Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the efficacy and the safety of epidural morphine or butorphanol combined with bupivacaine, 40 healthy parturients were studied during labor and delivery. All patients received an epidural test dose of 2 ml of 0.5% bupivacaine. Patients were then randomly assigned to receive one of four epidural regimens in a double-blind fashion: 0.25% bupivacaine + 1 mg butorphanol (Group I), 0.25% bupivacaine + 2 mg butorphanol (Group II), 0.25% bupivacaine + 2 mg morphine (Group III), or 0.25% bupivacaine alone (Group IV). Each group consisted of ten patients. All subsequent epidural injections were with plain 0.25% bupivacaine. Duration of analgesia was significantly longer for groups I, II, and III when compared to group IV (p less than or equal to .01); 139 +/- 111, 141 +/- 14, 199 +/- 29, and 96 +/- 6 minutes, X +/- SEM respectively. Quality of analgesia was significantly better in groups I, II, and III when compared with group IV. There were no differences between groups in duration of first and second stages of labor, uterine activity, or method of delivery. Thirty percent of patients in the morphine group (group III) developed mild pruritus that did not require any treatment. All neonates were vigorous at 5 minutes and had good Apgar Scores, umbilical cord acid base status, and Neurological Adaptive Capacity Scores. The authors conclude that adding small doses of either morphine or butorphanol to epidural bupivacaine during labor is effective and safe. Butorphanol may be preferable since none of the patients experienced pruritus.
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PMID:Epidural morphine or butorphanol augments bupivacaine analgesia during labor. 248 90

The etiology of the pruritus of cholestasis is unknown. It is inferred that the pruritogen(s) is produced in the liver, excreted in bile, and as a result of cholestasis it accumulates in plasma. It may follow, logically, that the removal of the substance(s) that mediate pruritus leads to its resolution. The problem with this approach, however, is that the substance(s) is unknown; thus, it is not possible to reduce its serum levels specifically. Oral cholestyramine, a resin that is not absorbed, is associated with increased fecal excretion of certain substances, including cholesterol and bile acids. Many patients respond to treatment with cholestyramine with a relief of pruritus, which unfortunately may be temporary, but is well tolerated in general and it seems reasonable to prescribe it as an initial therapy. When pruritus is not relieved by resins, the use of opiate antagonists (eg, naloxone and naltrexone) is supported by data from controlled clinical trials. Butorphanol is an agonist at the kappa opioid receptor and an antagonist at the mu opioid receptor with minimal or absent abuse potential. The use of butorphanol spray in selective patients may be a therapeutic alternative. In uncontrolled observations dronabinol, an agonist at the cannabinoid B1 receptor, and sertraline, a serotonin reuptake inhibitor, have been reported to be associated with the relief of pruritus. The cannabinoidergic and serotoninergic systems participate in the mediation of nociception; therefore, there appears to be a rationale for the use of these drugs to treat pruritus. Data from controlled clinical trials on the use of dronabinol and sertraline, however, are not available at present.
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PMID:Treatment of the Pruritus of Cholestasis. 1552 16

Opioid receptors in the central nervous system are important modulators of itch transmission. In this study, we examined the effect of mixed-action opioid butorphanol on histamine itch, cowhage itch, and heat pain in healthy volunteers. Using functional MRI, we investigated significant changes in cerebral perfusion to identify the critical brain centers mediating the antipruritic effect of butorphanol. Butorphanol suppressed the itch induced experimentally with histamine, reduced the intensity of cowhage itch by approximately 35%, and did not affect heat pain sensitivity. In comparison with the placebo, butorphanol produced a bilateral deactivation of claustrum, insula, and putamen, areas activated during itch processing. Analysis of cerebral perfusion patterns of brain processing of itch versus itch inhibition under the effect of the drug revealed that the reduction in cowhage itch by butorphanol was correlated with changes in cerebral perfusion in the midbrain, thalamus, S1, insula, and cerebellum. The suppression of histamine itch by butorphanol was paralleled by the activation of nucleus accumbens and septal nuclei, structures expressing high levels of kappa opioid receptors. In conclusion, important relays of the mesolimbic circuit were involved in the inhibition of itch by butorphanol and could represent potential targets for the development of antipruritic therapy.
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PMID:Butorphanol suppression of histamine itch is mediated by nucleus accumbens and septal nuclei: a pharmacological fMRI study. 2521 Nov 75