Posterior reversible encephalopathy syndrome in a melanoma patient with dabrafenib and trametinib treatment following immunotherapy

Stefanou, Maria‐Ioanna; Gepfner‐Tuma, Irina; Brendle, Cornelia; Kowarik, Markus C.; Meiwes, Andreas; Eigentler, Thomas; Müller, Alexandra; Garbe, Claus; Ziemann, Ulf; Tabatabai, Ghazaleh; Forschner, Andrea

doi:10.1111/ddg.13991

Cited by 6 publications

(6 citation statements)

References 17 publications

(26 reference statements)

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“…All cancer therapies were stopped, with PRES and DRESS resolution. Some resolute PRES are described after TT discontinuation, in second line after ICI, [4], but with fatal MM progression [7]. Immunoglobulin are used to treat acute encephalitis.…”

Section: Discussionmentioning

confidence: 99%

“…Severe grade III-IV adverse events are reported on both of therapies; immune-related adverse events (irAEs) may occur days, months, or years later [2]. Few cases of early acute posterior reversible encephalopathy syndrome (PRES) in metastatic melanoma [3,4], treated with TT are reported. We report an acute late-onset diffuse encephalopathy TT-induced, not resolving after treatment discontinuation in a CR-MM (metastatic melanoma with complete response).…”

Section: Introductionmentioning

confidence: 99%

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Acute Late-Onset Diffuse Encephalopathy Secondary to Target Therapies in Metastatic Melanoma

2023

Ann Case Report

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Immunotherapy and targeted therapies are both major drugs used for metastatic melanomas. Various severe adverse event are reported with both. Few cases of acute encephalopathy induced by targeted therapies are described, resolving after discontinuation, but it rarely occurs as a late adverse event. We report a severe acute late-onset diffuse encephalopathy induced by targeted therapy (BRAF and MEK inhibitors), not resolving after treatment discontinuation and immunosuppressive treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Acute Late-Onset Diffuse Encephalopathy Secondary to Target Therapies in Metastatic Melanoma

2023

Ann Case Report

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“…Consequently, enhanced fluid and cell diapedesis, and interstitial edema formation ensues. PRES manifestation and the dysfunction of microvasculature may be driven by the presence of checkpoint inhibitors (HSCT, chemotherapy, and immunosuppressive agent), by interactions with autoantibodies and autoreactive T-cells, and via abnormal secretion of angiogenic growth factors (VEGF) and proangiogenic cytokines (IL-8) (33,66,67), VEGF expression is increased, leading to increased vascular permeability and interstitial cerebral edema (33). Blood transfusion triggers a rapid increase in the hemoglobin, (Continued) FIGURE 4 | platelet, and viscosity levels, which is thought to trigger transfusion-associated circulatory overload (TACO) (68)(69)(70)(71).…”

Section: Discussionmentioning

confidence: 99%

Management and Clinical Outcome of Posterior Reversible Encephalopathy Syndrome in Pediatric Oncologic/Hematologic Diseases: A PRES Subgroup Analysis With a Large Sample Size

et al. 2021

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This study investigated the management and clinical outcomes along with associated factors of posterior reversible encephalopathy syndrome (PRES) in childhood hematologic/oncologic diseases. We present data from children with hematologic/oncologic diseases who developed PRES after treatment of the primary disease with chemotherapy and hematopoietic stem cell transplantation (HSCT) at 3 medical centers in Changsha, China from 2015 to 2020, and review all previously reported cases with the aim of determining whether this neurologic manifestation affects the disease prognosis. In the clinical cohort of 58 PRES patients, hypertension [pooled odds ratio (OR) = 4.941, 95% confidence interval (CI): 1.390, 17.570; P = 0.001] and blood transfusion (OR = 14.259, 95% CI: 3.273, 62.131; P = 0.001) were significantly associated with PRES. Elevated platelet (OR = 0.988, 95% CI: 0.982, 0.995; P < 0.001), hemoglobin (OR = 0.924, 95% CI: 0.890, 0.995; P < 0.001), and blood sodium (OR = 0.905, 95% CI: 0.860, 0.953; P < 0.001), potassium (OR = 0.599, 95% CI: 0.360, 0.995; P = 0.048), and magnesium (OR = 0.093, 95% CI: 0.016, 0.539; P = 0.008) were protective factors against PRES. Data for 440 pediatric PRES patients with hematologic/oncologic diseases in 21 articles retrieved from PubMed, Web of Science, and Embase databases and the 20 PRES patients from our study were analyzed. The median age at presentation was 7.9 years. The most common primary diagnosis was leukemia (62.3%), followed by solid tumor (7.7%) and lymphoma (7.5%). Most patients (65.0%) received chemotherapy, including non-induction (55.2%) and induction (44.8%) regimens; and 86.5% used corticosteroids before the onset of PRES. Although 21.0% of patients died during follow-up, in most cases (93.2%) this was not attributable to PRES but to severe infection (27.3%), underlying disease (26.1%), graft-vs.-host disease (14.8%), multiple organ dysfunction syndrome (8.0%), and respiratory failure (3.4%). PRES was more common with HSCT compared to chemotherapy and had a nearly 2 times higher mortality rate in patients with oncologic/hematologic diseases than in those with other types of disease. Monitoring neurologic signs and symptoms in the former group is therefore critical for ensuring good clinical outcomes following treatment of the primary malignancy.

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“…A recent pharmacological study reported 15 cases of peripheral neuropathy with two primary phenotypes: a symmetric, axonal, length-dependent polyneuropathy, and a demyelinating polyradiculoneuropathy (10). Additional neurological adverse events that have been reported include myasthenia, reversible posterior leukoencephalitis, and facial diplegia (11)(12)(13). Meirson et al observed that the combination of E/B was associated with an increased risk of peripheral neuropathy, including Guillain-Barrésyndrome (14).…”

Section: Case Reportmentioning

confidence: 99%

Case report: Parsonage-turner syndrome in a melanoma patient treated by BRAF/MEK inhibitors after immune checkpoint inhibitors

Bonnefin,

Duval,

Rouanet

et al. 2023

Front. Oncol.

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IntroductionCombination molecular BRAF/MEK inhibitors targeted therapy has been shown to improve overall survival in patients with BRAF V600 mutated unresectable or metastatic melanoma. Most patients treated with BRAF/MEK inhibitors will experience adverse events but neurological adverse events (nAEs) remain rare.Case reportA 42-year-old woman diagnosed with metastatic melanoma presented with an intense pain in the left shoulder 7 days after the beginning of encorafenib/binimetinib after immune checkpoint inhibitors (ICI) combination. No other triggering factors were identified. Electromyogram performed one month after the pain onset revealed a left brachial plexopathy suggestive of a Parsonage-Turner syndrome. The weakness slowly improved with intensive rehabilitation and targeted therapies were continued.ConclusionWe report the first case of Parsonage-Turner syndrome in a melanoma patient treated with encorafenib/binimetinib following checkpoint inhibitors combination.We cannot rule out the implication of ICI in the development of this syndrome but the rapid onset of the symptoms after the beginning of targeted therapies makes their involvment more likely.Given the increased use of BRAF/MEK inhibitors in managing of stage III and IV melanoma, as well as the development in stage II, clinicians should be aware of this potential side effect.

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Posterior reversible encephalopathy syndrome in a melanoma patient with dabrafenib and trametinib treatment following immunotherapy

Cited by 6 publications

References 17 publications

Acute Late-Onset Diffuse Encephalopathy Secondary to Target Therapies in Metastatic Melanoma

Acute Late-Onset Diffuse Encephalopathy Secondary to Target Therapies in Metastatic Melanoma

Management and Clinical Outcome of Posterior Reversible Encephalopathy Syndrome in Pediatric Oncologic/Hematologic Diseases: A PRES Subgroup Analysis With a Large Sample Size

Case report: Parsonage-turner syndrome in a melanoma patient treated by BRAF/MEK inhibitors after immune checkpoint inhibitors

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