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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The propensity to prefer and to consume salty foods varies considerably from person to person, and excessive salt intake has been linked to a number of pathological conditions. Extracellular dehydration occurs in humans after vomiting or diarrhea and is commonly observed during pregnancy. Because the hormonal responses to extracellular dehydration are known to increase salt appetite, we tested the hypothesis that extracellular dehydration during pregnancy increases the propensity of offspring to consume salt. Pregnant rats were treated with polyethylene glycol, which is known to produce extracellular dehydration and to exaggerate sodium appetite. The offspring of these treated pregnant rats showed an increase in salt appetite as compared with the offspring of control untreated dams. These results demonstrate that extracellular dehydration during pregnancy can enhance the natriophilic propensity in offspring and suggest that gravidic vomiting may contribute to the epidemiological factors of hypertension and other pathologies.
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PMID:Extracellular dehydration during pregnancy increases salt appetite of offspring. 230 41

The question of whether the HELLP syndrome exists as a distinct entity or is part of a spectrum of pregnancy complications, which have in common hemolysis, elevated liver enzymes, and thrombocytopenia, has long been a source of speculation and debate among obstetricians and internists. A review of the literature indicates a definite need for a uniform definition, diagnosis, and management of this syndrome. Patients manifesting this syndrome usually are seen before term (less than 36 weeks' gestation) complaining of malaise (90%), epigastric or right upper-quadrant pain (90%), and nausea or vomiting (50%), and some will have nonspecific viral-syndrome-like symptoms. Hypertension and proteinuria may be absent or slight. Thus some of these patients may have a variety of signs and symptoms, none of which are diagnostic of classic preeclampsia. In consideration of the high maternal and perinatal mortality and morbidity reported with the presence of this syndrome, I recommend that all pregnant women having any of these symptoms should have a complete blood cell count with platelet and liver enzyme determinations irrespective of maternal blood pressure.
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PMID:The HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets): much ado about nothing? 240 34

Long-term follow-up data on young patients receiving amiodarone is lacking, especially in relation to growth and late side effects. The records of 95 young patients (mean age 12.4 years; range 3 weeks to 31.5 years) who received amiodarone were reviewed. Minimal follow-up time for those continuing to take amiodarone was 1.5 years; the mean duration of therapy was 2.3 years (maximal 6.5). The mean maintenance dosage was 7.7 (1.5 to 25) mg/kg body weight per day. Initial success (based on symptoms and 24 h electrocardiogram) was achieved in 23 of 34 patients with ventricular tachycardia, in 32 of 33 with atrial flutter and in 21 of 28 patients with supraventricular tachycardia. However, in 7 of 33 patients with atrial flutter, the arrhythmia returned after 6 months. Patient growth continued in the same percentiles achieved before amiodarone in all but eight patients, improving in six and worsening in two with severe underlying disease. Proarrhythmia occurred in three patients: one had torsade de pointes that disappeared when amiodarone administration was stopped; two with severe anatomic heart disease died suddenly during the loading period (one with atrial flutter and one with ventricular tachycardia). Side effects occurred in 28 (29%) of the 95 patients: keratopathy (in 11), abnormal thyroid function test (in 6), chemical hepatitis (in 3), rash (in 3), peripheral neuropathy (in 2), hypertension (in 1) and vomiting (in 1). All side effects disappeared when amiodarone was discontinued or the dose was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term follow-up of amiodarone therapy in the young: continued efficacy, unimpaired growth, moderate side effects. 231 68

The authors report a case of toxic hepatitis in a woman of 22 years of age in the third trimester of her first pregnancy treated by methyldopa for hypertension of pregnancy which was diagnosed at 33 weeks of amenorrhoea. The prodromal symptoms were mild and consisted of nausea, vomiting and rise in temperature and this phase was associated with febrile jaundice without pruritus and it was only associated with coagulation disorders in the third stage of labour. This was a case of mixed cytolytic hepatitis (ASAT x 3N) and cholestasis (x 1.5N). The outcome was fatal. The patient died three days after delivery following haematemesis and renal failure as well as hepatic encephalopathy. The main diagnostic feature was acute hepatic stasis in spite of the absence of pruritus and the presence of a raised temperature after hematolytic, viral and obstructive causes had been eliminated. Histology confirmed that there was toxic hepatitis. This aetiology was suggested by the timing of the symptoms after MD (methyldopa) had been taken. Elkington described methyldopa hepato-toxicity in 1969. Fatal cases in the literature were in patients who were over 40 years of age. Methyldopa is used in pregnant women because of its safety as far as the fetus is concerned. Mechanism by which it causes toxic hepatitis is a combination of abnormal metabolism (the cytochrome P450 chain produces an antigen) and an immune reaction in response to this antigen and these explain why such severe and potentially fatal forms of the condition exist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Fatal toxic hepatitis in pregnancy. A discussion of the role of methyldopa]. 232 42

To evaluate the safety and possible efficacy of high-dose naloxone for the treatment of acute cerebral ischemia, 38 patients received a loading dose of 160 mg/m2 over 15 minutes followed by a 24-hour infusion at the rate of 80 mg/m2/hr. Nausea and/or vomiting were common side effects. Naloxone was discontinued in seven patients (because of hypotension in one, bradycardia and hypotension in two, myoclonus in one, focal seizures in two, and hypertension in one); all seven patients responded to treatment and no permanent sequelae to naloxone were noted. Twelve of the 38 patients showed early neurologic improvement (by completion of the naloxone loading dose). However, there was no correlation between such a loading dose response and clinical outcome at 3 months. Our experience suggests that naloxone is safe at the dose used, but data for efficacy are inconclusive.
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PMID:High-dose intravenous naloxone for the treatment of acute ischemic stroke. 233 51

Central nervous system is rarely involved in progressive systemic sclerosis (PSS) unless there are concomitant abnormalities in renal or lung function or hypertension. A 72-year-old woman with typical PSS developed cerebellar bleeding. Medical history records revealed, she had noted the onset of Raynaud's sign on her upper extremities at the age of 37. This was followed by necrosis and repeated infection, and as a result, shortening of her fingers in her 40's. The disease progressed and involved lower extremities, and then face and body in her 50's. Aortic valve stenosis was diagnosed at 69 year old, cardiac myopathy at 70 and at the age of 71 infectious dermatitis in both inguinal regions. Mild anemia, hypoalbuminemia and the decrease of serum Fe were discovered in June 1988. At the same time, prolonged ESR, positive C-reactive protein, RA, and anti-nuclear-antibody were also noticed. A chest roentgenogram revealed pulmonary fibrosis. Systemic hypertension was not noticed on the clinical course. She developed an onset of vertigo and vomiting in the morning of August 8, 1988. Consequently, she was brought to our hospital. She was alert but a physical examination showed a swallowing disturbance, dysarthria, right cerebellar ataxia, nystagmus and hypertension (192/100 mmHg). A CT examination on admission revealed a slightly low density area in right cerebellar hemisphere without mass effect. She was treated with dextran and mannitol and her condition improved on the 6th day of her admission. She was alert and blood pressure calm down to 120/70 mmHg without the use of anti-hypertension drugs on August 21.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of progressive systemic sclerosis associated with a hemorrhagic infarction of the cerebellum]. 235 21

We performed a retrospective review to investigate the safety of prehospital naloxone administration by paramedics as part of a protocol for all patients presenting with an acutely depressed level of consciousness (LOC). The prevalence of naloxone-induced vomiting, seizures, hypotension, hypertension, and cardiac arrest was sought from the prehospital records of 813 patients treated during a 12-month period. The mean age of the treated patients was 42.4 +/- 9.7 years. The initial dose of naloxone was 0.4 to 0.8 mg, and the mean total dose was 0.9 +/- 0.6 mg. No patients lost a pulse within ten minutes of receiving naloxone. Two patients (0.2%) experienced a significant drop in systolic blood pressure, and one patient (0.1%) demonstrated a significant rise in systolic blood pressure within five minutes of naloxone administration. Vomiting occurred in two patients (0.2%), and one patient (0.1%) suffered a tonic-clonic seizure within five minutes of naloxone administration. Of the 813 patients treated, 60 patients (7.4%: mean age, 32.3 +/- 6.7 years) were judged to have an improved LOC after naloxone, with 27 (3.3%) regaining a normal LOC. We conclude that in the above doses, naloxone is safe as part of prehospital protocols for paramedics treating patients with an acutely depressed LOC. However, the vast majority of patients treated empirically with naloxone in the field demonstrated no benefit.
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PMID:The safety of prehospital naloxone administration by paramedics. 237 73

Sixteen previously treated (with only one prior regimen) patients with histologically proven metastatic or locally recurrent colorectal carcinoma were treated with recombinant tumor necrosis factor (rTNF) administered by 30-minute i.v. infusions twice daily for 5 consecutive days every other week for 8 weeks. Patients received 100 micrograms/m2 twice daily on day 1 of cycle 1 with escalation to 150 micrograms/m2 twice daily thereafter. Patients were concomitantly treated with indomethacin 25 mg every 6 hours and acetaminophen 650 mg every 4 hours to obviate fever and chills. Toxicities included: nausea/vomiting (69%), headache (25%), chills (69%), pain at tumor sites (63%), hypotension (31%), and hypertension (38%). Hematologic toxicity included leukopenia less than 2000 cells/mm3 (38%) and thrombocytopenia less than 100,000 cells/mm3 (13%). Liver function abnormalities occurred independently of the site or extent of metastatic disease and inconsistently in each treatment cycle. Four patients developed bilirubinemia greater than 2.5 x baseline values (range, 2.5 to 10.3 U/L); five patients had greater than 2.5 x elevations in alkaline phosphatase (range, 624 to 1663 U/L). Two patients developed retinal vein thrombosis in the absence of hemostatic abnormalities. In both instances, this complication occurred several weeks after completion of therapy. No objective responses were noted in 14 evaluable patients (95% confidence interval: 0 to 0.23). Three patients had stable disease for a median duration of 4.5 months. In conclusion, i.v. rTNF at this dose and schedule has no demonstrable antitumor efficacy. Twice-daily i.v. administration of this agent is associated with more hepatotoxicity than previously reported in trials using subcutaneous or once daily i.v. administration. Retinal vein thrombosis may be a late complication of i.v. rTNF at this dose and schedule.
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PMID:A phase II trial of recombinant tumor necrosis factor in patients with advanced colorectal carcinoma. 238 95

Primary intraventricular hemorrhage (PIVH) imaged by magnetic resonance imaging (MRI) is reported. A fifty-seven-year-old man with long-standing hypertension suddenly developed severe headache, vomiting, and retrograde amnesia. A computed tomography scan on the same day revealed hematoma in the right posterior horn of the lateral ventricle and in the 4th ventricle. Angiography of the neck and head failed to demonstrate any vascular abnormalities. On the second day his neurological symptoms almost recovered except for the loss of the memory of the ictal day. High-field MRI on the sixteenth day demonstrated an isointense lesion surrounded by a hypointense area in the T1 weighted image or a hyperintense lesion in the T2 weighted image, suggesting subacute hematoma consistent with hypertension, just anterior to the right trigone of the lateral ventricle.
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PMID:Primary intraventricular hemorrhage imaged by high-field magnetic resonance imaging--a case report. 238 45

The pathophysiology and treatment of acute subarachnoid hemorrhage (SAH) are reviewed. SAH occurs when blood is released into the subarachnoid space, which surrounds the brain and spinal cord. Symptoms of SAH include severe headache, nausea, vomiting, neck pain, nuchal rigidity, and photophobia. The initial hemorrhage is fatal in 20-30% of patients. Complications of SAH include rebleeding, hydrocephalus, delayed cerebral ischemia associated with cerebral vasospasm, and seizures. The likelihood of rebleeding is increased by measures that rapidly lower intracranial pressure. The risk of developing hydrocephalus is associated with the volume of blood within the subarachnoid space and ventricular system. Cerebral vasospasm develops in 20-40% of patients, and up to 50% of affected patients die or suffer permanent neurological damage. Seizures occur in 5-15% of patients with SAH. Radiologic procedures form the foundation for the diagnosis of SAH. The most commonly used rating scale classifies the severity of SAH based on the clinical presentation of the patient. Surgery is the definitive treatment for the prevention of rebleeding. Hydrocephalus can only be treated surgically, most commonly by insertion of a drain. The only measures proved to be effective for treatment of delayed cerebral ischemia are volume expansion and the induction of hypertension. The calcium-channel blocker nimodipine was recently approved for treatment of arterial spasm in SAH. Intravenous nicardipine is also being studied for the same indication. These agents may improve clinical outcome substantially by limiting fixed neurological deficits. To prevent seizures, prophylactic antiepileptic therapy with phenytoin sodium is generally accepted. The SAH complications of rebleeding, hydrocephalus, delayed cerebral ischemia, and seizures are managed by surgical, drug, and fluid therapy.
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PMID:Pathophysiology and treatment of subarachnoid hemorrhage. 240 1


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