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)

Two children with osteosarcoma are presented in whom Wernicke encephalopathy with vomiting occurred during the chemotherapy. One of the children died with symptoms of toxic cardiomyopathy. Autopsy revealed Wernicke encephalopathy. The other child had similar symptoms (ocular signs, ataxia, somnolence). Parenteral thiamine had been given and after this therapy the child recovered from the encephalopathy. The authors emphasize the importance of the recognition of this neurological disorder occurring rarely in childhood: it can be cured with parenteral thiamine. Without thiamine treatment this condition is lethal.
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PMID:[Wernicke encephalopathy in childhood osteosarcoma]. 140 86

We report on a 3 3/4-year-old girl with acute lymphoblastic leukemia. Polychemotherapy caused a complete remission of the tumor. Six months after treatment was started, the patient developed vomiting and diarrhea necessitating parenteral nutrition. Disturbance of eye movements appeared 4 weeks later. The patient died suddenly 3 days after their manifestation. Autopsy revealed Wernicke's encephalopathy. This case demonstrates the need for thiamine substitution in infants with malignant diseases.
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PMID:Wernicke's encephalopathy in a child with acute lymphoblastic leukemia treated with polychemotherapy. 186 Feb 71

Patients (n = 104) were judged to be thiamine deficient by the criteria of erythrocyte transketolase activity (ETK) less than 0.6 U/g of hemoglobin, or greater than 17% increase in this activity on addition of thiamine pyrophosphate in vitro (TPP effect). ETK activated by TPP in vitro (AETK) was related to ETK by a linear regression of slope greater than or equal to 1, implying that transketolose apoenzyme (apoTK) was constant or decreased as ETK decreased. For most patient groups the value of apoTK was 0.1 U/g and the slope 1.033 to 1.050. In the subgroup of non-vomiting drinkers with Wernicke's encephalopathy (WE), the slope of the linear regression of AETK on ETK was 1.21, so that apoTK decreased as ETK decreased. Comparison of these data is consistent with a difference in the TK of WE drinkers from that of others. Generally, any variation of TPP effect was due only to variation of ETK. We recommend measurement of ETK, without TPP effect, for the assessment of thiamine nutrition.
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PMID:The relationship between erythrocyte transketolase activity and the 'TPP effect' in Wernicke's encephalopathy and other thiamine deficiency states. 207 41

Although the occurrence of Wernicke's encephalopathy (WE) in patients on dialysis is frequently alluded to, review of the literature reveals only 3 described cases. We describe 5 patients on dialysis who developed WE in the absence of alcoholism or other predisposing factors. The clinical diagnoses included uremic encephalopathy (2 patients), dysequilibrium syndrome (1), dialysis dementia (1), and brainstem hemorrhage (1). At postmortem examination, classic findings of WE were evident. The rarity of WE in patients on dialysis may in part be explained by studies indicating a genetic defect in transketolase activity. Patients on dialysis are also potentially at risk for thiamine deficiency because of anorexia, vomiting, and intravenous alimentation. Other factors altering thiamine requirements, such as glucose load or infections, may also contribute. Preventable and potentially curable, WE should be suspected in all patients on dialysis who have an unexplained neurological picture.
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PMID:Wernicke's encephalopathy in patients on peritoneal dialysis or hemodialysis. 382 16

A 29 year-old Japanese woman with hyperemesis gravidarum became comatose and died. The autopsy revealed a typical case of Wernicke's encephalopathy complicated by disseminated intravascular coagulation (DIC). Repeated vomiting and parenteral nutrition without vitamins led to Wernicke's encephalopathy and a spontaneous abortion 24 h before death triggered the induction of DIC.
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PMID:Wernicke's encephalopathy in early pregnancy complicated by disseminated intravascular coagulation. 641 34

Two weeks after gastric partitioning for morbid obesity, a 45-year-old woman experienced persistent vomiting that led to a weight loss of 30 kg over 6 weeks. Wernicke's encephalopathy and peripheral neuropathy developed. The Wernicke's encephalopathy responded well to the administration of thiamine. This is one of very few reported cases of Wernicke's encephalopathy following gastric partitioning.
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PMID:Wernicke's encephalopathy after gastric partitioning for morbid obesity. 670 23

3 cases of Wernicke's encephalopathy are reported with consecutive death in surgery patients. A long period of vomiting caused by tumors or inflammation in the upper intestinal tract, preceded. This probably causes a deficiency of thiamin. The deficiency was reinforced by high calorie parenteral nourishment. Caused by non-reversible shock and severe destruction of metabolism, only a period of 1-2 days lays between first neurological symptoms and death. in similar cases a sufficient supply of thiamine should be considered.
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PMID:[Non-alcoholic Wernicke's encephalopathy as a cause of death in 3 surgical patients]. 678 Apr 65

A case of Wernicke's encephalopathy with ataxia, confusion, memory loss, partial seizures of complex behavior and hypothermia, subsequent to thiamine depletion due to chronic malnourishment and triggered by an episode of acute vomiting and diarrhea, is reported, Computerized tomography (CT-scan) depicted small bilateral lesions in areas adjacent to the walls of the third ventricle, common location of the lesions seen in autopsy material of Wernicke's encephalopathy. Early diagnosis and treatment with vitamin B complex supplemented with intensive mnemonic and cognitive therapy led to complete recovery in a ten day period.
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PMID:Wernicke's encephalopathy. A case report with neurophysiologic and CT-scan studies. 686 52

A 25-year-old woman suffered from hyperemesis gravidarum when she was seven weeks pregnant. Since her vomiting continued, she received intravenous dextrose and electrolytes without thiamine in a hospital. One month later, she developed gait disturbance, followed by confusion and dysarthria. On admission to our department, she was confusional and had ataxic dysarthria. Spontaneous and gaze evoked nystagmus was present. Limb coordination was bilaterally ataxic. Based on her clinical course and symptoms, she was diagnosed as having Wernicke's encephalopathy. From the admission day, intravenous infusion of vitamin B1 (600 mg/day) was started. A few days later, her consciousness and limb ataxia began to improve. However, truncal ataxia and polyneuropathy became evident. Eight weeks after onset, she developed Korsakoff's psychosis such as anterograde and retrograde amnesia, disorientation and confabulation. We administered large amounts of corticosteroid (methylprednisolone 500 mg/day) in order to reduce brain edema or stabilize the impaired blood-brain barrier. Soon after, her psychosis began to improve gradually. She recovered remarkably from the psychosis, but she was left with persistent nystagmus, mild ataxic gait and polyneuropathy. The present case suggests that corticosteroid may have the beneficial effect on Wernicke-Korsakoff syndrome.
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PMID:[Beneficial effect of steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]. 795 22

The case of an 18-year-old woman with Wernicke's encephalopathy induced by hyperemesis gravidarum is reported. She had severe vomiting and received antiemetic therapy and intravenous administration of glucose and low-dose insulin solution without thiamine. She developed coma, nystagmus, ataxia and polyneuropathy. CT and MR imaging showed bilateral caudate lesions as well as symmetrical periventricular lesions of the thalamus and hypothalamus and periaqueductal gray matter. Caudate lesions are quite rare in Wernicke's encephalopathy.
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PMID:Wernicke's encephalopathy induced by hyperemesis gravidarum, associated with bilateral caudate lesions on computed tomography and magnetic resonance imaging. 803 46


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