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 is a potentially devastating neurologic illness seen predominantly in children following a viral prodrome. The cause is unknown. The clinical history and laboratory presentation are stereotypical and easy to recognize if the clinician considers the diagnosis. Neurologic dysfunction is characterized by lethargy, obtundation, persistent vomiting, agitated delirium, and coma. Death is secondary to severe cerebral swelling with elevation of intracranial pressure. Although no specific therapy has been clearly demonstrated to be superior in terms of outcome, most clinicians have adopted a management scheme aimed at lowering and controlling the elevated ICP. We have described the management protocol in use at the Children's Hospital of Philadelphia. The protocol is summarized in the Appendix for the convenience of the reader.
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PMID:Management of Reye's syndrome. 391 81

After reviewing the literature, a personal series of 10 adult patients with cerebellar infarction diagnosed by CT scan is described. The clinical picture in young adult men is characterized by rapid onset of headache, vomiting, vertigo, ataxia and blurred vision. After this sudden onset the patients may present a stable course or a rapid or delayed onset of brain stem compression, revealed by impairment of consciousness. CT scan is the diagnostic method of choice. The correlation between angiographic and CT localization of the infarction is not good. For therapy the following policy is suggested: in alert and clinically stable patients: medical treatment (mannitol, glycerol, dexamethason), ICP and serial CT monitoring; in alert patients with hydrocephalus or mass effect: medical treatment and monitoring as mentioned before; ventricular drainage if ICP surpasses 350 mm H2O; in patients with impaired consciousness and hydrocephalus or mass effect: immediate ventricular drainage. If it is not followed by prompt improvement of the level of consciousness, an emergency suboccipital craniectomy with removal of the infarcted tissue should be done.
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PMID:Surgical management of acute cerebellar infarction. 398 89

Benign recurrent intrahepatic cholestasis (BRIC or Summerskill-Walshe-Tygstrup-syndrome) is a rare autosomal recessive form of liver disease, which usually becomes manifest in childhood. Characteristic are recurrent episodes of jaundice and itching of different duration. Number and duration of episodic attack and asymptomatic period develop individually. For diagnosis of BRIC following criteria are proposed: At least three episodes of severe jaundice and pruritus with biochemical evidence of cholestasis, normal intra-and extrahepatic bile ducts on cholangiography, absence of a factor known to produce intrahepatic cholestasis and symptom-free intervals of several months or years. Often the diagnosis of BRIC is made very late and patients have to suffer invasive investigations (explorative laparotomy). Because of the unknown pathophysiological mechanism there is no specific treatment. We report on a 53-year-old patient with jaundice, severe pruritus, vomiting, loss of hair and weight, extreme sleeplessness and intractable cough. At the onset of the attack an increase of serum bilirubin concentration and serum alkaline phosphatase was observed, whereas aspartate and alanine aminotransferase and gamma-glutamyltransferase were normal. Histological findings of liver biopsy revealed accumulation of bile plugs in bile canaliculi. The long-term follow-up of our patient confirms that the prognosis is good.
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PMID:[Follow-up of benign recurrent intrahepatic cholestasis (Summerskill-Walshe-Tygstrup syndrome) over 46 years]. 965 5

Pseudotumor cerebri (PTC) presents with varied spectrum of manifestations, association with diverse pathological conditions and variable outcome. A preliminary observation on children presenting with PTC is being presented because of certain peculiarities, not observed earlier, like occurring in clusters during particular season, all were infants having close relationship with viral illness and all had extremely benign outcome. Children presenting with raised ICP were hospitalised and evaluated. The relevant investigations carried out included lumbar puncture, cranial ultrasonography, CT Scan and culture studies. Fifteen children, all in infancy with male-female ratio of 2:3 presented in clusters of 11 (73.3%) cases during late summer and early fall presented with bulging fontanelle, vomiting 11, fever 12, respiratory infection 5, diarrhea 5, lateral deviation of eye balls 4 and skin rashes 5 cases. Contact with viral illness in the family was found in 10 cases. Lumbar puncture showed high opening high CSF pressure in all. Results of this study suggest peculiar and perhaps different form of PTC seen recently which affected only the infants. These were closely related to viral illness and had benign outcome.
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PMID:Infantile pseudotumor cerebri related to viral illness. 1083 33

We report here a fatal intoxication case involving ammonium vanadate. A 24-year-old woman was admitted to the Emergency Department for abdominal pain, nausea, vomiting, multiple daily diarrheas, hypoglycaemia (0.2g/L) and severe acute renal failure with glomerular filtration rate estimated at 21 ml/min. This patient had taken an undetermined amount of ammonium vanadate 12h after ingesting. She died next morning in the context of respiratory distress despite intensive care and oxygen therapy. The autopsy revealed widespread asphyxia syndrome and erosive gastritis. Determination of vanadium concentration in blood was carried out by means of mass spectrometer (ICP-MS) using rhodium ((103)Rh) as the internal standard. The vanadium concentration was 6.22 mg/L, corresponding to 6000 times higher than normal concentration in the general population. The latency and the brutality of clinical picture degradation seem to be in consideration of systemic poisoning by vanadium leading to inhibition of the cellular respiratory process.
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PMID:Fatal poisoning by vanadium. 2113 May 88

Brain tumor symptoms vary greatly from person to person because of two factors: location and size of tumors. The size of a tumor, however, does not necessarily affect the severity of symptoms. Manifestations depend on the cause of the symptoms: an increase in ICP, direct compression of gray or white matter, shifting of intracranial contents, or secondary cerebral ischemia. Symptoms may be non-specific and include headache, altered mental status, ataxia, nausea, vomiting, weakness, and gait disturbance. Left-sided weakness may be seen in a patient with a tumor pressing on the contra-lateral motor strip or speech difficulties may occur if a tumor is in the dominant hemisphere. Up to a third of people report having seizures prior to being diagnosed with a brain tumor. Rarely, brain tumor can present with psychiatric symptoms but without other neurological signs or symptoms. Evaluation for brain tumor is indicated in any patient with chronic, persistent headache associated with protracted nausea, vomiting, seizures, changes in headache pattern, neurologic symptoms, and change in personality.
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PMID:Malignant gliomas: early diagnosis and clinical aspects. 2199 29