Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six severe epileptic patients developed stuporous encephalopathy with marked cognitive impairment when topiramate (TPM) and sodium valproate (VPA) were coprescribed for five patients, and when monotherapy with TPM was introduced for one patient. In four patients, ammonaemia increased and then returned to normal after TPM or VPA withdrawal. This severe potential side effect must be recognized. Moreover two distinct mechanisms might explain this toxicity: (1). a pharmacokinetic interaction between VPA and TPM, leading to hyperammonaemia, (2). a pharmacodynamic mechanism due to a direct toxicity of TPM in at-risk epileptic patients.
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PMID:Drug induced encephalopathy in six epileptic patients: topiramate? valproate? or both? 1507 54

Many patients develop confusion, lethargy, and cognitive and behavioral abnormalities during or after cardiac decompensation. Congestive heart failure and the accompanying elevation in systemic venous pressure and decrease in cardiac output can lead to changes within the cranial cavity that cause an encephalopathy. At times, excess cerebrospinal fluid accumulates within the cranium causing an apathetic state identical to that seen in patients with other causes of hydrocephalus. Awareness of the syndrome of cardiac encephalopathy and optimal management of congestive heart failure and body fluids can reverse the neurologic dysfunction. In some patients with excess cerebrospinal fluid, lumbar puncture with removal of cerebrospinal fluid can reverse the apathetic state.
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PMID:Cardiac Encephalopathy. 1509 13

This report describes 4 fatal cases of serum hepatitis associated with the administration of commercial plasma in the horse. Serum hepatitis in the horse is characterized by acute hepatic central lobular necrosis, and it has been associated with the administration of biological products of equine origin. None of these horses had a recent history of equine biologic-origin vaccination; however, they had received 1.5-5 L of commercial plasma, and in I horse, an additional 8 L of fresh blood. Acute, severe colic unresponsive to medical therapy, lethargy, or sudden death developed in these 4 horses 41 to 60 days later. Two of the horses developed encephalopathy, confirmed in 1 horse by the presence of severe diffuse Alzheimer type II astrocytes in the brain. Although the prevalence of serum hepatitis associated with the administration of commercial plasma appears to be low in the horse, it should be considered an uncommon but potentially fatal risk factor.
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PMID:Serum hepatitis associated with commercial plasma transfusion in horses. 1571 60

Glycine encephalopathy is a rare autosomal recessive metabolic disease characterized by glycine accumulation in body fluids owing to a defect in the glycine cleavage system. There are several forms of glycine encephalopathy. In the classic or neonatal form, symptoms usually develop as neurologic symptoms in the first few days of life. It characteristically presents with hypotonia, lethargy, apnea, and seizures and usually results in death by 1 year of age. In this report, we present two cases of neonatal glycine encephalopathy accompanied by isolated pes equinovarus deformity.
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PMID:Two cases of glycine encephalopathy accompanied by pes equinovarus. 1599 6

A previously healthy 4-year-old boy was admitted because of acute liver failure. He was icteric, lethargic, had elevated ammonia and abnormal liver function tests. Serology was negative for viral hepatitis. There was no history of hepatotoxic drugs. Family history was unremarkable. The child was taken to the operating room for a living-related hepatic transplant. Frozen section showed massive hepatic leukemic infiltration and hepatocellular necrosis. Bone marrow aspiration confirmed the diagnosis of acute lymphoblastic leukemia (ALL). Transplant was withheld and chemotherapy was attempted. He died the following day due to systemic leukemic infiltration, cerebral edema, and severe anoxic ischemic encephalopathy.
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PMID:Acute lymphoblastic leukemia presenting in fulminant hepatic failure. 1610 32

Respiratory syncytial virus (RSV) has been described as the single most important virus causing acute respiratory infections, especially bronchiolitis and pneumonia, in children. The most severe infections affect the youngest infants and well-defined high-risk groups, including infants with a history of premature birth, and those with chronic lung disease, congenital heart disease, cystic fibrosis and immunodeficiency. It has been reported that approximately 1/3 of high-risk children hospitalized with RSV infection are admitted to the intensive care unit, while the need for mechanical ventilation and mortality rate are increased in infants with underlying cardiac disease or chronic lung disease. The majority of infants hospitalized for RSV lower respiratory tract infection develop one complication or more, which have an impact on hospital length of stay and costs. A relatively uncommon complication consisting of seizures and other neurologic abnormalities such as lethargy, irritability and abnormal tone has been sporadically reported in infants and children with RSV respiratory infection. A recent study first focused on the association between RSV bronchiolitis and an encephalopathic process occurring in the form of a seizures disorder. This transient neurologic complication seems to be frequently associated with an abnormal EEG pattern, but no anatomic brain damages have been shown. Little is known about the long-term neurodevelopmental outcomes of children developing RSV-related encephalopathy, so a prolonged period of neurologic follow up can be recommended.
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PMID:Acute encephalopathy associated with respiratory syncytial virus infections in childhood. A literature review. 1617 Feb 98

We report the case of a 7-year-old girl with ornithine transcarbamylase deficiency whose quality of life (QOL) improved greatly after a living donor liver transplantation (LDLT). Ornithine transcarbamylase deficiency had been diagnosed when she was 2 years old and she finally underwent LDLT, with her father as the donor, when she was 7 years old. The patient had suffered episodes of hyperammonemic encephalopathy ranging from lethargy to coma, treated by hemodialysis twice before LDLT, and her intelligence quotient was borderline for her age. Preoperative magnetic resonance imaging (MRI) showed an atrophic area in the subcortical white matter of the frontal lobe. After LDLT, the patient suffered acute rejection with hyperamylasemia, but not hyperammonemia. Postoperative MRI and quantitative MR spectroscopy showed no changes in the subcortical lesion. She has been followed up carefully for 16 months and has had no further complications or any sign of hyperammonemia.
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PMID:Improved quality of life and unchanged magnetic resonance brain imaging after living donor liver transplantation for late-onset ornithine transcarbamylase deficiency: report of a case. 1634 94

Birth asphyxia is one of the common causes of mortality and morbidity in neonates and the incidence is 2-9 per 1,000 live borns. The present work is a retrospective hospital based observational study. Babies born at B.P. Koirala Institute of Health Sciences, Dharan, Nepal during the period from April 2002 to April 2003 with gestational age >or=37 weeks with Apgar score <or=6 at 5 minutes were included in the study. The aim was to study the clinical profile, the acid base parameters and the outcome of asphyxiated newborns. Babies with congenital defects, evidence of infection and maternal drug addiction were excluded from the study. All babies were resuscitated according to the guidelines of American Heart Association. Data on 50 birth asphyxia cases were tabulated and analysed. There were 10 (20%) cases of severe birth asphyxia (Apgar score: 1-3 ) and 40 (80%) cases of moderate birth asphyxia (Apgar score: 4-6). Staging of hypoxic ischaemic encephalopathy (HIE) was performed according to Sarnat's staging. Thirty percent of these cases presented with various stages of HIE and the incidence was higher in low Apgar score group. The common presentations of HIE cases had depressed neonatal reflexes, seizures, lethargy, and pupillary abnormalities. The common acid base disturbance was metabolic acidosis which was observed only in babies with HIE-3. Two neonates (4%) died during the hospital stay due to multiorgan failure and severe metabolic acidosis.
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PMID:Outcome of newborns with birth asphyxia. 1655 70

Although posterior reversible encephalopathy syndrome (PRES) is caused by various conditions, there have been no reports on PRES associated with bronchial asthma. We report a case with PRES during the treatment for severe asthmatic attack. A 4-year-old girl was treated for asthmatic attack with steroids. From the 10th hospital day, hypertension, pulmonary edema, and cardiomegaly were observed. In spite of treatment with furosemide, she became lethargic and had a generalized convulsion on the 23rd hospital day. CT showed low density areas in the bilateral occipital white matter and MRI on the 28th hospital day demonstrated high intensity areas in the same regions on T2-weighted and FLAIR images. After discontinuation of corticosteroid and further antihypertensive therapy, her consciousness improved. MRI on the 67th hospital day had no abnormalities and no neurological sequelae were seen at 2 years after the event. We should be aware that PRES is a rare but important adverse event related to steroid therapy, because hypertension and water retention are major adverse effects of steroids.
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PMID:Posterior reversible encephalopathy syndrome in a child with bronchial asthma. 1661 1

Valproate-induced hyperammonemic encephalopathy (VHE) is an unusual complication characterized by a decreasing level of consciousness, focal neurological deficits, cognitive slowing, vomiting, drowsiness, and lethargy. We have thoroughly reviewed the predisposing factors and their screening, the biochemical and physiopathological mechanisms involved, the different treatments described, and those that are being investigated. Etiopathogenesis is not completely understood, although hyperammonemia has been postulated as the main cause of the clinical syndrome. The increase in serum ammonium level is due to several mechanisms, the most important one appearing to be the inhibition of carbamoylphosphate synthetase-I, the enzyme that begins the urea cycle. Polytherapy with several drugs, such as phenobarbital and topiramate, seems to contribute to hyperammonemia. Hyperammonemia leads to an increase in the glutamine level in the brain, which produces astrocyte swelling and cerebral edema. There are several studies that suggest that treatment with supplements of carnitine can lead to an early favorable clinical response due to the probable carnitine deficiency induced by a valproate (VPA) treatment. Development of the progressive confusional syndrome, associated with an increase in seizure frequency after VPA treatment onset, obliges us to rule out VHE by screening for blood ammonium levels and the existence of urea cycle enzyme deficiency, such as ornithine carbamoyltransferase deficiency. Electroencephalography (EEG) is characterized by signs of severe encephalopathy with continuous generalized slowing, a predominance of theta and delta activity, occasional bursts of frontal intermittent rhythmic delta activity, and triphasic waves. These EEG findings, as well as clinical manifestations and hyperammonemia, tend to normalize after VPA withdrawal.
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PMID:Valproate-induced hyperammonemic encephalopathy. 1677 19


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