PM calls for ramping up of Covid testing, sero surveys
Coronavirus: 'Long Covid could be four different syndromes'
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The tragedy of the post-COVID “long haulers”
Suppose you are suddenly are stricken with COVID-19. You become very ill for several weeks. On awakening every morning, you wonder if this day might be your last.
And then you begin to turn the corner. Every day your worst symptoms — the fever, the terrible cough, the breathlessness — get a little better. You are winning, beating a life-threatening disease, and you no longer wonder if each day might be your last. In another week or two, you’ll be your old self.
But weeks pass, and while the worst symptoms are gone, you’re not your old self — not even close. You can’t meet your responsibilities at home or at work: no energy. Even routine physical exertion, like vacuuming, leaves you feeling exhausted. You ache all over. You’re having trouble concentrating on anything, even watching TV; you’re unusually forgetful; you stumble over simple calculations. Your brain feels like it’s in a fog.
Your doctor congratulates you: the virus can no longer be detected in your body. That means you should be feeling fine. But you’re not feeling fine.
The doctor suggests that maybe the terrible experience of being ill with COVID-19 has left you a little depressed, or experiencing a little PTSD. Maybe some psychiatric treatment would help, since there’s nothing wrong with you physically. You try the treatment, and it doesn’t help.
How common are lingering COVID symptoms?
Tens of thousands of people in the United States have such a lingering illness following COVID-19. In the US, we call them post-COVID “long haulers.” In the United Kingdom, they are said to be suffering from “long COVID.”
Published studies (see here and here) and surveys conducted by patient groups indicate that 50% to 80% of patients continue to have bothersome symptoms three months after the onset of COVID-19 — even after tests no longer detect virus in their body.
Which lingering symptoms are common?
The most common symptoms are fatigue, body aches, shortness of breath, difficulty concentrating, inability to exercise, headache, and difficulty sleeping. Since COVID-19 is a new disease that began with an outbreak in China in December 2019, we have no information on long-term recovery rates.
Who is more likely to become a long hauler?
Currently, we can’t accurately predict who will become a long hauler. As a recent article in Science notes, people only mildly affected by COVID-19 still can have lingering symptoms, and people who were severely ill can be back to normal two months later. However, continued symptoms are more likely to occur in people over age 50, people with two or three chronic illnesses, and people who became very ill with COVID-19.
There is no formal definition of the term “post-COVID long haulers.” In my opinion, a reasonable definition would be anyone diagnosed with the coronavirus that causes COVID-19, or very likely to have been infected by it, who has not returned to their pre-COVID-19 level of health and function after six months.
Long-haulers include two groups of people affected by the virus:
- Those who experience some permanent damage to their lungs, heart, kidneys, or brain that may affect their ability to function.
- Those who continue to experience debilitating symptoms despite no detectable damage to these organs.
Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, has speculated that many in the second group will develop a condition called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS can be triggered by other infectious illnesses — such as mononucleosis, Lyme disease, and severe acute respiratory syndrome (SARS), another coronavirus disease. The National Academy of Medicine estimates there are one million to two million people in the US with ME/CFS.
Dr. Tedros Ghebreyesus, director of the World Health Organization, also has expressed growing concern about the chronic illnesses that may follow in the wake of COVID-19, including ME/CFS.
What might cause the symptoms that plague long haulers?
Research is underway to test several theories. People with ME/CFS, and possibly the post-COVID long haulers, may have an ongoing low level of inflammation in the brain, or decreased blood flow to the brain, or an autoimmune condition in which the body makes antibodies that attack the brain, or several of these abnormalities.
The bottom line
How many people may become long haulers? We can only guess. Right now, more than seven million Americans have been infected by the virus. It’s not unthinkable that 50 million Americans will ultimately become infected. If just 5% develop lingering symptoms, and if most of those with symptoms have ME/CFS, we would double the number of Americans suffering from ME/CFS in the next two years. Most people who developed ME/CFS before COVID-19 remain ill for many decades. Only time will tell if this proves true for the post-COVID cases of ME/CFS.
For this and many other reasons, the strain on the American health care system and economy from the pandemic will not end soon, even if we develop and deploy a very effective vaccine by the end of 2021.
Virtually every health professional I know believes that the pandemic in the US could and should have been better controlled than it has been. Bad mistakes rarely lead to only temporary damage.
The post The tragedy of the post-COVID “long haulers” appeared first on Harvard Health Blog.
Stopping osteoarthritis: Could recent heart research provide a clue?
Here’s a recent headline that I found confusing: Could the first drug that slows arthritis be here?
It’s confusing because it depends on which of the more than 100 types of arthritis we’re discussing. We’ve had drugs that slow rheumatoid arthritis for decades. In fact, more than a dozen FDA-approved drugs can reduce, or even halt, joint damage in people with rheumatoid arthritis. We also have effective medications to slow or stop gout, another common type of arthritis.
But the headline refers to osteoarthritis, the most common type of arthritis. And currently, no medications can safely and reliably slow the pace of this worsening joint disease. That’s one reason so many knee and hip replacements are performed: more than 1.2 million each year in the US alone.
A drug that can slow down joint degeneration in osteoarthritis has long been the holy grail of arthritis treatments, because it could
- relieve pain and lessen suffering for millions of people
- help prevent the loss of function that accompanies osteoarthritis
- reduce the need for surgery, along with its attendant risks, expense, and time needed for recovery.
And, needless to say, such a drug would generate enormous profits for the pharmaceutical company that comes up with it first.
A study of heart disease might have identified a new treatment for osteoarthritis
According to new research published in Annals of Internal Medicine, it’s possible that such a treatment exists, and is already in use to treat other conditions. The researchers reanalyzed data on more than 10,000 people that originally looked at whether the drug canakinumab was beneficial for people with a previous heart attack — yes, heart attack, not arthritis.
Canakinumab inhibits interleukin-1, a substance closely involved with inflammation. And increasing evidence suggests that inflammation raises risk for cardiovascular disease, and may predict future cardiovascular trouble. All study participants had previously had a heart attack. Additionally, they had an elevated blood C-reactive protein (CRP) level, an indicator of inflammation in the body.
Every three months, each person received an injection of one of several doses of either canakinumab or a placebo. Canakinumab appeared to work for heart disease: those receiving the 150-mg dose of canakinumab had significantly fewer cardiovascular complications (repeat heart attack, stroke, or cardiovascular death) over about four years. Unfortunately, there was also a higher rate of fatal infections in the canakinumab-treated subjects.
Another look at this study of canakinumab
The reanalysis compares rates of hip or knee replacement due to osteoarthritis in those receiving canakinumab with rates among those who received a placebo. The study authors thought that since canakinumab reduces inflammation, it might help the inflammation found in the joints of people with osteoarthritis while also offering cardiovascular benefits.
Osteoarthritis has long been considered a wear-and-tear, age-related, and non-inflammatory form of joint disease. But over the last decade or so, research has demonstrated that some degree of inflammation occurs in osteoarthritis. So it’s not too much of a stretch to think a drug like canakinumab might be effective for osteoarthritis. This drug is already approved for a number of inflammatory conditions, including certain forms of pediatric arthritis.
The results of this new study surprised me: over about four years, those receiving canakinumab were at least 40% less likely to have a hip or knee replacement than those receiving placebo.
Warning: These results are preliminary
Before declaring victory over osteoarthritis with canakinumab treatment, it’s important to acknowledge that this trial doesn’t prove it actually works. That’s because the trial
- was not a treatment trial of people with osteoarthritis. More than 80% of participants had no history of osteoarthritis.
- did not compare x-rays or other imaging tests before and after treatment to confirm the diagnosis of osteoarthritis, or demonstrate that treatment slowed its progression
- did not assess whether joint pain was present before treatment or improved after treatment. It’s possible that the reason there were fewer joint replacements among people taking canakinumab is that the medication reduced pain, rather than slowing joint damage. Perhaps the medication can delay the need for joint replacement by reducing symptoms without slowing progression of joint damage.
- lasted about four years. The results could have been different if it had lasted longer.
- only included people who had prior heart attack and an elevated CRP. The results may not apply to people who have no history of cardiovascular problems or a normal CRP.
To learn whether canakinumab actually can slow osteoarthritis, we need a proper trial that enrolls people with osteoarthritis, and compares symptoms and x-rays after treatment with canakinumab or placebo.
Canakinumab is expensive, nearly $70,000/year (though discounts, insurance coverage, and copays vary), and only available by injection. It’s not clear how many people with osteoarthritis would accept such treatment. If it is proven highly effective at preventing the need for joint replacement surgery, its high cost might be easier to accept.
The bottom line
We need definitive information about the potential of canakinumab or related drugs to treat osteoarthritis and slow its progression. Until then, it’s unlikely to become a common option.
If you have osteoarthritis of the knees or hips, talk to your doctor about your options, including maintaining a heathy weight, staying active, and taking pain relievers as needed. Some people improve with walking aids (such as a cane) or knee braces (for knee arthritis). Joint replacement surgery can be considered as a last resort.
As for new treatments that can slow the progression of osteoarthritis, we should be hopeful. But we’re not there yet.
Follow me on Twitter @RobShmerling
The post Stopping osteoarthritis: Could recent heart research provide a clue? appeared first on Harvard Health Blog.
Stress and the heart: Lessons from the pandemic
The effects of COVID-19 have been extensive, with more than seven million confirmed cases and more than 200,000 deaths in the US alone. COVID-19 has caused additional impacts on healthcare; for example, patients have delayed seeking care for serious symptoms over fears of exposure to COVID-19. But the consequences of COVID-19 have reached beyond healthcare alone, with daily impacts on our financial, social, and emotional well-being.
As we attempt to cope and settle into this new normal, we will learn about the long-term effects of these hardships. Doctors have already begun to study the effects of COVID-related stress and anxiety on people around the world.
Physical effects of stress
Stress can have real physical effects on the body, and it has been linked to a wide range of health issues. Stress directly activates our sympathetic nervous system, initiating a fight-or-flight response that can elevate blood pressure and blood sugar. Though potentially useful in the short term from an evolutionary standpoint, stress can worsen hypertension and diabetes when it occurs chronically. Stress can disrupt our sleep, and can lead us to make unhealthy food choices, as we seek comfort foods or abandon portion control.
A recent study suggests that stress due to the pandemic may already be affecting our heart health.
The link between stress and heart health
Stress cardiomyopathy, also called Takotsubo cardiomyopathy and broken-heart syndrome, is a cardiac disorder characterized by a sudden onset of chest pain and heart dysfunction that mimics a heart attack. But, in contrast with what is seen during a heart attack, doctors are unable to find evidence of a blood clot or abnormalities with cardiac blood flow.
Typical stress cardiomyopathy patients are postmenopausal women experiencing sudden onset of chest pain and shortness of breath. The link between stress and stress cardiomyopathy is well documented; patients with stress cardiomyopathy often experience emotional or physical stress in the week preceding their illness. The exact mechanism of this reaction is not clearly understood, but researchers have found changes in blood flow to the brain and in signaling of stress-related hormones.
Emotional triggers of stress cardiomyopathy include death of a spouse or family member, divorce or interpersonal conflict, and natural disasters such as earthquakes and floods. It stands to reason that living with the chronic stress of a global pandemic could also trigger this syndrome.
Pandemic-related stress is already affecting heart health
A recent study published in JAMA Network Open attempted to measure the effect of COVID-19-related stress on our health by looking at the prevalence of stress cardiomyopathy during the pandemic. The researchers compared the incidence of stress cardiomyopathy during the COVID-19 pandemic (March 1 to April 30, 2020) to the incidence of stress cardiomyopathy during three prior periods (in 2018, 2019, and earlier in 2020). Importantly, all patients included in the study tested negative for COVID-19.
Researchers found that there was a significant rise in stress cardiomyopathy during the COVID-19 period, with stress cardiomyopathy occurring more than four times as often as usual during March and April 2020.
Fortunately, heart function typically recovers over one to two weeks in people with stress cardiomyopathy, and prognosis is generally good. However, affected patients do have an increased risk of recurrence.
Take steps to manage stress
This study is a cautionary tale regarding the impact of stress. It serves as a good reminder that we should all strive to minimize stress, even in these trying times, and improve how we handle it. Some practical tips for managing stress including choosing healthy foods, exercising regularly, getting enough sleep, and staying connected with friends and family.
The post Stress and the heart: Lessons from the pandemic appeared first on Harvard Health Blog.
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