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)

A 22-year-old male presented with a brief history of progressive encephalopathy. One week previously, he had developed an upper respiratory infection that resolved spontaneously and was followed by intractable vomiting. He had taken salicylates for several days during the viral syndrome. The diagnosis of Reye's syndrome was confirmed by hepatic histology. Aggressive conservative management was followed by complete metabolic and neurological recovery. There are fewer than 10 reported cases of Reye's syndrome in adults but this disease may be more common than is generally suspected. The diagnosis should be considered in patients presenting with emesis and obtundation, who have recently had a viral illness and exhibit elevated blood ammonia and transaminases with normal cerebrospinal fluid. Confirmation is achieved by liver biopsy. Therapy is directed toward aggressive reduction of increased intracranial pressure.
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PMID:Reye's syndrome in the adult: case report and review of the literature. 685 15

Primary amebic meningoencephalitis and granulomatous amebic encephalitis are well recognized clinicopathological entities caused by free-living amebas. Associated arteritis and "mycotic aneurysms" with infiltration of intracranial arteries by lymphocytes, amebic trophozoites and cysts have not been previously reported. A 26-month-old girl had a 3-week history of encephalitis, characterized, initially, by vomiting and low-grade fever. Subsequently, she developed ataxia, generalized weakness, lethargy, and esotropia. The first CSF showed 490 RBC/microliters, 705 WBC/microliters with 90% mononuclears. Her pupils reacted briskly to light. Moderate nuchal rigidity, nystagmus, fixed downward gaze, anisocoria, bilateral 6th nerve palsy, left arm monoparesis and left Babinski were present. CAT scan revealed slight symmetrical dilatation of anterior horns of lateral ventricles and an area of abnormal enhancement above the 3rd ventricle. She died 14 days after admission, 5 weeks after onset of symptoms. The brain showed focal necrotizing encephalopathy, involving thalami, cerebellum, brain stem, and cervical and upper thoracic spinal cord. Numerous free-living amebic trophozoites and cysts were present within a chronic granulomatous encephalitis. There were trombosis of basilar, posterior cerebral, and vertebral arteries with profuse chronic panarteritis, fibrinoid necrosis, and mycotic aneurysms.
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PMID:Granulomatous encephalitis, intracranial arteritis, and mycotic aneurysm due to a free-living ameba. 689 86

A short review is given of the pharmacokinetic characteristics and side effects of the nitroimidazoles: metronidazole, tinidazole and ornidazole. The drugs are well absorbed from the gastrointestinal tract, maximum plasma levels generally being obtained 1 to 4 h after oral intake. Metronidazole has been shown to be absorbed after rectal administration; vaginal absorption is documented for all three drugs. The nitroimidazoles are widely distributed in the body, cross the placenta and appear in breast milk. Therapeutically effective concentrations of e.g. metronidazole have been demonstrated in e.g. the central nervous system, middle ear discharges, bile, peritoneal fluid, and fluids and tissues of the female genital tract. The binding to plasma proteins is less than 20%. Available data suggest that the elimination half-lives of these drugs differ, being 7-8 h for metronidazole, about 12 h for tinidazole and 14-15 h for ornidazole. Both metronidazole and ornidazole, but not tinidazole, seem to be extensively metabolized before elimination. The nature and frequency of adverse reactions to this drug include encephalopathy in a few patients treated with doses between 5 and 10 g daily as an adjunct to radiotherapy, and peripheral neuropathy observed in patients treated for prolonged periods with high doses. Among the common side effects of the nitroimidazoles are symptoms from the gastrointestinal tract such as nausea, anorexia, vomiting and metallic or bitter taste. Dizziness, ataxia and headache have been reported. When given together with alcohol, a disulfiram-like intolerance reaction can be obtained.
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PMID:Pharmacokinetics of nitroimidazoles. Spectrum of adverse reactions. 694 57

Subacute lead encephalopathy due a chronic poisoning was present in a 6 year-old child. Neurologic features (coma, seizures, CSF abnormalities) began after 2 weeks of vomiting, abdominal pain and constipation. Diagnosis was confirmed by studies of porphyrin metabolism. Lead poisoning following pica in childhood has rarely been reported in France. Its pathogenesis, main features, diagnosis and treatment are reviewed.
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PMID:[Lead poisoning revealed by severe encephalopathy : pica does exist in France (author's transl)]. 731 73

Succinylated Acinetobacter glutaminase-asparaginase (SAGA) has broader antitumor activity than Escherichia coli L-asparaginase in experimental systems; moreover, drug resistance does not develop in tumor cell lines initially sensitive to this enzyme. We have investigated the pharmacology and toxicology of SAGA after both single-dose and serial daily dose injections in 20 adult patients. Glutaminase activity in plasma after i.v. injection of single doses did not follow simple first-order kinetics (half-life during the initial 24 hr was 21 +/- 9 hr. A linear relation was observed between increasing doses of SAGA and resultant levels of plasma enzyme activity and blood glutamate. Assay of whole blood which had been deproteinized immediately following phlebotomy showed that single doses of SAGA lowered glutamine only transiently to nondetectable levels; serial daily doses were required to achieve and maintain continuous glutamine depletion. Reversible depression of the central nervous system, ranging from encephalopathy to coma, occurred in a dose-related manner and was dose limiting. Other prominent reactions included respiratory alkalosis, hyperglycemia, nausea, and vomiting. Transient antitumor effects were noted in two patients with solid tumors and in two patients with leukemia. SAGA causes considerable neurotoxicity in adults which requires close patient monitoring. Phase II studies in leukemic patients are in progress.
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PMID:Phase I evaluation of succinylated Acinetobacter glutaminase-asparaginase in adults. 743 89

Your recent lead article on toxic shock and tampons (November 1, p. 1161) prompts me to report a case of pelvic infection and staphylococcal septicemia 8 days after the insertion of a Lippes loop. Pelvic infection is a recognized complication of IUDs; although there have been 2 reports of endocarditis occurring in susceptible patients following the insertion of an IUD, septicemia is rare. A previously healthy 31-year old married woman had a loop inserted at a family planning clinic. 3 days later she developed sweating, vomiting, confusion, and cough and during the following 48 hours became disoriented with hallucinations. She was referred to the hospital with suspected encephalitis and on admission was febrile (38.8 degrees Celsius) and stuporose but responded to simple commands. Blood pressure was 95/60 mmHg but there were no other abnormal signs. Hemoglobin was 12.2 g/dl, white blood count 4.0x109/1 (80% neutrophils), erythrocyte sedimentation rate 70mm in the 1st hour; cerebrospinal fluid normal. Chest x-ray examination revealed patchy consolidation in the upper lobes of both lungs and an electroencephalogram showed bilateral nonspecific abnormality. 3 blood cultures taken on admission yielded penicillin-resistant Staphylococcus aureus. She was treated with high-dose intravenous cloxacillin and 24 hours after starting the antibiotic had improved markedly and the IUD was removed. Culture from the coil and also from a high vaginal swab yielded Staph aureus with a similar antibiogram to that of the organism cultured from the blood. Subsequent recovery was uneventful, although repeat chest x-ray examination showed small abscess cavities in the upper lobes of both lungs. The patient was discharged 4 weeks after admission and serial chest radiographs have confirmed complete resolution of the pneumonia and abscesses. There is little doubt that this patients' septicemia with lung abscess formation and encephalopathy originated in the genital tract. The patient was both toxic and shocked but was different from patients with the recently described toxic shock syndrome in that her blood culture was positive for Staph aureus. The case provides another example of the importance of this organism as a cause of infection associated with the insertion of foreign bodies into or through the vagina.
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PMID:Staphylococcal septicaemia after insertion of an intrauterine contraceptive device. 744 49

Mitochondrial myopathy, encephalopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome is one of the mitochondrial encephalomyopathies that has distinct clinical features including stroke-like episodes with migraine-like headache, nausea, vomiting, encephalopathy and lactic acidosis. We report a 27-year-old woman who presented with partial seizure, stroke-like episodes including hemiparesis, hemianopia and hemihypethesia, sensorineural hearing loss, migraine-like headache, and lactic acidosis. Brain computed tomographic scan showed encephalomalacia in the right parieto-occipital area and recent hypodensity in the left temporoparieto-occipital area with cortical atrophy. Muscle biopsy revealed ragged-red fibers and paracrystaline inclusions in the mitochondria. Genetic study revealed an A to G point mutation at nucleotide position (np) 3243 of mitochondrial DNA. External ophthalmoplegia and ptosis were also found during two exaggerated episodes in this patient. Therefore, the overlapping syndrome of chronic progressive external ophthalmoplegia in the MELAS syndrome is considered in this case. Furthermore, we also found carnitine deficiency in this patient and she was responsive well to steroid therapy. Muscle biopsy also revealed excessive lipid droplets deposits. Therefore, the carnitine deficiency may occur in MELAS syndrome with the A to G point mutation at np 3243. We recommend the steroid or carnitine supplement therapy be applied to the MELAS syndrome with carnitine deficiency.
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PMID:CPEO and carnitine deficiency overlapping in MELAS syndrome. 748 81

Ornithine transcarbamylase deficiency is an X-linked recessive disorder of urea biosynthesis characterized by recurrent, often fatal, hyperammonemic encephalopathy in affected males; carrier females are usually asymptomatic. We report here the clinical and laboratory findings in five symptomatic heterozygous females with ornithine transcarbamylase deficiency. In each case, the onset of symptoms occurred in the 1st year of life, but diagnosis was delayed by up to 15 years. Symptoms included recurrent vomiting with lethargy (five patients), dietary protein intolerance (five), irritability (four), severe acute encephalopathy (three), ataxia (three), and acute hemiparesis (two). All eventually showed evidence of developmental delay or learning difficulties. Two of the three who experienced severe, acute, hyperammonemic encephalopathy suffered serious, permanent neurologic sequelae. Three of the patients showed decreased ornithine transcarbamylase activity in liver obtained by needle biopsy, and the other two had marked orotic aciduria associated with hyperammonemia. Neuroimaging studies demonstrated persistent abnormal lobar attenuation and abnormal signal on computed tomographic scan and magnetic resonance imaging. All patients showed marked symptomatic improvement on treatment with dietary protein restriction supplemented by pharmacologic measures to increase nonprotein nitrogen excretion. Ornithine transcarbamylase deficiency should be considered in the differential diagnosis of acute or chronic encephalopathy in females at any age.
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PMID:Ornithine transcarbamylase deficiency in females: an often overlooked cause of treatable encephalopathy. 749 56

Twenty one patients age ranging from 26-70 years, with biopsy proven recurrent/advanced carcinoma of the cervix were treated with bleomycin, cisplatinum and ifosfamide infusion therapy. 88% patients reported subjective improvement. The objective response rate was 66.6% (Complete 38% and partial 28.5%). Side effects were mainly nausea, vomiting, and alopecia. Treatment related fever was common. Hematuria and reversible encephalopathy with ifosfamide were seen in three and two patients respectively. These results indicate that BIP infusion chemotherapy is an active and safe combination for treatment of advanced/recurrent cervical cancer.
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PMID:Bleomycin, cisplatinum and ifosfamide infusion chemotherapy in advanced/recurrent cancer of cervix. 751 43

Toxic Shock Syndrome (TSS) is a potentially fatal illness caused by a particular strain of Staphylococcus aureus. The clinical presentation is similar to that of septic shock. The incidence of TSS peaked in the late 1970s and early 1980s, probably as a result of availability of super absorbent tampons. Although most commonly associated with menstruation, the overall incidence of menstrual and nonmenstrual TSS in men and women ranges from 1 to 3 per 100,000. There are almost equal numbers of menstrual and nonmenstrual cases of TSS identified annually. S aureus, the causative microorganism in cases of TSS, has been isolated from many body tissues. Toxic shock syndrome presents as a flu-like illness with high fever, vomiting, diarrhea, general malaise, and muscle weakness. Nursing and medical management focus on controlling or preventing potentially serious complications, such as adult respiratory distress syndrome, renal failure, electrolyte imbalances, disseminated intravascular coagulation, encephalopathy, and cardiomyopathy. Judicious use of tampons and barrier contraceptive devices may decrease the risk of developing TSS.
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PMID:Toxic shock syndrome: an opportunity for nursing intervention. 865


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