Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute liver failure (ALF) carries a high mortality in children. N-acetylcysteine (NAC), an antioxidant agent that replenishes mitochondrial and cytosolic glutathione stores, has been used in the treatment of late acetaminophen-induced ALF and non-acetaminophen-induced ALF. In our unit, NAC was introduced as additional treatment for non-acetaminophen-induced ALF in 1995. The aim of this study was to evaluate the safety and efficacy of NAC in children with ALF not caused by acetaminophen poisoning. A retrospective review of medical records of 170 children presenting with nonacetaminophen-induced ALF between 1989 and 2004 was undertaken. ALF was defined as either international normalized ratio of prothrombin time (INR) > 2 and abnormal liver function or INR >1.5 with encephalopathy and abnormal liver function. Children were divided into the following groups: Group 1 (1989-1994), standard care (n = 59; 34 [58%] male; median age 2.03 yr, range 0.003-15.8 yr); and Group 2 (1995-2004), standard care and NAC administration (n = 111; 57 [51%] male; median age 3.51 yr, range 0.005-17.4 yr). NAC was administered as a continuous infusion (100 mg/kg/24 hours) until INR < 1.4, death, or liver transplantation (LT). The median duration of NAC administration in Group 2 was 5 (range, 1-77) days. Complications were noted in 8 (10.8%) children: rash in 3, arrhythmia in 3, and dizziness and peripheral edema in 1. One child had an allergic reaction (bronchospasm) and NAC was stopped. A total of 41 (71%) children in Group 1 vs. 85 (77%) in Group 2 required admission to intensive care, P = not significant (ns). The length of intensive care stay was 6 (range, 1-58) days in Group 1 vs. 5 (range, 1-68) days in Group 2, P = ns and length of hospital stay was 25 (range, 1-264) days vs. 19 (range, 1-201) days, P = 0.05. The 10-yr actuarial survival was 50% in Group 1 compared to 75% in Group 2, P = 0.009. Survival with native liver occurred in 13 (22%) in Group 1 vs. 48 (43%) in Group 2, P = 0.005; 15 (25%) in Group 1 died without transplant vs. 21 (19%) in Group 2, P = ns; and LT was performed in 32 (54%) vs. 42 (38%), P = ns. Death after transplantation occurred in 15 (39%) in Group 1 vs. 8 (16%) in Group 2, P = 0.02. In conclusion, NAC is safe in non-acetaminophen-induced ALF. In this retrospective study NAC was associated with a shorter length of hospital stay, higher incidence of native liver recovery without transplantation, and better survival after transplantation.
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PMID:Safety and efficacy of N-acetylcysteine in children with non-acetaminophen-induced acute liver failure. 1816 97

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that may occur in people with normal liver-associated enzyme levels, despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl who had absence seizure and complained about progressive dizziness and general malaise several days after restarting valproate. Then, she presented vomiting and decreased consciousness three weeks after valproate use. Notably, her serum ammonia level was five times the upper limit of normal (184 micrommol/L), with normal liver-associated enzyme and supra-therapeutic valproate level. EEG showed continuous generalized slowing. The tandem mass analysis revealed carnitine deficiency. Consciousness improved after emergent hemodialysis. Ammonia level and EEG also returned to normal. Possible mechanisms, risk factors and the treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.
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PMID:Valproate-induced hyperammonemic encephalopathy treated by hemodialysis. 1879 59

Trichloroethane functions in cosmetics as a solvent. Although Trichloroethane has been reported to the Food and Drug Administration (FDA) to be used in cosmetic products, an industry survey found that it is not in current use in the cosmetic industry. Trichloroethane is considered a Class I ozone-depleting substance by the Environmental Protection Agency (EPA) and its use is prohibited in the United States, unless considered essential. The FDA has stated that Trichloroethane's use in cosmetics is considered nonessential. Trichloroethane is detected by gas chromatography, gas chromatography-mass spectrometry, and gas-liquid chromatography. In rats, Trichloroethane, whether inhaled or injected, is mostly expelled intact from the body through exhalation. A very small percentage is excreted in the urine. In humans, Trichloroethane is rapidly absorbed through the skin and eliminated in exhaled air and a very small percentage is excreted in urine. Inhaled Trichloroethane is eliminated in exhaled air. Acute oral LD(50) values have been reported as follows: 12.3 g/kg in male rats; 10.3 g/kg in female rats; 11.24 g/kg in female mice; 5.66 g/kg in female rabbits; and 9.47 g/kg in male guinea pigs. Acute toxicity studies using other routes of exposure, including subcutaneous injection and inhalation, produced no evidence of significant toxicity, except at very high exposure levels. Continuous inhalation exposure of rabbits to 750 mg/m(3) for 90 days did not produce any signs of toxicity. Continuous exposure of rats, guinea pigs, rabbits, and monkeys to 500 ppm Trichloroethane for 6 months did not produce any signs of toxicity. Other short-term and subchronic inhalation exposures confirmed acute and short-term exposure findings that the toxic effects of inhalation were a function of both concentration and time. Rats receiving 750 or 1500 mg/kg day(- 1) Trichloroethane in corn oil by oral gavage 5 days per week for 78 weeks had reduced body weights and early mortality. Reduced body weights, decreased survival rates, and early mortality (in females) were found in mice dosed with 3000 or 6000 mg/kg day(- 1) (over the last 58 weeks; lower doses were administered for the first 20 weeks). Mice exposed to prolonged periods of Trichloroethane in an inhalation chamber had increased motor activity at levels up to 5000 ppm. Further increase of concentration of exposure resulted in less of an increase of motor activity until motor activity began to fall below normal at 10,000 ppm. Adverse effects on motor activity in rats were seen at exposures as low as 3000 ppm for 4 h. Rabbits had slight reddening and scaling after 10 24-h applications to abdominal skin of Trichloroethane mixed with 2.4% to 3.0% dioxane, and slight to moderate erythema, slight edema, and slight exfoliation was observed when 75% Trichloroethane and 25% tetrachloroethylene were applied to rabbit ears for 11 days. Undiluted Trichloroethane applied to the clipped backs of guinea pigs produced histopathologic damage in the epidermis. A primary irritation index of 5.22 (out of 8) was reported in rabbits. Trichloroethane applied to the eyes of rabbits resulted in transient irritation and apparent pain, but no corneal damage. There was no effect on gestation, pup survival, or growth in mice given Trichloroethane in drinking water at up to 5.83 mg/ml during mating and/or gestation. Rats exhibited no or minimal effects of ingestion of Trichloroethane up to 30 ppm in drinking water during mating and/or gestation. There was no effect on gestation, pup survival, or growth in mice or rats inhaling 875 ppm Trichloroethane. However, prenatal exposure of rodents to Trichloroethane can produce developmental toxicity in the form of delayed development in the offspring. Trichloroethane has been found to be mutagenic in the Ames assay in some studies and not mutagenic in others. Trichloroethane induced transformations in Fischer rat embryo cell system at 99 mu M, was not mutagenic using the mouse lymphoma assay at up to 0.51 mu g/ml, was equivocal in that assay when tested with S9, and was also equivocal in a sister-chromatid exchange assay using Chinese hamster ovarian (CHO) cells with and without S9. Mice ingesting 80,000 ppm Trichloroethane in their drinking water had an increase in the frequency of micronucleated normochromatic erythrocytes. A peripheral blood micronucleus test in female mice was negative. Trichloroethane was not carcinogenic to rats when administered 1500 mg/kg by oral gavage 5 days/week for 78 weeks or in mice administered 6000 mg/kg. Exposure to 1500 ppm Trichloroethane vapor for 6 h/day, 5 days/week for 2 years likewise gave no indications of oncogenic effects in rats or mice. People who have been exposed to Trichloroethane have reported dizziness, lassitude, unconsciousness, respiratory depression, peripheral vascular collapse, impaired postural control, mild encephalopathy, perioral tingling, burning on the tongue and discomfort in the hands and feet. The Cosmetic Ingredient Review (CIR) Expert Panel recognizes that Trichloroethane (1,1,1-Trichloroethane) has been declared a Class I ozone-depleting substance by the EPA and its use is limited to essential products. The FDA has determined that use of Trichloroethane in aerosol cosmetic products is considered nonessential. At issue for this assessment is the safety of direct exposure to individuals as a result of exposure to cosmetic products that may contain Trichloroethane. The Expert Panel found the available data to be sufficient to support the safety of Trichloroethane as a solvent in cosmetic products.
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PMID:Final report on the safety assessment of Trichloroethane. 1910 34

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that can occur in people with normal liver-associated enzyme levels, and despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl suffering from absence seizures, who complained of progressive dizziness and general malaise several days after restarting valproate. She developed vomiting and decreased consciousness after 3 weeks of valproate use. She had a serum ammonia level five times higher than the upper normal limit, normal liver-associated enzymes, and a supra-therapeutic valproate level. Electroencephalography (EEG) showed continuous generalized slowing. Tandem mass spectrometry analysis revealed carnitine deficiency. Her consciousness improved after emergent hemodialysis. Her ammonia level and EEG also became normal. Possible mechanisms, risk factors and treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.
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PMID:Valproate-induced hyperammonemic encephalopathy. 1913 74

Two topics, related to mushroom poisoning of recent interest in Japan, have been presented. In autumn 2004, 59 cases of acute encephalopathy were reported across 9 prefectures in Japan (24 from Akita Prefecture with 8 deaths; age 48-93, average 70; female 14, male 10). Of 24 cases, 20 had kidney dysfunction. Four poisoned subjects showed no kidney trouble. Of the 24 poisoning cases, 23 people ate Pleurocybella porrigens, and one ate Grifola frondosa. The latter subject (female, late 40's) was receiving dialysis for more than 35 years. In August, she felt dizziness, headache and tinnitus. She visited hospital and asked to stay there. In the hospital she ate 5g of stewed G. frondosa and 10g of the same fungus boiled with chicken and taro on different days. Fourteen to 18 days after the eatings, she developed cramps and lost consciousness, and fell into a coma. Her cramp and coma continued for about 10 days almost until her death. Her symptoms caused by G. frondosa were similar to those observed for the above 23 cases of P. porrigens ingestion. Therefore, we concluded that encephalopathy experienced in Akita Prefecture caused by was the cyanogenic fungi such as P. porrigens , G. frondosa, Pleurotus eringii etc. Although the amounts of mushrooms eaten by poisoned subjects were not so clear, we estimated that the amounts of hydrogen cyanide (HCN) taken into human bodies exceeded the detoxication limit of HCN, resulting in HCN poisoning. However, it has not been proved that the encephalopathy is directly or indirectly caused by the HCN poisoning. Many typhoons came across Japan and landed 10 times in 2004, and mushroom size was larger than usual one, and HCN contents in fruit-bodies seemed to be increased especially in the late-stage of their growth. Thirteen species of magic mushrooms were prohibited by the law from 2002 in Japan. They include Copelandia (Panaeolus) cyanescens, Panaeolus papilionaceus, Panaeolus sphinctrinus, Panaeolus subbalteatus, Psilocybe argentipes, Psilocybe cubensis, Psilocybe fasciata, Psilocybe lonchophorus, Psilocybe subaeruginascens, Psilocybe subcaerulipes, Psilocybe subcubensis, Psilocybe tampanensis, and Psilocybe venenata.
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PMID:[Acute encephalopathy caused by cyanogenic fungi in 2004, and magic mushroom regulation in Japan]. 1934 63

A 58-year-old female receiving gemcitabine and cisplatin chemotherapy for stage IV gallbladder cancer developed the clinicoradiologic syndrome, posterior reversible encephalopathy syndrome (PRES). Just before the 4th gemcitabine chemotherapy cycle, she was admitted to the hospital with complaints of headache, dizziness, and generalized tonic-clonic seizures. A MRI was performed on the day when the seizure developed, and the findings showed patchy cortical and subcortical T2 hyperintensity without enhancement that involved both occipital and parietal lobes. Phenytoin loading and maintenance was started for prevention of recurrent seizures, which was successful. The follow-up brain MRI obtained 10 days after the seizure attack showed completely resolved radiologic findings. After the MRI findings revealed complete resolution, phenytoin maintenance was stopped. Even with discontinuation of phenytoin, she had no seizures or other clinical manifestations.
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PMID:A case of gemcitabine and cisplatin associated posterior reversible encephalopathy syndrome. 1968 73

This is the first case of virus-associated encephalitis/encephalopathy in which the pathogen was Hantaan virus. A 53-yr-old man presented fever, renal failure and a hemorrhagic tendency and he was diagnosed with hemorrhagic fever with renal failure syndrome (HFRS). In the course of his illness, mild neurologic symptoms such as dizziness and confusion developed and magnetic resonance images revealed a reversible lesion in the splenium of the corpus callosum. This case suggests that HFRS patients with neurologic symptoms like dizziness and mental slowing should be considered to have structural brain lesions and to require brain imaging studies.
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PMID:Reversible splenium lesion of the corpus callosum in hemorrhagic fever with renal failure syndrome. 2067 43

The fixed combination containing 5 mg of vinpocetine and 400 mg of pyracetam (vinpotropil) was prescribed to 349 patients with dyscirculatory encephalopathy, I-II stages in dose one capsule three times a day during 3 months. After this treatment, repeated neuropsychological testing showed significant diminishing of dysexecutive cognitive impairment linked with frontal lobes dysfunction. The cognitive improvement was associated with the regress of subjective neurological symptoms like headache, dizziness, tinnitus, fatigue and insomnia. Vinpotropil was safe and well tolerated in elderly patients with chronic cerebral vascular insufficiency.
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PMID:[Vinpotropil in the treatment of dyscirculatory encephalopathy with cognitive impairment without dementia]. 2118 16

We describe the case of a patient from the emergency ophthalmic clinic who presented with sudden, bilateral visual loss, headache and dizziness. The magnetic resonance imaging (MRI) showed bilateral parieto-occipital vasogenic edema of the white and grey brain matter consistent with the diagnosis of posterior reversible encephalopathy syndrome (PRES). This is a rare cause of sudden bilateral visual loss which describes a condition with bilateral edema of primarily the white but also the grey matter. The edema is usually detectable with MRI but not always with the less sensitive computed tomography (CT). Further clinical signs may be headache, seizure, nausea, character changes and reduced consciousness. Arterial hypertension, drugs inducing hypertension or drug side effects may cause PRES but sometimes the reason remains unknown. In most cases the symptoms resolve simultaneously with the edema but may also lead to severe complications. In suspected cases of PRES the blood pressure should be measured and a MRI performed, followed by intensive care and treatment of the hypertension, other symptoms and complications.
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PMID:[Acute bilateral loss of vision in posterior reversible encephalopathy syndrome]. 2273 65

BACKGROUND Little is known about adult-onset opsoclonus-myoclonus syndrome (OMS) outside of individual case reports. OBJECTIVE To describe adult-onset OMS. DESIGN Review of medical records (January 1, 1990, through December 31, 2011), prospective telephone surveillance, and literature review (January 1, 1967, through December 31, 2011). SETTING Department of Neurology, Mayo Clinic, Rochester, Minnesota. PATIENTS Twenty-one Mayo Clinic patients and 116 previously reported patients with adult-onset OMS. MAIN OUTCOME MEASURES Clinical course and longitudinal outcomes. RESULTS The median age at onset of the 21 OMS patients at the Mayo Clinic was 47 years (range, 27-78 years); 11 were women. Symptoms reported at the first visit included dizziness, 14 patients; balance difficulties, 14; nausea and/or vomiting, 10; vision abnormalities, 6; tremor/tremulousness, 4; and altered speech, 2. Myoclonus distribution was extremities, 15 patients; craniocervical, 8; and trunk, 4. Cancer was detected in 3 patients (breast adenocarcinoma, 2; and small cell lung carcinoma, 1); a parainfectious cause was assumed in the remainder of the patients. Follow-up of 1 month or more was available for 19 patients (median, 43 months; range, 1-187 months). Treatment (median, 6 weeks) consisted of immunotherapy and symptomatic therapy in 16 patients, immunotherapy alone for 2, and clonazepam alone for 1. Of these 19 patients, OMS remitted in 13 and improved in 3; 3 patients died (neurologic decline, 1; cancer, 1; and myocardial infarction, 1). The cause of death was of paraneoplastic origin in 60 of 116 literature review patients, with the most common carcinomas being lung (33 patients) and breast (7); the most common antibody was antineuronal nuclear antibody type 2 (anti-Ri, 15). Other causes were idiopathic in origin, 38 patients; parainfectious, 15 (human immunodeficiency virus, 7); toxic/metabolic, 2; and other autoimmune, 1. Both patients with N -methyl-D-aspartate receptor antibody had encephalopathy. Improvements were attributed to immunotherapy alone in 22 of 28 treated patients. CONCLUSIONS Adult-onset OMS is rare. Paraneoplastic and parainfectious causes (particularly human immunodeficiency virus) should be considered. Complete remission achieved with immunotherapy is the most common outcome.
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PMID:Adult-onset opsoclonus-myoclonus syndrome. 2369 54


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