LongCovid [+ CFS/ME]

patiëntengroep voor ouders van kinderen met long covid

There are striking parallels between the two syndromes – and scientists hope the link could help to unravel the mysteries of both.

In this longitudinal, case-controlled, cohort design study, authors show that post-exertional malaise is associated with severe exercise-induced myopathy, local and systemic metabolic disturbances and infiltration of amyloid-containing deposits in skeletal muscles of patients with long COVID.

Everyday tiredness is nothing like the depleting symptom that people with long COVID and ME/CFS experience.

Nature Reviews Cardiology - Graded exercise therapy should not be recommended for patients with post-exertional malaise

People with long COVID, ME/CFS and other chronic conditions are taking up science to find symptom relief and inspire new directions for professional scientists.

“More than a year on, I think I’m physically improving, but still feel nowhere near my baseline. I’ve felt a lot of frustration and anger, particularly when my reinfection set me back further, wishing that I could do the things I want to do. Mentally, it’s all taken a big toll, too.”

In this community-based cohort study, the risk of new-onset long COVID was 28% lower after a second infection compared with a first infection in participants ag

Some form of brain injury could be behind the symptoms reported by those with long COVID, according to a new study, and adapting tests and treatments to match could aid progress in tackling the condition.

As a new study shows, the answer lies in some long COVID sufferers’ muscle damage and their bodies’ ability to make energy.

### What you need to know This article updates and extends a previous BMJ Practice Pointer published in August 2020 when almost no peer reviewed research or evidence based guidance on the condition was available.1 In this update we outline how clinicians might respond to the questions that patients ask. The term “long covid”2 refers to prolonged symptoms following infection with SARS-CoV-2 that are not explained by an alternative diagnosis. It embraces the National Institute for Health and Care Excellence (NICE)’s terms “ongoing symptomatic covid-19” (symptoms lasting 4-12 weeks) and “post covid-19 syndrome” (symptoms beyond 12 weeks),3 the US Centers for Disease Control and Prevention’s group of “post-covid conditions,”4 and the World Health Organization’s “post covid-19 condition.”5 In mid-2022, approximately 70% of the UK adult population had been infected with SARS-CoV-2.6 Of these, almost 2 million report covid-19 symptoms persisting for more than four weeks; 807 000 (41% of all people with long covid) for more than a year; and 403 000 (19%) for more than two years.7 Based on workforce data from the British Medical Association,8 a full time equivalent general practitioner with an average list size (approximately 2000) has around 65 patients with long covid, 27 of whom will have been unwell for more than a year, and 12 for more than two years. Most general practices have far fewer patients with a long covid diagnostic code on their electronic health record9 for a combination of reasons, including lack of presentation, lack of recognition, and inadequate coding. These figures do not cover children, who are outside the …

The coronavirus disease 2019 (COVID-19) pandemic has caused significant medical, social, and economic impacts globally, both in the short and long term. Although most individuals recover within a few days or weeks from an acute infection, some experience longer lasting effects. Data regarding the postacute sequelae of severe acute respiratory syndrome coronavirus 2 infection (PASC) in children, or long COVID, are only just emerging in the literature. These symptoms and conditions may reflect persistent symptoms from acute infection (eg, cough, headaches, fatigue, and loss of taste and smell), new symptoms like dizziness, or exacerbation of underlying conditions. Children may develop conditions de novo, including postural orthostatic tachycardia syndrome, myalgic encephalomyelitis/chronic fatigue syndrome, autoimmune conditions and multisystem inflammatory syndrome in children. This state-of-the-art narrative review provides a summary of our current knowledge about PASC in children, including prevalence, epidemiology, risk factors, clinical characteristics, underlying mechanisms, and functional outcomes, as well as a conceptual framework for PASC based on the current National Institutes of Health definition. We highlight the pediatric components of the National Institutes of Health-funded Researching COVID to Enhance Recovery Initiative, which seeks to characterize the natural history, mechanisms, and long-term health effects of PASC in children and young adults to inform future treatment and prevention efforts. These initiatives include electronic health record cohorts, which offer rapid assessments at scale with geographical and demographic diversity, as well as longitudinal prospective observational cohorts, to estimate disease burden, illness trajectory, pathobiology, and clinical manifestations and outcomes.

The SARS-CoV-2 pandemic not only resulted in millions of acute infections worldwide, but also in many cases of post-infectious syndromes, colloquially referred to as “long COVID”. Due to the heterogeneous nature of symptoms and scarcity of available tissue samples, little is known about the underlying mechanisms. We present an in-depth analysis of skeletal muscle biopsies obtained from eleven patients suffering from enduring fatigue and post-exertional malaise after an infection with SARS-CoV-2. Compared to two independent historical control cohorts, patients with post-COVID exertion intolerance had fewer capillaries, thicker capillary basement membranes and increased numbers of CD169+ macrophages. SARS-CoV-2 RNA could not be detected in the muscle tissues. In addition, complement system related proteins were more abundant in the serum of patients with PCS, matching observations on the transcriptomic level in the muscle tissue. We hypothesize that the initial viral infection may have caused immune-mediated structural changes of the microvasculature, potentially explaining the exercise-dependent fatigue and muscle pain. Graphical Abstract

Current Clinical Microbiology Reports - Long COVID, or post-COVID Condition, is increasingly recognized in children and adolescents, despite being less studied compared with the adult population....

Molecular Psychiatry - Clinical improvement of Long-COVID is associated with reduction in autoantibodies, lipids, and inflammation following therapeutic apheresis

Analysis of blood revealed that Long COVID is characterized by changes to complement proteins and platelet activation.

IntroductionUpper respiratory tract infections (URTI) are the most common illnesses affecting athletes, causing absences from training and competition. Salivary immunoglobulin A (sIgA) is the main immune factor in saliva, and a consistent association between low concentrations of sIgA and an increased incidence of URTIs has been reported. The oral probiotic Streptococcus salivarius K12 has been suggested to have the potential to improve oral diseases and mucosal barrier function. However, the effects of this probiotic on active young subjects performing a high-intensity training (HIT) program have not been investigated.MethodsActive young students were randomised into a treated group (S. salivarius K12) and a control (placebo) group and asked to take the product daily for 30 days. After this period, participants performed a graded exercise test and five HIT sessions, all within 3 days. They were also asked to complete the Wisconsin Upper Respiratory Symptom Survey daily to monitor URTI’s presence. Before and after the 30 days, and at 0h, 24h and 72h after the last training session, saliva samples were collected to quantify sIgA level, secretion rate, and flow. The effect of S. salivarius K12 intake on these parameters was tested using an ANOVA for repeated measures.ResultsTwenty (M = 14, F = 6) young subjects (23.5 ± 2.3 years old) participated in the study. The total accumulated training load (sRPE) in the supplementation period was similar in the two groups (treated: 434...

Postural orthostatic tachycardia syndrome (POTS) is a form of dysautonomia that impacted an estimated 3 million Americans before COVID-19. Recent research shows that the number of POTS patients is now estimated to impact at least 6 million Americans since the pandemic began. POTS impacts millions of people around the world too, but we don?t have good epidemiology data in other countries. POTS is a form of orthostatic intolerance that is associated with the presence of excessive tachycardia and many other symptoms upon standing.1 Diagnostic Criteria The current diagnostic criteria for POTS is a heart rate increase of 30 beats per minute (bpm) or more, or over 120 bpm, within the first 10 minutes of standing, in the absence of orthostatic hypotension.1,2,3,4 In children and adolescents, a revised standard of a 40 bpm or more increase has recently been adopted.4,5 POTS is often diagnosed by a Tilt Table Test, but if such testing is not available, POTS can be diagnosed with bedside measurements of heart rate and blood pressure taken in the supine (laying down) and standing up position at 2, 5 and 10 minute intervals. Doctors may perform more detailed tests to evaluate the autonomic nervous system in POTS patients, such as Quantitative Sudomotor Axon Reflex Test (QSART, sometimes called Q-Sweat), Thermoregulatory Sweat Test (TST), skin biopsies looking at the small fiber nerves, gastric motility studies and more. Signs and Symptoms While the diagnostic criteria focus on the abnormal heart rate increase upon standing, POTS usually presents with symptoms much more complex than a simple increase in heart rate. It is fairly common for POTS patients to have a drop in blood pressure upon standing, but some POTS patients have no change or even an increase in blood pressure upon standing.1 POTS patients often have hypovolemia (low blood volume) and high levels of plasma norepinephrine while standing, reflecting increased sympathetic nervous system activation.3 Approximately 50% of POTS patients have a small fiber neuropathy that impacts their sudomotor nerves. Many POTS patients also experience fatigue, headaches, lightheadedness, heart palpitations, exercise intolerance, nausea, diminished concentration, tremulousness (shaking), syncope (fainting), coldness or pain in the extremities, chest pain and shortness of breath.1,3,4 Patients can develop a reddish purple color in the legs upon standing, believed to be caused by blood pooling or poor circulation. The color change subsides upon returning to a reclined position. Quality-of-Life and Disability Some patients have fairly mild symptoms and can continue with normal work, school, social and recreational activities. For others, symptoms may be so severe that normal life activities, such as bathing, housework, eating, sitting upright, walking or standing can be significantly limited.1,3 Physicians with expertise in treating POTS have compared the functional impairment seen in POTS patients to the impairment seen in chronic obstructive pulmonary disease (COPD) or congestive heart failure.1 Approximately 25% of POTS patients are disabled and unable to work.1 Researchers found that quality-of-life in POTS patients is comparable to patients on dialysis for kidney failure.21, 22 History of POTS The term POTS was coined in 1993 by a team of researchers from Mayo Clinic, led by neurologist Dr. Philip Low.8 However, POTS is not a new illness; it has been known by other names throughout history, such as DaCosta's Syndrome, Soldier's Heart, Mitral Valve Prolapse Syndrome, Neurocirculatory Asthenia, Chronic Orthostatic Intolerance, Orthostatic Tachycardia and Postural Tachycardia Syndrome.3 In the past, it was mistakenly believed to be caused by anxiety. However, modern researchers have determined that POTS is not caused by anxiety.2,6,7 It is caused by a malfunction of the patient's autonomic nervous system. Thankfully, in the last 20 years, researchers have gained much more insight into imbalances of the autonomic nervous system.1 POTS Classifications POTS researchers have classified POTS in various ways. Dr. Blair Grubb has described POTS as primary or secondary. Primary refers to POTS with no other identifiable medical condition (also known as idiopathic POTS). Secondary refers to POTS with the presence of another medical condition known to cause or contribute towards POTS symptoms.1 Dr. Julian Stewart has described high flow and low flow POTS, based upon the flow of blood in the patients lower limbs.9 Other researchers have described POTS based on some of its more prominent characteristics: hypovolemic POTS, which is associated with low blood volume; partial dysautonomic or neuropathic POTS which is associated with a partial autonomic neuropathy; and hyperandrenergic POTS which is associated with elevated levels of norepinephrine.1,3,4 These are not distinct medical conditions and many POTS patients have two or three of the different characteristics present. For example, one patient can have neuropathy, low blood volume and elevated norepineprhine. Who Develops POTS? POTS can strike any age, gender or race, but it is most often seen in women of child bearing age (between the ages of 15 and 50).2 Men and boys can develop it as well, but approximately 80% of patients are female.2 Is POTS Caused by Anxiety? While some of the physical symptoms of POTS overlap with the symptoms of anxiety, such as tachycardia and palpitations, POTS is not caused by anxiety. POTS patients are often misdiagnosed as having anxiety or panic disorder, but their symptoms are real and can severely limit a person's ability to function.1,3 Research has shown that POTS patients are similarly or even less likely to suffer from anxiety or panic disorder than the general public.3,5,6,7 Research surveys that evaluate mental health show similar results between POTS patients and national norms.20 What Causes POTS? POTS is a heterogeneous (meaning it has many causes) group of disorders with similar clinical manifestations.1,4 POTS itself is not a disease; it is simply a cluster of symptoms that are frequently seen together. This is why the 'S' in POTS stands for Syndrome. Since POTS is not a disease, it is fair to say that POTS is caused by something else. However, figuring out what is causing the symptoms of POTS in each patient can be very difficult, and in many cases, patients and their doctors will not be able to determine the precise underlying cause. When doctors cannot pinpoint the underlying cause of a patient's POTS, it may be called Primary or Idiopathic POTS.1 Idiopathic simply means of an unknown origin. While researchers are still working to identify the root causes and pathology of POTS, there are several underlying diseases and conditions that are known to cause or be associated with POTS or POTS like symptoms in some patients. This is a partial list: -Amyloidosis;1 -Autoimmune Diseases such as Autoimmune Autonomic Ganglionopathy, Sjogren's Syndrome, Lupus, Sarcoidosis, Antiphospholipid Syndrome;1,3, 22 -Chiari Malformation19 -Deconditioning;4 -Delta Storage Pool Deficiency13 -Diabetes and pre-diabetes -Ehlers Danlos Syndrome - a collagen protein disorder than can lead to joint hypermobility and stretchy veins;3,12 -Genetic Disorders/Abnormalities;3 -Infections such as Mononucleosis, Epstein Barr Virus, Lyme Disease, extra-pulmonary Mycoplasma pneumonia and Hepatitis C;1,2,3,4,10,11 -Multiple Sclerosis;14 -Mitochondrial Diseases;15 -Mast Cell Activation Disorders;3 -Paraneoplastic Syndrome - rare small tumors of the lung, ovary, breast and pancreas that produce antibodies;1 -Toxicity from alcoholism, chemotherapy and heavy metal poisoning.1 -Traumas, pregnancy or surgery;1,2,3 -Vaccinations;18 -Vitamin Deficiencies/Anemia;16,17 Treatment Each patient is different, thus consulting with a physician who has experience in treating autonomic disorders is important. The most common treatments for POTS include increasing fluid intake to 2-3 liters per day; increasing salt consumption to 3,000 mg to 10,000 mg per day; wearing compression stockings; raising the head of the bed (to conserve blood volume); reclined exercises such as rowing, recumbent bicycling and swimming; a healthy diet; avoiding substances and situations that worsen orthostatic symptoms; and finally, the addition of medications meant to improve symptoms.1,3 Many different medications are used to treat POTS, such as Fludrocortisone, Beta Blockers, Midodrine, Clonidine, Pyridostigmine, Benzodiazepines, SSRIs, SNRIs, Erythropoietin and Octreotide.1,3 If an underlying cause of the POTS symptoms can be identified, treating the underlying cause is very important as well. Prognosis Currently, there is no cure for POTS, however researchers believe that some patients will see an improvement in symptoms over time. Detailed long term follow up studies on the course of POTS are sparse, but Dysautonomia International is working with researchers to begin to collect long term follow up data. With proper lifestyle adjustments, exercise, diet and medical treatments, many patients see an improvement in their quality of life.1 If an underlying cause can be identified, and if that cause is treatable, the POTS symptoms may subside. While the prognosis is good for most patients, researchers have noted that some patients will not improve and may actually worsen over time.1 The longest follow-up study done to date comes from Mayo Clinic.20 Mayo Clinic did a survey of their pediatric POTS patients seen between 2003 and 2010. Of those who responded to the survey, 18.2% reported a complete resolution of their POTS symptoms, while 52.8% reported persistent but improved symptoms. Male patients were twice as likely to report recovery. The average survey respondent had been diagnosed for about 5 years. Both patients who fully recovered and those who did not had mental health scores similar to the national norm. Print out t

Collega Cordemans neemt zijn ervaringen als longarts-intensivist mee in zijn werk als gerechtsarts wanneer hij adviseert rondom long-COVID

Als longcovidpatiënten zich te veel inspannen, produceert hun lichaam eiwitten en enzymen die het lichaam zelf aanvallen, zo blijkt uit Amsterdams onderzoek.

Study finds biological changes may explain why those with lasting symptoms feel muscle pain and fatigue for weeks after working out

A study involving more than 450 people found that a mixture of prebiotics and probiotics alleviated some symptoms of long covid when taken daily for six months

Recent research suggests that vaccination after recovery from COVID-19 enhances T cell functionality. Learn more about the impact of vaccination on T cell response and immunity.

Treatment with SIM01 alleviates multiple symptoms of PACS. Our findings have implications on the management of PACS through gut microbiome modulation. Further studies are warranted to explore the beneficial effects of SIM01 in other chronic or post-infection conditions.

Getting a COVID-19 vaccine may not only reduce a person's risk of getting long-haul COVID, but also could mean fewer symptoms for people who develop the condition.

Long Coronavirus Disease-2019 (COVID-19), also known as post-COVID-19 conditions (PCC), has emerged as the next public health crisis with an estimated incidence of 10-30% in non-hospitalized and 50-70% in hospitalized individuals [1]. PCC is clinically heterogeneous, having been associated with over 200 symptoms [2]. In October 2021, the World Health Organization (WHO) defined PCC as ε1 symptom not explained by an alternate diagnosis, lasting at least 2 months, in individuals with probable or confirmed Severe Acute Respiratory-Coronavirus-2 (SARS-CoV-2) infection, 12 weeks from the onset of illness [3].

Genes, environment and lifestyle are some of the risk factors for serious diseases like Parkinson's and Alzheimer's. This is why scientists believe COVID-19 infection should be added to the list, writes Catherine Taylor.

Mast cells (MC) are ubiquitous in the body and are critical for allergic diseases, but also in immunity and inflammation, as well as potential involve…

Serotonin levels are depleted in long Covid patients, a new study says, pointing to a potential cause for “brain fog.”