Development of myasthenia gravis in a patient with chronic myeloid leukemia during treatment with nilotinib

Sanford, David; MacDonald, Maria; Nicolle, Michael W.; Xenocostas, Anargyros

doi:10.4081/hr.2014.5288

Cited by 7 publications

(8 citation statements)

References 14 publications

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“…Lorlatinib was continued given the favorable response of MG to immunosuppressants. AChR Ab positive MG cases have also been reported in two patients with chronic myeloid leukemia (CML) after starting nilotinib and imatinib, [ 36 , 37 ]. Both patients went into remission after treatment with pyridostigmine and prednisone.…”

Section: Drugs That Cause De Novo Mgmentioning

confidence: 99%

Drugs That Induce or Cause Deterioration of Myasthenia Gravis: An Update

Sheikh

Alvi

Soliven

et al. 2021

JCM

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Myasthenia gravis (MG) is an autoimmune neuromuscular disorder which is characterized by presence of antibodies against acetylcholine receptors (AChRs) or other proteins of the postsynaptic membrane resulting in damage to postsynaptic membrane, decreased number of AChRs or blocking of the receptors by autoantibodies. A number of drugs such as immune checkpoint inhibitors, penicillamine, tyrosine kinase inhibitors and interferons may induce de novo MG by altering the immune homeostasis mechanisms which prevent emergence of autoimmune diseases such as MG. Other drugs, especially certain antibiotics, antiarrhythmics, anesthetics and neuromuscular blockers, have deleterious effects on neuromuscular transmission, resulting in increased weakness in MG or MG-like symptoms in patients who do not have MG, with the latter usually being under medical circumstances such as kidney failure. This review summarizes the drugs which can cause de novo MG, MG exacerbation or MG-like symptoms in nonmyasthenic patients.

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Section: Drugs That Cause De Novo Mgmentioning

confidence: 99%

Drugs That Induce or Cause Deterioration of Myasthenia Gravis: An Update

Sheikh

Alvi

Soliven

et al. 2021

JCM

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“…The earliest reports were of 2 CML patients who developed MG after several years of treatment with busulfan. A summary of all cases of MPNs associated with MG is presented in Table 1 [14][15][16][17][18][19][20][21][22][23][24][25].…”

Section: Resultsmentioning

confidence: 99%

“…The authors of many reports had associated the onset of MG symptoms with the use of drugs to treat MPNs. Eg: TKI in [16], [17] and [18], busulfan in [24], [25] and [26], and interferon-alpha in [21]. However, there is no clarity in the mechanism of drug-induced MG in these reports.…”

Section: Discussionmentioning

confidence: 99%

Myasthenia Gravis and Myeloproliferative Neoplasms – Mere Association or Paraneoplastic Neurologic Syndrome: A Mini-Review

Sasi

Mohamed

et al. 2021

Preprint

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“…The patient was treated with pyridostigmine and prednisone with symptoms resolution and continued Nilotinib to achieve a major molecular response. The authors themselves were uncertain if the development of MG was related to Nilotinib, taking into account immunomodulatory effect reported by most of the TKI or to CML and related disturbed immune regulation [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

Neuromuscular complications following targeted therapy in cancer patients: beyond the immune checkpoint inhibitors. Case reports and review of the literature

et al. 2020

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Introduction In the last years, many new drugs have been developed targeting different oncology pathways, overall improving both quality of life and survival in several malignancies. However, the increase of those therapies is associated with novel toxicities, mainly immune-related adverse events (irAEs), never observed before. Different irAEs are now well characterized, and, among them, neuromuscular complications, following immune checkpoint inhibitor (ICPi) therapy, are increasingly studied and described. However, there are also neurological complications related to the use of other targeted therapies, less known and probably underestimated. Herein we describe two oncological patients who developed neuromuscular diseases after administration of targeted therapies, different from ICPi. Case reports The first patient was treated with the combination of Vemurafenib and Cobimetinib, BRAF and MEK inhibitors, respectively, for a cutaneous melanoma. One year after the beginning of the combined treatment, she developed a sub-acute motor neuropathy with predominant cranial nerve involvement. She was successfully treated with methylprednisolone. The second patient received therapy with Imatinib, tyrosine kinase inhibitor and precursor of the targeted therapy, for a gastrointestinal stromal tumour. Few days after the first administration, he developed generalized myasthenia gravis with respiratory failure. Clinical remission was obtained with plasma-exchange, intravenous immunoglobulins and steroids. Discussion and Conclusion We strengthen the relevance of neuromuscular complications which may occur long after treatment start or in patients receiving not only the latest ICPi but also "older" and apparently better-known targeted therapies. Also in the latter cases, an immune-mediated "off-target" pathogenic mechanism can be hypothesized, and consequences can be life threatening, if not promptly diagnosed and appropriately managed.

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Development of myasthenia gravis in a patient with chronic myeloid leukemia during treatment with nilotinib

Cited by 7 publications

References 14 publications

Drugs That Induce or Cause Deterioration of Myasthenia Gravis: An Update

Drugs That Induce or Cause Deterioration of Myasthenia Gravis: An Update

Myasthenia Gravis and Myeloproliferative Neoplasms – Mere Association or Paraneoplastic Neurologic Syndrome: A Mini-Review

Neuromuscular complications following targeted therapy in cancer patients: beyond the immune checkpoint inhibitors. Case reports and review of the literature

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