Neuromuscular complications of hematopoietic stem cell transplantation

Ruzhansky, Katherine; Brannagan, Thomas H.

doi:10.1002/mus.24724

Cited by 16 publications

(9 citation statements)

References 38 publications

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“…Severe hypophosphatemia, hypokalemia, or hypermagnesemia can also results in diffuse weakness, and Guillain-Barre syndrome has been described after surgery or with viral reactivation. Inflammatory myopathies may occur more frequently after HSCT, sometimes in associated with GVHD [53]. Polymyositis has also been described with tacrolimus exposure [54].…”

Section: Clinical Syndromesmentioning

confidence: 99%

Neurologic Complications of Transplantation

Dhar

2017

Neurocrit Care

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Neurologic disturbances including encephalopathy, seizures, and focal deficits complicate the course 10-30% of patients undergoing organ or stem cell transplantation. While much or this morbidity is multifactorial and often associated with extra-cerebral dysfunction (e.g., graft dysfunction, metabolic derangements), immunosuppressive drugs also contribute significantly. This can either be through direct toxicity (e.g., posterior reversible encephalopathy syndrome from calcineurin inhibitors such as tacrolimus in the acute postoperative period) or by facilitating opportunistic infections in the months after transplantation. Other neurologic syndromes such as akinetic mutism and osmotic demyelination may also occur. While much of this neurologic dysfunction may be reversible if related to metabolic factors or drug toxicity (and the etiology is recognized and reversed), cases of multifocal cerebral infarction, hemorrhage, or infection may have poor outcomes. As transplant patients survive longer, delayed infections (such as progressive multifocal leukoencephalopathy) and post-transplant malignancies are increasingly reported.

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Section: Clinical Syndromesmentioning

confidence: 99%

Neurologic Complications of Transplantation

Dhar

2017

Neurocrit Care

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“…Speci cally, among our AML patients, alloSCT was the strongest predictor for developing peripheral neuropathy. While rare, an association between alloSCT treatment and neurological complications, including peripheral neuropathy, has been observed in patients with hematologic malignacies [41][42][43][44] . This association is largely attributed to chronic graft versus host disease [41][42][43] , but contributing factors also include immune system reconstitution 41 , drug complications 41,44 , prior neurological disease 41,44 , the female sex 45 , and total-body irridation 45 .…”

Section: Discussionmentioning

confidence: 99%

Complex I inhibitor of oxidative phosphorylation in advanced solid tumors and acute myeloid leukemia: phase I trials

Yap

Daver

Mahendra

et al. 2023

Nat Med

123

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While targeting oxidative phosphorylation (OXPHOS) is a rational anticancer strategy, patient bene t with OXPHOS inhibitors in the clinic has yet to be achieved. Based on promising preclinical data, we advanced IACS-010759, a highly potent and selective small-molecule inhibitor of mitochondrial complex I, into two phase I trials in patients with acute myeloid leukemia (NCT02882321) or advanced solid tumors (NCT03291938). Clinical ndings revealed that IACS-010759 had a narrow therapeutic index with emergent dose-limiting toxicities that included elevated blood lactate and neurotoxicity, obstructing efforts to maintain target plasma exposure. Consequently, only modest on-target inhibition and limited antitumor activity were observed. Follow-up reverse translational studies uncovered that IACS-010759 reduced oxygen consumption rates in neurons and damaged myelin. Further, IACS-010759-treated mice displayed behaviors indictive of neuropathy, which were minimized with the co-administration of a histone deacetylase 6 inhibitor. Our ndings urge caution in the continued development of complex I inhibitors as antitumor agents.

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“…Recently, several reports have shown that rituximab, a monoclonal antibody against B cell surface antigen CD20, could be an effective treatment for patients with refractory MG [25, 26]. Rituximab therapy also reduces the incidence of GVHD following allogeneic HSCT and exhibits a beneficial effect on steroid-refractory GVHD [27].…”

Section: Discussionmentioning

confidence: 99%

A possible role of low regulatory T cells in anti-acetylcholine receptor antibody positive myasthenia gravis after bone marrow transplantation

et al. 2017

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Background: Chronic graft-versus-host disease (GVHD) appears several months following allogenic hematopoietic stem cell transplantation (HSCT) and is clinically analogous to autoimmune disorder. Polymyositis is a common neuromuscular disorder in chronic GVHD, but myasthenia gravis (MG) is extremely rare. Hence, its pathophysiology and treatment have not been elucidated. Case presentation: A 63-year-old man with a history of chronic GVHD presented with ptosis, dropped head, and dyspnea on exertion, which had worsened over the previous several months. He showed progressive decrement of compound muscle action potential in the deltoid muscle evoked by 3-Hz repetitive nerve stimulation, a positive edrophonium test, and elevated levels of serum anti-acetylcholine receptor antibodies, which suggested a diagnosis of generalized MG. No thymoma was found. Flow cytometric analysis revealed a remarkable depletion of peripheral Tregs (CD4

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Neuromuscular complications of hematopoietic stem cell transplantation

Cited by 16 publications

References 38 publications

Neurologic Complications of Transplantation

Neurologic Complications of Transplantation

Complex I inhibitor of oxidative phosphorylation in advanced solid tumors and acute myeloid leukemia: phase I trials

A possible role of low regulatory T cells in anti-acetylcholine receptor antibody positive myasthenia gravis after bone marrow transplantation

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