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)

Reye's syndrome (encephalopathy and fatty liver) is generally considered a disease of children. Four patients, aged 16, 18, 19, and 23 years, with Reye's syndrome were initially seen by internists. A viral prodrome followed by vomiting and encephalopathy without focal neurological signs or jaundice clinically suggested Reye's syndrome. Normal findings of CSF examination (except for increased opening pressure), abnormal findings of liver function tests, and increased blood ammonia further supported the diagnosis. None was hypoglycemic. Reye's syndrome was related to influenza B virus in three patients and to Varicella in another. Three patients survived. Reye's syndrome may be seen intially by general practitioners, emergency room physicians, internists, or psychiatrists. The importance of considering this syndrome in the differential diagnosis of unexplained encephalopathy in adults is stressed.
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PMID:Reye's syndrome in nonpediatric age groups. 48 May 58

We report a patient who developed delayed gastric emptying with vomiting and weight loss simultaneously with herpes zoster in the sixth right thoracic dermatome. Sequential radionuclide solid egg meal gastric emptying studies were used to document gastroparesis, the response to metoclopramide and its transient nature. We present a possible explanation for this phenomenon within the context of the known pathophysiology of varicella-zoster infection.
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PMID:Transient gastroparesis associated with cutaneous herpes zoster. 381 85

Clinicians and nurses should obtain a history of antecedent illness occurring within 2 weeks of the onset of vomiting. Ninety percent of school-age children will give a history of an antecedent illness (varicella or influenza-like respiratory illness) within 1 week of the onset of vomiting. The vomiting of Reye's syndrome is usually persistent, lasting for 24 to 96 hours before the onset of serious brain signs. We believe that any child with the history of flu or chickenpox within 1 week of the onset of vomiting, which lasts for more than 12 hours, and is unusually severe or is associated with lethargy, should have an SGPT (alanine aminotransferase). This laboratory measure is clearly elevated in most cases of Reye's syndrome.
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PMID:Management of Reye's syndrome: need for early diagnosis and intravenous treatment of stage I non-comatose cases. 402 67

Serum salicylate concentration was measured at admission in 130 children with liver-biopsy-confirmed Reye's disease. Mean serum salicylate was 12.3 mg/dl and mean salicylate concentrations by neurological grade (Lovejoy) were: stage I, 12, stage II, 13, stage III, 11, stage IV, 13, and stage V, 13 mg/dl. However, mean serum salicylate (15 mg/dl) at admission in 21 patients who died or had serious neurological deficits was significantly higher than that in 103 patients who survived without neurological sequelae (10 mg/dl). Serum salicylate in a group of 27 age-matched, community-matched control children collected consecutively over the period 1978-80 was less than 2 mg/dl, and children with varicella or influenza had salicylate concentrations indistinguishable from apparently well classmates or siblings. It is impossible to determine from this data whether salicylates are involved in the aetiology of or in determining the outcome of Reye's disease. Increased concentrations of salicylates at admission could be the result of excessive dosage because of a greater severity of the prodromal illness, or to diminished excretion because of impaired hepatic metabolism. It seems likely that serum salicylate concentrations entered the toxic range in many patients with Reye's disease before they presented for treatment. Most had been vomiting and had diminished oral intake for 33-55 h before hospital admission. Since the average number of hours from the beginning of vomiting to admission was no different in non-comatose and comatose cases, the time at which salicylate concentration was measured in relation to the last dose was probably similar in the two groups and therefore does not account for the higher levels in children with poor outcome. Salicylates are mitochondrial toxins and mitochondria are known to be significantly injured in Reye's disease; therefore, it seems wise to avoid the use of aspirin in children during outbreaks of Reye's disease.
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PMID:Serum salicylate concentrations in Reye's disease. A study of 130 biopsy-proven cases. 611 59

In a one-year prospective study we assessed the incidence of Reye's syndrome in children presenting with the acute onset of vomiting after a prodromal upper-respiratory-tract infection or varicella, and with serum alanine or aspartate aminotransferase levels at least three times higher than normal, and a paucity of neurologic findings. Of 25 patients meeting the above criteria, 19 had liver biopsies yielding adequate tissue for diagnostic purposes. Biopsy specimens from 14 of these 19 patients (74 per cent) were diagnostic of Reye's syndrome, according to rigorous light-microscopical, histochemical, and ultrastructural criteria. None of the biopsy specimens contained evidence of other acute pathologic processes, including hepatitis. A wide spectrum of mitochondrial alterations existed at the ultrastructural level, ranging from mild to severe lesions that were indistinguishable from those seen in comatose patients with Reye's syndrome. Our findings suggest that the clinical complex of vomiting, hepatic dysfunction, and minimal neurologic impairment after varicella or an upper-respiratory-tract infection usually represents Reye's syndrome. This syndrome occurs more frequently than previously recognized.
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PMID:Grade I Reye's syndrome. A frequent cause of vomiting and liver dysfunction after varicella and upper-respiratory-tract infection. 686 12

Two previously healthy men, aged 54 and 41 years, fell ill with headaches and increased fatiguability, one also with vomiting, the other with fever, transitory visual disturbances and slight weakness of the left hand. Both of them had a stiff neck and clouded consciousness. The EEG had moderate to severe dysrhythmia, predominantly over the temporal area, CSF showed an increased cell count of 1000/3, predominantly lymphocytes, and increased protein. The younger patient also had global aphasia and the computed tomography indicated an area of decreased density in the left temporal region. In the CSF there were locally produced IgG. The clinical findings were similar to those of herpes encephalitis, but were milder and regressed more quickly. Severe months later only a few minor organic behavioural changes were present. Antibody findings in CSF and serum suggest varicella-zoster virus as the causative agent, although in both instances no rash was observed throughout the entire period of observation.
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PMID:[Zoster encephalitis without rash: report of two cases (author's transl)]. 707 5

A case is reported of a patient who had previously undergone autologous bone marrow transplantation for recurrent Hodgkin's disease. The patient developed a generalised vesicular skin eruption. The clinical diagnosis was of disseminated shingles. Herpes viral particles were identified within the vesicular fluid by electron microscopy and using a specific monoclonal antibody to varicella zoster virus (VZV), positive immunofluorescence was detected in scrapings from the base of a vesicle. Gastroscopy and biopsy were performed because of severe abdominal pain and vomiting. The histological features were of non-specific active inflammation. Despite the histological absence of viral inclusions electron microscopy of the gastric biopsy revealed the presence of intranuclear herpes viral particles with a diameter of 90-100 nm. VZV specific DNA was detected by the polymerase chain reaction in the gastric biopsy extract. The patient was treated with acyclovir and made a full recovery.
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PMID:Varicella zoster gastritis in a bone marrow transplant recipient. 782 87

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

We report here our findings in two Japanese siblings who experienced recurrent bacterial and viral infections since early infancy. Recent symptoms included diarrhoea, conjunctivitis, rashes, headache, sore throat, joint pain, vomiting and vertigo, all similar to those seen in toxic shock syndrome, except for shock. These symptoms improved following gammaglobulin treatment. Staphylococcus aureus with coagulase type IV was continuously isolated from nasal smears producing toxic shock syndrome toxin-1 (TSST-1). Serum antibodies did not or only poorly responded to TSST-1, diphtheria toxoid, varicella virus and rubella virus, whereas total and subclass levels of serum immunoglobulin and in vitro DNA synthesis of lymphocytes stimulated by TSST-1, Staph. aureus, varicella vaccine and mitogens were normal. In the family, ten other members in three generations (five males: five females) including the mother had similar clinical symptoms. Thus, the disease may be inherited in an autosomal dominant fashion.
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PMID:A family of selective immunodeficiency with normal immunoglobulins: possible autosomal dominant inheritance. 803 20

A nine months old boy was admitted to the hospital with the diagnosis of meningoencephalitis 15 days after having a clinically diagnosed chickenpox. Lumbar puncture showed clear CSF with 0.23 g/l of proteins, 57 mg/dl of glucose, 30 red cells/mm3 and 5 leukocytes/mm3. Blood count showed a packed red cell volume of 22%, a hemoglobin of 7 g/dl, 14800 leukocytes with 1% eosinophils, 5% band and 39% segmented neutrophils, 50% lymphocytes and 5% monocytes and a decreased platelet count. On the fourth hospitalization day, the patient had vomiting, irritability and stiff neck. A new lumbar puncture showed a clear CSF that differed from the former only in the glucose level that increased to 102 mg/dl. The patient died and the necropsy showed a congestive and enlarged brain and congestive meninges infiltrated with lymphocytes. There was lymphoid follicle hyperplasia in the small bowel and enlarged mesenteric lymph nodes. Samples of brain, brain stem, spinal cord and stools were sent for virological study. A Coxsackie B-5 virus was isolated from the spinal cord sample.
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PMID:[Isolation of Coxsackieviruses B5 in a fatal case of meningoencephalitis]. 873 69


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