Asthma associated with the use of cocaine, heroin, and marijuana: A review of the evidence.

OBJECTIVE: A review of the evidence was conducted regarding asthma associated with the use of cocaine, heroin, and marijuana. DATA SOURCES: A search of the English literature was performed via PubMed/Medline and EMBASE using the search terms asthma AND cocaine, heroin, and marijuana. When pertinent articles were found, salient references in those articles were assessed. STUDY SELECTION: Due to the relatively small number of studies, we included all studies and cases. RESULTS: For several decades, case reports, retrospective studies, and laboratory investigations have demonstrated that inhalation of cocaine or heroin is associated with increased asthma symptoms and reduced pulmonary function. Smoking crack cocaine, nasal insufflation of cocaine or heroin, and smoking heroin increases the risk of emergency department visits and hospitalizations for asthma. Although frequent smoking of marijuana may cause symptoms of cough, sputum production, and wheezing in the general population, more studies are needed specifically in patients with asthma. Smoking marijuana with concomitant tobacco use is common and further worsens the respiratory symptoms. CONCLUSIONS: Use of cocaine and heroin in patients with asthma should be avoided. Pending further studies, it would be prudent for patients with asthma to avoid smoking marijuana. Clinicians need to be vigilant regarding use of these drugs in their patients with hyperreactive airway disease.

Evaluation of Chronic Obstructive Pulmonary Disease (COPD) and reduced ejection fraction heart failure (HFrEF) discharge medication prescribing: Is drug therapy concordant with national guidelines associated with a reduction in 30-day readmissions?

INTRODUCTION: Approximately 1 in 5 hospitalized COPD patients are readmitted within 30 days of discharge. CHF coexists in more than 20% of patients with COPD, and is associated with early readmission for COPD. Reducing 30-day hospital readmissions for COPD is of intense current interest. METHODOLOGY: A retrospective chart review was performed to identify patients discharged with COPD exacerbation and HFrEF. The primary objective was to evaluate if discharge medication prescribing following guidelines for both COPD and HFrEF correlates with reduced 30-day readmission rates. RESULTS: The study included 281 admissions with 39.1% prescribed appropriate discharge medications for both COPD and HFrEF; 30-day readmission rate was 24.5% for these patients compared to 31.1% that were not prescribed appropriate medications (p = 0.24). Beta blockers, ACE inhibitors or ARBS, and aldosterone antagonists were under-prescribed, but this did not significantly associate with increased readmission (p = 0.51, p = 0.23 or 0.99, and p = 0.18, respectively). Those prescribed hydralazine or nitrates were more likely to readmit (both p = 0.01). Diabetes and hyperlipidemia were associated with increased readmission (p = 0.01 and 0.05). CONCLUSIONS: This study did not show a significant difference in 30-day readmission rate based on appropriate discharge medications for both COPD and HFrEF. The comorbidities diabetes and hyperlipidemia and prescription of hydralazine or nitrates were significantly associated with increased readmission rate. Larger patient populations may be needed to assess if guideline based discharge medication prescribing is associated with reduced 30-day readmissions for COPD.

Effect of diseases on response to vitamin K antagonists.

INTRODUCTION: The purpose of this review article is to summarize the literature on diseases that are documented to have an effect on response to warfarin and other VKAs. METHODS: We searched the English literature from 1946 to September 2015 via PubMed, EMBASE, and Scopus for the effect of diseases on response vitamin K antagonists including warfarin, acenocoumarol, phenprocoumon, and fluindione. DISCUSSION: Among many factors modifying response to VKAs, several disease states are clinically relevant. Liver disease, hyperthyroidism, and CKD are well documented to increase response to VKAs. Decompensated heart failure, fever, and diarrhea may also elevate response to VKAs, but more study is needed. Hypothyroidism is associated with decreased effect of VKAs, and obese patients will likely require higher initial doses of VKAs. CONCLUSION: In order to minimize risks with VKAs while ensuring efficacy, clinicians must be aware of the effect of disease states when prescribing these oral anticoagulants.

Effect of Body Weight on Dose of Vitamin K Antagonists.

OBJECTIVES: Numerous factors are well documented to affect the response to vitamin K antagonists (VKA), including dietary vitamin K, other drugs, age, pharmacogenetics, and disease states. Body weight is perhaps not as well known as a variable affecting VKA dose. Our aim was to review the literature regarding body weight and VKA dose requirements. METHODS: We reviewed the English-language literature via PubMed and Scopus using the search terms VKA, warfarin, acenocoumarol, phenprocoumon, fluindione, AND body weight. RESULTS: Among 32 studies conducted since the widespread use of the international normalized ratio, 29 found a correlation with body weight or body surface area and VKA dose requirement. Warfarin was evaluated in 27 studies and acenocoumarol, phenprocoumon, or fluindione were assessed in 5 investigations. CONCLUSIONS: Because of varying study methodologies, further study is warranted. Based on current evidence, clinicians should include body weight, along with other established variables when dosing VKA. Most important, obese and morbidly obese patients may require a 30% to 50% increase with the initial dosing of VKA.

Fever as a risk factor for increased response to vitamin K antagonists: a review of the evidence and potential mechanisms.

Numerous factors affect the response to vitamin K antagonists (VKA) including age, dietary vitamin K, other drugs, pharmacogenetics, and disease states. In antithrombotic guidelines, fever is mentioned as a factor that may increase response to VKA. The purpose of this article is to review the available evidence regarding the effect of fever on response to VKA, and to discuss possible mechanisms of this effect. We performed a search of the English literature from 1943 to June 2014, using the key words fever AND warfarin, acenocoumarol, phenprocoumon, coumarin anticoagulants and VKA; fever AND vitamin K dependent clotting factors II, VII, IX, and X. One animal investigation and 6 studies in humans suggest fever increases response to VKA, but one study did not find a significant effect. The magnitude of this effect is variable. Possible mechanisms for the increased effect of VKA associated with fever are increased catabolism of vitamin K dependent clotting factors, decreased vitamin K intake, and inhibition of VKA metabolism. More rigorous studies are needed to confirm that fever increases response to warfarin and other VKA.

Comparison of initial warfarin response in obese patients versus non-obese patients.

Achieving therapeutic anticoagulation with warfarin is complicated by substantial inter-patient and intra-patient variability with numerous factors known to influence dose requirements. Obesity is one factor for which there remains no study to date investigating its initial effect on warfarin response assessed by INR, stratified by BMI category in hospitalized patients. To compare initial warfarin response between obese and non-obese patients by evaluating average daily dose (ADD), time required to attain therapeutic INR, and mean discharge dose (MDD), stratified by BMI category. A retrospective review was conducted to evaluate initial warfarin response in hospitalized patients of different BMI categories initiated on warfarin with ≥4 consecutive days of therapy and managed by pharmacy dosing service. 211 patients were included (10 underweight, 45 normal weight, 48 overweight, 71 obese, 37 morbidly obese). Across BMI categories, the percentage of patients attaining therapeutic INR prior to discharge differed (p = 0.0004) with 71.1 % of normal weight therapeutic compared to 42.3 % of obese and 38 % of morbidly obese. Within BMI categories, when comparing ADD between patients therapeutic and subtherapeutic at discharge, no differences were observed, except among overweight patients (5.6 ± 0.3 vs. 7 ± 0.4 mg, p = 0.0143). Compared to normal weight, obese and morbidly obese required a significantly longer median time to achieve therapeutic INR (8 and 10 days vs. 6 days) and a higher ADD (6.6 ± 0.3 and 7.6 ± 0.5 vs. 5 ± 0.3 mg) and MDD (6.7 ± 0.5 and 6.7 ± 0.7 vs. 4.4 ± 0.5 mg). Compared to normal weight, obese and morbidly obese patients had a decreased initial response to warfarin.