Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a boy 5 years old we admitted to our PICU with signs of impending hepatic failure (hypertransaminasemia, hyperammonemia, prolonged PT) following mild upper respiratory infection and irrepressible vomiting. We observed no neurological abnormalities excepting slight lethargy; on the contrary, EEG findings showed severe diffuse slowing and high-voltage Delta activity. Our diagnosis of Reye's syndrome was later confirmed by liver biopsy. Clinical and electrophysiological signs recovered after 48-72 hours and no explication was found for this anomalous Reye's syndrome presentation. Further studies are needed for understanding the basis of neurological involvement of stage I Reye's syndrome.
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PMID:[Clinical-instrumental dissociation in a case of Reye's syndrome]. 770 45

The clinicopathological features of a previously unrecognised type of acute encephalopathy prevalent among Japanese children is described by reviewing the records of 13 consecutive patients treated and 28 previously reported cases. The hallmark of this encephalopathy, proposed to be a novel entity termed acute necrotising encephalopathy of childhood, is multiple, necrotic brain lesions showing a symmetric distribution. The encephalopathy was noted in previously healthy children after respiratory tract infections, with presenting symptoms of coma, convulsions, vomiting, hyperpyrexia, and hepatomegaly. Laboratory examinations disclosed liver dysfunction, uraemia, and hypoproteinaemia. The histological appearance of the liver was variable and non-specific. Cerebrospinal fluid contained an increased amount of protein. Computed tomography and MRI showed the presence of symmetrically distributed brain lesions of the thalamus, cerebral white matter, brainstem, and cerebellum. Necropsy examination confirmed extensive fresh necrosis of these regions with evidence of local breakdown of the blood-brain barrier. Based on the characteristic combination of clinical and pathological findings, acute necrotising encephalopathy of childhood can be distinguished from previously known encephalopathies, including Reye's syndrome.
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PMID:Acute necrotising encephalopathy of childhood: a new syndrome presenting with multifocal, symmetric brain lesions. 2996 23

Reye's syndrome is considered a disease of the pediatric age. It is characterized by a prodrome of viral illness followed by vomiting and encephalopathy with associated hepatic dysfunction. This syndrome is potentially life-threatening with high morbidity and mortality rates. There are 27 other cases of adult onset Reye's syndrome reported in the literature. We describe a 18-year-old woman who developed varicella and four days later started with vomiting, delirium and in the following day she became comatose. Laboratory tests of liver function and pathology of a liver biopsy proved the diagnosis. The patient survived. A review of the proposed pathogenic mechanisms are presented. Our patient represents case the number 28 in world literature and the first in the mexican literature.
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PMID:[Reye's syndrome in an adult. Review of pathogenic mechanisms]. 783 23

This article describes the metabolic investigations to be applied in any clinical situation consistent with a late acute form of inborn error of metabolism: unexplained coma with or without focal neurological manifestations, recurrent vomiting with lethargy, episodes of ataxia with or without behaviour disorder, fits of psychiatric troubles. In each of these situations, careful medical history is of major importance searching for previous clinical manifestations such as episodes of coma, ataxia or vomiting, anorexia, failure to thrive, developmental delay, all very suggestive of metabolic disorder. The association of neurological symptoms and abnormal hepatic tests is also of great value and must not lead to the diagnosis of Reye's syndrome without considering a metabolic defect of fatty acid oxidation, urea cycle, respiratory chain, or Wilson's disease. When looking for an etiological origin, it is mandatory to collect all the biological information at the same time, also knowing that metabolic abnormalities may be mild and transitory, and that many of them are non specific (metabolic acidosis, hyperlactacidemia, hyperammonemia, hepatic tests disturbances) being encountered in collapsus, shock and multiple organ failure syndrome.
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PMID:[Diagnosis of metabolic coma in children]. 784 29

The medium-chain acylcoenzyme-A dehydrogenase enzyme (MCAD) is involved in the initial stages of breakdown of medium-chain-length fatty acids in mitochondria. A deficiency of this enzyme can become symptomatic during a catabolic state and may resemble Reye syndrome. We report the case of a 17-month-old white girl whose 1-day history of vomiting and agitation followed by generalized unresponsiveness caused her to be brought to a local emergency department. She died after resuscitative efforts failed, and an autopsy revealed severe cerebral edema, marked hepatic steatosis, and steatosis of the renal tubule epithelia. Electron microscopy of the liver showed cytoplasmic lipid spherules and mitochondria with dense matrices, changes similar to Reye syndrome; however, postmortem examination of the decedent's blood revealed elevated medium-chain-length acylcarnitines diagnostic of an MCAD deficiency. Although uncommon, a deficiency of this enzyme should be considered in apparent Reye syndrome victims.
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PMID:Medium-chain acylcoenzyme-A dehydrogenase deficiency. Not just another Reye syndrome. 811 90

Defects in mitochondrial beta-oxidation may result in severe metabolic crisis after metabolic stress. The combination of hypoketotic hypoglycaemia and concurrent collapse of mitochondrial metabolic function may be very similar to that in Reye syndrome. Chronic effects on cardiac and skeletal muscle may be seen in some patients with defective long-chain fatty acid oxidation. Less common symptoms include peripheral neuropathy, pigmentary retinopathy, and failure to thrive with recurrent diarrhoea or vomiting. Collectively, such disorders are relatively common and their association with sudden infant death leads to a considerable demand for laboratory investigation. Currently the laboratory methods available are not capable of dealing with this demand in a rational and cost-effective manner and it is necessary to have careful clinically- and pathologically-based selection procedures if a useful service is to result.
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PMID:Defects in mitochondrial fatty acid oxidation: clinical presentations and their role in sudden infant death. 844 23

Aspirin, Neem oil, valproic, adipic, benzoic, isovaleric, 3-mercaptopropionic and 4-pentenoic acids are implicated in the pathogenesis of Reye's syndrome, Jamaican vomiting sickness, and related chemical toxicities. These disorders are characterized by hyperammonemia, hypoglycemia, microvesicular steatosis and encephalopathy. The goal of this study was to determine whether chemicals implicated in Reye's-related disorders induce the mitochondrial permeability translation (MPT). The MPT is induced by opening of a high-conductance, cyclosporin-sensitive pore in the mitochondrial inner membrane, causing swelling, depolarization and uncoupling of oxidative phosphorylation. In freshly isolated rat liver mitochondria, unhydrolyzed aspirin (300 microM) did not induce the MPT in the presence of 50 microM CaCl2. Salicylate, the hydrolysis product of aspirin and its active metabolite, was much more potent causing dose-dependent onset of the MPT in a therapeutic range of concentrations (37.5-300 microM). Similarly, Neem oil and valproic, adipic, benzoic, isovaleric, 3-mercaptopropionic and 4-pentenoic acids induced onset of the MPT. In all cases, cyclosporin A (200 nM), a specific inhibitor of the permeability transition pore, blocked the MPT caused by these inducers. Induction of the MPT by these agents was not caused by mitochondrial depolarization because concentrations of valproic acid and salicylate inducing the MPT had little effect on mitochondrial delta psi. Moreover, equivalent uncoupling caused by 5 nM carbonyl cyanide p-trifluoromethoxyphenylhydrazone did not induce an MPT. These data suggest that induction of the MPT is a common pathophysiological mechanism causing mitochondrial injury in Reye's syndrome and Reye's-related drug toxicities.
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PMID:The mitochondrial permeability transition: a new pathophysiological mechanism for Reye's syndrome and toxic liver injury. 881 78

A case of sudden unexpected natural death in a 6-year-old girl was reported. She was found in dead with vomiting on her bed in the morning on 24. December. Autopsy did not reveal any injuries and abnormalities on her appearance. Small amount of light yellowish mucus in her nose, trachea and bronchus was found. Brain was slightly edematous (1395 g in weight). Liver was 750 g in weight and focal yellowish lesions were observed on its cut surfaces. Microscopically fatty degeneration (granulous fatty deposits) was observed in hepatocytes. Immunohistochemical staining of mitochondria in heart showed no staining microscopically, and degeneration and breakdown of mitochondria were found electromicroscopically. From the results of autopsy and histopathological findings, her cause of death was diagnosed as the Reye's syndrome.
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PMID:[An autopsy case of the Reye's syndrome]. 899 87

Reye's syndrome (RS) is a biphasic illness that occurs predominately in children and adolescents. A prodromal viral illness (frequently influenza A or B or chicken pox) is followed by protracted vomiting and neurologic changes that start 3 to 5 days later, just when the child seems to be recovering. Aspirin has been identified as one factor contributing to the metabolic disorder that occurs. Since 1986 the FDA has required labels on all aspirin products warning about the association of aspirin use and RS. Media messages heightened public awareness regarding the alternatives to aspirin for analgesia and antipyretic use. Since 1988, the incidence of RS has decreased dramatically. RS is now more prevalent in older adolescents who may self-medicate. Because early recognition of the disease is associated with decreased morbidity and mortality, it is important for health care providers to recognize the symptoms of RS. Unexpected vomiting and disturbed brain functioning following a viral illness are symptoms of RS in children and adolescents. In infants, the symptoms of RS may be more subtle, including diarrhea, respiratory disturbances, and seizures.
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PMID:Reye's syndrome: an update. 943 71

Reye syndrome (RS) is an acute encephalopathy in childhood, and is very rare in adulthood. Here we report a 21-year-old woman with RS. Because of her dysmenorrhea, she took 3 tablets of diclofenac sodium (25 mg) per day in 3 divided doses for two days. Two days after the last intake of the medicine, she developed high fever, nausea, vomiting, and disturbance of consciousness with delirium, i.e., acute encephalopathy. She did not have seizure, hemiplegia, or other focal neurological manifestations. The serum GOT level was normal at onset, but in 12 hours dramatically increased up to 8,632 IU/L. The serum bilirubin level was normal. The cerebrospinal fluid revealed normal cell count, and protein. Although the liver biopsy was not performed because of thrombocytopenia, we diagnosed her as an adult case of RS according to the clinical criteria of the Center for Disease Control. In addition to treatment for the brain edema, plasma exchange was performed once treat the encephalopathy at the onset. The next day, her consciousness level and serum GOT level markedly improved. She completely recovered from acute encephalopathy in a week after her admission. In conclusion, diclofenac sodium, as well as aspirin, should be considered as a possible causal agent for RS, and early plasma exchange may be beneficial.
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PMID:[An adult case of Reye syndrome induced by diclofenac sodium, and recovered by plasma exchange]. 974 77


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