Safety of Low-Dose Oral Dantrolene Sodium on Hepatic Function

Kim, Jung Yoon; Chun, Sohyun; Bang, Moon Suk; Shin, Hyung Ik; Lee, Shi-Uk

doi:10.1016/j.apmr.2011.04.012

Cited by 15 publications

(11 citation statements)

References 14 publications

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“…Dantrolene inhibits ryanodine receptors in the ER and functions to suppress efflux of calcium from the ER to the cytosol ( Figure 1 ) [ 42 ]. Hepatotoxicity, even with sporadic short-term use, is a known side effect of this drug that may range from asymptomatic transaminase elevations to fulminant hepatic failure [ 16 ]. Previous reports of dantrolene-related fatal hepatotoxicity have been associated with daily doses greater than 300 mg/day [ 42 , 43 ].…”

Section: Discussionmentioning

confidence: 99%

“…Previous reports of dantrolene-related fatal hepatotoxicity have been associated with daily doses greater than 300 mg/day [ 42 , 43 ]. More recently it has been suggested that lower daily doses (i.e., <200 mg/day) may be safely used in patients without coexisting liver dysfunction or coingestion of hepatotoxic medications [ 16 ]. It is important to systematically evaluate dantrolene safety prior to it becoming usual care for WS because reduced cytosolic calcium in the setting of neuronal stimulation in WS in vitro neuronal models has been linked with poor mitochondrial function [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

“…In WFS1 deficient cells ATF-6 is no longer under negative inhibition and is permitted to constitutively activate genes that promote cellular apoptosis and decrease insulin gene expression [ 31 ]. Ⓑ ER calcium channels, such as the ryanodine receptor (RyR), but most importantly the inositol triphosphate receptor (IP3R), permit efflux of calcium from the ER to the cytosol [ 16 , 28 ]. It is believed that increased cytoplasmic calcium levels activate the calcium-dependent protease, calpain-2, which promotes cellular apoptosis [ 16 , 34 ].…”

Section: Figurementioning

confidence: 99%

“…Ⓑ ER calcium channels, such as the ryanodine receptor (RyR), but most importantly the inositol triphosphate receptor (IP3R), permit efflux of calcium from the ER to the cytosol [ 16 , 28 ]. It is believed that increased cytoplasmic calcium levels activate the calcium-dependent protease, calpain-2, which promotes cellular apoptosis [ 16 , 34 ]. Potential therapeutic targets include molecules which inhibit calcium efflux from the ER, such as dantrolene, via inhibition of the RyR [ 35 ], and rapamycin and pioglitazone, via inhibition of IP3R [ 34 ].…”

Section: Figurementioning

confidence: 99%

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Wolfram Syndrome: A Case Report and Review of Clinical Manifestations, Genetics Pathophysiology, and Potential Therapies

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McMillan

et al. 2018

Case Reports in Endocrinology

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Background Classical Wolfram syndrome (WS) is a rare autosomal recessive disorder caused by mutations in WFS1, a gene implicated in endoplasmic reticulum (ER) and mitochondrial function. WS is characterized by insulin-requiring diabetes mellitus and optic atrophy. A constellation of other features contributes to the acronym DIDMOAD (Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy, and Deafness). This review seeks to raise awareness of this rare form of diabetes so that individuals with WS are identified and provided with appropriate care. Case We describe a woman without risk factors for gestational or type 2 diabetes who presented with gestational diabetes (GDM) at the age of 39 years during her first and only pregnancy. Although she had optic atrophy since the age of 10 years, WS was not considered as her diagnosis until she presented with GDM. Biallelic mutations in WFS1 were identified, supporting a diagnosis of classical WS. Conclusions The distinct natural history, complications, and differences in management reinforce the importance of distinguishing WS from other forms of diabetes. Recent advances in the genetics and pathophysiology of WS have led to promising new therapeutic considerations that may preserve β-cell function and slow progressive neurological decline. Insight into the pathophysiology of WS may also inform strategies for β-cell preservation for individuals with type 1 and 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

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Wolfram Syndrome: A Case Report and Review of Clinical Manifestations, Genetics Pathophysiology, and Potential Therapies

Toppings

McMillan

et al. 2018

Case Reports in Endocrinology

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“…Therefore, for patients taking a high dose of dantrolene, it is helpful to consider the half life of the medication when making decisions about the timing of medication discontinuation [8,15]. However, there are individual differences in pharmacokinetics.…”

Section: Discussionmentioning

confidence: 99%

The effect of long-term oral dantrolene on the neuromuscular action of rocuronium: a case report

Jeon

Song

Kim

et al. 2014

Korean J Anesthesiol

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Oral dantrolene causes a dose-dependent depression of skeletal muscle contractility. A 52-year-old man treated with oral dantrolene for spasticity after spinal cord injury was scheduled to undergo irrigation and drainage of a thigh abscess under general anesthesia. He had taken 50 mg oral dantrolene per day for 3 years. Under standard neuromuscular monitoring, anesthesia was performed with propofol, rocuronium, and sevoflurane. A bolus dose of ED95 (0.3 mg/kg) of rocuronium could not depress T1 up to 95%. An additional dose of rocuronium depressed T1 completely and decreased the train-of-four (TOF) count to zero. There was no apparent prolongation of the neuromuscular blocking action of rocuronium. The TOF ratio was recovered to more than 0.9 within 40 minutes after the last dose of rocuronium. A small dose of oral dantrolene does not prolong the duration of action and recovery of rocuronium.

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