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Dopaminergic Mechanisms in Gastrointestinal Motility
Published in T. S. Gaginella, Regulatory Mechanisms — in — Gastrointestinal Function, 2017
John W. Wiley, Takahashi Toku, Owyang Chung
Administration of dopamine intrathecally (it), the nonselective dopamine agonist apomorphine subcutaneously (sc) or it, and the preferential DA-2 receptor agonist bromocriptine (sc) decreased gastrointestinal transit, which was significantly antagonized by the DA-2 receptor antagonists domperidone and alizapride administered sc but not by SCH23390 (sc), supporting participation of peripheral DA-2 receptors in mediating this action.45
Development of palliative medicine in the United Kingdom and Ireland
Published in Eduardo Bruera, Irene Higginson, Charles F von Gunten, Tatsuya Morita, Textbook of Palliative Medicine and Supportive Care, 2015
Neuroaxially administered opioids, especially morphine, have higher pruritus risk, and appears not to be mediated via histamine, but via mu-opioid receptors. Â 114-118 Pruritus invoked by intrathecal morphine is of longer duration and is difficult to treat. Â 119 Treatment options remain a challenge, and much of the research has emerged from surgical patients who received neuro-axial opioids, and have looked at agents as prophylaxis rather than treatment. Â 116 Naloxone and naltrexone, both mu-opioid receptor antagonists, have demonstrated anti-pruritic effects, but their usage is limited by decreased analgesic effects. Â 119-121 Nalbuphine, a mixed opioid-receptor agonist-antagonist, was shown to be effective without compromising analgesia, but its usage is limited due to its sedating effects. Â 122-124 Serotonin (5-HT3) receptor antagonists (ondasetron, dolasetron) have demonstrated mixed results with respect to their effectiveness in pruritus management, with some studies suggesting benefit, Â 125-128 and others that do not. Â 129-131 Dopamine D2-receptor agonists, droperidol and alizapride, have demonstrated some benefit in the management of pruritus prophylaxis. Â 132,133
Human Herpesvirus 6A, 6B, and 7 Encephalitis
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Joseph Ongrádi, Balázs Stercz, Valéria Kövesdi, Károly Nagy, Joshua Prichett, Dharam V. Ablashi, Steven Jacobson
The use of drugs associated with HHV-6 reactivation—especially in patients with CIHHV-6—should be carefully considered and potential effects on the virus should be monitored (Pellett et al. 2011). CIHHV-6 can be reactivated from PBMCs by 12-O-tetradecanoy1-13-acetate (Arbuckle et al. 2010). The antiarrhythmic drug mex-iletine can reactivate HHV-6 and HHV-7 in DIHS. Histone deacetylase inhibitors such as hydroxamic acids (e.g., anticancer trichostatin A, a compound known to reactivate latent herpesviruses) can also reactivate CIHHV-6. Aliphatic acid compounds including the anticonvulsants carbamazepine and sodium valproate, benzamides including analgesic and antipyretic salicylamide, ethenzamide, antiemetic drugs containing alizapride and domperidone, and several others (e.g., phenobarbital) have also been shown to reactivate HHV-6 in vitro and in vivo. Although many seizures are controlled with intravenous phenytoin, this drug is not ideal in cases of HHV-6-or HHV-7-associated encephalitis because it is known to reactivate latent HHV-6 in vivo. The anesthetic trichloroethane activates latent HHV-6 in vivo. HHV-6 activity has been reported more frequently in SCT recipients who received anti-T-cell antibodies as part of their preconditioning regimen. Also, prevention and treatment of secondary microbial infections of the lung and urinary tract need frequent intervention. Besides amoxicillin, minocycline, sulfadiazine, and dapsone have also been reported to reactivate latent HHV-6 in vivo. Several of the HHV-6 reactivating drugs listed above also act in additive or synergistic fashion, such as phenobarbital and phenytoin with carbamazepine (Pellett et al. 2011).
Influence of pretreatment with everolimus or sunitinib on the subacute hematotoxicity of 177Lu-DOTATATE PRRT
Published in Acta Oncologica, 2020
Eva Medaer, Chris Verslype, Eric Van Cutsem, Jeroen Dekervel, Paul M. Clement, Kristiaan Nackaerts, Annouschka Laenen, Olivier Gheysens, Karolien Goffin, Sander Jentjens, Koen Van Laere, Christophe M. Deroose
The intended cumulative activity was 29.6 GBq, administered in four cycles of 7.4 GBq with an interval of 8 weeks. Reasons to reduce the injected activity or end the therapy were persistent or recurrent grade 3 or 4 hematotoxicity and disease progression. To prevent renal toxicity, an intravenous infusion of 2 L of an amino acid solution (Proteinsteril Hepa 8% (Fresenius, Bad Homburg, Germany), with among others 6.88 g/L lysine and 10.72 g/L arginine) was started at least 30 min before the administration of 177Lu-DOTATATE, and continued up to 4 h later. To prevent amino-acid induced nausea, ondansetron 8 mg was injected intravenously before the 177Lu-DOTATATE and an continuous infusion of alizapride was given. The radiopharmaceutical was administered in 15 min using a second pump system.
Foxglove poisoning: diagnostic and therapeutic differences with medicinal digitalis glycosides overdose
Published in Acta Clinica Belgica, 2022
Koen R. Maes, Pieter Depuydt, Joris Vermassen, Peter De Paepe, Walter Buylaert, Cathelijne Lyphout
She was treated with 10 ml of a glucose 30% solution with 10 IU of rapidly acting insulin intravenously (IV) and as well as an aerosol of salbutamol 5 mg/1 ml in 2 ml of NaCl 0,9% solution by inhalation to lower the serum potassium. For the nausea, she was given 50 mg of alizapride and 4 mg of ondansetron IV. One milligram of atropine was administered IV for an episode of bradycardia of 35 bpm (with a normal blood pressure). A short episode of a sinus tachycardia of 122 bpm with normal PR duration occurred, followed by a relapse of the second-degree AV block (30–40 bpm) after 10 minutes. The patient was transferred to the intensive care unit (ICU) of the university hospital for further follow-up and treatment.