Cocaine 25% / Adrenaline (base) 0.1% oromucosal paste

Background: The simultaneous use of cocaine and alcohol is highly prevalent and is associated with high numbers of emergency department admissions, primarily due to cardiovascular complications. Aims: To answer the question of whether the co-use of cocaine and alcohol increases the cardiovascular risk compared to the use of cocaine alone. Method: A systematic review of human studies comparing the cardiovascular risk of co-used cocaine and alcohol with the use of cocaine alone. Results: Despite a higher myocardial workload induced by the co-use of cocaine and alcohol and the potentiation of cocaine's cardiovascular effects by alcohol, the findings on the risk and severity of cardiovascular symptoms due to combined use are inconsistent. However, the co-use of cocaine and alcohol clearly leads to higher mortality. Interestingly, the presence of cocaethylene, a unique metabolite generated only via a pharmacokinetic interaction between alcohol and cocaine, carries an 18- to 25-fold increase over the absence of cocaethylene (cocaine-alone users) in the risk of sudden death and is associated with myocardial injury and cardiac arrest, probably due to the inhibition of cardiac ion channels by cocaethylene. Conclusion: Despite the inconsistency in some of the results, it is concluded that the co-use of cocaine and alcohol poses an additional risk of cardiovascular fatalities compared to the use of cocaine alone.

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BackgroundNasotracheal intubation is associated with a risk of epistaxis. Decongestion of the nasal mucosa reduces the risk of epistaxis, and different vasoconstrictors may be used. Cocaine has both decongestive and analgesic properties, but it also has side effects. In this systematic review, we aimed to evaluate if cocaine decreases the occurrence and severity of epistaxis when administered topically to the nasal mucosa before nasotracheal intubation.MethodsWe conducted a systematic review and meta-analysis following the PRISMA guidelines based on a predefined protocol. We included randomized clinical trials comparing nasal cocaine to active comparators or placebo for nasotracheal intubation. Two reviewers independently screened studies for eligibility and performed data extraction. Relative risk with 95% confidence intervals was calculated. Predefined primary outcome measures were the occurrence and severity of epistaxis. Secondary outcomes were pain, mechanical complications, and patient-centered side effects. The risk of bias was evaluated using the revised Cochrane Risk of Bias 2 tool for randomized trials, and certainty of evidence on outcome level was assessed according to GRADE.ResultsSix trials (n = 457) were included; one trial was judged as having a low risk of bias. All six trials provided information on the occurrence of epistaxis. The meta-analysis did not support a difference in the occurrence of epistaxis between cocaine and its comparators (fixed effect: relative risk 0.90 [95% confidence interval 0.75 to 1.09, I2 of 0%, certainty of evidence: low]). The severity of epistaxis was evaluated on incompatible scales and thus not suitable for meta-analysis. No studies reported on pain or mechanical complications associated with nasotracheal intubation, and data on patient-centered side effects were sparse.ConclusionThis systematic review with meta-analysis demonstrated that the quantity and certainty of evidence on cocaine used for nasotracheal intubation is low and that there is no firm evidence for the benefits and harms of cocaine compared to other vasoconstrictors and topical analgetics or placebo. Consequently, sufficiently powered randomized trials assessing patient-centered outcomes, including outcomes on side effects, should be conducted before firm conclusions on cocaine for nasotracheal intubation can be drawn.Editorial commentEpistaxis can occur with nasotracheal intubation, and topical drug vasoconstrictor effects have been used to reduce this risk. This analysis shows that the evidence base supporting the use of cocaine for reducing the risk of epistaxis in nasotracheal intubation is uncertain.

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IntroductionThis article provides a current narrative review of the medications that may cause halitosis as a side effect. Halitosis is frequently associated with important social, psychological, and emotional aspects of life; therefore, it is crucial for health care providers to be able to diagnose and manage it effectively.MethodsA literature review was conducted using the PubMed and EMBASE/OVID databases between January 2015 and December 2024 to find the latest relevant articles, focusing on systematic reviews and literature published between 2020 and 2025.ResultsMedications can lead to halitosis (bad breath) either intra- or extra-orally. Research has identified several medications that may cause extra-oral halitosis as a side effect. These include ranitidine, cysteamine, certain antifungals, peppermint oil, aspirin and other NSAIDs, PX-12, silybin, disulfiram, suplatast tosilate, dimethyl sulfoxide, levocarnitine, nitrates and nitrites, paraldehyde, chloral hydrate, and iodine-containing medications. Intra-oral halitosis is mostly related to medications that cause xerostomia and MRONJ as side effects.DiscussionMultiple groups of medications can cause intra- or extra-oral halitosis. prior knowledge about these medications and their underlying mechanisms that will lead to halitosis will enable clinicians to diagnose and manage this condition more effectively. It is also wise for clinicians to consider recreational drugs like crack, cocaine, and smokeless tobacco when looking for the underlying reason for halitosis.SummaryMultiple groups of medications can act as an underlying cause for halitosis. However, more research is needed to monitor halitosis as an independent side effect and to investigate the mechanism by which each medication causes halitosis.

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BackgroundA systematic review was conducted following PRISMA guidelines to identify human studies investigating pharmacological interventions and reported sleep outcomes among individuals with CUD or MUD.MethodsPubMed and APA PsycInfo were searched from inception to January 2025 and risk of bias was assessed. Articles were included if they included human participants with either cocaine or methamphetamine dependence, administered a pharmacological treatment, and reported night-time sleep as an outcome using at least one rigorous measurement tool. Articles were excluded if they included animals, did not include pharmacological intervention (e.g., supplements or behavioral treatments), or only assessed baseline sleep or if sleep was only reported as a side effect rather than as a formal outcome.ResultsEighteen studies (N = 678) met inclusion criteria, eleven in CUD and seven in MUD. The results of the risk-of-bias assessment indicated good-to-excellent interrater reliability (ICC range=0.85-0.90), and overall methodological quality across studies was moderate to high. For CUD, modafinil, buprenorphine, and suvorexant were preliminarily associated with improvements in sleep parameters, with modafinil linked to higher abstinence rates. Results for mirtazapine, lisuride, lorazepam, tiagabine, and cannabidiol were mixed. For MUD, mirtazapine and modafinil demonstrated modest initial benefits, while quetiapine and suvorexant showed preliminary promise in smaller studies.ConclusionsOverall, pharmacological interventions targeting sleep disturbances showed emerging but inconsistent benefits in CUD and MUD, which could be due to small sample sizes, short treatment durations, side effects, or comorbidities. Addressing sleep dysregulation may represent a novel and clinically meaningful pathway to improve recovery outcomes in stimulant use disorders.

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