Hyperammonemic Encephalopathy After Chemotherapy

Rosario, Michael Del; Sl, Werlin; Lauer, Stephen J.

doi:10.1097/00004836-199712000-00026

Cited by 23 publications

(6 citation statements)

References 9 publications

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“…Urea cycle defects should be excluded by measurement of urinary amino acids and orotic acid. Effective therapies are lacking but hemodialysis or sodium benzoate to trap ammonia have been attempted [62].…”

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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“…Several strategies have been proposed to control hyperammonemia (Table 2) [15]. Some pharmacological agents (sodium benzoate and sodium phenylacetate) have been proposed to promote the elimination of ammonia, with variable outcomes [16]. In addition to ammonia-trapping agents, hemodialysis should be initiated early to promote ammonia elimination [17].…”

Section: Discussionmentioning

confidence: 99%

Fatal Idiopathic Hyperammonemia after Induction Chemotherapy for Acute Myeloid Leukemia

Angelo

Vincent

Komuta

et al. 2020

Case Reports in Hematology

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Idiopathic hyperammonemia is a rare but potentially fatal complication occurring in patients with acute leukemia or bone marrow transplantation. The role of some specific anticancer drugs may be discussed, but the etiology of hyperammonemia is often multifactorial. We report the case of a 40-year-old woman who developed fatal idiopathic hyperammonemia two weeks after induction chemotherapy with idarubicin-aracytine for acute myeloid leukemia. Despite intensive care management and extrarenal epuration, the patient was declared brain dead two days after hyperammonemia onset.

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“…Hyperammonemia has also been described in rare cases after heart-lung or lung transplantation [ 17 , 18 ]. Pathogenesis of hyperammonemia in these situations is believed to be multifactorial involving increased protein catabolism, parenteral nutrition, gastrointestinal hemorrhage, sepsis or mucositis [ 19 ], and transient acquired enzyme reductions affecting urea synthesis [ 20 ], as well as drug effects from chemotherapy agents [ 20 ].…”

Section: Pathophysiology Of Hyperammonemiamentioning

confidence: 99%

Hyperammonemia: What Urea-lly Need to Know: Case Report of Severe Noncirrhotic Hyperammonemic Encephalopathy and Review of the Literature

Upadhyay

Bleck

Busl

2016

Case Reports in Medicine

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Purpose. A 66-year-old man who presented with coma was found to have isolated severe hyperammonemia and diagnosed with a late-onset urea-cycle disorder. He was treated successfully and had full recovery. Methods. We report a novel case of noncirrhotic hyperammonemia and review the literature on this topic. Selected literature for review included English-language articles concerning hyperammonemia using the search terms “hyperammonemic encephalopathy”, “non-cirrhotic encephalopathy”, “hepatic encephalopathy”, “urea-cycle disorders”, “ornithine transcarbamylase (OTC) deficiency”, and “fulminant hepatic failure”. Results. A unique case of isolated hyperammonemia diagnosed as late-onset OTC deficiency is presented. Existing evidence about hyperammonemia is organized to address pathophysiology, clinical presentation, diagnosis, and treatment. The case report is discussed in context of the reviewed literature. Conclusion. Late-onset OTC deficiency presenting with severe hyperammonemic encephalopathy and extensive imaging correlate can be fully reversible if recognized promptly and treated aggressively.

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Hyperammonemic Encephalopathy After Chemotherapy

Abstract: A 16-year-old boy had hyperammonemia and encephalopathy develop after high-dose chemotherapy for acute lymphoblastic leukemia. He was treated successfully with the ammonia-trapping agents sodium benzoate and sodium phenylacetate.

Cited by 23 publications

References 9 publications

Neurologic Complications of Transplantation

Neurologic Complications of Transplantation

Fatal Idiopathic Hyperammonemia after Induction Chemotherapy for Acute Myeloid Leukemia

Hyperammonemia: What Urea-lly Need to Know: Case Report of Severe Noncirrhotic Hyperammonemic Encephalopathy and Review of the Literature

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