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Lithium therapy in the treatment of manic-depressive illness. Present status and future perspectives. A critical review.

This article reviews critically the present status of lithium in the treatment and prophylaxis of manic-depressive illness compared to the two anticonvulsant drugs, carbamazepine and valproic acid. Lithium is used successfully in the prophylaxis and treatment of manic-depression. The mechanism by which it exerts its effects is still not very clear. There is much evidence to indicate that lithium may exert its therapeutic action by interfering with the metabolism of phosphoinositides which play an important role in synaptic transmission. Because of lithium's narrow therapeutic/toxic ratio, blood concentration monitoring is crucial. Published data suggest that, compared to lithium, carbamazepine is similar in its relative specificity in treating mania. It is often faster in achieving its antimanic effects and best established as an alternative for patients not responding or intolerant to lithium. Carbamazepine is a good substitute for lithium when severe renal problems exclude the use of lithium. The therapeutic profile of valproic acid in manic-depression, although less extensively studied, appears to be similar to that of carbamazepine. As carbamazepine, it seems to be best indicated in patients with rapid cycles. Whereas lithium inhibits myo-inositol monophosphatase, carbamazepine shows a stimulating effect and valproic acid has no effect on this biochemical target. The implication of the inositol pathway in the pathogenesis of adverse effects, such as neurotoxicity and dermatological irritation, is discussed. A further understanding of this pathway is important for the future development of new lithium-like compounds in order to maximize the therapeutic benefits without the adverse effects.

Anticonvulsants↗
PubMed1996

Lithium neurotoxicity at low therapeutic doses Hypotheses for causes and mechanism of action following a retrospective analysis of published case reports.

Lithium has been the pharmacologic treatment for the management of manic-depressive illness for many years. While the therapeutic efficacy of lithium is invaluable, it can cause a variety of neurotoxicities at normal therapeutic doses or concentrations. A systematic search through the Medline database was performed. 41 Cases of neurotoxic adverse effects of lithium at low therapeutic concentrations were observed (< 65 years, 14 males & 21 females/> 65 years, 6 females). Although a higher percentage of female subjects experienced lithium neurotoxicity, no statistically significant difference between the two groups was noted (Fisher's exact test, P = 0.07). The analysis of the data shows that among case reports of lithium neurotoxicity, drug interaction effect is an important factor. More than 50% (51.2%) of the patients received at least one neuroleptic medication with their lithium treatment, 22% received concomitantly an antidepressant, 22% an antiepileptic (carbamazepine) and 17% an anxiolytic. It is our hypothesis that these drug associations are an important contributing factor to lithium neurotoxicity. The high percentage of neurotoxicity which is associated with neuroleptics warrant caution in the daily clinical practice when these two classes of medications are combined. It is hypothesised that neuroleptics, in particular the phenothiazines, might increase lithium influx in red blood cells and that the enhanced levels of lithium in the tissue may possibly be responsible for the neurotoxic effects. Concomitant administration of medications such as neuroleptics with lithium require caution with regular clinical observations and drug plasma concentration monitoring.

Adult↗
PubMed2006

Role of nitric oxide in the gastro-protective effect of lithium.

BACKGROUND AND AIM: Lithium is widely used for the management of neuropsychiatric symptoms in bipolar disorders. A few studies have shown that lithium has a protective effect against gastric damage with an unknown mechanism. Some of the actions of lithium are mediated through nitric oxide (NO), which has an important role in the regulation of gastric wall blood flow as well as gastric mucosal integrity. The aim of this study was to test the hypothesis if the gastro-protective effect of lithium is mediated through NO. METHODS: Male Wistar rats were pre-treated with either a non-selective NO synthase inhibitor (N(G)-nitro-l-arginine, 10mg/kg), a selective inducible NO synthase inhibitor (aminoguanidine, 100mg/kg) or saline. Lithium carbonate (10, 20, 50 and 100mg/kg) was then administered intraperitoneally 1h before the induction of gastric mucosal damage. Gastric damage was induced by either water immersion stress or ethanol gavage in rats. RESULTS: Lithium had a significant protective effect in both stress and ethanol-induced gastric damage, but it needed in ethanol-induced gastric damage a higher dose than in the stress induced lesion. Lithium carbonate doses 20 and 50mg/kg produced plasma concentrations that were in the range of human therapeutic Li levels (0.6-1.0muM). Pre-treatment of animals with N(G)-nitro-l-arginine (20 and 40mg/kg) reduced the protective effect of lithium against ethanol-induced gastric damage, but not in stress-induced damage. Aminoguanidine administration showed no effect on the damage reduction either in control or lithium treated rats. CONCLUSIONS: The results indicate that NO might play a role in the gastro-protective effect of lithium against ethanol-induced gastric damage in rats.

Journal Article↗
PubMed2003

Lithium gluconate 8% vs ketoconazole 2% in the treatment of seborrhoeic dermatitis: a multicentre, randomized study.

BACKGROUND: Lithium significantly improved seborrhoeic dermatitis symptoms in comparison with placebo. Objectives This randomized controlled trial was designed to show a non-inferiority of 15% (primary end-point) of lithium gluconate 8% ointment compared with ketoconazole 2% emulsion. METHODS: The study population comprised out-patients who had facial seborrhoeic dermatitis for at least 2 months, with moderate to severe erythema and desquamation at inclusion. The primary end-point was complete remission, defined as the disappearance of both erythema and desquamation. The non-inferiority of lithium was assessed on the 95% confidence interval (CI) of the difference between treatments. RESULTS: The intent-to-treat analysis (ITT) involved 288 patients and the per protocol (PP) analysis 269 patients. Treatment groups were comparable at baseline on age, sex, disease duration and symptoms. For the main criterion, the success rate was 52.0% (lithium) vs. 30.1% (ketoconazole) in the ITT population and 53.2% (lithium) vs. 30.7% (ketoconazole) in the PP population. The non-inferiority of lithium was demonstrated with differences of 21.9% (95% CI 10.0-33.7%) and 22.5% (95% CI 10.2-34.8%), respectively, in the ITT and PP population. As the lower limit of the 95% CI was > 0, the superiority of lithium was shown. Lithium also showed better results on other symptoms: burning and dryness. Adverse events were reported by 26.3% (lithium) and 25% (ketoconazole) of patients. CONCLUSIONS: Lithium was 22% more effective than ketoconazole in giving complete remission of seborrhoeic dermatitis, with comparable safety.

Adolescent↗
PubMed2004

Lithium acetate therapy in a maintenance hemodialysis patient.

BACKGROUND/AIMS: Single cases of lithium carbonate dosing in hemodialysis patients have been published. We investigate the dose-serum level relationship after single and multiple lithium acetate dosing in a hemodialysis patient and review the literature. METHODS: Lithium acetate was administered orally over a period of 11 months in a patient with major depressive episodes after being placed on hemodialysis three times a week. The serum trough levels of lithium before and after hemodialysis were analyzed. The data were compared with those reported in the literature, and potential drug interactions and the importance of the residual renal function are discussed. RESULTS: No adverse events due to the lithium therapy were documented. Steady state levels of between 0.6 and 0.8 mmol/l of lithium acetate were achieved 17 days after initiating the therapy, using 24 mmol/l of lithium three times a week, in a patient with a residual diuresis of about 400 ml/day. In contrast, data reported in the literature implicate that only 9.6-14.4 mmol/l of lithium (450-600 mg of lithium carbonate) is sufficient to achieve adequate serum levels. CONCLUSIONS: The residual renal function can be important for lithium clearance. The creatinine clearance does not reflect this point.

Acetates↗
PubMed1981

Lithium carbonate and granulocyte production: dose optimization.

To determine the optimal dose of lithium for inducing granulocytosis, the authors administered lithium carbonate to normal volunteers at five dose levels. The authors performed assessments of circulating and marginated blood pools of granulocytes and of marrow reserve granulocytes to confirm that the early granulocytosis following lithium administration is due to increased granulocyte production rather than redistribution. At 300 mg/day and 600 mg/day, lithium had no significant effect on granulocyte production. Doses of 900, 1200, and 1500 mg/day, corresponding to lithium levels of 0.55 to 1.50 mEq/liter, were associated with increased granulocyte production. Within this therapeutic range, no correlation between lithium level and granulocyte production was demonstrated. This study suggests that any lithium dose which achieves a lithium level of greater than 0.55 mEq/liter, i.e., doses greater than or equal to 900 mg/day, is adequate to induce granulocytosis. While lithium did not increase platelet production, doses of 900 mg/day to 1500 mg/day were associated with decreased bleeding times.

Adult↗
PubMed1987

Status epilepticus is produced by administration of cholinergic agonists to lithium-treated rats: comparison with kainic acid.

Electroencephalographic techniques were used to study generalized convulsive status epilepticus induced by administration of subconvulsive doses of cholinomimetics (e.g., pilocarpine) to rats pretreated with lithium chloride. Status epilepticus induced by this treatment was compared with status epilepticus induced by kainic acid. Lithium/pilocarpine-induced status epilepticus developed within 10 min of initial paroxysmal spike activity, 24 +/- 1 min (N = 20) after administration of pilocarpine, and continued uninterrupted for more than 3 h. Kainic acid (10 mg/kg)-induced status epilepticus developed approximately 60 min after initial spike activity, 96 +/- 3 min (N = 7) after kainate administration, and continued for 0.5 h. Thus, the interval of intermittent seizure activity and the duration of status epilepticus differed markedly between these two models. The potentiation by lithium (3 meq/kg) of the convulsant effect of cholinergic agonists was found to be 10 to 13-fold for two direct-acting cholinomimetics, pilocarpine and arecoline, whereas the convulsant effect of the indirect-acting agonist, physostigmine, was potentiated by 50%. The full proconvulsant effect of lithium lasted from 2 to 24 h after a single acute treatment (3 meq/kg). The dose response of the proconvulsant effect of lithium was determined and the EC50 of lithium was approximately 1.5 meq/kg when pilocarpine (30 mg/kg) was administered 20 h later. Chronic treatment with lithium for 4 weeks potentiated the convulsant effect of pilocarpine by more than 26-fold. These results demonstrated that both acute and chronic administration of lithium enhance cholinergic function in vivo. Potentiation of cholinergic function by lithium may play a role in the therapeutic action of lithium in affective disorders.

Animals↗
PubMed1988

Lithium: evidence for reduction in circulating testosterone levels in mice following chronic administration.

Lithium, the widely-used antipsychotic drug, is known to exert adverse effects on a number of endocrine organs. In the present investigations, the effects of chronic lithium administration on circulating levels of testosterone and plasma and pituitary levels of luteinizing hormone (LH) were evaluated in order to examine whether or not the pituitary-gonadal axis is a probable target of lithium action. Adult male C57BL/6 mice, maintained on a fixed photoperiodism (LD 14:10), were administered lithium orally, by being fed on a specially prepared chow containing 0.4% lithium chloride for 15 or 30 days, while their matched controls were maintained on standard laboratory chow. At the termination of the respective experimental schedules, the animals were decapitated, their blood collected, and plasma was separated and stored frozen. Pituitaries were quickly removed, weighed, homogenized, centrifuged and their supernatants were stored frozen. Testosterone in plasma and LH in pituitary and plasma were quantitated by standard RIA methods. Plasma Li concentration was determined by using flame photometric methods. A significant suppression in testosterone levels was noted after both 15 (p less than .01) and 30 (p less than .05) days of lithium treatment, but both pituitary and plasma LH levels remained unchanged at both the periods. It is, therefore, suggested that lithium exerts its effect directly at the level of the Leydig cells rather than through the pituitary-gonadal axis. Since the noted lithium-induced reduction of testosterone was manifested when the plasma lithium levels were within (or around) the therapeutic range, these results may have important clinical implications.

Animals↗
PubMed1982

Lithium ratio and maintenance treatment response.

Erythrocyte/plasma lithium ratios were determined in 41 polar manic depressive outpatients maintained on lithium for a mean of 64 months. Sixteen patients experienced affective episodes requiring additional pharmacologic intervention during periods when their plasma lithium averaged 0.7 meq/l or above for at least 3 preceding months and they were on no concurrent medication known to induce depression or mania. These patients considered to be a homogeneous group of non-responders to lithium, had a mean lithium ratio of 0.50 (range 0.15-1.16). Seven patients experienced affective symptoms at plasma levels below 0.7 meq/1 and/or while taking concurrent medication known to induce affective symptoms, and therefore could not be categorized clinically as lithium non-responders or responders. Eighteen remaining patients, who had no affective episodes during lithium maintenance, were found to have a mean erythrocyte/plasma ratio of 0.52 (range 0.19-1.05). This latter group of apparent responders should be considered heterogeneous in that it may include spontaneous remitters. The difference in mean ratios between the non-responder group and the apparent responder group was not statistically significant. These findings support the contention that the erythrocyte/plasma lithium ratio does not correlate with response of bipolar outpatients to maintenance lithium.

Bipolar Disorder↗
PubMed1988

The effects of intravenous theophylline infusion versus intravenous sodium bicarbonate infusion on lithium clearance in normal subjects.

Ten normal subjects ingested lithium carbonate (600 mg p.o. b.i.d.) for three 1-week intervals. At the end of each weekly interval, subjects' lithium clearances were randomly perturbed for 12 hours with the subject in a supine position by infusing either normal saline (308 mEq), sodium bicarbonate (350 mEq) in normal saline (308 mEq), or theophylline (mean = 14.0 micrograms/ml) in normal saline (308 mEq). Subjects were placed on a 200 mEq/day sodium diet during the lithium clearance perturbation stages of the study. When each patient's normal saline lithium clearance was used as a control, it was found that the theophylline produced a significantly greater % increase in lithium clearance than did the sodium bicarbonate. Theophylline infusions increased patients' individual lithium clearances by 51 +/- 52%, while sodium bicarbonate infusions increased lithium clearances by 0.6 +/- 33%. Theophylline infusions ought to be investigated as an alternative to hemodialysis in lithium intoxications requiring the immediate reduction of lithium concentrations.

Adult↗
PubMed1992

Ontogenic study of lithium-pilocarpine-induced status epilepticus in rats.

Lithium is known to potentiate the ability of pilocarpine to induce status epilepticus in rats. The goal of this study was to determine whether lithium could potentiate pilocarpine-induced seizures in developing animals. Behavioral, electroencephalographic (EEG), and histopathological changes induced by systemic administration of lithium (3 meq/kg) followed 20 h later by pilocarpine (3, 10, 30, 60 mg/kg) were studied in 3-30-day-old rats. Lithium followed by pilocarpine (30 and 60 mg/kg) induced hyperactivity, tremor, loss of postural control and scratching but no electrographic seizures in 3-8-day-old rats. In the 7-10-day-old animals pretreatment with lithium and pilocarpine 60 mg/kg induced status epilepticus with sustained myoclonus and continuous bilateral synchronous spike and sharp wave, but doses of pilocarpine lower than 60 mg/kg had no effect. The susceptibility to lithium-pilocarpine-induced status epilepticus increased markedly during the third postnatal week of life. During this time period, rats treated with lithium (3 meq/kg) plus pilocarpine 10 mg/kg exhibited behavioral and EEG manifestations of status epilepticus. The same combination of lithium and pilocarpine failed to induce status epilepticus either before or after the third week of life. Histopathological analysis of the brains of the animals used in these studies failed to demonstrate the widespread damage reported in adult rats that have undergone lithium-pilocarpine-induced status epilepticus.

Aging↗
PubMed1991

Effect of a single test dose of lithium carbonate on sodium and potassium excretion in man.

1. The possible natriuretic and kaliuretic effects of a single dose of lithium, as used in lithium clearance studies, were investigated in 15 healthy subjects on fixed sodium (100 mmol/24 h) and potassium (70 mmol/24 h) intakes. Lithium carbonate (300 mg or 600 mg) or placebo tablets were administered, double-blind and in random order, midway through a 48 h urine collection (divided into six 8 h periods), at 23.00 hours. 2. During the three 24 h periods which preceded the administration of lithium or placebo (control days), rates of sodium and potassium excretion followed normal circadian patterns, but no differences in excretion rates between the 3 control days were observed. Placebo tablets did not affect excretion rates. 3. After the 300 mg dose of lithium carbonate, 24 h sodium excretion increased by approximately 17 mmol (P less than 0.05); almost all of the natriuretic effect occurred during the first two 8 h periods. No effect on potassium excretion was observed. 4. After the 600 mg dose of lithium carbonate, 24 h sodium excretion increased by approximately 48 mmol (P less than 0.001) and 24 h potassium excretion increased by approximately 19 mmol (P less than 0.01). These effects were confined to the first two 8 h periods and thus occurred before and during the usual lithium clearance period. 5. Plasma renin activity, measured in 10 subjects, increased after the 600 mg dose of lithium carbonate (P less than 0.005), but plasma concentrations of aldosterone and atrial natriuretic peptide were not significantly affected. Neither the 300 mg dose of lithium carbonate nor the placebo tablets affected hormone levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

Lithium-induced alterations in the testis of the male roseringed parakeet (Psittacula krameri) : evidence for significant structural changes and disruption in the spermatogenetic activity.

In this report, we have examined the effects of lithium on testicular morphology in a male subtropical wild avian species, the roseringed parakeet (Psittacula krameri). Adult male birds were collected during the months of February-March, a time when the testicular gametogenic activity in these seasonally breeding birds is at its peak. They were injected, intramuscularly, twice daily (07:00 and 19:00 h) with lithium chloride (Sigma Chemical Company) at a dosage of 0.5 mEq/Kg body weight either for 5 or 10 days. A significant decrease in both the absolute and relative testicular weights was evident in the lithium-treated birds as compared to those of the saline-injected control animals. Light microscopic studies of the testis in the lithium-treated animals showed a wide range of degenerative changes. These included a) a significant reduction in the diameter of seminiferous tubules; b) necrosis and exfoliation of most of the germ cells in the seminiferous tubular lumen with the exception of the spermatogonia; and c) a significant reduction in the number of mature spermatozoa in the tubular lumen. These degenerative changes were dependent on the duration of lithium treatment and were evident when the plasma lithium concentrations were well below the human therapeutic range. Leydig cell morphology was not affected by lithium however. Our results provide the first experimental evidence of lithium's adverse reproductive function in an avian species. These data provide further support to the view that lithium adversely affects the male reproductive system and that these effects extend beyond mammalian species.

Animals↗
PubMed1982

Lithium enhances growth of human leukaemia cells in vitro.

Lithium is known to cause leucocytosis in normal humans, and lithium salts have been used therapeutically in attenuating leucopenia in patients undergoing chemotherapy. Recent reports also described leukaemia development during lithium treatment. We have investigated the effect of lithium chloride on the proliferation of human myeloid, erythroblastic, and T- and B-lymphoblast leukaemia cells in vitro. Colony formation by cells of the myeloid leukaemia lines HL-60 and KG-1 was enhanced by lithium chloride, and maximal stimulation was seen at 5 X 10(-4) M. Lithium also increased the proliferation of KG-1a cells, a subline of KG-1 cells that does not respond to colony-stimulating factor, indicating a direct growth-promoting effect on myeloid leukaemia cells. Lithium was found to enhance colony formation by the T-lymphoblast cell line MOLT 4 and the B-lymphoblast line IM-9 at concentrations between 10(-6) and 10(-3) M. The addition of lithium chloride to murine Friend or human K-562 erythroleukaemia cells also caused an augmentation in colony formation. These observations may have relevance to the therapeutic use of lithium in patients with haematological malignancies.

Animals↗
PubMed2005

Lithium-induced NDI in rats is associated with loss of alpha-ENaC regulation by aldosterone in CCD.

Lithium-induced nephrogenic diabetes insipidus (Li-NDI) is associated with increased urinary sodium excretion and decreased responsiveness to aldosterone and vasopressin. Dysregulation of the epithelial sodium channel (ENaC) is thought to play an important role in renal sodium wasting. The effect of 7-day aldosterone and spironolactone treatment on regulation of ENaC in rat kidney cortex was investigated in rats with 3 wk of Li-NDI. Aldosterone treatment of rats with Li-NDI decreased fractional excretion of sodium (0.83 +/- 0.02), whereas spironolactone did not change fractional excretion of sodium (1.10 +/- 0.11) compared with rats treated with lithium alone (1.11 +/- 0.05). Plasma lithium concentration was decreased by aldosterone (0.31 +/- 0.03 mmol/l) but unchanged with spironolactone (0.84 +/- 0.18 mmol/l) compared with rats treated with lithium alone (0.54 +/- 0.04 mmol/l). Immunoblotting showed increased protein expression of alpha-ENaC, the 70-kDa form of gamma-ENaC, and the Na-Cl cotransporter (NCC) in kidney cortex in aldosterone-treated rats, whereas spironolactone decreased alpha-ENaC and NCC compared with control rats treated with lithium alone. Immunohistochemistry confirmed increased expression of alpha-ENaC in the late distal convoluted tubule and connecting tubule and also revealed increased apical targeting of all three ENaC subunits (alpha, beta, and gamma) in aldosterone-treated rats compared with rats treated with lithium alone. Aldosterone did not, however, affect alpha-ENaC expression in the cortical collecting duct (CCD), which showed weak and dispersed labeling similar to that in rats treated with lithium alone. Spironolactone did not affect ENaC targeting compared with rats treated with lithium alone. This study shows a segment specific lack of aldosterone-mediated alpha-ENaC regulation in the CCD affecting both alpha-ENaC protein expression and trafficking, which may explain the increased sodium wasting associated with chronic lithium treatment.

Aldosterone↗
PubMed1985

The influence of lithium chloride on experimental autoimmune thyroid disease.

Lithium administration is known to be associated with the development of thyroid dysfunction; it also exerts an effect on the immune system. The effect of lithium on experimental autoimmune thyroid disease was studied in female August rats. Following immunization with rat thyroglobulin in Freund's complete adjuvant, lithium chloride was administered i.p. for 30 days to four groups at varying stages of the disease. Control animals received i.p. saline. Anti-thyroglobulin antibody levels (measured by ELISA) were significantly increased in rats given lithium immediately post-immunization (group B) compared to control animals (661 +/- 42 OD vs 448 +/- 68; mean +/- s.e., P less than 0.02). In contrast, animals which received lithium during the spontaneous resolution of the disease (group D) showed a significant fall in anti-TG antibody compared to controls (99 +/- 15 vs 27 +/- 15; P less than 0.001). Anti-TG antibody levels remained undetectable in animals which received lithium but were not immunized. The splenic T cell blastogenic response (as measured following phytohaemagglutinin stimulation) was significantly increased in rats receiving lithium prior to and during immunization (group A) (stimulation index 63.4 +/- 6.9 vs 10.2 +/- 2.4; P less than 0.001). Spontaneous cell proliferation of splenic lymphocytes was decreased in two lithium treated groups (group A P less than 0.005, group C P less than 0.05). There was no alteration in splenic weight or the degree of thyroid lymphocytic infiltration in any of the treated group. Lithium exerted both positive and negative influences on the immune system in rats immunized with thyroglobulin in adjuvant but did not induce autoantibody production in normal rats.

Animals↗
PubMed2003

Cortical myoclonus during lithium exposure.

BACKGROUND: Myoclonus can occur in association with lithium therapy at toxic and therapeutic dosages, and can be a predominant and disabling adverse effect. Moreover, myoclonus has been reported when lithium has been combined with cyclic antidepressants and with the neuroleptic clozapine. Although clinical case reports exist, no electrophysiologic data are available that provide a source or a neurophysiological mechanism for the myoclonus seen in lithium therapy. OBJECTIVE: To describe the electrophysiologic characteristics and source of the myoclonus associated with lithium therapy. DESIGN AND METHODS: We retrospectively analyzed 5 cases of myoclonus during lithium therapy. We reviewed the clinical features and results of previous electrophysiologic testing. Four patients received lithium monotherapy; and 1, sertraline hydrochloride and nefazodone hydrochloride in addition to lithium. The electrophysiologic data that had been gathered included multichannel surface electromyographic (EMG) recordings with simultaneous electroencephalography (EEG), somatosensory evoked potentials, and elicitation of long-latency EMG reflexes to median and digital nerve stimulation. RESULTS: All 5 patients showed multifocal action myoclonus without reflex activation and only rare occurrence at rest. In each case, back-averaging created a focal EEG transient over the contralateral sensorimotor area preceding the myoclonus EMG discharge. In 2 of the patients receiving lithium monotherapy, the therapy was discontinued and the myoclonus disappeared. CONCLUSIONS: Lithium, by itself, can be associated with prominent clinical myoclonus, short-duration (<50-millisecond) myoclonus EMG discharges and cortical action myoclonus without the presence of epileptiform abnormalities on the routine EEG. This myoclonus is different from the most common form that is well documented to occur with tricyclic antidepressant therapy by clinical and electrophysiologic means.

Adult↗
PubMed2001

Lithium use in octogenarians.

OBJECTIVES: To assess the tolerability and side-effect profile of lithium use in a group of octogenarians attending a specialized lithium clinic. METHODS: This is a cross-sectional study looking at all patients of eighty years and over attending a lithium clinic. Charts were examined to assess renal function, thyroid function and level of side-effects during their course of lithium treatment in order to assess the tolerability of this medication in octogenarians. RESULTS: Twelve patients of 80 years and over (with an average age of 83.6 years) were taking lithium for an average period of 53.7 months. They had a mean serum level of 0.42 mmol/l. No patient had to discontinue lithium therapy because of side-effects, even though some patients did develop transient abnormalities of renal function. One patient developed diabetes insipidus. One female patient developed hypothyroidism. CONCLUSIONS: Lithium was well tolerated and was administered safely to this cohort of octogenarians. Monitoring of serum lithium levels and kidney and thyroid function should preferably be done in the setting of a specialized lithium clinic.

Aged↗