Lithium poisoning: Is determination of the red blood cell lithium concentration useful?

Balkhi, Souleiman El; Mégarbane, Bruno; Poupon, Joël; Baud, Frédéric J.; Galliot-Guilley, M.

doi:10.1080/15563650802392398

Cited by 47 publications

(30 citation statements)

References 49 publications

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“…Despite the obvious advantages of chronic lithium therapy, its clinical use is often curtailed by its narrow therapeutic index and its devastating overdose-induced toxicity. Furthermore, it should be noted that in spite of therapeutic lithium serum levels, wide variations between serum lithium levels and intracellular concentrations of lithium have been reported [22,23]. However, low dose levels have scantly been assessed in animal and clinical studies.…”

Section: Discussionmentioning

confidence: 99%

Effect of lithium on ventricular remodelling in infarcted rats via the Akt/mTOR signalling pathways

2017

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Activation of phosphoinositide 3-kinase (PI3K)/Akt signalling is the molecular pathway driving physiological hypertrophy. As lithium, a PI3K agonist, is highly toxic at regular doses, we assessed the effect of lithium at a lower dose on ventricular hypertrophy after myocardial infarction (MI). Male Wistar rats after induction of MI were randomized to either vehicle or lithium (1 mmol/kg per day) for 4 weeks. The dose of lithium led to a mean serum level of 0.39 mM, substantially lower than the therapeutic concentrations (0.8–1.2 mM). Infarction in the vehicle was characterized by pathological hypertrophy in the remote zone; histologically, by increased cardiomyocyte sizes, interstitial fibrosis and left ventricular dilatation; functionally, by impaired cardiac contractility; and molecularly, by an increase of p-extracellular-signal-regulated kinase (ERK) levels, nuclear factor of activated T cells (NFAT) activity, GATA4 expression and foetal gene expressions. Lithium administration mitigated pathological remodelling. Furthermore, lithium caused increased phosphorylation of eukaryotic initiation factor 4E binding protein 1 (p-4E-BP1), the downstream target of mammalian target of rapamycin (mTOR). Blockade of the Akt and mTOR signalling pathway with deguelin and rapamycin resulted in markedly diminished levels of p-4E-BP1, but not ERK. The present study demonstrated that chronic lithium treatment at low doses mitigates pathological hypertrophy through an Akt/mTOR dependent pathway.

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Section: Discussionmentioning

confidence: 99%

Effect of lithium on ventricular remodelling in infarcted rats via the Akt/mTOR signalling pathways

2017

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“…One answer may be differences between individuals in the penetration of lithium into brain tissues, which is determined by two factors: 14 1. Slow diffusion across the blood-brain barrier, with delayed transfer from plasma, and delayed exit back out.…”

Section: Commentary By David a Kahn MDmentioning

confidence: 99%

A Case With Reversible Neurotoxicity After 2 Years of Dementia Secondary to Maintenance Lithium Treatment

Soriano-Barceló

Alonso

Traba

et al. 2015

Journal of Psychiatric Practice

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Chronic neurotoxicity caused by lithium salts can be reversible or irreversible and may appear after years of treatment, even at serum levels considered within the usual therapeutic range. The authors present the case of a patient with bipolar disorder who developed dementia at the age of 54 after being treated with lithium carbonate at therapeutic levels for 4 years. Nevertheless, lithium treatment was continued. At age 56, the patient presented with an acute encephalopathy caused by toxic lithium levels, which resolved only after lithium carbonate was discontinued. Full recovery from the dementia, which had started 2 years earlier, occurred only after cessation of lithium. The authors conclude that when patients treated with lithium develop subacute cognitive impairment, the possibility of lithium toxicity should be considered, even if the serum levels are considered within the therapeutic range. A long duration of neurotoxicity associated with lithium treatment does not necessarily indicate an irreversible prognosis.

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“…However, toxic symptoms do not always correlate with plasma concentrations [24]. There is some correlation between Li serum levels and the severity of symptoms of intoxication [1].…”

Section: Discussionmentioning

confidence: 99%

Unrecognized acute lithium toxicity: a case report

et al. 2012

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AbstractWe report a case of a 63-year-old male who has been admitted to the Emergency department with nonspecific symptoms. Lithium toxicity was not at first recognized. When we obtained sufficient information about previous medication and medical history, we measured lithium levels found to be 1.46 mmol/L. Although the value of lithium was mildly elevated, nephrotoxicity was produced leading to severe renal insufficiency and neurological symptoms. Hemodialysis was started, and we succeed to treat the patient without squeals. This case illustrates some of the factors that lead to lithium toxicity as well as the need to consider lithium toxicity to the differential diagnosis of a patient presenting with renal insufficiency with or without change in mental status and neurologic symptom.

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Lithium poisoning: Is determination of the red blood cell lithium concentration useful?

Cited by 47 publications

References 49 publications

Effect of lithium on ventricular remodelling in infarcted rats via the Akt/mTOR signalling pathways

Effect of lithium on ventricular remodelling in infarcted rats via the Akt/mTOR signalling pathways

A Case With Reversible Neurotoxicity After 2 Years of Dementia Secondary to Maintenance Lithium Treatment

Unrecognized acute lithium toxicity: a case report

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