Severe acute axonal neuropathy following treatment with arsenic trioxide for acute promyelocytic leukemia: a case report

Kühn, Marcus; Sammartin, Kety; Nabergoj, Mitja; Vianello, Fabrizio

doi:10.4084/mjhid.2016.023

Cited by 16 publications

(8 citation statements)

References 17 publications

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“…The neuropathy has been characterized as both mild and reversible, but sensory and motor polyneuropathy has been observed chronically. The pathogenesis is not well understood, but findings of acute axonal damage with demyelination have been reported previously in addition to associations with thiamine deficient states [ 30 ].…”

Section: Chemotherapeutic Agentsmentioning

confidence: 99%

Drug-Induced Peripheral Neuropathy: A Narrative Review

Jones

Urits

Wolf

et al. 2020

CCP

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Background: Peripheral neuropathy is a painful condition deriving from many and varied etiologies. Certain medications have been implicated in the iatrogenic development of Drug Induced Peripheral Neuropathy (DIPN) and include chemotherapeutic agents, antimicrobials, cardiovascular drugs, psychotropic, anticonvulsants, among others. This review synthesizes current clinical concepts regarding the mechanism, common inciting medications, and treatment options for drug-induced peripheral neuropathy. Methods: The authors undertook a structured search of bibliographic databases for peer-reviewed research literature using a focused review question and inclusion/exclusion criteria. The most relevant and up to date research was included. Results: Drug-induced peripheral neuropathy is a common and painful condition caused by many different and frequently prescribed medications. Most often, DIPN is seen in chemotherapeutic agents, antimicrobials, cardiovascular drugs, psychotropic, and anticonvulsant drugs. Certain drugs exhibit more consistent neuropathic side effects, such as the chemotherapeutic compounds, but others are more commonly prescribed by a larger proportion of providers, such as the statins. DIPN is more likely to occur in patients with concomitant risk factors such as preexisting neuropathy, diabetes, and associated genetically predisposing diseases. DIPN is often difficult to treat, however medications including duloxetine, and gabapentin are shown to reduce neuropathic pain. Advanced techniques of neuromodulation offer promise though further randomized and controlled studies are needed to confirm efficacy. Conclusion: Awareness of the drugs covered in this review and their potential for adverse neuropathic effect is important for providers caring for patients who report new onset symptoms of pain, paresthesia, or weakness. Prevention of DIPN is especially important because treatment often proves challenging. While many pharmacologic therapies have demonstrated analgesic potential in the pain caused by DIPN, many patients remain refractive to treatment. More studies are needed to elucidate the effectiveness of interventional, neuromodulating therapies.

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Section: Chemotherapeutic Agentsmentioning

confidence: 99%

Drug-Induced Peripheral Neuropathy: A Narrative Review

Jones

Urits

Wolf

et al. 2020

CCP

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“… 94–97 Thiamine deficiency may exacerbate heavy metal toxicity, as both arsenic trioxide and mercury can inhibit the pyruvate dehydrogenase complex, leading to irreversible axonal neuropathy. 98 …”

Section: Neuropathy and Statin Drugsmentioning

confidence: 99%

Pathophysiology, prevention, and treatment of beriberi after gastric surgery

Wilson

2020

Nutrition Reviews

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Beriberi is a nutritional complication of gastric surgery, caused by deficiency of vitamin B1, or thiamine. Thiamine deficiency leads to impaired glucose metabolism, decreased delivery of oxygen by red blood cells, cardiac dysfunction, failure of neurotransmission, and neuronal death. This review describes the history and pathophysiology of beriberi as well as the relationship between beriberi and nutritional deficiencies after gastric surgery. A literature review of the history and pathophysiology of beriberi and the risk factors for thiamine deficiency, particularly after gastric resection or bariatric surgery, was performed. Recommendations for nutritional follow-up post gastric surgery are based on current national guidelines. Patients may have subclinical thiamine deficiency after upper gastrointestinal surgery, and thus beriberi may be precipitated by acute illness such as sepsis or poor dietary intake. This may occur very soon or many years after gastrectomy or bariatric surgery, even in apparently well-nourished patients. Prompt recognition and administration of supplemental thiamine can decrease morbidity and mortality in patients with beriberi. Dietary education post surgery and long-term follow-up to determine nutritional status, including vitamin and mineral assessment, is recommended for patients who undergo gastric surgery.

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“…The onset of arsenic neuropathy can be acute, as in arsenic poisoning or during treatment of APL with arsenic trioxide (Kühn, Sammartin, Nabergoj, & Vianello, 2016); chronic, as in environmental arsenic exposure; or acute-on-chronic, as in ORAI (Dani, 2013). The diagnosis of acute arsenic neuropathy is straightforward and based on the association of gastrointestinal disorders, encephalopathy and mood disorders (Bahiga, Kotb, & El-Dessoukey, 1978;Campbell & Alvarez, 1989;Ratnaike, 2003).…”

Section: Arsenic Neuropathymentioning

confidence: 99%

Chronic arsenic intoxication diagnostic score (CAsIDS)

Dani

Walter

2017

J of Applied Toxicology

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Arsenic and its compounds are well-established, potent, environmentally widespread and persistent toxicants with metabolic, genotoxic, mutagenic, teratogenic, epigenetic and carcinogenic effects. Arsenic occurs naturally in the Earth's crust, but anthropogenic arsenic emissions have surmounted the emissions from important natural sources such as volcanism. Inorganic arsenicals exhibit acute and chronic toxicities in virtually all cell types and tissues, and hence arsenic intoxication affects multiple systems. Whereas acute arsenic intoxication is rare and relatively easy to diagnose, chronic arsenic intoxication (CAsI) is common but goes often misdiagnosed.Based on a review of the literature as well as our own clinical experience, we propose a chronic arsenic intoxication diagnostic score (CAsIDS). A distinctive feature of CAsIDS is the use of bone arsenic load as an essential criterion for the individual risk assessment of chronic arsenic intoxication, combined with a systemic clinical assessment. We present clinical examples where CAsIDS is applied for the diagnosis of CAsI, review the main topics of the toxicity of arsenic in different cell and organ systems and discuss the therapy and prevention of disease caused or aggravated by chronic arsenic intoxication. CAsIDS can help physicians establish the diagnosis of CAsI and associated conditions.

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Severe acute axonal neuropathy following treatment with arsenic trioxide for acute promyelocytic leukemia: a case report

Cited by 16 publications

References 17 publications

Drug-Induced Peripheral Neuropathy: A Narrative Review

Drug-Induced Peripheral Neuropathy: A Narrative Review

Pathophysiology, prevention, and treatment of beriberi after gastric surgery

Chronic arsenic intoxication diagnostic score (CAsIDS)

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