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

Ears are special sense organs whose principal functions are hearing and maintaining equilibrium. Aminoglycoside antibiotics, erythromycin, polymyxin B, and cisplatin can affect either or both of these functions by binding with, injuring, and/or destroying special receptor cells associated with these functions. Severe hearing loss manifests itself as deafness, whereas loss of equilibrium will present as abnormal righting reflexes, nausea, and vomiting. Damage is proportional to levels of these ototoxins in the endolymphatic fluids. Evidence suggests that toxicity may be influenced by endolymphatic calcium concentrations, and levels of cAMP and cGMP are altered in specialized cochlear cells during ototoxicity, suggesting an additional mechanism for ototoxicity. The administration of salicylates and loop diuretics may potentiate the action of ototoxins, especially aminoglycoside antibiotics, probably by increasing the levels of these toxins in the endolymphatic fluid. Although many of these assessments have been made in laboratory animals, applicability may also be expected in small domestic animals, and extreme care should be taken in prescribing potentially ototoxic drugs to small animals. Cochlear damage from ototoxic compounds occurs initially in the cells detecting high-frequency sounds located at the lower basal region. In aging dogs and humans, this sensitivity of receptors in the lower basal region is enhanced. Early auditory damage is detectable by BAER and cochlear microphonic potentials. Vestibular responses can also be detected early as vestibular ocular reflexes and visual-vestibulo-ocular reflexes. Early detection is especially important because early changes can sometimes be reversible. Cavinton (apovincaminic acid) and fosfomycin represent examples of experimental agents being evaluated in laboratory animals for application as potential treatments to limit the ototoxicity associated with various drugs.
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PMID:Ototoxicity in dogs and cats. 845 3

To characterize otologic causes for vertigo, data on 564 patients with the six most common diseases involving vertigo were retrieved from the database of a computer-aided diagnostic system for neurotologic diseases. The diseases were Meniere's disease, vestibular schwannoma, benign paroxysmal positional vertigo, vestibular neuritis, sudden deafness, and traumatic vertigo. The prevalence of tinnitus in the study population was 76%. The most severe forms of vertigo and nausea were found in vestibular neuritis, whereas the most severe case of tinnitus appeared in Meniere's disease. Of the patients with vestibular schwannoma, 49% had had vertigo. A linear discrimination analysis using case history classified 90% of the patients into correct groups. The key questions discriminating between the diseases concerned the frequency and duration of vertigo attacks, the duration of hearing loss and vertigo, and the occurrence of head injury. Making a correct diagnosis during the first office visit can be difficult, especially for sudden deafness, vestibular schwannoma, and Meniere's disease. Neurotologic and audiometric information was of minor value in distinguishing between these six diseases. Vestibular schwannoma had significantly greater asymmetry in electronystagmography and smaller gains in smooth pursuit in comparison with the other disease. Factorial analysis did not aid the clustering of these diseases.
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PMID:Characteristics of six otologic diseases involving vertigo. 909 90

Between 1981 and 1994, 58 bioequivalence studies (b.s.) were performed in 885 healthy volunteers. 93.1 per cent were single-dose, mainly of two way cross-over design. According to ATC groups, 13 were of cardiovascular drugs(C), 11 musculoskeletal (M), nine alimentary (A), seven urogenital (G), seven antimicrobial (J), six haematological (B), three nervous (N) and two respiratory (R). 97.2 per cent of volunteers finished the studies. Out of 25 withdrawals, 14 did it by their own will, seven were excluded because of lack of compliance with the protocol, one because of an adverse drug reaction (ADR) (preputial oedema), one because of intercurrent illness, and two for other objective reasons. In 35 studies the probants have been males, in 23 both sexes. Subjects were between 18 and 40 years. 209 adverse events were reported in 18 studies (31 per cent). From 885 volunteers that came to first session at the time, 115 (13 per cent) had ADRs. The association of the drug and ADRs was defined as probable in 91 ADRs (45.9 per cent), definite in 66 (33.4 per cent) and possible in 41 (20.7 per cent). 73 (63.5 per cent) volunteers had one ADR, 22 (19.1 per cent) had two and 20 (17.4 per cent) more than two ADRs. The majority -117 (56 per cent)-of ADRs were mild, 78 (37.3 per cent) moderate and 14 (6.7 per cent) severe. The most frequent ADR was headache (22.9 per cent), followed by nasal congestion (12.9 per cent), sweating (12.4 per cent), nausea (6.7 per cent), restlessness (6.7 per cent), deafness and tinnitus (6.2 per cent), change of biochemical or haematological parameters (5.3 per cent) and other. An unusual and rare ADR was impotence and preputial oedema (two volunteers on frusemide). All studies of G group (7-100 per cent) had ADRs, followed by C group (5-38 per cent) and A (3-33 per cent). Glipizide (5 mg) had highest number of ADRs (64-30.6 per cent), bromocriptine (10 mg) had 31 (14.8 per cent) and frusemide (500 mg) 22 (10.6 per cent). The largest number of subjects with ADRs were on frusemide (13-72 per cent), glipizide (17-68 per cent) and bromocriptine (15-52 per cent). At a time when generic drugs are of increasing importance, the safety of b.s. is of considerable interest. Our data confirm their safety and indicate that the majority of ADRs are mild.
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PMID:How safe are bioequivalence studies in healthy volunteers? 895 18

Tirapazamine (SR 4233; 3-amino-1,2,4-benzotriazine-1,4-di-N-oxide) is a bioreductive agent exhibiting up to 200 x greater toxicity for hypoxic cells as compared to oxygenated cells. In murine studies, a selective increase in tumor kill was observed when tirapazamine was coadministered with other agents, notably cisplatin. A Phase I study of single-agent tirapazamine administered i.v. every 3 weeks was conducted to determine the toxicity of a schedule for use with systemic chemotherapy. A total of 28 patients were given 50 courses of tirapazamine at doses ranging from 36-450 mg/m2. No tumor responses were observed. Reversible deafness and tinnitus were dose-limiting, with ototoxicity observed in 1 of 6 patients treated at 330 mg/m2, 1 of 4 patients treated at 390 mg/m2, and 3 of 3 patients treated at 450 mg/m2. Muscle cramps, nausea, and vomiting were also observed. Pharmacokinetic studies revealed a greater than dose-proportional increase in the area under the plasma concentration x time curve (AUCs) of the two major metabolites. Patients who developed ototoxicity generally showed higher plasma AUC values for the parent drug and metabolites. The mean plasma tirapazamine AUC at 330 mg/m2 was 1026.5 microgram/ml x min (range 863. 8-1252.3), but no pharmacokinetic data are available for the solitary patient who developed otoxicity at this dose level. These AUC values were in the (estimated) range required for therapeutic effect in murine studies. Ototoxicity was not observed when the AUC of tirapazamine was equal to or less than 1252 microgram/ml x min. The dose of 330 mg/m2 was therefore chosen as an appropriate level for combination chemotherapy studies.
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PMID:Phase I and pharmacokinetic study of tirapazamine (SR 4233) administered every three weeks. 981 34

The standard first-line treatment for malaria in adults in Papua New Guinea is chloroquine; for severe and treatment-failure malaria standard therapy is a combination of quinine and Fansidar (sulphadoxine-pyrimethamine). These standard treatments are currently under revision. The present study evaluated the effect of halofantrine in treatment-failure falciparum malaria in adults in Port Moresby compared to standard therapy. In the halofantrine group all parasites were cleared by day 5 after starting therapy, in the quinine-Fansidar group by day 7. There was no evidence of recurrence of parasitaemia during the 21-day follow-up in either group. Nausea was associated with halofantrine use in 68% of patients. In the quinine-Fansidar group 79% had muffled deafness, 32% tinnitus and 26% dizziness; 32% of patients withdrew from treatment on day 2 because of intolerance to quinine. Halofantrine in this study population provided an efficacy against treatment-failure falciparum malaria similar to that of quinine-Fansidar, with a more favourable profile of adverse effects.
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PMID:Halofantrine versus quinine-Fansidar combination in the treatment of post-chloroquine falciparum parasitaemia. 1093 52

Our objective was to determine the maximum tolerated doses of tirapazamine and cyclophosphamide given i.v. in combination. Eligible patients had advanced solid tumors refractory to conventional treatment. Tirapazamine (escalated from 80 to 390 mg/m(2)) was given i.v. over 2 h and followed by cyclophosphamide over 1 h. The cyclophosphamide dose was fixed at 1000 mg/m(2) until the tirapazamine dose of 390 mg/m(2) was reached. Once that dose of tirapazamine was reached, the cyclophosphamide dose was escalated to 1250 and 1500 mg/m(2). Twenty-eight patients were enrolled. The dose-limiting toxicity was granulocytopenia. One patient had transient deafness for 2 days. Four other patients had grade 1 ototoxicity. Grade 1 and 2 muscle cramps were observed at all dose levels. Other toxic effects observed included fatigue, nausea, vomiting, headache, diarrhea, drug fever, elevated transaminases and elevated creatine phosphokinase. Three patients had stable disease and the longest time to progression was 5 months. The combination of tirapazamine and cyclophosphamide is feasible, and the dose-limiting toxicity is granulocytopenia. The use of growth factors could possibly allow escalation of tirapazamine doses in future phase II trials. Without growth factor support, the recommended doses of tirapazamine and cyclophosphamide when administered in this schedule are 260 and 1000 mg/m(2), respectively.
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PMID:Phase I trial of i.v. administered tirapazamine plus cyclophosphamide. 1145 95

A 52-year-old woman was admitted to our hospital with sudden diplopia, right ophthalmalgia, and occipital pain. The nature of her headache was continuous, and changing her position provided no relief. Three weeks before her admission, she experienced continuous cough and rhinorrhea during a few days. On admission, her neurological examination revealed right abducens paralysis, and right lateral gaze aggravated diplopia. Brain magnetic resonance imaging scan demonstrated diffuse pachymeningeal enhancement by gadolinium. Radioisotope cisternography showed a leak of cerebrospinal fluid from near the third lumbar vertebra. The first lumbar puncture revealed an initial pressure of 0 mm H2O. She was given a diagnosis of spontaneous intracranial hypotension due to a leak of the cerebrospinal fluid. During her hospitalization, she complained of vertigo and nausea. We found horizontal gaze nystagmus to left side and sensorineural deafness in her left ear, which improved in a few days. After treatment by a lumbar epidural continuous infusion of saline and a lumbar epidural blood patch, her headache and abnormal MRI findings had improved. The continuous cough before her admission may be the cause of the leak of cerebrospinal fluid. We had difficulty in diagnosis only by the history and clinical examination, because she had no history of orthostatic headache.
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PMID:[A case of spontaneous intracranial hypotension without any history of positional headache]. 1251 25

Tinnitus is an otological symptom that is encountered often, yet its treatment is difficult. If tinnitus is of cochlear origin, a reasonable assumption is that a total depression of the cochlear function will abolish cochlear tinnitus. To achieve this depression, transtympanic infusion of a local anesthetic (4% lidocaine) to anesthetize the inner ear was conducted in a patient suffering from tinnitus. Transtympanic infusion of 4% lidocaine was performed as a treatment for cochlear tinnitus, and its efficacy was investigated. The overall efficacy rate for the 292 patients with 369 affected ears was 81%. In the investigation of the treatment results in cases of different underlying ear diseases, the efficacy rate was high for tinnitus accompanying sudden deafness and labyrinthine vertigo. However, vestibular symptoms, such as vertigo and nausea, developed after lidocaine infusion. No permanent side effects were noted. Lidocaine infusion is thought to be a useful treatment option for tinnitus and should be considered before surgical treatment. Inner ear anesthesia into the tympanic cavity has been carried out in patients who had cochlear tinnitus and in whom conservative methods of therapy, such as oral medication, had proved unsuccessful. This treatment method is useful as a local therapy for cochlear tinnitus.
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PMID:Treatment of cochlear tinnitus with transtympanic infusion of 4% lidocaine into the tympanic cavity. 1496 56

This study presents two cases of Arnold-Chiari malformation type I. In a 26-year old man, right side deafness and left side sensorineural hearing loss at high frequencies occurred. Another patient, a 48-year old man also complained of sensorineural hearing loss and dizziness, that appeared a year and half ago. In addition, this patient had episodes of vertigo with nausea and vomit that occurred about one year before main symptoms. In both patients ENT examinations were performed as well as an audiological diagnostic battery including tonal- and impedance-audiometry, auditory brainstem responses, distortion product otoacoustic emissions and electroencephalography. Magnetic resonance imaging (MRI) showed pathological changes in the cerebello-pontine angle region that allowed diagnosing Arnold-Chiari malformation in both cases. Additionally, angio-MRI performed in patient with right side deafness revealed cochleovestibular nerve compression syndrome on the same side. Presumably, both anomalies occurring simultaneously in this patient might be responsible for deafness in the right ear, instead of mild or moderate hearing loss and tinnitus usually expected according to the literature. The paper presented two cases of Arnold-Chiari malformation with co-existing cochleovestibular nerve compression syndrome in one case. The importance of both audiological diagnostic battery and MRI in diagnostic procedures of this malformation has been demonstrated.
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PMID:[Otoneurologic symptoms associated with Arnold-Chiari syndrome type I]. 1530 73

Chronic myeloid leukemia (CML) is one of the etiologic causes of sudden hearing loss and vertigo. However, deafness in association with vestibular symptoms rarely occurs in CML as the first sign. In this article, a 50-year-old male with CML whose first signs and symptoms were unilateral sudden hearing loss and tinnitus in the right ear, vertigo and nausea was presented. Aetiopathogenetic mechanisms, clinical and radiological aspects and therapeutic options for CML with deafness and vertigo were discussed reviewing the literature.
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PMID:Unilateral sudden hearing loss as the first sign of chronic myeloid leukemia. 1761 73


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