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PubMed2001

[Lithium treatment and hyperparathyroidism].

BACKGROUND: Lithium treatment, which is extensively used in bipolar affective disorders, may give rise to hypercalcaemia and sometimes to irreversible hyperparathyroidism. MATERIAL AND METHODS: We present a patient who developed hyperparathyroidism following long-term treatment with lithium. RESULTS: After 15 years on lithium the patient was diagnosed with hypercalcaemia; at the same time the patient stopped her lithium medication. Two years later she developed depression with psychotic symptoms and was given electroconvulsive treatment. Measurements of serum calcium and parathormon showed that she had developed hyperparathyroidism. Neck exploration was performed, and two parathyroid adenomas (weight 650 mg and 880 mg), which had been detected by scintigraphy, were removed. Lithium treatment was restarted. One year later she was normocalcaemic and her mood was normal. INTERPRETATION: In lithium-induced hyperparamyroidism, lithium should be replaced with other mood stabilizers, preferably an antiepilepticum. If cessation of lithium therapy does not lead to normocalcaemia, parathyroidectomy is indicated.

Antidepressive Agents↗
PubMed2001

[Mortality in patients with affective disorder who commenced treatment with lithium. A 16-year follow-up].

INTRODUCTION: Lithium treatment is claimed to reduce mortality in patients with affective disorder, but the evidence is conflicting. The aim of this study was to estimate mortality rates from a cohort of such patients, who commenced treatment with lithium, over an observation period of 16 years. MATERIAL AND METHODS: The mortality rates of affectively ill patients, who commenced lithium treatment, were compared with the mortality rates in the general Danish population, standardised for age, sex, and a time to death from all causes, suicide, and cardiovascular death. Comparison of the time from a two-year follow-up to death from any cause between patients compliant and non-compliant with two years of lithium treatment was performed with the Cox regression analysis. RESULTS: Forty of the 133 patients who participated in the study died during the 16-year observational period; 11 from suicide. Mortality in the patients was twice that of the background population. This statistically significantly higher mortality was predominantly caused by the number of suicides, whereas mortality from all other causes was similar to the background population. Thirty-two patients died after the first two years of observation and were included in the analysis of association between death and two years of compliance with lithium. Suicide occurred more frequently in the lithium non-compliant patients than in the lithium compliant patients. DISCUSSION: Mortality, particularly death from suicide, was significantly increased in unselected affective disorder patients, who commenced lithium treatment, as compared with the background population.

Adolescent↗
PubMed2003

[Lithium intoxication in a patient with severe motor and intellectual disabilities].

A severaly retarded 30-year-old woman developed acute lithium intoxication. Since the age of 22, she had been treated with neuroleptics for her aggressive behavior. At 30 years of age, lithium carbonate was added to arrest self-injurious behavior, at an initial dosage of 300 mg/day and a maintenance dosage of 900 mg/day. She subsequently developed anorexia and weight loss, and was admitted to our hospital. After 7 months of lithium therapy, she suddenly had a high fever (38.3 degrees C), diabetes inspidus, severe hypernatremia, and became akinetic and mute. Under the suspicion of lithium intoxication, all medication was discontinued, and mannitol to increase renal lithium clearance. She was given gradually improved over a month, but remained hypothyroid. This case shows the importance of interaction of lithium carbonate and other drugs which may cause lithium intoxication. In patients with severe intellectual disabilities who are unable to complain their symptoms, lithium therapy requires particularly close attention to signs of early toxicity.

Adult↗
PubMed2003

Partial involvement of c-jun protooncogene in growth enhancing and cytotoxic effects of lithium in vitro.

The AP-1 transcription factor is comprised of homo- and heterodimers of the Fos and Jun families of proteins. Literature reports indicate that AP-1 is activated in lithium treated mammalian cells suggesting a role in lithium induced growth stimulation and apoptosis. In these studies, an antisense c-jun plasmid blocked the stimulation of HL-60 cell growth by lithium. Furthermore, antisense c-jun caused a 60% reduction in cell viability at 48 hr post-transfection but did not influence DNA fragmentation in the presence of lithium. The levels of c-jun mRNA, as determined by RT-PCR, were not affected by lithium treatment. Nevertheless, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) blocked the induction of apoptosis by lithium suggesting the involvement of the protein kinase C (PKC) signaling pathway. In RAJI cells, antisense c-jun mimicked lithium by inhibiting cell proliferation with only a marginal loss in cell viability. This study therefore suggests that PKC is involved in the effects of lithium on cells in culture and provides evidence for differential effects of antisense c-jun on hemotopoietic lineages.

Cell Division↗
PubMed2004

[Acute poisoning with lithium carbonate in a young woman--case report].

In the clinical practice there are three types of lithium intoxication: acute poisoning in patients not previously treated with lithium, acute on chronic poisoning, i.e., an acute overdose in patients who are under lithium treatment and chronic poisoning that occurs in patients who are under lithium treatment. Threats and the clinical management in these types are different. The paper describes a case of a young woman acutely intoxicated with lithium carbonate, never treated lithium before. Plasma concentration of lithium, 15 hours after ingestion of 9.75 g lithium carbonate, was 2.56 mmol/L. Only minor clinical symptoms were observed. Calculated elimination half-life was 15-26.8 hours.

Adult↗
PubMedDate not supplied

The influence of lithium on biokinetics and biodistribution of 65Zn under different dietary protein regimens in rats.

The present study was designed to evaluate the effect of lithium on the biological half-lives of 65Zn in the rat liver and whole body and also its biodistribution under different dietary protein regimens. To carry out these investigations, each rat after three weeks of different treatments was injected with 1.85 MBq of 65Zn, intraperitoneally (ip) and its radioactivity was recorded in liver as well as in whole body by using gamma ray spectrometer. The radionuclide 65Zn showed two kinetic components indicating its biological half-life: Tb1 the initial fast component and the Tb2 or slow component. Protein deficiency led to a significant elevation of both components in the whole body but not in the liver when compared to the control group. High protein (HP) diet in rats resulted in marked reduction in both components in the liver but not in the whole body. Lithium treatment alone to normal rats caused a significant reduction in the Tb2 but not in the Tb1 component in the whole body as well as in the liver. The administration of lithium normalized the observed increase in both components in the whole body of protein deficient rats. On the contrary, in rats fed with low protein (LP) diet after lithium treatment the Tb(2) component was significantly reduced in the liver. Lithium treatment to HP fed rats, showed a significant decrease in both components in the liver when compared to normal rats: however this decrease was less pronounced in comparison to the HP group that had not been given lithium. Furthermore, one day prior to the end of the treatment period, the rats were injected ip with a tracer dose of 0.37 MBq 65Zn and 24 h later, various organs were excised for 65Zn biodistribution measurements in vitro. Under different dietary protein regimens as well as after administration of lithium the percent uptake values of 65Zn varied in various organs viz: the brain, liver, kidney, small intestine and large intestine as well as in the blood. In conclusion, different protein dietary conditions on co-administration with lithium in the rats seemed to have a dominant role for the retention of 65Zn in the liver the whole body and in other organs.

Administration, Oral↗
PubMed2006

The effect of lithium on the adrenoceptor-mediated second messenger system in the rat brain.

OBJECTIVE: Lithium remains the most widely used treatment for bipolar disorder; however, the molecular mechanisms underlying its therapeutic actions have not been fully elucidated. We studied the in-vivo effect of lithium on the density of alpha-adrenoceptor (alpha-AR) and beta-AR subtypes and linked second messenger systems in the rat brain. METHODS: The densities of alpha(1)-ARs, alpha(2)-ARs, and beta(1)-ARs and beta(2)-ARs in the cortex and cerebellum of rats treated with lithium (0.4%), orally, for 30 days were measured using [(3)H]prazosin, [(3)H]clonidine and [(3)H]CGP-12177, respectively. The activity of adenylyl cyclase (AC) and levels of inositol trisphosphate (IP3), both second messengers linked to these receptors, were estimated using [(3)H]ATP and [(3)H]myoinositol, respectively. RESULTS: A significant decrease in the densities of cortical alpha(1)-ARs (85%, p < 0.0001), alpha(2)-ARs (50%, p < 0.0001), beta(1)-ARs (26%, p < 0.0001) and beta(2)-ARs (25%, p < 0.0001) was observed after lithium treatment. However, only the density of alpha(1)-ARs was significantly decreased (25%, p < 0.0001) in the cerebellum. The affinity of [(3)H]prazosin for cerebellar alpha(1)-ARs was increased. A small, but statistically significant, increase (19%, p < 0.0001) in the density of total beta-ARs was seen in the cerebellum, without altering the affinity of the radioligand for these receptors. Basal AC activity was not altered in the lithium-treated rat cortex. However, the norepinephrine-stimulated AC activity, which represents alpha(2)-AR-linked and beta-AR-linked AC, was significantly increased (66%, p < 0.0001). Both basal IP3 formation and norepinephrine-stimulated IP3, which represents alpha(1)-AR-linked phospholipase C activity, were significantly decreased (50%, p < 0.0001) in the lithium-treated rat cortex. CONCLUSION: Our results suggest that long-term administration of lithium treatment downregulates the cortical, but not cerebellar, alpha(1)-ARs, alpha(2)-ARs, beta(1)-ARs and beta(2)-ARs. Thus, it may be concluded that lithium induces region-specific and differential functional downregulation of alpha-AR and beta-AR subtypes in the rat brain.

Adenylyl Cyclases↗
PubMed1991

Myo-inositol attenuates two specific behavioral effects of acute lithium in rats.

Acute and chronic lithium treatment reduces levels of brain myo-inositol in rats. Several biological effects of lithium can be reversed in vitro by addition of myo-inositol. The ability of myo-inositol to reverse behavioral effects of lithium was tested using chronic inositol administration or acute intracerebroventricular (i.c.v.) injections. Chronic myoinositol elevated activity during the first 10 min in an open field, but did not reverse lithium-induced hypokinesia. Myo-inositol (i.c.v.) reversed the suppression of rearing behavior 24 hrs after an acute dose of lithium (5 mEq/kg) but did not attenuate hypokinesia 24 hrs after a high dose of lithium (10 mEq/kg). Myo-inositol, but not the inactive isomer chiro-inositol (i.c.v.), also significantly prolonged the latency to clonus in the lithium pilocarpine seizure model. These studies suggest that reduction of brain myo-inositol may be a critical mechanism for the behavioral effects of lithium.

Animals↗
PubMedDate not supplied

[Irreversible neurologic sequelae caused by lithium].

Lithium therapy can induce acute toxic reactions especially during overdosage. Exceptionally, permanent neurologic sequelae persist after the acute toxic reaction. These sequelae are more often cerebellar symptoms. Dementia, parkinsonian syndromes, choreoathetosis, brain stem syndromes and peripheral neuropathies have also been described. They are defined as irreversible if they persist more than two months after the interruption of lithium treatment. These neurologic complications occur frequently after voluntary or accidental poisoning but they may be observed even if the serum lithium dosage is below toxic level. Risk factors other than overdose are not well identified. Neurologic lesions induced by lithium can occur in the first days of the treatment as well as after years of maintenance therapy. Age and psychiatric diagnosis do not seem to be correlated with an increased risk of lithium induced neurotoxicity. Sex may be a risk factor, because of an overrepresentation of women among the case reports. The lithium-neuroleptic combination is another possible (although controversial) risk factor precipitating the occurrence of irreversible neurologic sequelae. Haloperidol was first implicated, but it has been shown that others neuroleptics, in combination with lithium, can induce similar toxic reactions. Intercurrent somatic illness with pyrexia often precedes the acute toxic reaction, and special attention must be paid to patients treated by lithium when they become hyperthermic. Major surgery, concurrent treatment with diuretics, renal failure, low food intake or low-salt diet are more uncommon precipitating factors. Available pharmacological treatments have not yet proved to be helpful. Even when the lesions are irreversible, a functional improvement can be obtained by rehabilitation. Thirty one cases of irreversible neurologic sequelae are reviewed.

Female↗
PubMed1990

Kainate receptors coupled to the evoked release of [3H]-gamma-aminobutyric acid from striatal neurons in primary culture: potentiation by lithium ions.

The pharmacological properties and modulation by lithium of the kainate (KA) receptor system coupled to the evoked release of [3H]-gamma-aminobutyric acid [( 3H]GABA) from purified populations of striatal neurons in primary culture were examined. KA evoked a dose-dependent (EC50, 100 microM) and saturable increase in [3H]GABA release from striatal neurons that was unaffected by the removal of extracellular calcium and resistant to the actions of tetrodotoxin. The release of [3H]GABA evoked by 100 microM KA was attenuated in a dose-dependent manner by the following excitatory amino acid antagonists (IC50):6-cyano-2, 3-dihydroxy-7-nitroquinoxaline (2 microM),2,3-dihydroxy-6,7-dinitroquinoxaline (2 microM), kynurenate (0.3 mM), and gamma-D-glutamylglycine (2 mM). The antagonist properties of 6-cyano-2,3-dihydroxy-7-nitroquinoxaline, kynurenate, and gamma-D-glutamylglycine were competitive in nature, inducing parallel rightward shifts of the KA dose-response curves. At concentrations at which it did not significantly increase basal levels of [3H]GABA release, quisqualate attenuated in a dose-dependent manner (IC50, 10 microM) the release due to 100 microM KA. The quisqualate receptor agonist alpha-amino-3-hydroxyisoxazolepropionic acid (AMPA), however, exerted a biphasic effect on 100 microM KA-evoked release of [3H]GABA. At lower concentrations of AMPA (0.1-10 microM), the release due to 100 microM KA was potentiated 25-50%; at higher concentrations (greater than 10 microM) AMPA induced a dose-dependent (IC50, 100 microM) attenuation of KA-evoked release. The release of [3H]GABA due to 100 microM KA was significantly potentiated by the replacement of sodium with lithium in the extracellular medium. A significant potentiation (20-30%) was detected with as little as 5-10 mM lithium, and maximal effects (100-110% increase) were obtained with 50-75 mM lithium. Replacement of sodium with choline or N-methyl-D-glucamine could not mimic the actions of lithium. Lithium (25 mM) also induced a 4-fold increase in the levels of endogenous GABA release due to 100 microM KA. Whole-cell voltage-clamp recordings of these striatal neurons indicated that the 100 microM KA-induced inward current was not significantly altered in the presence of 25 mM lithium. Lithium attenuated vasoactive intestinal polypeptide-stimulated cyclic AMP formation by 50%, with a dose dependence similar to that of its actions on KA-evoked release. The results of this study demonstrate a distinct pharmacological profile for the KA receptor system coupled to the evoked release of [3H]GABA from striatal neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

The clinical significance of lithium-nonsteroidal anti-inflammatory drug interactions.

There is conclusive evidence that nonsteroidal anti-inflammatory drugs can increase serum lithium levels, diminish renal lithium clearance, and possibly induce lithium toxicity. Such an interaction has occurred in patients with normal renal function. The effect on serum lithium levels varies greatly among different nonsteroidal anti-inflammatory drugs, indomethacin seeming most potent. On the other hand, there is no convincing evidence that sulindac and aspirin affect serum lithium levels to a clinically significant degree. Ibuprofen and naproxen can significantly increase serum lithium levels, but there is marked interindividual variation. Patients receiving nonsteroidal anti-inflammatory drugs must have their serum lithium levels checked every 4-5 days until the extent of drug interaction is assessed. A reduction in lithium dosage may be needed in some cases.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1989

Lithium increases rat striatal beta- and gamma-preprotachykinin messenger RNAs.

Previous reports indicate that the antimanic drug, lithium, increases substance P-like immunoreactivity (SP-LI) in the basal ganglia. The aim of this study was to use lithium as a pharmacological tool to further understand the mechanism of this process. We have used solution hybridization-nuclease protection assays to quantitate the specific preprotachykinin (PPT) mRNAs and radioimmunoassays and immunocytochemistry to assess SP-LI levels in the striatum of male Fisher F-344 rats. A regimen of subchronic administration of lithium (4 mEq/kg i.p. for 1, 2, 4 or 6 days) increased SP-LI in a time-dependent fashion. Concurrent administration of a dopamine receptor antagonist, haloperidol (1 mg/kg s.c. for 4 days) with a 4-day lithium regimen partially blocked the lithium-induced increase in SP-LI as well as neurokinin A-like immunoreactivity. An analysis of the abundance of individual PPT mRNAs indicated that lithium increases beta- and gamma-PPT mRNAs in the striatum; coadministration of haloperidol attenuates the lithium-induced increases. These results indicate that lithium affects the tachykinin biosynthetic process by accelerating transcriptional and/or translational processes in striatonigral neurons and that the dopaminergic system appears to be partly involved in this process.

Animals↗
PubMed1979

Lithium and granulocytopenia during induction therapy of acute myelogenous leukemia.

Twenty-seven patients receiving a standard cytosine arabinoside and daunorubicin regimen as induction of reinduction therapy of acute myelogenous leukemia were randomly assigned to receive lithium carbonate, 300 mg t.i.d., or no lithium. Treatment groups were comparable with respect to age and baseline granulocyte counts. All patients developed granulocyte nadirs below 100/cu mm. By actuarial analysis, the median duration of granulocytopenia, less than 1000/cu mm, was 16.0 days in the lithium group and 24.6 days in the no-lithium group, p = 0.013. The median duration of granulocytes less than 500/cu mm also favored the lithium group but only approached statistical significance: 14.0 days versus 20.5 days, p = 0.054. Lithium levels between 0.5 and 1.0 meq/liter were easily maintained in 11 of 12 patients receiving lithium, 300 mg t.i.d., and toxicity directly attributable to lithium was not observed. Despite the shortened duration of neutropenia, the incidence of infections and the rate of remission were not affected.

Agranulocytosis↗
PubMed1978

Effect of lithium on granulopoiesis in culture.

Lithium carbonate therapy is associated with polymorphonuclear leukocytosis. In vitro studies have shown that lithium ions stimulate formation of granulocytic colonies. In a study undertaken to determine how lithium acts, colony-forming cells uncontaminated by monocytes (which elaborate colony-stimulating factor [CSF] in vitro) were obtained by means of a two-step cell separation procedure. The effects of lithium on colony formation were then studied in (a) cultures stimulated by humoral CSF, (b) cultures in which monocytes were relied upon to synthesize CSF de novo and (c) unstimulated cultures. Lithium enhanced the action of CSF but did not stimulate colony formation in the absence of CSF. In monocyte-stimulated cultures, colony formation increased with lithium concentrations up to 1 mmol/L but this increase paralleled that in CSF-stimulated cultures and therefore was not due to increased CSF production by monocytes. At higher concentrations of lithium, colony formation decreased in the monocyte-stimulated cultures but increased in the CSF-stimulated cultures. A lithium concentration of 4 mmol/L gave the greatest enhancing effect on colony formation in CSF-stimulated cultures and a concentration greater than 1 mmol/L inhibited de novo synthesis of CSF by monocytes.

Cells, Cultured↗
PubMed1987

[The effect of lithium treatment on the activity of central dopaminergic neurons].

In the terminal regions of various dopaminergic neurons (i.e., median eminence, neurointermediate lobe, striatum, accumbens, prefrontal cortex, hippocampus, and amygdala, respectively), maintenance of rats on a diet containing lithium carbonate (0.23%) for 3, 7 or 21 days resulted in a significant increase in the accumulation of dihydroxyphenylalanine (DOPA) after the inhibition of the activity of aromatic l-amino acid decarboxylase with 3-hydroxybenzylhydrazine (NSD 1015, 100 mg/kg). There was also a significant increase in the concentrations of dopamine metabolites; dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 3-methoxytyramine (3-MT), in these brain regions of animals given lithium for 21 days when compared to control animals, suggesting a possible enhancement in dopamine synthesis and release. Furthermore, there was a significant increase in dopamine concentrations in anterior pituitary glands, but no significant change in other brain regions of lithium-treated animals. The inclusion of lithium in the diet resulted in a significant reduction of prolactin concentrations in serum and anterior pituitary glands. There was also a significant decrease in the secretion of prolactin from anterior pituitary tissues in vitro of lithium-treated rats. Chronic lithium consumption led to a significant decrease in beta-adrenergic receptor binding in selected regions of the rat brain, with no changes noted in alpha 2-adrenergic, dopaminergic D1 or D2 receptor binding. These results are suggestive that lithium treatment enhances the activity of various dopaminergic neurons. An increased release of dopamine from tuberoinfundibular dopaminergic neuron may account for the lithium-induced reduction of prolactin concentrations in serum and anterior pituitary glands, and the suppressed secretion of prolactin in vitro from anterior pituitary tissue.

Animals↗
PubMed1988

Lithium determined in serum with an ion-selective electrode.

We evaluated the performance of the lithium ion-selective electrode (ISE) in the Du Pont Na/K/Li analyzer. Lithium concentrations in 106 serum samples from patients being treated with lithium were measured in duplicate with the ISE and by flame photometry. The slope of the regression line for the two methods was 1.004 with a standard error of the estimate of 0.049 mmol/L (x = flame photometry, y = ISE). Lithium measurements by the ISE method in serum or aqueous standards were linear to greater than 2.0 mmol/L. Within-run CVs for low (0.31 mmol/L) and high (1.15 mmol/L) lithium controls were 5.9% and 1.7%, respectively (n = 20). Day-to-day CVs for the same controls were 9.8% and 3.3%, respectively (n = 20). There was no significant interference when the concentrations of sodium, potassium, calcium, or magnesium were varied, nor did intervening urinary lithium analyses affect the measurement of serum lithium. Results for lithium measurement in four serum-based survey materials compared well with results by isotope dilution/mass spectrometry.

Electrodes↗
PubMed1986

The renal lithium clearance and its correlations with other biological variables: observations in a large group of physically healthy persons.

The lithium clearance (CLi) is a measure of the delivery of fluid from the proximal tubules to the loop of Henle. We determined the correlations between CLi and a number of variables on 350 occasions in 164 physically healthy persons in lithium treatment for manic-depressive illness. CLi was significantly correlated (p less than 0.001) with sex, age, body surface, urine flow, sodium clearance, potassium clearance, serum lithium concentration, and lithium dosage. Correlations with sex, age and body surface lost statistical significance when the renal variables and the surface were divided by creatinine clearance; these correlations are indirect and caused by common correlations with the filtration rate. The findings show that the fractional delivery of fluid from the proximal tubules is independent of sex, age and body surface. Correlations with urine flow, serum lithium, and lithium dosage could be explained by circumstances connected with the lithium treatment. These variables do not seem to affect CLi. It is concluded that factors which should be taken into account if the assessment of lithium clearance values include the creatinine clearance, the sodium clearance, and the potassium clearance.

Adult↗
PubMed1985

[Lithium in the therapy of hematologic diseases in childhood].

The literature as well as the author's data of this topic are reviewed. Lithium stimulates myelopoesis in vitro, especially via CSF-production. This effect is associated with a modulation of cyclic nucleotides. Lithium stimulates leukemic cell lines too. However, according to epidemiological data lithium does not play an etiological role in leukemia. Furthermore, lithium does not stimulate several tumor cell lines in culture. The effect of cytostatic drugs as well as remission rates are not lessened by lithium. In spite of increased production the functions of the granulocytes are not impaired. Because of the wide range of serum level variation serum level determinations are mandatory. To treat hematological disorders a serum level between 0.7 and 1.2 mmol/l should be achieved. Flame emission photometry and atomic absorption photometry are equivalent methods for determination of the serum level. CNS, thyroid gland, kidney, electrolyte balance, gastrointestinal tract have to be monitored for side effects. Lithium therapy has not be given in pregnancy and to breast feeding mothers. In neutropenia with increased susceptibility to infections lithium therapy including serum level monitoring can be given. Lithium reduces leukopenia and infections following cytotoxic chemotherapy for solid tumors. Current pediatric studies are investigating whether patients with chemotherapy induced neutropenia benefit from this effect in terms of increased and prolonged remission rates.

Anemia, Aplastic↗