They examined the records of nearly 300,000 adults in the U.S. who had an initial atherosclerotic cardiovascular disease event between 2007 and 2016. These were divided into three groups: coronary heart disease, ischemic stroke or transient ischemic attack, or peripheral artery disease.
When people left the hospital or emergency department in 2007 following a first diagnosis in one of these categories, about half began taking statins within 30 days. By 2016, statin use increased to approximately 60%.
“Based on the guidelines, we hoped to see a much higher uptake among this entire group,” says Dr. Noseworthy. “Statin intolerance was only noted for 4%-5% of the patients, which means as many as 35% of patients are not receiving treatment according to the guidelines.”
Xiaoxi Yao, Nilay D. Shah, Bernard J. Gersh, Francisco Lopez-Jimenez, Peter A. Noseworthy. Assessment of Trends in Statin Therapy for Secondary Prevention of Atherosclerotic Cardiovascular Disease in US Adults From 2007 to 2016. JAMA Network Open, 2020; 3 (11): e2025505 DOI: 10.1001/jamanetworkopen.2020.25505
Vaccine candidate was found to be more than 90% effective in preventing COVID-19 in participants without evidence of prior SARS-CoV-2 infection in the first interim efficacy analysis
Analysis evaluated 94 confirmed cases of COVID-19 in trial participants
Study enrolled 43,538 participants, with 42% having diverse backgrounds, and no serious safety concerns have been observed; Safety and additional efficacy data continue to be collected
Submission for Emergency Use Authorization (EUA) to the U.S. Food and Drug Administration (FDA) planned for soon after the required safety milestone is achieved, which is currently expected to occur in the third week of November
Clinical trial to continue through to final analysis at 164 confirmed cases in order to collect further data and characterize the vaccine candidate’s performance against other study endpoints
“There was always a discussion: Is the spike protein the right target? Well, now we know it’s the right target,” Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, told STAT on Monday. “So, it’s not only immediate good news, it really is optimistic about what’s going to roll out in the next several months with the other vaccines.”
Attention-deficit/hyperactivity disorder (ADHD) exerts lifelong impairment, including difficulty sustaining employment, poor credit, and suicide risk. To date, however, studies have assessed selected samples, often via self-report. Using mental health data from the entire Swedish population (N = 11.55 million) and a random sample of credit data (N = 189,267), we provide the first study of objective financial outcomes among adults with ADHD, including associations with suicide. Controlling for psychiatric comorbidities, substance use, education, and income, those with ADHD start adulthood with normal credit demand and default rates. However, in middle age, their default rates grow exponentially, yielding poor credit scores and diminished credit access despite high demand. Sympathomimetic prescriptions are unassociated with improved financial behaviors. Last, financial distress is associated with fourfold higher risk of suicide among those with ADHD. For men but not women with ADHD who suicide, outstanding debt increases in the 3 years prior. No such pattern exists for others who suicide.
Here in the US we’ve seen an steady increase in ADHD diagnoses.
And an alarming increase in suicide.
Then my mind wanders to drugs (to drugs, not due to drugs).
To summarize, the psychiatric side effects of methylphenidate are quite similar to those of cocaine and amphetamines, giving more support to the idea that almost all CNS stimulants will produce a similar clinical picture. A person using cocaine can experience nervousness,57,58 restlessness,58 agitation,57 suspiciousness,60 paranoia,61–63 hallucinations and delusions,61,63 impaired cognitive functions,64 delirium,65 violence,57,58,62,65,66 suicide,67 and homicide.67–70
A high dose of favipiravir, however, had a potent effect. A few days after the infection, the virologists detected hardly any infectious virus particles in the hamsters that received this dose and that had been infected intranasally. Moreover, hamsters that were in a cage with an infected hamster and had been given the drug did not develop an obvious infection. Those that had not received the drug all became infected after having shared a cage with an infected hamster.
Favipiravir: A new and emerging antiviral option in COVID-19
Favipiravir was first used against SARS-CoV-2 in Wuhan at the very epicenter of the pandemic. Then, as the pandemic spread to Europe, this drug received approval for emergency use in Italy, and currently has been in use in Japan, Russia, Ukraine, Uzbekistan, Moldova, and Kazakhstan. Approval has also recently been granted in Saudi Arabia and the UAE. Thereafter, Turkey, Bangladesh, and most recently Egypt have also seen recent commercial launches. In June 2020, favipiravir received the DCGI approval in India for mild and moderate COVID-19 infections. As of the 23rd of July, 2020; there are 32 studies registered on clinicaltrials.gov to assess the utility of this drug in the management of COVID-19 (3 completed, 12 recruiting).1
The current investigators analyzed national healthcare claims from the US Medicaid program from 2001 to 2010 for 39,582 Medicaid beneficiaries (mean age, 44.5 years; 78.5% women) diagnosed with depression. Patients with alternative indications for anti-psychotic therapy, such as schizophrenia, psychotic depression or bipolar disorder, were excluded.
After a period of at least 3 months of treatment with a single antidepressant, more than half of the patients (56.6%) augmented their treatment with one of these atypical anti-psychotics: quetiapine, risperidone, aripiprazole or olanzapine. The remaining patients (43.4%) added a second antidepressant. The average chlorpromazine-equivalent starting dose for all atypical anti-psychotics was 68 mg/day, which increased to 100 mg/day during follow-up.
A total of 153 patients died during 13,328 person-years of follow-up, including 105 who augmented with an atypical anti-psychotic and 48 who augmented with a second antidepressant.
Compared with those who added a second antidepressant, those who added an anti-psychotic had a 45% increased risk of dying during follow up (adjusted hazard ratio,1.45; 95% CI, 1.02 – 2.06).
Many widely used medications may cause or exacerbate a variety of arrhythmias. Numerous antiarrhythmic agents, antimicrobial drugs, psychotropic medications, and methadone, as well as a growing list of drugs from other therapeutic classes (neurological drugs, anticancer agents, and many others), can prolong the QT interval and provoke torsades de pointes. Perhaps less familiar to clinicians is the fact that drugs can also trigger other arrhythmias, including bradyarrhythmias, atrial fibrillation/atrial flutter, atrial tachycardia, atrioventricular nodal reentrant tachycardia, monomorphic ventricular tachycardia, and Brugada syndrome. Some drug-induced arrhythmias (bradyarrhythmias, atrial tachycardia, atrioventricular node reentrant tachycardia) are significant predominantly because of their symptoms; others (monomorphic ventricular tachycardia, Brugada syndrome, torsades de pointes) may result in serious consequences, including sudden cardiac death. Mechanisms of arrhythmias are well known for some medications but, in other instances, remain poorly understood. For some drug-induced arrhythmias, particularly torsades de pointes, risk factors are well defined. Modification of risk factors, when possible, is important for prevention and risk reduction. In patients with nonmodifiable risk factors who require a potentially arrhythmia-inducing drug, enhanced electrocardiographic and other monitoring strategies may be beneficial for early detection and treatment. Management of drug-induced arrhythmias includes discontinuation of the offending medication and following treatment guidelines for the specific arrhythmia. In overdose situations, targeted detoxification strategies may be needed. Awareness of drugs that may cause arrhythmias and knowledge of distinct arrhythmias that may be drug-induced are essential for clinicians. Consideration of the possibility that a patient’s arrythmia could be drug-induced is important.
Statins remain our safest and most effective drug for primary and secondary prevention of coronary artery disease. However, a cult of statin deniers has taken hold on the internet and their efforts often result in patients inappropriately stopping statins, an outcome which can have lethal consequences. Early in the pandemic a patient of mine in…
Note to my readers: I encourage you to follow the link and read the entire post and the comments to fully understand Dr. Pearson’s message. And if you’re a statin denier don’t bother reading the full post because we’re not here to engage in an argument or to change your opinion on this medication.
Based on the results of the Diabetes Prevention Program Outcomes Study (DPPOS), in which metformin significantly decreased the development of diabetes in individuals with baseline fasting plasma glucose (FPG) concentrations of 110–125 vs. 100–109 mg/dL (6.1–6.9 vs. 5.6–6.0 mmol/L) and A1C levels 6.0–6.4% (42–46 mmol/mol) vs. <6.0% and in women with a history of gestational diabetes mellitus, it has been suggested that metformin should be used to treat people with prediabetes. Since the association between prediabetes and cardiovascular disease is due to the associated nonglycemic risk factors in people with prediabetes, not to the slightly increased glycemia, the only reason to treat with metformin is to delay or prevent the development of diabetes. There are three reasons not to do so. First, approximately two-thirds of people with prediabetes do not develop diabetes, even after many years. Second, approximately one-third of people with prediabetes return to normal glucose regulation. Third, people who meet the glycemic criteria for prediabetes are not at risk for the microvascular complications of diabetes and thus metformin treatment will not affect this important outcome. Why put people who are not at risk for the microvascular complications of diabetes on a drug (possibly for the rest of their lives) that has no immediate advantage except to lower subdiabetes glycemia to even lower levels? Rather, individuals at the highest risk for developing diabetes—i.e., those with FPG concentrations of 110–125 mg/dL (6.1–6.9 mmol/L) or A1C levels of 6.0–6.4% (42–46 mmol/mol) or women with a history of gestational diabetes mellitus—should be followed closely and metformin immediately introduced only when they are diagnosed with diabetes.
This is now the third anti-viral therapy to disappoint us within a few weeks (preliminary data on lopinavir/ritonavir and remdesivir were both unimpressive). This raises a question of whether any anti-viral therapies will be beneficial. Especially among the critically ill, patients often present relatively late (at a time-point when viral load is already falling anyway). Much of the pathogenesis of critical illness seems to result from dysregulated inflammation, rather than direct viral cytopathic effect. This raises a question of whether any antiviral treatment will be beneficial for late-presenting patients with severe illness.
Benadryl causes significant sedation. One study in a driving simulator showed an ordinary adult dose of Benadryl caused worse driving than a blood alcohol level of 0.1 percent (that’s between buzzed-drunk and frat-party drunk). Ordinary doses of Benadryl can also cause urinary retention, dizziness, trouble with coordination, dry mouth, blurry vision, and constipation. Especially in older individuals, diphenhydramine can cause delirium and contribute to long term dementia.