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[PMID]:29187686
[Au] Autor:Matsuda M; Takesako S; Nakazaki M; Nandate T; Umehara F
[Ad] Endereço:Department of Neurology, Nanpuh Hospital.
[Ti] Título:[Portal-systemic encephalopathy with bilateral thalamic and internal capsule lesions using diffusion-weighted MRI in a super-aged patient].
[So] Source:Rinsho Shinkeigaku;57(12):759-763, 2017 Dec 27.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:We describe the case of a 90-year-old woman who was hospitalized in July 2016 and subsequently experienced a sudden decline in consciousness level resulting in a state of deep coma. Involuntary movements were not observed, and bilateral Babinski signs were inconclusive. Diffusion-weighted MRI (DWI) of the brain showed bilateral hyperintensity in the thalamus and internal capsule, laboratory testing detected high levels of plasma ammonia, and an electroencephalogram showed delta waves and triphasic waves predominantly in the frontal lobe. Based on these results, treatment for hepatic encephalopathy was administered, which led to an improvement in consciousness level, a decrease in plasma ammonia levels, and a normalization in the DWI scan. Abdominal computed tomography scan showed no abnormality in the liver, but revealed an abnormal blood vessel leading from the ileocolic vein to the inferior vena cava; the patient was diagnosed with portal-systemic encephalopathy. In deep coma patients, acute encephalopathy with hyperammonemia is important for differential diagnosis when DWI shows high-density legions in the thalamus and internal capsule.
[Mh] Termos MeSH primário: Imagem de Difusão por Ressonância Magnética
Encefalopatia Hepática/diagnóstico por imagem
Cápsula Interna/diagnóstico por imagem
Tálamo/diagnóstico por imagem
[Mh] Termos MeSH secundário: Idoso de 80 Anos ou mais
Diagnóstico Diferencial
Eletroencefalografia
Feminino
Encefalopatia Hepática/complicações
Seres Humanos
Hiperamonemia/etiologia
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-001068


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[PMID]:27771289
[Au] Autor:Dercksen M; Duran M; IJlst L; Kulik W; Ruiter JP; van Cruchten A; Tuchman M; Wanders RJ
[Ad] Endereço:Laboratory Genetic Metabolic Diseases, Departments of Pediatrics and Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Human Metabonomics, North-West University, Potchefstroom Campus, South Africa. Electronic address: marli.dercksen@nwu.ac.za.
[Ti] Título:A novel UPLC-MS/MS based method to determine the activity of N-acetylglutamate synthase in liver tissue.
[So] Source:Mol Genet Metab;119(4):307-310, 2016 12.
[Is] ISSN:1096-7206
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: N-acetylglutamate synthase (NAGS) plays a key role in the removal of ammonia via the urea cycle by catalyzing the synthesis of N-acetylglutamate (NAG), the obligatory cofactor in the carbamyl phosphate synthetase 1 reaction. Enzymatic analysis of NAGS in liver homogenates has remained insensitive and inaccurate, which prompted the development of a novel method. METHODS: UPLC-MS/MS was used in conjunction with stable isotope (N-acetylglutamic-2,3,3,4,4-d acid) dilution for the quantitative detection of NAG produced by the NAGS enzyme. The assay conditions were optimized using purified human NAGS and the optimized enzyme conditions were used to measure the activity in mouse liver homogenates. RESULTS: A low signal-to-noise ratio in liver tissue samples was observed due to non-enzymatic formation of N-acetylglutamate and low specific activity, which interfered with quantitative analysis. Quenching of acetyl-CoA immediately after the incubation circumvented this analytical difficulty and allowed accurate and sensitive determination of mammalian NAGS activity. The specificity of the assay was validated by demonstrating a complete deficiency of NAGS in liver homogenates from Nags -/- mice. CONCLUSION: The novel NAGS enzyme assay reported herein can be used for the diagnosis of inherited NAGS deficiency and may also be of value in the study of secondary hyperammonemia present in various inborn errors of metabolism as well as drug treatment.
[Mh] Termos MeSH primário: Aminoácido N-Acetiltransferase/genética
Carbamoil-Fosfato Sintase (Amônia)/genética
Hiperamonemia/diagnóstico
Distúrbios Congênitos do Ciclo da Ureia/diagnóstico
[Mh] Termos MeSH secundário: Acetilcoenzima A/metabolismo
Aminoácido N-Acetiltransferase/metabolismo
Animais
Carbamoil-Fosfato Sintase (Amônia)/deficiência
Seres Humanos
Hiperamonemia/genética
Hiperamonemia/metabolismo
Hiperamonemia/fisiopatologia
Fígado/enzimologia
Camundongos
Camundongos Knockout
Espectrometria de Massas em Tandem
Distúrbios Congênitos do Ciclo da Ureia/genética
Distúrbios Congênitos do Ciclo da Ureia/metabolismo
Distúrbios Congênitos do Ciclo da Ureia/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
72-89-9 (Acetyl Coenzyme A); EC 2.3.1.1 (Amino-Acid N-Acetyltransferase); EC 2.3.1.1 (NAGS protein, human); EC 6.3.4.16 (Carbamoyl-Phosphate Synthase (Ammonia))
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28745680
[Au] Autor:Belousova ED
[Ad] Endereço:Department of Psychoneurology and Epileptology ,Research and Clincal Institute of Pediatrics, Pirogov Russian National Research Medical University, Moscow, Russia.
[Ti] Título:[The decreased level of plasma carnitine in patients with epilepsy].
[Ti] Título:Snizhenie kontsentratsii karnitina u patsientov s épilepsiei..
[So] Source:Zh Nevrol Psikhiatr Im S S Korsakova;117(6):106-110, 2017.
[Is] ISSN:1997-7298
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Antiepileptic drugs (AEDs) have long been known to affect carnitine metabolism, dropping the plasma free carnitine. Valproate (VPA) was considered to be the strongest carnitine-reducing agent. VPA-induced hyperammonemic encephalopathy and hepatotoxicity are well known, and pre-existing carnitine deficiency can be a predisposing factor, especially in congenital metabolic disorders. Several studies have shown that carnitine supplementation in patients receiving VPA to result in subjective and objective improvements and to prevent VPA-induced hepatotoxicity and encephalopathy, in parallel with increases in carnitine serum concentrations. Level of free plasma carnitine <20 micromol/l (syn. carnitine deficiency) in patients with epilepsy (in 15-30% of cases) may occur not only with administration of VPA but with administration of other AEDs (phenobarbital, phenytoin, carbamazepine) and low nutritional intake of carnitine. Some findings indicate that the number of AEDs used is a risk factor for carnitine deficiency. It was established that body weight, height and multidrug therapy are significantly associated with low level of free plasma in epileptic patients. Carnitine deficiency can have severe consequences; but most epileptic patients suffering from it are asymptomatic. Although carnitine deficiency is not uncommon among patients receiving AEDs, it seems not necessary to routinely monitor carnitine levels in epileptic ambulatory patients, this is reasonable only in groups of risk. L-carnitine supplementation is clearly indicated in case of VPA-induced hepatotoxicity (i.v. administration) VPA overdose (i.v. administration), primary carnitine-transporter defect and is strongly recommended in specific secondary carnitine deficiency syndromes, symptomatic VPA-associated hyperammonemia, infants and young children receiving VPA, especially those younger than 2 years, patients with a complex neurologic disorder, who are receiving multiple AEDs, patients who have risk factors for hepatotoxicity and carnitine insufficiency. In the absence of double blind trials, clinical practice is based on empiric observation, clinical experience, and theory. Well-designed studies of specific and general uses of L-carnitine replacement therapy in patients with epilepsy are needed.
[Mh] Termos MeSH primário: Anticonvulsivantes/efeitos adversos
Cardiomiopatias/induzido quimicamente
Carnitina/sangue
Carnitina/deficiência
Epilepsia/sangue
Epilepsia/tratamento farmacológico
Hiperamonemia/induzido quimicamente
Doenças Musculares/induzido quimicamente
[Mh] Termos MeSH secundário: Anticonvulsivantes/uso terapêutico
Peso Corporal
Carbamazepina/efeitos adversos
Carbamazepina/uso terapêutico
Cardiomiopatias/tratamento farmacológico
Carnitina/uso terapêutico
Criança
Feminino
Seres Humanos
Hiperamonemia/tratamento farmacológico
Lactente
Masculino
Doenças Musculares/tratamento farmacológico
Síndromes Neurotóxicas/tratamento farmacológico
Síndromes Neurotóxicas/etiologia
Fatores de Risco
Ácido Valproico/efeitos adversos
Ácido Valproico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticonvulsants); 33CM23913M (Carbamazepine); 614OI1Z5WI (Valproic Acid); S7UI8SM58A (Carnitine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/jnevro201711761106-110


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[PMID]:28953637
[Au] Autor:Cattaneo CI; Ressico F; Valsesia R; D'Innella P; Ballabio M; Fornaro M
[Ad] Endereço:aAsl Novara, Department of Mental Health - Outpatient Unit bAsl Novara, Department of Mental Health - Inpatient Unit- Borgomanero, Novara cDepartment of Neuroscience, University School of Naples "Federico II", Naples, Italy.
[Ti] Título:Sudden valproate-induced hyperammonemia managed with L-carnitine in a medically healthy bipolar patient: Essential review of the literature and case report.
[So] Source:Medicine (Baltimore);96(39):e8117, 2017 Sep.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Valproic Acid is a commonly used psychiatric drug primarily used as a mood stabilizer. Mild hyperammonemia is a Valproic Acid common adverse effect. This report presents an example of treated hyperammonemia on Valproic acid therapy managed with L-carnitine administration in BD patients characterized by sudden vulnerability. PATIENT CONCERNS: We report the case of a 29-year-old man suffering from bipolar disorder (BD) and substance use disorder who exhibited sudden altered mental status upon admittance to the inpatient unit. The patient was started on Valproic acid with no improvement. DIAGNOSES: The patient had remarkably high ammonia levels (594 µg/dL) without hepatic insufficiency, likely due to his valproate treatment. INTERVENTIONS: The patient was administered lactulose, intravenous hydration, and i.v. levocarnitine supplementation 4.5 g/day. OUTCOMES: The administration leads to reduction of ammonia levels to 99 µg/dL within 12 hours upon initiation of carnitine therapy and progressive restore of his mental status within 24 hours. LESSONS: Resolution of hyperammonemia caused by Valproic acid therapy may be enhanced with the administration of L-carnitine. An interesting aspect of this case was how rapidly the patient responded to the carnitine therapy.
[Mh] Termos MeSH primário: Antimaníacos/efeitos adversos
Transtorno Bipolar/tratamento farmacológico
Carnitina/administração & dosagem
Hiperamonemia/tratamento farmacológico
Transtornos Relacionados ao Uso de Substâncias/tratamento farmacológico
Ácido Valproico/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Seres Humanos
Hiperamonemia/induzido quimicamente
Masculino
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antimanic Agents); 614OI1Z5WI (Valproic Acid); S7UI8SM58A (Carnitine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008117


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[PMID]:28592010
[Au] Autor:Guan HZ; Ding Y; Li DX; Dong H; Song JQ; Jin Y; Zhu ZJ; Sun LY; Yang YL
[Ad] Endereço:Department of Neonatology, Shanxi Provincial Children's Hospital, Taiyuan 030013, China.
[Ti] Título:[Clinical diagnosis and treatment of three cases with hyperornithinemia-hyperammonemia-homocitrullinuria syndrome].
[So] Source:Zhonghua Er Ke Za Zhi;55(6):428-433, 2017 Jun 02.
[Is] ISSN:0578-1310
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To study the clinical characteristics, methods of diagnosis and treatment of hyperornithinemia-hyperammonemia- homocitrullinuria (HHH) syndrome. From July 2011 to August 2016, 3 Chinese patients with HHH syndrome were enrolled in this study. The clinical course, biochemical features, brain MRI findings, and gene mutations were analyzed. The three patients' age at onset of symptoms was 3 months to 7 years, and the age of diagonosis was 3 years and 10 months to 9 years and 10 months. All of them presented with intolerance to protein-rich foods from the infant period, development retardation and abnormal posture. Case 1 and 2 had moderate mental retardation. Serum ammonia 25-276 µmol/L (reference range<60 µmol/L), alanine aminotransferase (ALT) 20-139 IU/L (reference range 9-50 IU/L), ornithine 29.12-99.44 µmol/L(reference range 15-100 µmol/L), urinary orotic acid 1.49-29.75 mmol/mol Cr (reference range 0-7 mmol/mol Cr), uracil 6.09-103.97 mmol/mol Cr (reference range 0-1.5 mmol/mol Cr). The cranial MRI revealed lesions in the basal ganglia, abnormal white matter signal, progressive demyelination and cerebral atrophy. On their SLC25A15 gene, a novel homozygous missense mutation c. 416A>G (p.E139G) was identified in case 1, a known pathogenic homozygous nonsense mutation c. 535C>T was found in case 2 and 3. Liver transplantation had been performed when case 1 was 6 years old. Significant improvements were observed in dietary habit, mental and motor functions, and biochemical parameters. After the dietary intervention with the supplements of arginine, L-carnitine, case 2 was improved, spastic paraplegia of case 3 had no mitigation. Liver transplant was recommended. HHH syndrome has an aversion to protein-rich food, and the patients have recurrent vomiting and progressive neurological dysfunction. Clinical diagnosis of HHH syndrome is difficult and patients may present with incomplete biochemical phenotype. The genetic analysis is key for the diagnosis. Depending on their condition, individuals with HHH syndrome can be treated with a low-protein diet, drugs and liver transplantation.
[Mh] Termos MeSH primário: Dieta com Restrição de Proteínas
Hiperamonemia/diagnóstico
Mutação
Ornitina/deficiência
Fenótipo
Distúrbios Congênitos do Ciclo da Ureia/diagnóstico
[Mh] Termos MeSH secundário: Arginina
Grupo com Ancestrais do Continente Asiático
Carnitina
Criança
Pré-Escolar
Testes Genéticos
Homozigoto
Seres Humanos
Lactente
Ornitina/uso terapêutico
Ácido Orótico
Proteínas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proteins); 61H4T033E5 (Orotic Acid); 94ZLA3W45F (Arginine); E524N2IXA3 (Ornithine); S7UI8SM58A (Carnitine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0578-1310.2017.06.007


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[PMID]:28562536
[Au] Autor:Mitani S; Kadowaki S; Komori A; Sugiyama K; Narita Y; Taniguchi H; Ura T; Ando M; Sato Y; Yamaura H; Inaba Y; Ishihara M; Tanaka T; Tajika M; Muro K
[Ad] Endereço:aDepartment of Clinical Oncology bDepartment of Diagnostic and Interventional Radiology cDepartment of Endoscopy, Aichi Cancer Center Hospital, Nagoya, Japan.
[Ti] Título:Acute hyperammonemic encephalopathy after fluoropyrimidine-based chemotherapy: A case series and review of the literature.
[So] Source:Medicine (Baltimore);96(22):e6874, 2017 Jun.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute hyperammonemic encephalopathy induced by fluoropyrimidines (FPs) is a rare complication. Its pathophysiology remains unclear, especially given the currently used regimens, including intermediate-doses of 5-fluorouracil (5-FU) or oral FP agents. We aimed to characterize the clinical manifestations in cancer patients who developed hyperammonemic encephalopathy after receiving FP-based chemotherapy.We retrospectively reviewed 1786 patients with gastrointestinal or primary-unknown cancer who received FP-based regimens between 2007 and 2012. Eleven patients (0.6%) developed acute hyperammonemic encephalopathy. The incidence according to the administered anticancer drugs were as follows: 5-FU (8 of 1176, 0.7%), S-1 (1 of 679, 0.1%), capecitabine (2 of 225, 0.9%), and tegafur-uracil (UFT) (0 of 39, 0%). Ten patients (90.9%) had at least 1 aggravating factor, including infection, dehydration, constipation, renal dysfunction, and muscle loss. All the 10 patients met the definition of sarcopenia. Median time to the onset of hyperammonemic encephalopathy in the cycle was 3 days (range: 2-21). Three patients (27.3%) developed encephalopathy during the first cycle of the regimen and the remaining 8 patients during the second or more cycles. Seven patients (63.6%) had received at least 1 other FP-containing regimen before without episodes of encephalopathy.All patients recovered soon after immediate discontinuation of chemotherapy and supportive therapies, such as hydration, infusion of branched-chain amino acids, and oral lactulose intake, with a median time to recovery of 2 days (range: <1-7). Four patients (36.4%) received FP-based regimens after improvement of symptoms; 3 patients were successfully managed with dose reduction, and 1 patient, who had developed encephalopathy due to S-1 monotherapy, received modified FOLFOX-6 therapy without encephalopathy later.FP-associated acute hyperammonemic encephalopathy is extremely rare, but a possible event at any time and even during the administration of oral FP agents. Particular attention is warranted when giving FP-based therapy for patients with aggravating factors, such as sarcopenia. This complication can be properly managed with early detection.
[Mh] Termos MeSH primário: Antimetabólitos Antineoplásicos/efeitos adversos
Encefalopatias/induzido quimicamente
Hiperamonemia/induzido quimicamente
Pirimidinas/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Idoso
Antimetabólitos Antineoplásicos/uso terapêutico
Encefalopatias/diagnóstico
Encefalopatias/terapia
Feminino
Seres Humanos
Hiperamonemia/diagnóstico
Hiperamonemia/terapia
Masculino
Meia-Idade
Pirimidinas/uso terapêutico
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (Pyrimidines)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170601
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006874


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[PMID]:28425418
[Au] Autor:Li H; Ma Z; Xie Y; Tian F
[Ad] Endereço:Department of gastroenterology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
[Ti] Título:Recurrent Hyperammonemia After Abernethy Malformation Type 2 Closure: a Case Report.
[So] Source:Ann Hepatol;16(3):460-464, 2017 May - Jun.
[Is] ISSN:1665-2681
[Cp] País de publicação:Mexico
[La] Idioma:eng
[Ab] Resumo:The Abernethy malformation is a rare congenital malformation defined by the presence of an extrahepatic portosystemic shunt. Although most patients are asymptomatic, clinical encephalopathy is present in 15% of cases. We present a patient with type 2 Abernethy malformation, hyperammonemia, and encephalopathy. Shunt closure was performed successfully using interventional angiography; however, hyperammonemia recurred 3 months later. The diagnosis of Abernethy malformation can be made easily, but the ideal patient management strategy has not yet been established. This is the first reported patient with recurrence of hyperammonemia after interventional treatment; we discuss the therapeutic options for Abernethy malformation.
[Mh] Termos MeSH primário: Embolização Terapêutica
Hiperamonemia/etiologia
Veias Mesentéricas/anormalidades
Veia Porta/anormalidades
Malformações Vasculares/terapia
[Mh] Termos MeSH secundário: Angiografia por Tomografia Computadorizada
Feminino
Encefalopatia Hepática/etiologia
Seres Humanos
Hiperamonemia/diagnóstico
Veias Mesentéricas/diagnóstico por imagem
Meia-Idade
Flebografia/métodos
Veia Porta/diagnóstico por imagem
Radiografia Intervencionista
Recidiva
Resultado do Tratamento
Malformações Vasculares/complicações
Malformações Vasculares/diagnóstico por imagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.5604/16652681.1235492


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[PMID]:28422839
[Au] Autor:Quirino M; Rossi S; Schinzari G; Basso M; Strippoli A; Cassano A; Barone C
[Ad] Endereço:aDepartment of Medical Oncology, Catholic University of Sacred Heart, Rome bDepartment of Medical Oncology, Humanitas Clinical and Research Center, Rozzano, Milan, Italy.
[Ti] Título:Unexpected side effect in mCRC: A care-compliant case report of regorafenib-induced hyperammonemic encephalopathy.
[So] Source:Medicine (Baltimore);96(16):e6522, 2017 Apr.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Regorafenib represents a treatment option in heavily pretreated patients affected by metastatic colorectal cancer (mCRC). Its safety profile is typical of small-molecule tyrosine-kinase inhibitors (TKIs) and most adverse events are manageable. PATIENT CONCERNS: A 56 years-old Caucasian man affected by mCRC with normal hepatic reserve was treated with regorafenib as second-line treatment. After only 2 days of therapy, the patient presented to the emergency department due to impairment of both spatial and temporal orientation and motor function with bradylalia. INTERVENTIONS: Serum ammonia level was 191 mmol/L, liver function tests and complete blood count were normal. Regorafenib was withheld and branched chain amino acids and lactulose were administered. OUTCOMES: Serum ammonia level returned within the normal range, but when regorafenib was restarted at a lower dose level, a new episode of acute confusion arised. MAIN LESSON: Discontinuation of regorafenib after confirmation of hyperammonemia is strongly recommended; reintroduction of the therapy at lower doses after resolution of symptoms related to hyperammonemic encephalopathy has to be discouraged.
[Mh] Termos MeSH primário: Antineoplásicos/efeitos adversos
Encefalopatias/etiologia
Hiperamonemia/etiologia
Compostos de Fenilureia/efeitos adversos
Piridinas/efeitos adversos
[Mh] Termos MeSH secundário: Antineoplásicos/uso terapêutico
Encefalopatias/fisiopatologia
Neoplasias Colorretais/tratamento farmacológico
Neoplasias Colorretais/fisiopatologia
Seres Humanos
Hiperamonemia/fisiopatologia
Masculino
Meia-Idade
Compostos de Fenilureia/uso terapêutico
Piridinas/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Phenylurea Compounds); 0 (Pyridines); 24T2A1DOYB (regorafenib)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006522


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[PMID]:28403092
[Au] Autor:Guo X; Wei J; Gao L; Xing B; Xu Z
[Ad] Endereço:Department of Neurosurgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, People's Republic of China.
[Ti] Título:Hyperammonemic coma after craniotomy: Hepatic encephalopathy from upper gastrointestinal hemorrhage or valproate side effect?: Case report and literature review.
[So] Source:Medicine (Baltimore);96(15):e6588, 2017 Apr.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Postoperative coma is not uncommon in patients after craniotomy. It generally presents as mental state changes and is usually caused by intracranial hematoma, brain edema, or swelling. Hyperammonemia can also result in postoperative coma; however, it is rarely recognized as a potential cause in coma patients. Hyperammonemic coma is determined through a complicated differential diagnosis, and although it can also be induced as a side effect of valproate (VPA), this cause is frequently unrecognized or confused with upper gastrointestinal hemorrhage (UGH)-induced hepatic encephalopathy. We herein present a case of valproate-induced hyperammonemic encephalopathy (VHE) to illustrate the rarity of such cases and emphasize the importance of correct diagnosis and proper treatment. PATIENT CONCERNS AND DIAGNOSES: A 61-year-old woman with meningioma was admitted into our hospital. Radical resection of the tumor was performed, and the patient recovered well as expected. After administration of valproate for 7 days, the patient was suddenly found in a deep coma, and her mental state deteriorated rapidly. The diagnoses of hepatic encephalopathy was confirmed. However, whether it origins from upper gastrointestinal hemorrhage or valproate side effect is uncertain. INTERVENTIONS AND OUTCOMES: The patient's condition fluctuated without improvement during the subsequent 3 days under the treatment of reducing ammonia. With the discontinuation of valproate treatment, the patient regained complete consciousness within 48 hours, and her blood ammonia decreased to the normal range within 4 days. LESSONS SUBSECTIONS: VHE is a rare but serious complication in patients after craniotomy and is diagnosed by mental state changes and elevated blood ammonia. Thus, the regular perioperative administration of VPA, which is frequently neglected as a cause of VHE, should be emphasized. In addition, excluding UGH prior to providing a diagnosis and immediately discontinuing VPA administration are recommended.
[Mh] Termos MeSH primário: Anticonvulsivantes/efeitos adversos
Coma/diagnóstico
Encefalopatia Hepática/diagnóstico
Hiperamonemia/diagnóstico
Complicações Pós-Operatórias/diagnóstico
Ácido Valproico/efeitos adversos
[Mh] Termos MeSH secundário: Coma/induzido quimicamente
Craniotomia
Diagnóstico Diferencial
Feminino
Hemorragia Gastrointestinal/complicações
Hemorragia Gastrointestinal/diagnóstico
Encefalopatia Hepática/induzido quimicamente
Seres Humanos
Hiperamonemia/induzido quimicamente
Neoplasias Meníngeas/tratamento farmacológico
Neoplasias Meníngeas/cirurgia
Meningioma/tratamento farmacológico
Meningioma/cirurgia
Meia-Idade
Complicações Pós-Operatórias/induzido quimicamente
Período Pós-Operatório
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticonvulsants); 614OI1Z5WI (Valproic Acid)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170430
[Lr] Data última revisão:
170430
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006588


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[PMID]:28400468
[Au] Autor:Hogrel JY; Janssen JBE; Ledoux I; Ollivier G; Béhin A; Stojkovic T; Eymard B; Voermans NC; Laforet P
[Ad] Endereço:Institute of Myology, Pitié-Salpêtrière Hospital, Paris, France.
[Ti] Título:The diagnostic value of hyperammonaemia induced by the non-ischaemic forearm exercise test.
[So] Source:J Clin Pathol;70(10):896-898, 2017 Oct.
[Is] ISSN:1472-4146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: The non-ischaemic forearm exercise test (NIFET) is used as a diagnostic tool for the screening of patients with exercise intolerance and for the diagnosis of various metabolic muscle disorders. The production of lactate and ammonia are generally analysed to guide the diagnosis. The aim of this retrospective study was to determine the level of ammonia rise, which can be suggestive of a muscle disease. METHODS: This retrospective study involved 1440 patients who underwent NIFET. The clinical files of the patients with hyperammonaemia were methodically studied. Normal values were derived from 60 healthy controls. RESULTS: 110 patients with hyperammonaemia were detected. They were classified as either having mild (between 94 and 141 µmol/L) or severe (more than 141 µmol/L) hyperammonaemia. Their diagnosis was studied with respect to the increase in lactate induced by the NIFET. CONCLUSIONS: Severe postexercise hyperammonaemia, even in the presence of a normal lactate response, is strongly suggestive of a muscle glycogen storage disease. Mild hyperammonaemia in the absence of other abnormalities is most likely non-specific and not indicative of a muscle disease.
[Mh] Termos MeSH primário: Teste de Esforço/métodos
Doença de Depósito de Glicogênio/diagnóstico
Hiperamonemia/etiologia
Doenças Musculares/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Feminino
Antebraço
Força da Mão
Seres Humanos
Masculino
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170413
[St] Status:MEDLINE
[do] DOI:10.1136/jclinpath-2017-204324



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