Tacrolimus-induced Permanent Asymptomatic Pontine Myelinolysis after Liver Transplantation

Bao, Jianfeng; Liang, Hui

doi:10.2169/internalmedicine.53.2418

Cited by 7 publications

(6 citation statements)

References 2 publications

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“…Our patient presented with an asymptomatic pontine lesion and diabetic amyotrophy almost simultaneously after the rapid treatment of poor glycemic control. Some asymptomatic cases with pontine lesions have been reported as ODS/CPM (16-18), but the histological confirmation of demyelination was not performed in those cases. Therefore, we simply described the cranial MRI abnormality in this case as a “asymptomatic pontine lesion”.…”

Section: Discussionmentioning

confidence: 99%

Asymptomatic Pontine Lesion and Diabetic Amyotrophy after Rapid Improvement of Poor Glycemic Control in a Patient with Type 1 Diabetes

et al. 2019

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We herein report a 28-year-old woman with type 1 diabetes with an asymptomatic pontine lesion and diabetic amyotrophy. She had suffered from diabetes from 10 years old. Treatment in a hospital reduced the hemoglobin A1c level from 14.2% to 7.2% for approximately 2 months. She suffered from acute-onset pain and weakness of the lower limb muscles without central nervous system manifestations. Magnetic resonance imaging showed high-intensity lesions at the brainstem and lower limb muscles on T2-weighted images. These findings and symptoms gradually resolved. Rapid treatment of poor glycemic control might increase the risk of asymptomatic pontine lesions and diabetic amyotrophy.

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Section: Discussionmentioning

confidence: 99%

Asymptomatic Pontine Lesion and Diabetic Amyotrophy after Rapid Improvement of Poor Glycemic Control in a Patient with Type 1 Diabetes

et al. 2019

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“…Osmotic demyelination syndrome (ODS) represents a severe complication which is usually attributed to a rapid correction of hyponatremia and/or surgery related complications [ 3 ]. Symptoms of ODS occur early after surgery and may manifest with various and not rarely atypical course [ 7 , 9 ]. To date, only few cases reporting the tacrolimus-associated central pontine myelinolysis have been reported in literature [ 9 – 12 ].…”

Section: Discussionmentioning

confidence: 99%

Tacrolimus-induced parkinsonism in a patient after liver transplantation – case report

et al. 2018

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BackgroundHepatic encephalopathy may manifest by a wide spectrum of neuropsychiatric symptoms, including cognitive impairment, seizures or extrapyramidal symptoms. The liver transplant can lead to improvement of the signs of encephalopathy but subsequent immunosuppressive treatment might possess pronounced neurotoxicity.Case presentationWe present a case report of a patient with chronic liver disease who developed signs of Parkinsonism after an orthotopic liver transplant, with consecutive immunosuppressant treatment with tacrolimus. Despite the improvement of liver functions due to the cytostatic treatment, a progressive worsening of neuropsychiatric symptoms associated with the presence of tremor was observed. Metabolic as well as endocrine dysfunctions were excluded as the primary causes of this condition. A brain CT did not reveal structural pathology. Signs of severe, symmetric Parkinsonism - with resting tremor, bradykinesia, rigidity and severe postural instability were observed. A brain MRI was performed with the presence of T2- hyperintensities in basal ganglia bilaterally. Tacrolimus blood concentration was elevated; hence the dose was reduced and later switched to less toxic sirolimus. Subsequently, clinical signs markedly improved after treatment modification. Improvement of clinical symptomatology after tacrolimus discontinuation supports the drug-induced etiology of this neurological condition.ConclusionsCytostatic treatment after solid organ transplantation often leads to signs of encephalopathy. If necessary, the dose of cytostatics needs to be reduced, or a less toxic agent must be chosen for the therapy. This modification is usually efficient with no further need for neurological intervention.

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“…Brain PET scan revealed no abnormalities of FDG-PET uptake. Based on few reports in the literature of tacrolimus-induced neurotoxicity, [1][2][3][4][5] we hypothesized that this was the potential culprit and changed to cyclosporine. Tacrolimus levels were therapeutic throughout his hospitalization (6.3-9.0 ng/mL).…”

Section: Oy-stersmentioning

confidence: 99%

“…[1][2][3][4][5] Tacrolimus is an immunosuppressive agent that inhibits calcineurin phosphatase activity and T lymphocyte activation. 7 Neurologic adverse effects range from tremors and headaches to cortical blindness and status epilepticus.…”

Section: Oy-stersmentioning

confidence: 99%

“…In a prospective study of 14 patients with tacrolimus neurotoxicity, 5 had white matter abnormalities on brain MRI, one had putaminal hemorrhage, and 8 were normal. 10 We found only 5 prior reports describing tacrolimus neurotoxicity presenting as a pontine predominant lesion with hyperintense signal on T2-weighted MRI, [1][2][3][4][5] and in these cases, the clinical presentations varied widely.…”

Section: Oy-stersmentioning

confidence: 99%

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Pearls & Oy-sters: Tacrolimus neurotoxicity presenting as an isolated brainstem lesion

Saadi

Schmahmann

2016

Neurology

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Tacrolimus-induced Permanent Asymptomatic Pontine Myelinolysis after Liver Transplantation

Abstract: A 57-year-old man presented to our clinic with mild dizziness. He had undergone liver transplantation due to chronic severe hepatitis two months previously. There had been no significant fluctuations in the serum sodium concen-

Cited by 7 publications

References 2 publications

Asymptomatic Pontine Lesion and Diabetic Amyotrophy after Rapid Improvement of Poor Glycemic Control in a Patient with Type 1 Diabetes

Asymptomatic Pontine Lesion and Diabetic Amyotrophy after Rapid Improvement of Poor Glycemic Control in a Patient with Type 1 Diabetes

Tacrolimus-induced parkinsonism in a patient after liver transplantation – case report

Pearls & Oy-sters: Tacrolimus neurotoxicity presenting as an isolated brainstem lesion

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