Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 17-year-old female case of ornithine transcarbamylase (OTC) deficiency who died of brain edema due to hyperammonemic attack. The patient had a brother with OTC deficiency who had died of hyperammonemia at 17 years of age. She firstly had a symptom of headache, nausea, vomiting and myalgia at 14 years old and twice thereafter. On admission she had a severe disorientation and vomiting. The plasma ammonia level was 89 micrograms/dl, then increased to 400 micrograms/dl in five hours. In addition to plasma exchange, hemodialysis and then peritoneal dialysis for next 5 days, parenteral sodium benzoate and arginine were administered. Although the plasma ammonia level improved gradually, her consciousness never returned and she died of severe brain edema with uncontrollable hypotension on day 8. Histology of a necropsy liver sample showed fatty metamorphosis of hepatocytes mainly with fine lipid droplets. Electron micrograph of hepatocytes showed crystalloid inclusions in mitochondria. Significance of the clinical course and the treatment during hyperammonemic crisis was discussed.
 ...
PMID:[Abrupt onset and rapid deterioration in the course of congenital ornithine transcarbamylase deficiency: a case report]. 221 May 91

Described here is a fatal case of accidental aconitine poisoning following the ingestion of aconite, Torikabuto, mistaken for an edible grass, Momijigasa. A 61-year-old man developed symptoms of nausea, diarrhea, and discomfort of the body about 2 h after the ingestion and was taken to an emergency room. Resuscitation and antiarrhythmic drugs were ineffective, and ventricular tachycardia and fibrillation developed and lasted for 6 h. He was transferred to a coronary care unit and complete sinus rhythm was obtained on an electrocardiogram 30 h after his admission. The patient fell into a coma and died of brain edema diagnosed by CT on the 6th day. Consent for autopsy was denied by the family but was given for gas chromatography/selected ion monitoring (GC/SIM) to analyze the toxicity of aconitine alkaloids in the blood and the urine. Only a faint amount of jesaconitine was detected, while aconitine, mesaconitine and hypaconitine were not detectable in the blood 24 h after ingestion. On the other hand, aconitine and its related alkaloids such as mesaconitine, jesaconitine, and hypaconitine were clearly detected in the urine.
 ...
PMID:A case of aconitine poisoning with analysis of aconitine alkaloids by GC/SIM. 883 86

Reye syndrome (RS) is an acute encephalopathy in childhood, and is very rare in adulthood. Here we report a 21-year-old woman with RS. Because of her dysmenorrhea, she took 3 tablets of diclofenac sodium (25 mg) per day in 3 divided doses for two days. Two days after the last intake of the medicine, she developed high fever, nausea, vomiting, and disturbance of consciousness with delirium, i.e., acute encephalopathy. She did not have seizure, hemiplegia, or other focal neurological manifestations. The serum GOT level was normal at onset, but in 12 hours dramatically increased up to 8,632 IU/L. The serum bilirubin level was normal. The cerebrospinal fluid revealed normal cell count, and protein. Although the liver biopsy was not performed because of thrombocytopenia, we diagnosed her as an adult case of RS according to the clinical criteria of the Center for Disease Control. In addition to treatment for the brain edema, plasma exchange was performed once treat the encephalopathy at the onset. The next day, her consciousness level and serum GOT level markedly improved. She completely recovered from acute encephalopathy in a week after her admission. In conclusion, diclofenac sodium, as well as aspirin, should be considered as a possible causal agent for RS, and early plasma exchange may be beneficial.
 ...
PMID:[An adult case of Reye syndrome induced by diclofenac sodium, and recovered by plasma exchange]. 974 77

Because of their variety of uses, corticosteroids are frequently prescribed in advanced cancer patients. Two patients who developed neuropsychiatric complications on corticosteroids and their subsequent management are described. The first patient, who had a known history of steroid-induced psychotic depression, required corticosteroids to treat recurrent brain edema from a malignant meningioma. The patient was managed by using low-dose corticosteroids and concomitant haloperidol. The second patient was prescribed corticosteroids for a constellation of symptoms, including pain and nausea from a possible bowel obstruction, and developed a severe delirium that required discontinuation of the corticosteroids. The difficulties of diagnosing steroid-related cognitive and mood changes in advanced cancer patients who often have multisystem disease are discussed, as well as strategies for minimizing the effects of corticosteroids' neuropsychological complications.
 ...
PMID:Difficulties in diagnosing neuropsychiatric complications of corticosteroids in advanced cancer patients: two case reports. 1079 97

DMSO is an amphipathic molecule with a highly polar domain and two apolar methyl groups, making it soluble in both aqueous and organic media. It is one of the most common solvents for the in vivo administration of several water-insoluble substances. Despite being frequently used as a solvent in biological studies and as a vehicle for drug therapy, the side-effects of DMSO (undesirable for these purposes) are apparent from its utilization in the laboratory (both in vivo and in vitro) and in clinical settings. DMSO is a hydrogen-bound disrupter, cell-differentiating agent, hydroxyl radical scavenger, intercellular electrical uncoupler, intracellular low-density lipoprotein-derived cholesterol mobilizing agent, cryoprotectant, solubilizing agent used in sample preparation for electron microscopy, antidote to the extravasation of vesicant anticancer agents, and topical analgesic. Additionally, it is used in the treatment of brain edema, amyloidosis, interstitial cystitis, and schizophrenia. Several systemic side-effects from the use of DMSO have been reported, namely nausea, vomiting, diarrhea, hemolysis, rashes, renal failure, hypertension, bradycardia, heart block, pulmonary edema, cardiac arrest, and bronchospasm. Looking at the multitude of effects of DMSO brought to light by these studies, it is easily understood how many researchers working with DMSO (or studying one of its specific effects) might not be fully aware of the experiences of other groups who are working with it but in a different context.
 ...
PMID:Multidisciplinary utilization of dimethyl sulfoxide: pharmacological, cellular, and molecular aspects. 1266 39

A postherpetic-neuralgia patient abruptly discontinued pregabalin. Thirty hours later, unexplained nausea, headache, and ataxia developed, progressing to delirium 8 days later. Magnetic resonance imaging indicated T2-hyperintense lesions of her splenium. Similar magnetic resonance imaging abnormalities, interpreted as focal vasogenic edema, develop in some epileptic patients after rapid anticonvulsant withdrawal. Patients with high-altitude cerebral edema have similar splenial-predominant magnetic resonance imaging abnormalities that accompany these same neurological symptoms. This case is the first to associate anticonvulsant-withdrawal splenial abnormalities with neurological symptoms, with gabapentin-type anticonvulsants, and is among the first in nonepileptic patients, suggesting that sudden anticonvulsant withdrawal alone, unaccompanied by seizures, can initiate symptomatic focal brain edema. The similarity of this syndrome to high-altitude cerebral edema suggests a possible common pathophysiology and offers potential therapies.
 ...
PMID:Pregabalin-withdrawal encephalopathy and splenial edema: a link to high-altitude illness? 1637 25

We report the first case of an obstructive hydrocephalus after intraventricular hemorrhage in a woman with HELLP syndrome and eclampsia. A 25-year-old primiparaous woman had severe preeclampsia at 36 weeks of gestation. She complained of epigastric pain and nausea. The levels of AST, ALT, and LDH were 539, 560, and 1051 IU/L, respectively; the platelet count was 101 x 109/L. Cesarean section was promptly performed. Intraoperatively, she had a first convulsion. The CT scan revealed only mild brain edema. The platelet count deteriorated to 30 x 109/L at 5 hour after the operation, and she had a second convulsion with an intraventricular hemorrhage. On the 6th post-cesarean day, she complained severe headache followed by coma. The CT scan revealed the enlargement of both lateral ventricles, indicating the occurrence of obstructive hydrocephalus. Drainage into cerebral ventricle was performed, resulting in the recovery of consciousness to a normal level.
 ...
PMID:Hydrocephalus after intraventricular hemorrhage in eclamptic woman with HELLP syndrome. 1706 45

Deliberate hyperthermia has been used clinically as experimental therapy for neoplastic and infectious diseases. Several case fatalities have occurred with this form of treatment, but most were attributable to systemic complications rather than central nervous system toxicity. Nonetheless, demyelating peripheral neuropathy and neurological symptoms of nausea, delirium, apathy, stupor, and coma have been reported. Temperatures exceeding 40 degrees C cause transient vasoparalysis in humans, resulting in cerebral metabolic uncoupling and loss of pressure-flow autoregulation. These findings may be related to the development of brain edema, intracerebral hemorrhage, and intracranial hypertension observed after prolonged therapeutic hyperthermia. Furthermore, deliberate hyperthermia critically worsens the extent of histopathological damage in animal models of traumatic, ischemic, and hypoxic brain injury. However, it is unknown whether these findings translate to episodes of spontaneous fever in neurologically injured patients. In a clinical setting fever is a strong prognostic marker of a patient's primary degree of neuronal damage, and a causal relation with long-term functional neurological outcome has not been established for most types of brain injury. Furthermore, in the neurosurgical intensive-care unit fever is extremely common whereas antipyretic therapy is only poorly effective. Therefore maintaining strict normothermia may be an impossible goal in many patients. Although there are several physiological arguments for avoiding exogenous hyperthermia in neurologically injured patients, there is no evidence that aggressive attempts at controlling spontaneous fever can improve clinical outcome.
 ...
PMID:Cerebral pathophysiology and clinical neurology of hyperthermia in humans. 1764 19

The key elements in acclimatization aim at securing the oxygen supply to tissues and organs of the body with an optimal oxygen tension of the arterial blood. In acute exposure, ventilation and heart rate are elevated with a minimum reduction in stroke volume. In addition, plasma volume is reduced over 24-48 h to improve the oxygen-carrying capacity of the blood, and is further improved during a prolonged sojourn at altitude through an enhanced erythropoiesis and larger Hb mass, allowing for a partial or full restoration of the blood volume and arterial oxygen content. Most of these adaptations are observed from quite low altitudes [approximately 1000 m above sea level (m a.s.l.)] and become prominent from 2000 m a.s.l. At these higher altitudes additional adaptations occur, one being a reduction in the maximal heart rate response and consequently a lower peak cardiac output. Thus, in spite of a normalization of the arterial oxygen content after 4 or more weeks at altitude, the peak oxygen uptake reached after a long acclimatization period is essentially unaltered compared with acute exposure. What is gained is a more complete oxygenation of the blood in the lungs, i.e. SaO(2) is increased. The alteration at the muscle level at altitude is minor and so is the effect on the metabolism, although it is debated whether a possible reduction in blood lactate accumulation occurs during exercise at altitude. Transient acute mountain sickness (headache, anorexia, and nausea) is present in 10-30% of subjects at altitudes between 2500 and 3000 m a.s.l. Pulmonary edema is rarely seen below 3000 m a.s.l. and brain edema is not seen below 4000 m a.s.l. It is possible to travel to altitudes of 2500-3000 m a.s.l., wait for 2 days, and then gradually start to train. At higher altitudes, one should consider a staged ascent (average ascent rate 300 m/day above 2000 m a.s.l.), primarily in order to sleep and feel well, and minimize the risk of mountain sickness. A new classification of altitude levels based on the effects on performance and well-being is proposed and an overview given over the various modalities using hypoxia and altitude for improvement of performance.
 ...
PMID:General introduction to altitude adaptation and mountain sickness. 1866 47

The authors report a rare case of pial single-channel arteriovenous fistula presenting with significant brain edema. A 51-year-old woman was admitted with a 5-day history of headache and nausea, followed by consciousness disturbance. Computed tomography showed cerebellar swelling with obstructive hydrocephalus. Magnetic resonance imaging revealed extensive vasogenic edema in the cerebellum bilaterally. Angiography demonstrated 2 different arteriovenous shunts (AVSs) at peripheral branches of the right anterior inferior cerebellar artery. One was located on the suboccipital surface. It drained through a dilated inferior vermian vein and emptied retrogradely into the contralateral cerebellar veins with marked stagnation. Focal stenosis of the dilated draining vein was present. The other AVS was located on the petrosal surface, which had a slow flow with no angiographic evidence of venous congestion. Given that the latter was believed to be asymptomatic, the former AVS was excised, and histological examination revealed that the lesion consisted of a direct communication of multiple arterial feeding vessels with a single vein, consistent with a diagnosis of pial single-channel arteriovenous fistula. The restriction of venous drainage presumably caused venous hypertension, leading to the brain edema and neurological symptoms.
 ...
PMID:Intracranial pial single-channel arteriovenous fistula presenting with significant brain edema. 1875 83


1 2 Next >>