Lithium Articles 10

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The effect of inositol supplements on the psoriasis of patients taking lithium: a randomized, placebo-controlled trial.
            (Allan et al., 2004) Download
BACKGROUND:  Lithium carbonate is the most widely used long-term treatment for bipolar affective disorders, but its ability to trigger and exacerbate psoriasis can become a major problem in patients for whom lithium is the only treatment option. Inositol depletion underlies the action of lithium in bipolar affective disorders and there are good theoretical reasons why the use of inositol supplements might be expected to help this group of patients. OBJECTIVES:  To determine whether inositol supplements improve the psoriasis of patients on lithium therapy. METHODS:  Fifteen patients with psoriasis, who were taking lithium, took part in a randomized, double-blind, placebo-controlled, crossover clinical trial comparing the effect of inositol supplements with those of a placebo (lactose). Changes in the severity of their psoriasis were measured by Psoriasis Area and Severity Index scores recorded before and after the different courses of treatment. The effect of inositol supplements on the psoriasis of 11 patients who were not taking lithium was evaluated in the same way. RESULTS:  The inositol supplements had a significantly beneficial effect on the psoriasis of patients taking lithium. No such effect was detected on the psoriasis of patients not on lithium. CONCLUSIONS:  The use of inositol supplements is worth considering for patients with intractable psoriasis who need to continue to take lithium for bipolar affective disorders.

Lithium use and primary hyperparathyroidism.
            (Broome and Solorzano, 2011) Download
OBJECTIVE:  To review suspected causes of lithium-induced hyperparathyroidism, disease presentation, underlying pathology, and current recommendations and trends in medical and surgical treatment. METHODS:  Relevant literature was reviewed. RESULTS:  Lithium carbonate therapy has continued to be a mainstay of treatment for bipolar disease and schizoaffective disorder since its introduction into clinical use. Several metabolic consequences are associated with its long-term use, including hypercalcemia and hyperparathyroidism. CONCLUSIONS:  Until further data become available, the surgeon should remain vigilant for the presence of pathologically active glands that may manifest their function at different times during the disease course.


Lithium monotherapy increases ACTH and cortisol response in the DEX/CRH test in unipolar depressed subjects. A study with 30 treatment-naive patients.
            (Bschor et al., 2011) Download
BACKGROUND:  Distorted activity of the hypothalamic-pituitary-adrenocortical (HPA) system is one of the most robustly documented biological abnormalities in major depression. Lithium is central to the treatment of affective disorders, but little is known about its effects on the HPA system of depressed subjects. OBJECTIVE:  To assess the effects of lithium monotherapy on the HPA system of patients with major depression by means of the combined DEX/CRH test. METHOD:  Thirty drug-naive outpatients with major depression (single episode or unipolar recurrent; SCID I- and II-confirmed) were treated with lithium monotherapy for four weeks. The DEX/CRH test was conducted directly before intake of the first lithium tablet and four weeks thereafter. Weekly ratings with the HDRS(21) were used to determine response (≥50% symptom reduction) and remission (HDRS ≤7). RESULTS:  Lithium levels within the therapeutic range were achieved rapidly. Tolerability was good; no patient terminated the treatment prematurely. Response and remission rates were 50% and 33% respectively. Compared to the DEX/CRH test before the start of the treatment, a considerable and significant increase in all CRH-stimulated ACTH and cortisol parameters could be detected in the second DEX/CRH test. When analysed with particular regard to responders and non-responders, that significant increase was only present in the responders. CONCLUSIONS:  We were able to demonstrate that lithium leads to a significant activation of the HPA system. This is possibly connected to stimulation of hypothalamic arginine vasoporessin (AVP), to direct intracellular effects of lithium on pituitary cells and to an induction of gene expression. TRIAL REGISTRATION:  drks-nue.uniklinik-freiburg.de DRKS00003185.

Lithium for maintenance treatment of mood disorders
            (Burgess et al., 2001) Download
BACKGROUND: Mood disorders are common, disabling and tend to be recurrent. They carry a high risk of suicide. Maintenance treatment, aimed at the prevention of relapse, is therefore of vital importance. Lithium has been used for some years as the mainstay of maintenance treatment in bipolar affective disorder, and to a lesser extent in unipolar disorder. However, the efficacy and effectiveness of prophylactic lithium therapy has been disputed. Low suicide rates in lithium-treated patients have led to claims that lithium has a specific anti-suicidal effect. If so, this is of considerable importance as treatments for mental disorders in general have not been shown convincingly to be effective in suicide prevention. OBJECTIVES: 1. To investigate the efficacy of lithium treatment in the prevention of relapse in recurrent mood disorders. 2. To examine the effect of lithium treatment on consumers' general health and social functioning, its acceptability to consumers, and the side-effects of treatment. 3. To investigate the hypothesis that lithium has a specific effect in reducing the incidence of suicide and deliberate self-harm in persons with mood disorders. SEARCH STRATEGY: The Cochrane Collaboration Depression, Anxiety and Neurosis Controlled Trials Register (CCDANCTR) and The Cochrane Controlled Clinical Trials Register (CCTR) were searched. Reference lists of relevant papers and major text books of mood disorder were examined. Authors, other experts in the field and pharmaceutical companies were contacted for knowledge of suitable trials, published or unpublished. Specialist journals concerning lithium were hand searched. SELECTION CRITERIA: Randomised controlled trials comparing lithium with placebo, where the stated intent of treatment was maintenance or prophylaxis. Participants were males and females of all ages with diagnoses of mood disorder. Discontinuation studies (in which all participants had been stable on lithium for some time before being randomised to either continued lithium treatment or placebo substitution) were excluded. DATA COLLECTION AND ANALYSIS: Data were extracted from the original reports independently by two reviewers. The main outcomes studied were related to the objectives stated above. Data were analysed for all diagnoses of mood disorder and for bipolar and unipolar disorder separately. Data were analysed using Review Manager version 4.0. MAIN RESULTS: Nine studies were included in the review, reporting on 825 participants randomly allocated to lithium or placebo. Lithium was found to be more effective than placebo in preventing relapse in mood disorder overall, and in bipolar disorder. The most consistent effect was found in bipolar disorder (random effects OR 0.29; 95% CI 0.09 to 0.93 ). In unipolar disorder, the direction of effect was in favour of lithium, but the result (when heterogeneity between studies was allowed for) did not reach statistical significance. Considerable heterogeneity was found between studies in all groups of patients. The direction of effect was the same in all studies; no study found a negative effect for lithium. Heterogeneity may have been due to differences in selection of participants, and to differing exposures to lithium in the pre-study phase resulting in variable influence of a discontinuation effect. There was little reported data on overall health and social functioning of participants under the different treatment conditions, or on the participants' own views of their treatment. Descriptive analysis showed that assessments of general health and social functioning generally favoured lithium. Small absolute numbers of deaths and suicides, and the absence of data on non-fatal suicidal behaviours, made it impossible to draw meaningful conclusions about the place of lithium therapy in suicide prevention. REVIEWER'S CONCLUSIONS: This systematic review indicates that lithium is an efficacious maintenance treatment for bipolar disorder. In unipolar disorder the evidence of efficacy is less robust. This review does not cover the relative efficacy of lithium compared with other maintenance treatments, which is at present unclear. There is no definitive evidence from this review as to whether or not lithium has an anti-suicidal effect. Systematic reviews and large scale randomised studies comparing lithium with other maintenance treatments (e.g. anti-convulsants, antidepressants) are necessary. Outcomes relating to death and suicidal behaviour should be included in all future maintenance studies of mood disorder.


Lithium and hematology: established and proposed uses
            (Focosi et al., 2009) Download
Lithium (as lithium carbonate) is an inexpensive drug, widely used in psychiatry for over 50 years in treatment of mood instability (bipolar disorder) and as an adjunct to antidepressants. Hematological effects of neutrophilia and increased circulating CD34+ cells of marrow origin have long been known. Lithium was at the center of hematological investigations in the 1980s, but no definitive use in hematology has yet emerged. We review evidence that lithium increases G-CSF and augments G-CSF effects. We suggest possible therapeutic uses of lithium in neutropenia. In bone marrow transplantation, preharvest lithium-assisted hematopoietic stem cell mobilization may be useful as well.

Age as a factor affecting lithium therapy.
            (Hewick et al., 1977) Download
1 We examined the case notes of 82 psychiatric out-patients (aged 21-84 years) receiving lithium prophylaxis and with steady-state plasma lithium levels. 2 The mean weight-related daily dose of lithium prescribed decreased by about 50% between the third and eight decades. 3 The corresponding steady-state plasma lithium levels showed a less marked tendency to decrease, this only being seen in the seventh and eighth decades. 4 In patients aged 50 years or over the daily lithium dose required to give a plasma level of 1 mmol l-1 (0.50 mmol kg-1) was significantly lower than that (0.65 mmol kg-1) in patients aged under 50 years (P less than 0¿5, Student's t-test). In patients aged 70-79 years this dose was 31% lower than in patients under 50 years. However, interindividual variation was great and it was estimated that age only contributed about 14% to the total interpatient variation. 5 Of the 36 patients under 50 years of age, 42% had minor lithium side-effects and 17% were not optimally controlled with lithium. The corresponding figures for the 46 'older' patients were 46% and 28%. 6 Generally the 50% dosage reduction seemed necessary to compensate for an age-related decrease in lithium excretion and to reduce lithium side effects to a level comparable to that acceptable in younger patients.

Using lithium as a neuroprotective agent in patients with cancer.
            (Khasraw et al., 2012) Download
Neurocognitive impairment is being increasingly recognized as an important issue in patients with cancer who develop cognitive difficulties either as part of direct or indirect involvement of the nervous system or as a consequence of either chemotherapy-related or radiotherapy-related complications. Brain radiotherapy in particular can lead to significant cognitive defects. Neurocognitive decline adversely affects quality of life, meaningful employment, and even simple daily activities. Neuroprotection may be a viable and realistic goal in preventing neurocognitive sequelae in these patients, especially in the setting of cranial irradiation. Lithium is an agent that has been in use for psychiatric disorders for decades, but recently there has been emerging evidence that it can have a neuroprotective effect.This review discusses neurocognitive impairment in patients with cancer and the potential for investigating the use of lithium as a neuroprotectant in such patients.

Lithium: a review of its metabolic adverse effects.
            (Livingstone and Rampes, 2006) Download
Treatment with lithium has long been recognized to be associated with metabolic adverse effects notably hypothyroidism, hyperparathyroidism, weight gain and nephrogenic diabetes insipidus. It is important that clinicians prescribing lithium are aware of these adverse effects and have a strategy for their detection and management. We review aspects of these actions of lithium including their prevalence, risk factors, biochemical changes involved and management, and discuss some advances that have been made in their understanding in recent years.

The use of lithium carbonate to reduce infection and leukopenia during systemic chemotherapy.
            (Lyman et al., 1980) Download
To investigate whether lithium ameliorates the infectious complications that accompany systemic chemotherapy, we studied 45 patients with small-cell bronchogenic carcinoma receiving combination chemotherapy and radiation therapy. Twenty received lithium carbonate, and 25 received no additional therapy. Control subjects experienced more days with neutropenia than the lithium-treated group (2.17 days per 100 patient-days vs. 0.29), more severe febrile episodes (seven patients vs. one patient), more days hospitalized with fever and neutropenia (1.92 per 100 patient-days vs. 0.18), and more infection-related deaths (five vs. none). Infection-free survival was significantly longer in the lithium-treated group than in controls (P less than 0.05). Delay in subsequent chemotherapy was longer (P less than 0.01) and the number of dose reductions greater (P less than 0.01) in the control group. For both leukocytes and neutrophils, the first cycle nadir, mean of all treatment nadirs, and the lowest nadir observed during treatment were significantly higher in the lithium group. Mean mid-cycle monocyte counts were greater in the lithium group (P less than 0.05) and correlated with concurrent serum lithium levels (rs = 0.74, P less than 0.05). We believe that lithium carbonate shows promise as a means of lowering the risk of infection among patients receiving cytotoxic therapy.


 

Adjuvant lithium improves the efficacy of radioactive iodine treatment in Graves' and toxic nodular disease.
            (Martin et al., 2012) Download
CONTEXT:  Lithium increases iodine retention in the thyroid gland and inhibits thyroid hormone release. Although lithium has been reported to improve the efficacy of radioactive iodine (RAI) treatment in Graves' disease, its role as an adjunct to RAI treatment of hyperthyroidism, particularly in toxic nodular disease, remains contentious. OBJECTIVE:  To assess whether adjuvant lithium increases the efficacy of a fixed dose RAI regimen in Graves' and toxic nodular hyperthyroid patients. DESIGN AND SETTING:  Retrospective cohort study in a tertiary referral centre. Two hundred and four hyperthyroid patients (163 Graves' disease, 26 toxic multinodular goitre and 15 solitary toxic thyroid adenoma). INTERVENTION:  One hundred and three patients received RAI alone (median dose 558 MBq). One hundred and one patients received RAI (median dose 571 MBq) with adjuvant lithium (800 mg/day for 10 days). MAIN OUTCOME MEASURE:  Proportion of patients cured at any time over a 1-year period following RAI treatment. Cure was defined as sustained (two or more sequential time points) biochemical euthyroidism or hypothyroidism during the follow-up period. RESULTS:  The likelihood of cure at any time was 60% greater in all hyperthyroid patients (Graves' plus toxic nodular disease) receiving adjuvant lithium (n = 204, P = 0·003). In patients with Graves' disease receiving RAI + lithium, there was a similar occurrence in cure (n = 163, P = 0·006). Cure was twice as likely in patients with toxic nodular (non-Graves') disease receiving RAI + lithium compared with RAI alone (n = 41, P = 0·01). CONCLUSIONS:  This study supports the use of adjuvant lithium to improve the efficacy of RAI in the treatment of Grave's disease and suggests a novel role in the management of toxic nodular (non-Graves') disease.

Lithium use in special populations.
            (Mohandas and Rajmohan, 2007) Download
Lithium, a monovalent cation, was first used for the treatment of mania in the 1940s. Half a century into its use, the drug continues to be the preeminent choice for bipolar disorder with antimanic, antidepressant (modest) and antisuicidal property. Lithium is the “gold standard” mood stabilizer against which potential mood stabilizer agents are judged. The therapeutic uses of lithium also include use as an augmenting agent in depression, schizoaffective disorder, aggression, impulse control disorder, eating disorders, attention deficit disorder and in certain subsets of alcoholism. Lithium has been used in many medical disorders, especially cluster headache and dermatological disorders (seborrheic dermatitis, eczematoid dermatitis, genital herpes).[1] The drug is however associated with neurologic, endocrine, cardiovascular, renal, dermatologic and gastrointestinal adverse effects and possible teratogenicity.


Adult hippocampal neurogenesis and its role in Alzheimer's disease
            (Mu and Gage, 2011) Download
The hippocampus, a brain area critical for learning and memory, is especially vulnerable to damage at early stages of Alzheimer's disease (AD). Emerging evidence has indicated that altered neurogenesis in the adult hippocampus represents an early critical event in the course of AD. Although causal links have not been established, a variety of key molecules involved in AD pathogenesis have been shown to impact new neuron generation, either positively or negatively. From a functional point of view, hippocampal neurogenesis plays an important role in structural plasticity and network maintenance. Therefore, dysfunctional neurogenesis resulting from early subtle disease manifestations may in turn exacerbate neuronal vulnerability to AD and contribute to memory impairment, whereas enhanced neurogenesis may be a compensatory response and represent an endogenous brain repair mechanism. Here we review recent findings on alterations of neurogenesis associated with pathogenesis of AD, and we discuss the potential of neurogenesis-based diagnostics and therapeutic strategies for AD.

The effect of lithium carbonate on the electroencephalogram of patients with affective disorders.
            (Platman and Fieve, 1969) Download
This paper examines the degree of electroencephalogram abnormality among the three phases of manic-depressive disease and the changes brought about by lithium carbonate. A double-blind study was performed on forty-five manic-depressive patients. There was no difference in the number of abnormal EEG patterns. Fifteen of 28 showed increasing abnormal EEGs when placed on lithium carbonate.

The dynamics of cortical and hippocampal atrophy in Alzheimer disease
            (Sabuncu et al., 2011) Download
OBJECTIVE: To characterize rates of regional Alzheimer disease (AD)-specific brain atrophy across the presymptomatic, mild cognitive impairment, and dementia stages. DESIGN: Multicenter case-control study of neuroimaging, cerebrospinal fluid, and cognitive test score data from the Alzheimer's Disease Neuroimaging Initiative. SETTING: Research centers across the United States and Canada. PATIENTS: We examined a total of 317 participants with baseline cerebrospinal fluid biomarker measurements and 3 T1-weighted magnetic resonance images obtained within 1 year. MAIN OUTCOME MEASURES: We used automated tools to compute annual longitudinal atrophy in the hippocampus and cortical regions targeted in AD. We used Mini-Mental State Examination scores as a measure of cognitive performance. We performed a cross-subject analysis of atrophy rates and acceleration on individuals with an AD-like cerebrospinal fluid molecular profile. RESULTS: In presymptomatic individuals harboring indicators of AD, baseline thickness in AD-vulnerable cortical regions was significantly reduced compared with that of healthy control individuals, but baseline hippocampal volume was not. Across the clinical spectrum, rates of AD-specific cortical thinning increased with decreasing cognitive performance before peaking at approximately the Mini-Mental State Examination score of 21, beyond which rates of thinning started to decline. Annual rates of hippocampal volume loss showed a continuously increasing pattern with decreasing cognitive performance as low as the Mini-Mental State Examination score of 15. Analysis of the second derivative of imaging measurements revealed that AD-specific cortical thinning exhibited early acceleration followed by deceleration. Conversely, hippocampal volume loss exhibited positive acceleration across all study participants. CONCLUSIONS: Alzheimer disease-specific cortical thinning and hippocampal volume loss are consistent with a sigmoidal pattern, with an acceleration phase during the early stages of the disease. Clinical trials should carefully consider the nonlinear behavior of these AD biomarkers.

A pathophysiological framework of hippocampal dysfunction in ageing and disease
            (Small et al., 2011) Download
The hippocampal formation has been implicated in a growing number of disorders, from Alzheimer's disease and cognitive ageing to schizophrenia and depression. How can the hippocampal formation, a complex circuit that spans the temporal lobes, be involved in a range of such phenotypically diverse and mechanistically distinct disorders? Recent neuroimaging findings indicate that these disorders differentially target distinct subregions of the hippocampal circuit. In addition, some disorders are associated with hippocampal hypometabolism, whereas others show evidence of hypermetabolism. Interpreted in the context of the functional and molecular organization of the hippocampal circuit, these observations give rise to a unified pathophysiological framework of hippocampal dysfunction.

The effect of lithium carbonate on leukopenia after chemotherapy.
            (Steinherz et al., 1980) Download
To evaluate the efficacy of lithium carbonate in ameliorating leukopenia, 37 patients (3 to 26 years old, mea (less than or equal to 1,000/mm3) over 40% of the time were designated at random on the last day of 82 separate chemotherapy courses to receive lithium or no treatment. Four could not take the drug because of the size of the capsules. There were 39 controls and 39 patients given lithium. Blood levels were maintained at 0.2 to 1.2 mEq/1 (median 0.7). The median drop of WBC in the treated group was 3,400/mm3 with a nadir of 1,800/mm3 vs 5,000 and 1,400, respectively, for the untreated patients (P LESS THAN 0.01). Eight patients (21%) in the lithium-treated group became severly leukopenic (less than or equal to 1,000/mm3) while 14 (36%) in the control group became leukopenic to that extent. Twenty-four patient days were spent with the WBC less than or equal to 1,000/mm3 after lithium and 57 days in the control group. Three patients required admission for 24 hospital days for fever while leukopenic after lithium, whereas seven patients spent 62 days in the hospital in the control group. Lithium reduces the period of leukopenia after chemotherapy during which time the patients may acquire infections.

 

Thyrotoxicosis

Lithium carbonate in the treatment of thyrotoxicosis. A controlled trial.
            (Kristensen et al., 1976) Download
Of 24 patients with newly diagnosed thyrotoxicosis, 13 were randomly selected for treatment with methimazole 40 mg per day, and 11 for treatment with lithium carbonate in such doses that the serum lithium lay between 0-5 and 1-3 meq. per litre. The lithium treatment brought about a fall in serum-thyroxine iodine (T4I) of 27.0%, and in the free-thyroxine index (F.T.I.) of 38.1% after 10 days. A comparison of the two patient groups with regard to the fall in F.T.I. after 3 and 10 days showed no statistically significant difference; similarly the calculated confidence limits appeared to exclude any difference of clinical importance. 8 of the 11 patients subjected to lithium treatment had side-effects, so that the general condition, which was already affected by the hyperthyroidism, was worsened. It is concluded that lithium cannot be considered superior to thiocarbamides for the rapid control of thyrotoxicosis.

Treatment of thyrotoxicosis with lithium carbonate.
            (Lazarus et al., 1974) Download
Eleven patients with a long history of Graves’ disease received lithium carbonate for 6 months as the sole therapy. Mean follow-up was 7-8 months. Eight patients were clinically euthyroid 2 weeks after starting therapy. Serum thyroxine iodine and triiodothyronine fell by 35 % during this period, but radioiodine uptakes did not fall to normal until 6-8 weeks after lithium therapy started. There was a significant reduction in absolute iodine uptake over 6 months but no consistent change in plasma-inorganic-iodine concentration. Seven patients relapsed 1-4 weeks after stopping therapy. It is concluded that lithium rapidly reduces thyroid function in hyperthyroid patients and can maintain the euthyroid state for up to 6 months. Lithium therapy does not seem to affect the course of the disease. It is suggested that lithium could be used in place of iodides in the management of hyperthyroidism in some cases.


 

Iatrogenic thyrotoxicosis: causal circumstances, pathophysiology, and principles of treatment-review of the literature.
            (Meurisse et al., 2000) Download
Thyrotoxicosis is the clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormones. In most instances thyrotoxicosis is due to hyperthyroidism, a term reserved for disorders characterized by overproduction of thyroid hormones by the thyroid gland. Nevertheless, thyrotoxicosis may also result from a variety of conditions other than thyroid hyperfunction. The present report focuses on the etiologies, pathophysiology, and treatment of iatrogenic thyrotoxicosis. Iatrogenic thyrotoxicosis may be caused by (1) subacute thyroiditis (a result of lymphocytic infiltration, cellular injury, trauma, irradiation) with release of preformed hormones into circulation; (2) excessive ingestion of thyroid hormones ("thyrotoxicosis factitia"); (3) iodine-induced hyperthyroidism (radiologic contrast agents, topical antiseptics, other medications). Among these causes of iatrogenic thyrotoxicosis, that induced by the iodine overload and cytotoxicity associated with amiodarone represents a significant challenge. Successful management of amiodarone-induced thyrotoxicosis requires close cooperation between endocrinologists and endocrine surgeons. Surgical treatment may have a leading yet often underestimated role in view of the potential life-threatening severity of this disease, whereas others kinds of iatrogenic thyrotoxicosis are usually treated conservatively.

Lithium as an adjunct to radioiodine therapy for thyrotoxicosis.
            (Turner et al., 1976) Download
16 patients with diffuse thyroid hyperplasia were given lithium carbonate (400 mg daily) for 1 week before and 1 week after a standardised 5 mCi therapy dose of 131I. A comparable control group of 16 patients were treated with 5 mCi of 131I without lithium therapy. The % retention of the therapy dose was measured in all patients at 7 days (168-hour 131I uptake). In the lithium-treated group the 24-hour 131I uptake showed no significant change after the first week of lithium therapy. The mean 48-hour protein-bound 131I, however, fell considerably from 1-21 to 0.55%/dose/1. The mean 24-168 hour % thyroidal 131I uptake drop was significantly less in the lithium group. These results show that low-dosage lithium therapy increases the retention of a standard-therapy dose of 131I. Lithium promises to be a useful adjunct to 131I therapy in patients with a rapid thyroidal iodine turnover and particularly in young patients where the total body-radiation dose must be kept to a minimum.

 


References

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Bschor, T, et al. (2011), ‘Lithium monotherapy increases ACTH and cortisol response in the DEX/CRH test in unipolar depressed subjects. A study with 30 treatment-naive patients.’, PLoS One, 6 (11), e27613. PubMed: 22132117
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