Tizanidin-Absetzsymptome bei Stress-Kardiomyopathie

Mörkl, Sabrina; Bengesser, Susanne; Schöggl, Helmut; Bayer, Dietmar; Kapfhammer, H. P.

doi:10.1055/s-0034-1399167

Cited by 9 publications

(9 citation statements)

References 6 publications

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“…20 There have been international reports of sympatholytic withdrawal from either β-blockers or α-2-agonists leading to TCM; each case concluded a hyperadrenergic state was likely responsible. [21][22][23][24][25] Two cases of withdrawal from the antispasmodic baclofen and 1 case of antidepressant withdrawal leading to TCM were also reported. [26][27][28]…”

Section: Discussionmentioning

confidence: 99%

The Connection Between Opioid Withdrawal and Takotsubo Cardiomyopathy: Case Reports of ‘Opioid Octopus Heart’

Hack

Ojeniyi

Mamzhi

et al. 2022

Georgetown Medical Review

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Case PresentationsHere, we present 2 cases of TCM in patients who chronically used opioids, both at the same institution within 1 month of each other. The first patient is a 68-year-old man who presented with a chronic obstructive pulmonary disease exacerbation and did not disclose his long-standing opioid use disorder. One day after admission, he was found to be in opioid withdrawal and, soon after, developed TCM. He was originally treated for non-ST elevation myocardial infarction and opioid withdrawal but decompensated. He was sent to the intensive care unit (ICU) to receive pressors and fluid resuscitation. He soon recovered and his cardiac function returned to baseline. The second patient is a 33-year-old woman with opioid use disorder taking methadone who presented with lower extremity weakness, edema, and pain. She was diagnosed with infective endocarditis. While awaiting surgery and receiving antibiotics, she developed respiratory failure and was upgraded to the ICU. There was a lapse in her opioid treatment, and she subsequently developed TCM. She was treated with pressors and fluids in the ICU, and eventually recovered with reduced cardiac function at the time of discharge. ConclusionsWhile clinical evidence indicated opioid withdrawal as the likely provoking factor for development of TCM in the first case, the second patient's symptoms from other clinical complications confounded the cause of her TCM. Twelve similar cases have been reported in the literature, suggesting that opioid withdrawal may be associated with development of TCM. Further quantitative research is required to establish this relationship. Our findings contribute to the theoretical pathophysiology of TCM and offer important considerations for clinical management of opioid withdrawal.

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Section: Discussionmentioning

confidence: 99%

The Connection Between Opioid Withdrawal and Takotsubo Cardiomyopathy: Case Reports of ‘Opioid Octopus Heart’

Hack

Ojeniyi

Mamzhi

et al. 2022

Georgetown Medical Review

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“…THC is an α2-adrenergic receptor agonist, used to alleviate symptoms of spasticity associated with multiple muscle sclerosis, spinal cord injury, or neurodegenerative disease. 17 It is also used in treatment of painful muscle spasm associated with musculoskeletal damage, as well as low back pain. 18 We found that THC could inhibit U2 OS cell proliferation, invasion, and migration.…”

Section: Discussionmentioning

confidence: 99%

Tizanidine hydrochloride exhibits a cytotoxic effect on osteosarcoma cells through the PI3K/AKT signaling pathway

et al. 2019

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Objectives α2-adrenergic receptors are reportedly involved in cancer cell proliferation, invasion, and apoptosis through regulation of diverse molecules, which implies that it contributes to tumor progression. However, the functional significance of α2-adrenergic receptors in osteosarcoma (OS) is unclear. Tizanidine hydrochloride (THC), an α2-adrenergic receptor agonist, is often used to alleviate symptoms of spasticity. This study investigated the functional implications of THC treatment on human OS cells and the underlying mechanisms of resulting changes. Methods The proliferation of U2 OS cells was assessed by Cell Counting Kit-8; the migration and invasion capacities of U2 OS cells were then analyzed by transwell assay. Moreover, apoptosis in U2 OS cells was evaluated by flow cytometry and western blot analyses. Additionally, expression levels of key proteins in the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway were measured. Results THC inhibited the proliferation, migration, and invasion of U2 OS cells, but promoted apoptosis within these cells. Expression levels of p-AKT, p-mTOR, and p-P70S6K were reduced by exposure to THC, suggesting involvement of PI3K/AKT signaling in THC-induced cytotoxicity within OS cells. Conclusions THC may play a novel role in OS cell cytotoxicity, and these findings suggest a potent therapeutic strategy for OS treatment.

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“…The incidence of tizanidine withdrawal is difficult to ascertain as there are only 2 published case reports of its management. 2 , 3 Mörkl et al 2 described a 53-year-old patient who developed serious withdrawal syndrome after long-term high-dose treatment in the context of stress cardiomyopathy (with reflex tachycardia, hypertension, tremor, hypertonicity, and anxiety). They concluded that tizanidine dose should be gradually reduced under the supervision of a psychiatrist.…”

Section: Discussionmentioning

confidence: 99%

“…This episode of sudden adrenergic discharge suggested tizanidine withdrawal syndrome. We searched for other cases of tizanidine withdrawal in the literature (PUBMED and MEDLINE databases) and found only 2 reports 2 , 3 in which withdrawal was managed by restarting medication at low dose to reduce symptoms and then reduced progressively until it was fully stopped. Based on this literature, we restarted medication with tizanidine 2 mg every 8 hours (her previous regimen was 2 mg 8 times a day) and tapered down for 12 days (2 mg every 8 hours for 4 days, 2 mg every 12 hours for the next 4 days and 2 mg per day for the last 4 days).…”

Section: Case Reportmentioning

confidence: 99%

Management of Tizanidine Withdrawal Syndrome: A Case Report

Suárez-Lledó

Padullés

Lozano

et al. 2018

Clin Med Insights Case Rep

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Most drugs that act on the central nervous system (CNS) require dose titration to avoid withdrawal syndrome. Tizanidine withdrawal syndrome is caused by adrenergic discharge due to its α2-agonist mechanism and is characterized by hypertension, reflex tachycardia, hypertonicity, and anxiety. Although tizanidine withdrawal syndrome is mentioned as a potential side effect of cessation, it is not common and there have been few reports. We present the case of a 31-year-old woman with tizanidine withdrawal syndrome after discontinuing medication prescribed for a muscle contracture (tizanidine). She showed high adrenergic activity with nausea, vomiting, generalized tremor, dysthermia, hypertension, and tachycardia. Symptoms were reversed and successful reweaning was achieved by restarting tizanidine followed by slow downward titration. Withdrawal syndrome should be considered when drugs targeting the CNS are suddenly stopped. Weaning regimens should be closely monitored for acute withdrawal reactions.

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Tizanidin-Absetzsymptome bei Stress-Kardiomyopathie

Cited by 9 publications

References 6 publications

The Connection Between Opioid Withdrawal and Takotsubo Cardiomyopathy: Case Reports of ‘Opioid Octopus Heart’

The Connection Between Opioid Withdrawal and Takotsubo Cardiomyopathy: Case Reports of ‘Opioid Octopus Heart’

Tizanidine hydrochloride exhibits a cytotoxic effect on osteosarcoma cells through the PI3K/AKT signaling pathway

Management of Tizanidine Withdrawal Syndrome: A Case Report

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