to its effect on circadian clocks. Identifying the targets for lithium's action on circadian clocks would therefore be important both for understanding the mechanisms of its therapeutic effect and also in further understanding disease mechanisms in bipolar disorders. Using Drosophila melanogaster as a model system, we show that long-term administration of lithium results in lengthening of the free-running period (tau) of circadian locomotor activity rhythm of flies in constant darkness (DD). This effect occurs at concentrations similar to the plasma levels of lithium used in the treatment of bipolar disorder. The lithium-treated flies also show reduced activity of one of the previously reported targets of lithium action, Glycogen Synthase Kinase 3beta (GSK 3beta). GSK 3beta has been shown to be involved in the regulation of circadian clocks as the down regulation of this protein results in an elongation of tau. The tau elongation resembles the effect seen with lithium administration in a number of organisms including man, and taken together with the earlier observations our results suggest that lithium inhibits the activity of GSK 3beta to produce its effect on circadian clocks.

Animals↗
PubMed1995

5-HT efflux from rat hippocampus in vivo produced by 4-aminopyridine is increased by chronic lithium administration.

Effects of lithium on central 5-HT function have been shown using electrophysiological, behavioural and neurochemical approaches. Chronic lithium administration, for example, enhances both electrophysiological and behavioural responses mediated by postsynaptic 5-HT1A receptors as well as increasing potassium-evoked and electrically evoked release of 5-HT from the hippocampus in in vitro slices and in vivo. Our studies have shown that potassium-channel blocking drugs increase 5-HT release in vivo, and others have shown that lithium suppresses potassium currents in some cell types. We therefore investigated in the rat the effect of short-term (3 days) and long-term (21 days) lithium on 5-HT release evoked by potassium-channel blockade, using in vivo microdialysis. Long-term lithium treatment enhanced 5-HT efflux in rat hippocampus produced by 4-aminopyridine (4-AP) perfused in microdialysis fluid by as much as 100% within 40 min, compared with non-lithium-treated control rats. Short-term lithium treatment did not enhance 4-AP-induced 5-HT efflux. The effect of local tetraethylammonium chloride (TEA) on hippocampal 5-HT release was unaltered by long-term lithium treatment. In addition, neither the effect of local perfusion with 4-AP on efflux of striatal 5-HT, or dopamine in nucleus accumbens, was altered by chronic lithium treatment. These results show that long-term lithium treatment enhances 4-AP-stimulated efflux of 5-HT in the hippocampus, but not in the striatum, nor dopamine output in the nucleus accumbens.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1988

Lithium and renal function in relation to concomitant theory.

Two hundred and fourteen patients (99 men, 115 women, age 21-87 years) were treated with lithium during the period 1963-1984 at the Psychiatric Unit, Danderyd Hospital. The patients were diagnosed as having bipolar depression (97), unipolar depression (54), cycloid psychosis (21), schizoaffective psychosis and depressive neurosis (42). Sixty patients were treated with lithium salt only, 73 patients received neuroleptic drugs in addition to lithium and 51 antidepressant drugs. Sixteen patients were treated with a combination of neuroleptic drugs, antidepressant drugs and lithium. Fourteen patients were treated with lithium and benzodiazepines. The aim of this retrospective lithium study was to examine the renal function in these different treatment groups. The results show that patients treated with a lithium salt and neuroleptic drugs have significantly lower urinary osmolality than those treated with a lithium salt only. Also tricyclic antidepressants in combination with a lithium salt appear to have an influence on renal function. The duration of concomitant therapy seems to be of importance for the effect on renal function. Eleven patients with the lowest osmolality values were investigated at the Renal Unit, Danderyd Hospital, but in no case was it necessary to withdraw the lithium treatment.

Adult↗
PubMed2000

Prediction of lithium response using. m-chlorophenylpiperazine challenge test: A preliminary finding.

It is important to be able to predict a response to lithium before lithium administration because it usually takes 2 or 3 weeks for lithium to manifest its effect sufficiently. We hypothesized that lithium responders have a high post-synaptic serotonergic receptor function, whereas non-responders have low one. This is because it has been suggested that lithium's primary actions on the serotonergic neuron may be presynaptic and several reports have shown that lithium enhances serotonin synthesis and secretion at the presynaptic serotonergic neuron. As a preliminary study, we investigated the relationship between several responses to meta-chlorophenylpiperazine (a serotonergic agonist) reflecting the serotonergic receptor function and the clinical lithium response of 10 patients. No significant relationship between hormone responses and improvement ratios was found. However, there were significant relationships found between 'anger' during the challenge test and the improvement ratio and between 'tension' during the test and the improvement ratio. Thus, it seems that the hormone response to a serotonergic agonist is not useful for predicting lithium response. However, subjective responses such as anger and tension to a serotonergic agonist are possible candidates for predicting lithium response. In any case, further studies with larger numbers of participants are required to investigate whether subjective responses to a serotonergic agonist are useful for predicting lithium response.

Adult↗
PubMed2006

Effects of lamotrigine and lithium on body weight during maintenance treatment of bipolar I disorder.

OBJECTIVE: The effect of lamotrigine maintenance therapy on body weight was assessed retrospectively in analyses of data from two double-blind, placebo- and lithium-controlled, 18-month studies in patients with bipolar I disorder (n = 227 for lamotrigine, 190 for placebo, 166 for lithium). METHODS: Endpoints included mean change in weight, the percentage of patients with > or = 7% change (increase, decrease, fluctuation) in weight, and the percentage of patients with weight-related adverse events during double-blind treatment. RESULTS: Mean weight remained stable during maintenance therapy with lamotrigine. In a mixed-model repeated-measures analysis, mean changes in weight (kg) at week 52 were -1.2 with lamotrigine, +0.2 with placebo, and +2.2 with lithium [estimated difference (95% CI) lamotrigine minus placebo = -1.3 (-3.6, 0.9), p = 0.237; lithium minus placebo = +2.0 (-0.3, 4.4), p = 0.094; lithium minus lamotrigine = +3.4 (1.4, 5.4), p < 0.001]. Analyses were truncated at week 52 because of the high incidence of missing data at later time points. The percentages of patients with a >/=7% weight gain, during randomized treatment, were 10.9%, 7.6% and 11.8% for the lamotrigine, placebo, and lithium groups, respectively. The percentages of patients with a > or = 7% weight loss, during randomized treatment, were 12.1%, 11.5%, and 5.1% for the lamotrigine, placebo, and lithium groups, respectively. The percentage of patients with a > or = 7% weight loss did not significantly differ between lamotrigine and placebo but was significantly higher with lamotrigine than lithium. The incidences of > or = 7% weight changes and of weight changes reported as adverse events were comparable between active treatments and placebo. CONCLUSION: Lamotrigine was associated with stable body weight during 1 year of treatment and was comparable to placebo in mean weight change, incidence of clinically significant weight change, and incidence of weight changes reported as adverse events in patients with bipolar disorder. Lithium was associated with weight gain, but the magnitude of lithium-associated weight gain was lower in the current analysis than in previous studies.

Adult↗
PubMed2006

Decreased risk of suicides and attempts during long-term lithium treatment: a meta-analytic review.

OBJECTIVES: To update and extend comparisons of rates of suicides and suicide attempts among patients with major affective disorders with versus without long-term lithium treatment. METHODS: Broad searching yielded 45 studies providing rates of suicidal acts during lithium treatment, including 34 also providing rates without lithium treatment. We scored study quality, tested between-study variance, and examined suicidal rates on versus off lithium by meta-analytic methods to determine risk ratios (RRs) and 95% confidence intervals (CI). RESULTS: In 31 studies suitable for meta-analysis, involving a total of 85,229 person-years of risk-exposure, the overall risk of suicides and attempts was five times less among lithium-treated subjects than among those not treated with lithium (RR = 4.91, 95% CI 3.82-6.31, p < 0.0001). Similar effects were found with other meta-analytic methods, as well as for completed versus attempted suicide, and for bipolar versus major mood disorder patients. Studies with higher quality ratings, including randomized, controlled trials, involved shorter exposures with somewhat lesser lithium superiority. Omitting one very large study or those involving lithium-discontinuation had little effect on the results. The incidence-ratio of attempts-to-suicides increased 2.5 times with lithium-treatment, indicating reduced lethality of suicidal acts. There was no indication of bias toward reporting positive findings, nor were outcomes significantly influenced by publication-year or study size. CONCLUSIONS: Risks of completed and attempted suicide were consistently lower, by approximately 80%, during treatment of bipolar and other major affective disorder patients with lithium for an average of 18 months. These benefits were sustained in randomized as well as open clinical trials.

Bipolar Disorder↗
PubMed1992

Lithium effects on inositol phospholipids and inositol phosphates: evaluation of an in vivo model for assessing polyphosphoinositide turnover in brain.

Administration of lithium chloride to rats injected intracerebrally with [3H]inositol led to time- and dose-dependent increases in levels of labeled inositol monophosphates in brain. Quantitative analysis of the inositol phosphates by ion chromatography revealed 37- and 20-fold increases in the mass of myo-inositol 1-phosphate and 4-phosphate, respectively, at 4 h intraperitoneal after injections of 6 mEq/kg of lithium chloride. Albeit to a much lesser extent, lithium administration also resulted in an increase in the level of myo-inositol, 1,4-bisphosphate in brain. The lithium-induced increase in content of labeled inositol monophosphates was marked by a concomitant decrease in content of labeled inositol, and after injections of high doses of lithium, e.g., 10 mEq/kg, this was followed by a general decrease in labeling of the inositol phospholipids. In general, animals injected with [3H]inositol but not lithium did not reveal obvious differences in labeling of inositol monophosphates on stimulation by mecamylamine or pilocarpine. However, when animals were injected with [3H]inositol and then lithium, there were large increases in the levels of labeled inositol monophosphates on administration of these compounds. Administration of atropine to the lithium-treated mice led to a partial reduction in the amount of labeled inositol monophosphates accumulated due to the administration of lithium alone. Furthermore, atropine was able to block the pilocarpine-induced increase in level of labeled inositol monophosphates. These results demonstrate the suitable use of the radiotracer technique together with lithium administration for assessing the effects of drugs and receptor agonists on the signaling system involving polyphosphoinositide turnover in brain.

Animals↗
PubMed1999

The effect of lithium administration in animal models of depression: a short review.

The aim of this short review was to collate the data involving the effects of lithium alone, or in combination, with antidepressant drugs in several animal models of depression. It has been shown that lithium administration reduced immobility in the mouse forced swimming test when given 30 min, but not 45 min, before testing. Further studies indicated that this activity was probably a result of an activity on serotonin (5-HT) 1A and 1B receptor subtypes. Lithium treatment has been shown to reverse helpless behaviour in the learned helplessness model of depression after chronic treatment (30 days), where lithium was administered in the drinking water. Further studies showed that acute (5 days) administration of lithium failed to reverse behavioural deficits. In the olfactory bulbectomised rat model of depression, several immunological and enzymatic functions have been shown to be altered and these changes are regularised by antidepressant treatment as well as lithium administration for 15 days. Hypokinesia (reduced locomotor activity) is a phenomenon observed following immobilisation stress in rats. This behavioural deficit was attenuated by lithium together with a wide range of antidepressant drugs used in the treatment of unipolar depression at non-stimulant doses. In addition, a single administration of lithium slightly inhibited midbrain raphe lesion-induced muricidal behaviour (25%); however, repeated treatment (5 days) significantly attenuated this behavioural deficit. Lithium treatment has also been shown to reverse behavioural and biochemical deficits induced by reserpine together with those induced by acute administration of single intracerebroventricular (i.c.v.) dose of the Na, K-ATPase-inhibiting compound, ouabain. Long-term studies of lithium augmentation have not been performed, so that no clear recommendations for the duration of this therapy can be made. The points raised in this short review endorse the commencement of such studies.

Animals↗
PubMed1978

The pharmacokinetics of lithium in the brain, cerebrospinal fluid and serum of the rat.

1 Addition of lithium carbonate (55 mmol/kg dry wt.) to the diet of rats for 4 days resulted in ratios between lithium in the brain and serum and between the cerebrospinal fluid (CSF) and serum of approx. 1 and 0.4, respectively. The relationships between the concentrations were linear. 2 After single intraperitoneal injections of lithium chloride (5 mmol/kg body wt.) the concentration of lithium in the CSF was greater than that of the brain for 2 h. 3 Repeated subcutaneous injections of lithium chloride (0.9 mmol/kg body wt.) resulted in steady state ratios corresponding to those observed when lithium was given in the diet. The rate of elimination from the CSF was intermediate between that of the serum and cerebral tissue until a new equilibrium was reached after approx. 24 h. At that time the ratios between lithium in the brain and serum, and in the CSF and serum were increased to approx. 5 and 0.8, respectively. 4 These results are consistent with passive transfer kinetics of lithium in the CSF and elimination of lithium from the cerebral tissue via the CSF. 5 The results may explain some of the phenomena observed in patients during intoxication with lithium.

Animals↗
PubMed1993

Characterization of the effects of lithium on phosphatidylinositol (PI) cycle activity in human muscarinic m1 receptor-transfected CHO cells.

1. The effects of lithium on [3H]-inositol and [3H]-cytidine incorporation into [3H]-inositol monophosphates ([3H]-InsP1) and [3H]-cytidine monophosphorylphosphatidate ([3H]-CMP-PA), respectively, and inositol 1,4,5-trisphosphate (InsP3) and inositol 1,3,4,5-tetrakisphosphate (InsP4) mass were studied in carbachol-stimulated human m1 muscarinic receptor-transfected Chinese hamster ovary cells (m1 CHO cells). 2. Lithium alone (10 mM) had no appreciable effects on any of the four parameters measured; it was only in carbachol-stimulated cells that the effects of lithium became apparent. 3. In the presence of carbachol (1 mM), lithium (10 mM) caused a relatively rapid (within 5 min) accumulation of [3H]-InsP1 and [3H]-CMP-PA which continued up to about 20-30 min, after which accumulation slowed down. On the other hand, the elevation in InsP3 and InsP4 levels produced by carbachol was not altered by lithium in the short-term and only at later times (> 20-30 min) was the response attenuated, with InsP3 and InsP4 levels approaching basal. 4. The effects of lithium on carbachol-stimulated [3H]-InsP1 and [3H]-CMP-PA accumulation and the attenuation of the carbachol-induced elevation of InsP3 and InsP4 were all dose-dependent, with EC50s in the region of 1 mM. 5. The lithium-induced effects on [3H]-CMP-PA and InsP3 and InsP4 in carbachol-stimulated cells could be reversed, in a dose-dependent manner, by preincubation with exogenous myo-inositol (EC50 = 2-3 mM) but not by the inactive analogue scyllo-inositol, indicating that these effects occur as a consequence of depletion of inositol. 6. The temporal effects of lithium are consistent with lithium inhibiting inositol monophosphatase,causing accumulation of InsP1, resulting in lower free inositol levels. This leads to accumulation of CMP-PA and reduced PI synthesis which, once agonist-linked membrane inositol phospholipids are depleted, produces attenuated InsP3 and InsP4 responses.7. These results in ml CHO cells support the hypothesis that lithium affects the PI cycle cell signalling pathway by depletion of inositol due to inhibition of inositol monophosphatase.

Animals↗
PubMed1995

Absence of a losartan interaction with renal lithium excretion in the rat.

1. The interaction of losartan, a non-peptide specific AT1 receptor antagonist with the renal handling of lithium was analysed in conscious normotensive Wistar rats and compared with the known increase in renal tubular lithium reabsorption induced by the non-steroidal anti-inflammatory drug, indomethacin. 2. The rats were treated for five days with losartan (10 mg kg-1 day-1, orally), indomethacin (2.5 mg kg-1 day-1, intramuscularly) or their solvents. Lithium chloride (16.7 mg kg-1, i.p.) was given as a single dose on the fifth day; renal functions were then measured. 3. Indomethacin, in the absence of any effect on creatinine clearance, increased renal fractional lithium reabsorption and led to an increase in plasma lithium levels. 4. Losartan did not modify renal lithium handling and its plasma level. No change was observed in renal lithium clearance, the quantity of filtered lithium or the fractional reabsorption of the metal. As expected, losartan had no effect on systolic blood pressure in normotensive rats. 5. In conclusion, our results indicate that losartan, when given orally in the rat at a dose of 10 mg kg-1 day-1 over five days, does not modify renal lithium handling. They suggest that blockade of the angiotensin II receptors does not interfere with renal lithium reabsorption, which occurs mainly at a proximal tubular site.

Angiotensin I↗
PubMed1981

Functional and structural rat kidney changes caused by peroral or parenteral lithium treatment.

Renal functional and structural changes were studied in rats treated with lithium for 5 months. The lithium was administered in two different ways: in the food or as a daily intraperitoneal injection. In the perorally treated rats serum lithium was relatively constant during the day. In the injected rats serum lithium reached a high peak value just after the injection followed by a decrease to very low values. In all rats an increased water consumption and a reduced renal concentration ability were seen during lithium treatment. Light microscopy showed focal degenerative changes in the distal convoluted tubule and collecting ducts. These changes comprised nuclear and cellular polymorphism and tubular dilatation. The functional as well as the structural changes were most pronounced in the rats treated with peroral lithium, and a correlation between the functional and morphological changes was present. It is concluded that lithium is more harmful to the kidney when the administrations give a relatively constant serum lithium level, such as in peroral administration, than when administration causes great variations, including peak values and very low minimum levels in serum lithium. The reason for this might be that a number of regenerative processes occur only in periods with low lithium concentrations.

Administration, Oral↗
PubMed1985

Lithium effects on ophthalmological-electrophysiological parameters in young healthy volunteers.

The effects of lithium on the visual system in man have been tested. Ten healthy volunteers followed a 10-day lithium regimen. Lithium plasma levels in the range of 0.6-0.8 mmol/l were obtained. Clinically used ophthalmological-electrophysiological tests were performed. Most of the tests showed no significant change during the lithium treatment. The lithium regimen resulted in a strong reduction of the slow phase. Also the "Arden-ratio", measured by electrooculogram (EOG), was influenced by lithium. The "Arden-ratio" reflects the corneo-fundal potential in retinal illumination and dark adaptation and is influenced by the state of adaptation. All the demonstrated effects were fully reversible at the end of lithium administration. Possible mechanisms of the action of lithium are discussed (for example Ca2+-fluxes, c-AMP, cGMP). These lithium-induced effects on the visual system in man may give some hint of the individual responsiveness to lithium.

Adult↗
PubMed1988

Prospective studies on a lithium cohort. 1. General features.

Since 1979, patients started on long-term lithium treatment at the Psychiatric Hospital in Risskov have been followed systematically with recording of clinical and laboratory variables before the start of treatment, after 6 and 12 months of treatment, and thereafter at yearly intervals. By June 1987, 480 examinations had been carried out before the start of lithium treatment, 236 after treatment for 6 months, and decreasing numbers up to 7 years of lithium treatment. The total lithium exposure time was 548 years. The mean lithium dose was 23.2 mmol/d and the mean serum lithium concentration 0.68 mmol/l. These values are about 30% lower than the corresponding values in patients given lithium treatment prior to 1979. About one half of the patients who had gone through the pre-lithium examinations did not reach the 6-month examination. This was because they did not start lithium, or because they stopped it again before 6 months of treatment or before they had reached that point. Thereafter there was a drop-out rate of about 25% per year during the first 2 years of lithium treatment and about 10% per year after 4-5 years of treatment. More men than women left the cohort.

Adult↗