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Psychotropic Drugs
Published in Diana Riley, Perinatal Mental Health, 2018
Two authors84,85 assert that therapeutic doses of tranylcypromine (Parnate) are secreted in breast milk in doses too small to affect the child. Another100 states that no ill effects have been noted in the infants of mothers taking isocarboxazid (Marplan), but goes on to say that animal studies on nialamide (Niamid) have shown that the maturation of young is affected, and that there is a high mortality rate in the offspring. In view of the potential for interaction of this group of drugs with other medication or dietary factors, it would be unwise to continue breast-feeding while taking this group of drugs.
MAO Inhibitors: Predicting Response/Maximizing Efficacy
Published in Mark S. Gold, R. Bruce Lydiard, John S. Carman, Advances in Psychopharmacology: Predicting and Improving Treatment Response, 2018
Support for the efficacy of this combined treatment also comes from Gutierrez and Alino45 who combined (IV) nialamide with tryptophan, in a severely depressed, hospitalized group. They reported a 79% satisfactory response for combination treatment, as contrasted with 53% for MAOI alone. In a more indirect way, Pare46 and Shopsin et al.47 provide support for combined treatment. Pare administered tryptophan to a group of patients that had responded to MAOI but had relapsed when dosage was decreased. Of 14 patients, 6 promptly recovered on tryptophan but relapsed again when placebo was substituted. Shopsin et al.47 noted that addition of small doses of parachlorophenylanine (PCPA), a serotonin synthesis inhibitor, caused relapse in depressed patients who had responded to tranylcypromine. This adds support to the involvement of serotonin in MAOI antidepressant effects and the expectation that tryptophan, its precursor, should potentiate MAOI treatment.
Psychopathology
Published in Allan Hobson, Psychodynamic Neurology, 2014
When I was a resident in psychiatry in the early 1960s, amine reuptake blockers were not available to treat depression, but monoamine oxidase inhibitors (MAOIs) like nialamide were. Although there were undesirable side effects, MAOI drugs often worked wonders and I remember my astonishment when periodically depressed patients insisted on electroconvulsive treatment (ECT) instead of taking drugs for their depression. I had naively assumed that these patients would do anything to avoid having a seizure induced by electric current passed across their temples. In order to suppress the motor output of the seizure produced by ECT, the patients also had to undergo general anesthesia and intravenous neuromuscular blockade using life-threatening anticholinergic drugs. Despite these risks some patients elected ECT. Why? I wondered. Because, they said, the antidepressant effects of ECT were much more immediate than those of medication, occurring within a few days instead of several weeks.
The role of gut microbiota in the modulation of drug action: a focus on some clinically significant issues
Published in Expert Review of Clinical Pharmacology, 2018
β-Glucuronidase-producing intestinal bacteria have been involved in the pathophysiological mechanisms underlying the delayed diarrhea induced by irinotecan and the lower gastrointestinal toxicity caused by NSAIDs. These enzymes hydrolyze the ether or ester linkages between glucuronic acid and SN-38, the active metabolite of irinotecan, or some NSAIDs (including diclofenac, indomethacin, and ketoprofen), respectively, releasing the active molecules in the gut, which then trigger the pathogenic pathways leading to the toxic mucosal damage. So far, only experimental data obtained using mouse models of SN-38- and NSAID-induced toxicities have shown that bacterial β-glucuronidase inhibition significantly reduces the intestinal mucosa injury produced by irinotecan [38,39] and NSAIDs [48,49], and prevents the delayed diarrhea induced by irinotecan [38,39]. A molecule named Inhibitor-1 is the β-glucuronidase inhibitor most commonly used in these studies. It is highly selective for the bacterial enzyme and does not seem to induce any toxic effects on prokaryotic or eukaryotic cells. The pharmacokinetics of this compound have been investigated in mice and have been shown to be favorable (low bioavailability and short t1/2). Other bacterial β-glucuronidase inhibitors have been identified by high-throughput screening [39,40]. In addition, old drugs such as amoxapine, isocarboxazid, and nialamide have been shown to inhibit bacterial β-glucuronidases [41]. The therapeutic effects of some of these old and new drugs have been evaluated with success in the irinotecan-induced delayed diarrhea mouse model [39,42]. The big hope is now that these drugs will be shown to be effective in clinical trials also. Positive clinical results would significantly change the safety profiles of drugs such as NSAIDs, which are very frequently used and have important rates of serious complications.
Reemergence of monkeypox: prevention and management
Published in Expert Review of Anti-infective Therapy, 2022
Sahaya Nadar, Tabassum Khan, Abdelwahab Omri
CP-COV03 developed by Hyundai Bioscience for the treatment of Covid-19 is currently Phase II clinical trial as a broad-spectrum antiviral agent. Researchers at the Kansas State University in the US in a study proved CP-COV03 with nialamide as the active agent to significantly reduce vaccinia virus proliferation at a low concentration. By inducing autophagy in the host-cells, CP-COV03 eliminates the viruses that penetrate within the cells, proving it effective even in mutation [86,87].