Browsing by Subject "Benzodiazepines"

Now showing 1 - 4 of 4
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    Alcohol and medication interactions
    (U.S. National Institute on Alcohol Abuse and Alcoholism, 1999) Weathermon, Ron; Crabb, David W.; Medicine, School of Medicine
    Many medications can interact with alcohol, thereby altering the metabolism or effects of alcohol and/or the medication. Some of these interactions can occur even at moderate drinking levels and result in adverse health effects for the drinker. Two types of alcohol-medication interactions exist: (1) pharmacokinetic interactions, in which alcohol interferes with the metabolism of the medication, and (2) pharmacodynamic interactions, in which alcohol enhances the effects of the medication, particularly in the central nervous system (e.g., sedation). Pharmacokinetic interactions generally occur in the liver, where both alcohol and many medications are metabolized, frequently by the same enzymes. Numerous classes of prescription medications can interact with alcohol, including antibiotics, antidepressants, antihistamines, barbiturates, benzodiazepines, histamine H2 receptor antagonists, muscle relaxants, nonnarcotic pain medications and anti-inflammatory agents, opioids, and warfarin. In addition, many over-the-counter and herbal medications can cause negative effects when taken with alcohol.
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    Efficacy of Benzodiazepines or Antihistamines for Patients With Acute Vertigo: A Systematic Review and Meta-analysis
    (American Medical Association, 2022) Hunter, Benton R.; Wang, Alfred Z.; Bucca, Antonino W.; Musey, Paul I., Jr.; Strachan, Christian C.; Roumpf, Steven K.; Propst, Steven L.; Croft, Alexander; Menard, Laura M.; Kirschner, Jonathan M.; Emergency Medicine, School of Medicine
    Importance: Acute vertigo can be disabling. Antihistamines and benzodiazepines are frequently prescribed as "vestibular suppressants," but their efficacy is unclear. Objective: To assess the efficacy of antihistamines and benzodiazepines in the treatment of acute vertigo from any underlying cause. Data sources: We searched the PubMed, CENTRAL, EMBASE, CINAHL, Scopus, and ClinicalTrials.gov databases from inception to January 14, 2019, without language restrictions. Bibliographies of the included studies and relevant reviews were also screened. Study selection: We included randomized clinical trials (RCTs) comparing antihistamine or benzodiazepine use with another comparator, placebo, or no intervention for patients with a duration of acute vertigo for 2 weeks or less. Studies of healthy volunteers, prophylactic treatment, or induced vertigo were excluded, as were studies that compared 2 medications from the same class. Data extraction and synthesis: Following Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines, data were extracted and risk of bias was assessed by 2 authors independently for each study. Data were pooled using a random-effects model. Main outcomes and measures: The predefined primary outcome was change in 10- or 100-point vertigo or dizziness visual analog scale (VAS) scores at 2 hours after treatment. Secondary outcomes included change in nausea VAS scores at 2 hours, use of rescue medication at 2 hours, and improvement or resolution of vertigo at 1 week or 1 month. Results: Of the 27 trials identified in the systematic review, 17 contributed to the quantitative meta-analysis and involved a total of 1586 participants. Seven trials with a total of 802 participants evaluated the primary outcome of interest: single-dose antihistamines resulted in significantly more improvement on 100-point VAS scores compared with benzodiazepines (difference, 16.1 [95% CI, 7.2 to 25.0]) but not compared with other active comparators (difference, 2.7 [95% CI, -6.1 to 11.5]). At 1 week and 1 month, neither daily benzodiazepines nor antihistamines were reported to be superior to placebo. RCTs comparing the immediate effects of medications (at 2 hours) after a single dose generally had a low risk of bias, but those evaluating 1-week and 1-month outcomes had a high risk of bias. Conclusions and relevance: Moderately strong evidence suggests that single-dose antihistamines provide greater vertigo relief at 2 hours than single-dose benzodiazepines. Furthermore, the available evidence did not support an association of benzodiazepine use with improvement in any outcomes for acute vertigo. Other evidence suggested that daily antihistamine use may not benefit patients with acute vertigo. Larger randomized trials comparing both antihistamines and benzodiazepines with placebo could better clarify the relative efficacy of these medications.
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    Olanzapine for the Prevention of Chemotherapy-Induced Nausea and Vomiting
    (Massachusetts Medical Society, 2016-07-14) Navari, Rudolph M.; Qin, Rui; Ruddy, Kathryn J.; Liu, Heshan; Powell, Steven F.; Bajaj, Madhuri; Dietrich, Leah; Biggs, David; Lafky, Jacqueline M.; Loprinzi, Charles L.; Department of Medicine, IU School of Medicine
    BACKGROUND We examined the efficacy of olanzapine for the prevention of nausea and vomiting in patients receiving highly emetogenic chemotherapy. METHODS In a randomized, double-blind, phase 3 trial, we compared olanzapine with placebo, in combination with dexamethasone, aprepitant or fosaprepitant, and a 5-hydroxytryptamine type 3–receptor antagonist, in patients with no previous chemotherapy who were receiving cisplatin (≥70 mg per square meter of body-surface area) or cyclophosphamide–doxorubicin. The doses of the three concomitant drugs administered before and after chemotherapy were similar in the two groups. The two groups received either 10 mg of olanzapine orally or matching placebo daily on days 1 through 4. Nausea prevention was the primary end point; a complete response (no emesis and no use of rescue medication) was a secondary end point. RESULTS In the analysis, we included 380 patients who could be evaluated (192 assigned to olanzapine, and 188 to placebo). The proportion of patients with no chemotherapy-induced nausea was significantly greater with olanzapine than with placebo in the first 24 hours after chemotherapy (74% vs. 45%, P = 0.002), the period from 25 to 120 hours after chemotherapy (42% vs. 25%, P = 0.002), and the overall 120-hour period (37% vs. 22%, P = 0.002). The complete-response rate was also significantly increased with olanzapine during the three periods: 86% versus 65% (P<0.001), 67% versus 52% (P = 0.007), and 64% versus 41% (P<0.001), respectively. Although there were no grade 5 toxic effects, some patients receiving olanzapine had increased sedation (severe in 5%) on day 2. CONCLUSIONS Olanzapine, as compared with placebo, significantly improved nausea prevention, as well as the complete-response rate, among previously untreated patients who were receiving highly emetogenic chemotherapy. (Funded by the National Cancer Institute; ClinicalTrials.gov number, NCT02116530.)
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    Towards precision medicine for anxiety disorders: objective assessment, risk prediction, pharmacogenomics, and repurposed drugs
    (Springer Nature, 2023) Roseberry, K.; Le-Niculescu, H.; Levey, D. F.; Bhagar, R.; Soe, K.; Rogers, J.; Palkowitz, S.; Pina, N.; Anastasiadis, W. A.; Gill, S. S.; Kurian, S. M.; Shekhar, A.; Niculescu, A. B.; Psychiatry, School of Medicine
    Anxiety disorders are increasingly prevalent, affect people's ability to do things, and decrease quality of life. Due to lack of objective tests, they are underdiagnosed and sub-optimally treated, resulting in adverse life events and/or addictions. We endeavored to discover blood biomarkers for anxiety, using a four-step approach. First, we used a longitudinal within-subject design in individuals with psychiatric disorders to discover blood gene expression changes between self-reported low anxiety and high anxiety states. Second, we prioritized the list of candidate biomarkers with a Convergent Functional Genomics approach using other evidence in the field. Third, we validated our top biomarkers from discovery and prioritization in an independent cohort of psychiatric subjects with clinically severe anxiety. Fourth, we tested these candidate biomarkers for clinical utility, i.e. ability to predict anxiety severity state, and future clinical worsening (hospitalizations with anxiety as a contributory cause), in another independent cohort of psychiatric subjects. We showed increased accuracy of individual biomarkers with a personalized approach, by gender and diagnosis, particularly in women. The biomarkers with the best overall evidence were GAD1, NTRK3, ADRA2A, FZD10, GRK4, and SLC6A4. Finally, we identified which of our biomarkers are targets of existing drugs (such as a valproate, omega-3 fatty acids, fluoxetine, lithium, sertraline, benzodiazepines, and ketamine), and thus can be used to match patients to medications and measure response to treatment. We also used our biomarker gene expression signature to identify drugs that could be repurposed for treating anxiety, such as estradiol, pirenperone, loperamide, and disopyramide. Given the detrimental impact of untreated anxiety, the current lack of objective measures to guide treatment, and the addiction potential of existing benzodiazepines-based anxiety medications, there is a urgent need for more precise and personalized approaches like the one we developed.