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)

CBT-1, a natural product, was studied as an MDR modulator with Taxol (135 mg/m2) in an escalating dose Phase I clinical trial. CBT-1 was administered orally at doses from 300 mg/m2 to 500 mg/m2 daily x 7. The MTD was determined to be 500 mg/m2 with moderate nausea and occasional emesis. Side effects were mainly attributable to Taxol rather than the study drug. A total of 18 patients were registered on study with only one patient determined to be intolerant of CBT-1 due to nausea and emesis. In this Phase I study four patients (3 breast, 1 NSCLC) remained stable for greater than two cycles of treatment. No complete or partial responses were seen in this Taxol resistant population of patients with advanced cancer.
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PMID:Phase I study of CBT-1 and Taxol in patients with Taxol resistant cancers. 1080 20

CBT-1, a natural product, was studied in an escalating dose Phase I clinical trial with doxorubicin at 60 mg/m2. CBT-1 was administered by mouth at doses from 200 mg/m2 to 600 mg/m2. The drug was given for 7 days and doxorubicin administered intravenously on day 6. The MTD was determined to be 500 mg/m2 although some patients did tolerate 600 mg/m2 with moderate nausea and occasional vomiting. Side effects were otherwise mild in the 23 patients treated. Pharmacokinetic determinations in an additional 11 patients demonstrated that CBT-1 did not significantly alter the pharmacokinetics of doxorubicin. In this Phase I study, 25 of 34 patients were evaluable for response and 5 patients demonstrated tumor shrinkage.
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PMID:A phase I and pharmacokinetic study of CBT-1 as a multidrug resistance modulator in the treatment of patients with advanced cancer. 1085 Mar 43

Anxiety disorders and alcohol dependence have a higher co-occurence than expected by chance only. This association has a double origin, as the presence of alcohol dependence increases by 6 the risk of any anxious disorder, and the presence of an anxious disorder multiply by 3 the risk of alcohol-dependence. Interestingly, a large population-based epidemiological study performed 10 years apart clearly showed that anxiety disorders moderatly increase the risk of regular consumption in non-consumers or irregular drinkers (by 70%), does not increase ther risk of abuse in regular drinkers, but has a strong impact on the risk of alcohol dependence while already an abuser (OR = 2.7). Assessing the kinetic of symptoms of anxiety and focusing on some symptoms that are more specific than others (for example nausea, vomiting and/or shaking hands in the morning, all being relieved by the first drink) is helpful. Treating anxiety symptoms in alcohol dependence means, whatever the type of relationship they have, to begin with a detoxification program. Indeed, antidepresants have a larger liver-toxicity in alcohol dependence, and benzodiazepine loose most of their benefits with high level of alcohol consumption. Furthermore, when benzodiazepines are taken with large doses of alcohol, the risk of severe withdrawal symptoms is increased (such as seizures). The same trend could be proposed for psychotherapy, as cognitive behavioural therapy sollicitates a lot executive functions. The neurotoxicity of alcohol explains the damages on executive functions, CBT therefore should have larger efficacy after the detoxification program, helping to reduce the risk of relapse.
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PMID:[Alcohol dependence and anxious disorders: dangerous liaisons]. 2062 97