Decreased Lithium Clearance in Patients with Hyperthyroidism

Owada, Akira; Tomita, Kimio; Ujiie, Kazutomo; Akiba, Takashi; Marumo, Fumiaki

doi:10.1159/000187275

Cited by 9 publications

(7 citation statements)

References 21 publications

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“…40 Conversely hyperthyroidism can increase lithium reabsorption thereby reducing lithium excretion. 41 Hypothyroidism is associated with the development of severe neurotoxicity from lithium with an adjusted OR of 9.30 (95% CI 1.36-63.66). 9 Hyperparathyroidism : This is a known complication of lithium therapy 38 and may lead to volume depletion secondary to the osmotic effects of hypercalcemia. …”

Section: Risk Assessmentmentioning

confidence: 99%

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Lithium Poisoning

Baird-Gunning

Lea‐Henry

Hoegberg

et al. 2016

J Intensive Care Med

118

125

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Lithium is a commonly prescribed treatment for bipolar affective disorder. However, treatment is complicated by lithium's narrow therapeutic index and the influence of kidney function, both of which increase the risk of toxicity. Therefore, careful attention to dosing, monitoring, and titration is required. The cause of lithium poisoning influences treatment and 3 patterns are described: acute, acute-on-chronic, and chronic. Chronic poisoning is the most common etiology, is usually unintentional, and results from lithium intake exceeding elimination. This is most commonly due to impaired kidney function caused by volume depletion from lithium-induced nephrogenic diabetes insipidus or intercurrent illnesses and is also drug-induced. Lithium poisoning can affect multiple organs; however, the primary site of toxicity is the central nervous system and clinical manifestations vary from asymptomatic supratherapeutic drug concentrations to clinical toxicity such as confusion, ataxia, or seizures. Lithium poisoning has a low mortality rate; however, chronic lithium poisoning can require a prolonged hospital length of stay from impaired mobility and cognition and associated nosocomial complications. Persistent neurological deficits, in particular cerebellar, are described and the incidence and risk factors for its development are poorly understood, but it appears to be uncommon in uncomplicated acute poisoning. Lithium is readily dialyzable, and rationale support extracorporeal treatments to reduce the risk or the duration of toxicity in high-risk exposures. There is disagreement in the literature regarding factors that define patients most likely to benefit from treatments that enhance lithium elimination, including specific plasma lithium concentration thresholds. In the case of extracorporeal treatments, there are observational data in its favor, without evidence from randomized controlled trials (none have been performed), which may lead to conservative practices and potentially unnecessary interventions in some circumstances. More data are required to define the risk-benefit of extracorporeal treatments and their use (modality, duration) in the management of lithium poisoning.

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Section: Risk Assessmentmentioning

confidence: 99%

Section: Risk Assessmentmentioning

confidence: 99%

Lithium Poisoning

Baird-Gunning

Lea‐Henry

Hoegberg

et al. 2016

J Intensive Care Med

118

125

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show abstract

“…Alterations in thyroid function impact significantly on lithium excretion [24]. Hyperthyroidism induces avid tubular resorption of lithium, and subsequently results in a significant reduction in lithium clearance [25]. Interestingly, lithium may alter thyroid hormone receptor binding and potentially mask the signs of thyroid hormone excess [26], such that biochemical markers of thyroid function may be a better indicator of thyroid status than clinical examination.…”

Section: Effect Of Thyroid Functionmentioning

confidence: 99%

Lithium Toxicity: An Iatrogenic Problem in Susceptible Individuals

Oakley

Whyte

Carter

2001

Aust N Z J Psychiatry

100

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Severe lithium neurotoxicity occurs almost exclusively in the context of chronic therapeutic administration of lithium, and rarely results from acute ingestion of lithium, even in patients currently taking lithium. As such it is an iatrogenic illness, occurring in patients who have identifiable clinical risk factors: nephrogenic diabetes insipidus, older age, abnormal thyroid function and impaired renal function. Although administration of drugs which impair lithium clearance appeared to contribute minimally to chronic lithium poisoning in the absence of other factors, these drugs may well 'uncover' the predisposing risk factors and certainly should not be considered safe to use as a consequence of this study. The serious morbidity suffered by lithium toxic patients, and the cost to society due to long hospital stays, might be reduced by careful prescribing, vigilant monitoring and awareness of these factors, as they develop in otherwise stable patients. Review of existing therapeutic guidelines may be warranted.

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“…Cardiac symptoms are rare, but prolonged QTc intervals and/or severe bradycardia have been reported (13). Owada et al (7) reported that increased TRP and decreased FELi were observed in patients with hyperthyroidism and reverted to normal after antithyroid drug therapy. Therefore, it is quite likely that an important reason why the patient's lithium level increased and remained persistently high, particularly early in her course, was her thyrotoxicosis-which was probably recent in onset, as she had features that were consistent with silent thyroiditis.…”

Section: Sato Et Almentioning

confidence: 99%

“…In 1993, it was reported that reduced lithium clearance and increased tubular reabsorption of phosphate are observed in patients with hyperthyroidism and that these phenomena return to normal in the euthyroid state (7). Therefore, lithium toxicity might easily be observed when patients treated with lithium develop thyrotoxicosis, unless the lithium dose is reduced in order to maintain the serum lithium in the normal range (8).…”

Section: Introductionmentioning

confidence: 99%