Long COVID for the Rheumatologist





There are estimated tens of millions of individuals throughout the world suffering from a variety of postinfectious sequela following infection with severe acute respiratory syndrome coronavirus 2 also commonly referred to as long coronavirus disease (COVID). Long COVID is providing an opportunity for the field of rheumatology to explore the relationship between similar syndromes including fibromyalgia seen in patients with underlying inflammatory and noninflammatory rheumatic diseases, as well as other postacute infectious sequela and bring our field’s traditional skill sets to bear on improving our understanding of these disorders and the care of such patients.


Key points








  • Long COVID lacks a uniform definition and diagnostic criteria, posing many challenges to its study as well as unclear estimates of prevalence.



  • To date, identified risk factors for long COVID include female gender, older age, and severity of initial infection.



  • Patients with long COVID may present with a wide array of symptoms, with the most common being fatigue, pain, and sleep dysfunction.



  • There exist many similarities among long COVID, fibromyalgia, and myalgic encephalitis/chronic fatigue syndrome, and this warrants further study.



  • There are currently no approved therapies for long COVID, thus treatment guidelines are largely derived from expert opinion and consensus guidelines.




Introduction


Long COVID-19 is a term coined in 2020 by patients suffering from seeming states of incomplete recovery following infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Notably, it took some time for the medical establishment to forthrightly embrace this new syndrome, which has contributed to ongoing tensions between patient advocacy groups, health care providers, and research efforts on long COVID. Over the past 4 years, however, long COVID, also referred to as postacute sequelae of SARS-CoV-2 infection (PASC), has become firmly established as a disorder of high priority worldwide. The exact number suffering from long COVID has been difficult to ascertain; earlier estimates by the World Health Organization (WHO) ranged between 10% and 20%, while more recent estimates by the Center for Disease Control and Prevention (CDC) range from 1.9% to 10.6% of the infected population. It is estimated that up to 65 million people were afflicted globally as of 2022. Regardless of its exact prevalence, there is near-universal agreement that it is a formidable public health issue; accordingly, long COVID is now generating an intense effort in biomedical research. As of April 2024, long COVID has been cited in the peer-reviewed medical literature over 5500 times; for those working in the field, the pace of emerging data from both traditional as well as the gray literature is both humbling and at times disarming. Four years into the pandemic, the field of long COVID research remains unsettled. Still lacking are accepted classification criteria for comparative research as well as diagnostic criteria to give clinicians and patients confidence in their care. Furthermore, while much has been discovered in terms of associated biomedical findings among cohorts of diverse patient groups with long COVID, , they have not yet led to a successful controlled clinical trial. This review will attempt to summarize the clinical spectrum of long COVID, its current epidemiology, the leading pathogenic theories surrounding it and, finally, discuss some best practices for its diagnosis and management.


What is long COVID and how is it defined?


Long COVID, in its most reductionist form, is a state where signs, symptoms, and conditions either continue or develop after a reasonable period following an episode of coronavirus disease 2019 (COVID-19). At one extreme, this may represent the organ damage as sequelae of clinically severe infection (ie, which required hospital and/or intensive care unit admission with resultant well-defined pathologic damage to host tissues) and is referred to as nonsyndromic long COVID. At the other end of the spectrum are people who have experienced mild, even possibly, asymptomatic COVID-19 and have persistent new-onset symptoms in the wake of the infectious episode for a given period (ie, 4, 8, 12 weeks, or longer). Patients with this form of long COVID (which we and others refer to as syndromic long COVID) will form the basis of this discussion.


Patients with syndromic long COVID characteristically have numerous subjective symptoms dominated by fatigue, neurocognitive dysfunction, pain, sleep disturbances, and a myriad of other complaints that, by some estimates, number over 200. Critical to the concept of syndromic long COVID is the absence of traditional pathologic findings, which can explain the symptoms; screening laboratory studies are typically normal.


Currently, there are a number of proposed definitions for syndromic long COVID from organizations such as the CDC, the WHO, and the National Institute for Health and Care Excellence, all of which have been recently summarized and critically appraised for their limitations. Each of these definitions requires that symptoms have no other explanation and remain medically unexplained but differ as to length of persistence (4–12 weeks or more). For the purposes of this review, we will confine our comments to those with persistent or new onset symptoms for greater than 12 weeks, the WHO definition, since this longer lasting form is more likely to require clinical assessment and intervention. It should be acknowledged that there is high heterogeneity of severity, organ involvement, and underlying endotypes in this definition.


Challenges in assessing epidemiology of long COVID?


The current lack of a widely endorsed case definition poses a marked challenge for the epidemiologic investigation of long COVID. The case definitions most generally used (eg, CDC and WHO) have been considered overly broad by some, which lowers their specificity thus threatening diagnostic accuracy and compromising case tracking. The implications of these methodologic limitations are that, for now, it is perilous to compare studies from the diagnostic, pathophysiologic, or therapeutic perspectives. Furthermore, the most common clinical manifestations of long COVID (fatigue, pain, neurocognitive dysfunction, and sleep disorders) are highly nonspecific and appear to be equally prevalent following non-COVID respiratory illnesses. , They are also highly prevalent in the general population even in the pre-COVID era. Encouragingly, however, the national institute of health (NIH)-sponsored researching COVID to enhance recover (RECOVER) Consortium has recently launched a massive study with the potential to mark a new beginning in standardizing the case definition of long COVID. As of this writing, however, it has not been widely used for investigation since it requires a specific questionnaire at a specific timing in the post-COVID disease course.


Risk factors for long COVID


Given the lack of widely accepted classification criteria for long COVID, investigations to assess risk factors for its development are inexact. Despite this, certain trends appear consistent across a wide range of investigations. Female gender, older age, belonging to an ethnic minority, socioeconomic deprivation, smoking, obesity, and a wide range of comorbidities were all identified in a large United Kingdom database assessing 115 symptoms in a cohort of nearly 2 million patients with nearly one-quarter having COVID-19. , Severity of initial infection has also been repeatedly noted as a risk for both syndromic and nonsyndromic post-COVID-19 sequelae. , It should be emphasized that a number of pathologically defined sequelae and possibly long COVID may occur in patients with mild or even asymptomatic infection and in previous states of good health. , Pre-existing mental health issues have been suggested as a predisposing factor to post-COVID sequelae but the relationship to long COVID is as yet unclear. Similar findings have also been demonstrated in medically unexplained illness after other non-SARS-CoV-2-related infections. The risk of long COVID appears to be greatest following infection with originator strains and possibly less likely following infection with SARS-CoV-2 variants of reduced pathogenicity. Growing evidence for some level of protection from vaccination has been suggested. , The potential for early antiviral therapy for mild-to-moderate COVID-19 to reduce the likelihood of long COVID has been suggested, and clinical trials are now ongoing examining the effectiveness of antivirals as therapy for long COVID. , The role of pre-existing inflammatory rheumatic diseases as a risk factor for long COVID is a critical question and under active investigation.


Pathogenesis of long COVID


A full discussion of the pathogenesis of long COVID is beyond the scope of this review, but it has been the subject of previous reviews. , , Numerous pathophysiologic mechanisms have been proposed as initiators and/or drivers of the long COVID state, but as of now, these remain passive biologic associations and await further confirmation. Fig. 1 displays the leading candidate theories of pathobiology, all with varying degrees of evidence with many observations now duplicated albeit in unmatched cohorts. Of particular interest to rheumatologists are the observations of low level systemic and tissue specific inflammation as well as the documentation of robust autoantibody responses, including antinuclear antibody positivity following COVID-19 infection. , , These proposed mechanisms have generated interest in anti-inflammatory and immunomodulatory therapies for long COVID.




Fig. 1


Potential pathogenic pathways in Long Covid. Reprinted with permission, Cleveland Clinic Foundation ©2024. All Rights Reserved.


An overview of clinical manifestations of long COVID


Given that there is a marked diversity among the unexplained symptomatologies ascribed to syndromic long COVID, with some studies asserting that over 200 such symptoms may be accounted for under the description of medically unexplained complications, it is logical and necessary to focus on the major symptoms of the disorder based both upon their incidence and contribution to morbidity. This marked variation in individual symptoms across studies may be explained by a multitude of factors including differences in recruitment strategies ranging from one extreme of prospective preinfection-based cohorts that are microbiologically documented, interviewed, and examined, to Internet-based surveys among self-identified patients with no documentation of infection status. Despite such marked heterogeneity, numerous meta-analyses have demonstrated that certain manifestations are reproducibly common and clinically important. , The prevalence of symptoms within these epidemiologic studies vary greatly with the highest frequencies described in self-reported cases. Despite such differences, there is a consistency within these large databases emphasizing a core set of symptoms including fatigue, pain, and sleep disturbances. This is important for rheumatologists, as this constellation of findings is highly reminiscent of those observed in fibromyalgia. Similarly, the presence of fatigue complicated by postexertional malaise (PEM), nonrestorative sleep, and pain is also highly consistent with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).


Fatigue and Postexertional Malaise


Among all symptoms associated with long COVID (regardless of case definition), fatigue is the most commonly reported with an incidence of 22% to over 95% described in several meta-analyses, systematic reviews, and international cohort investigations. , Fatigue remains one of the most poorly understood physiologic states, and there is an intense amount of controversy regarding its nature and treatments in the setting of long COVID. Numerous studies assessing the impact of fatigue on quality of life have shown a range from mild to totally disabling. , The fatigue of long COVID is generally associated with descriptions of recurrent flu-like symptoms, nonrefreshing sleep, and, at the extreme, disabling fatigue with features of PEM. PEM is a biologic state characterized by a worsening of fatigue and/or other associated somatic symptoms after physical, cognitive, or psychological stressors and is often delayed 24 to 72 hours or more. , It is a characteristic and required symptom for the diagnosis of ME/CFS ; its presence is the basis for the increasing interest between the parallels of long COVID and ME/CFS. Unfortunately, there is no simple diagnostic tool for PEM; currently, the ascertainment of the presence of PEM must be done through medical history, preferably in conjunction with patient-reported outcome instruments such as the de Paul symptom questionnaire PEM subscale. The implications of PEM complicating chronic fatigability and long COVID are clinically important and a topic of considerable controversy with vocal concern from patient advocacy groups about the potential harms of unsupervised exercise. The lack of a high-efficiency diagnostic biomarker and the fact that PEM is not routinely ascertained by clinicians leave gaps in our understanding of its prevalence and clinical significance. Other factors contributing to fatigability in long COVID may include deconditioning, sleep disturbances, and intercurrent mood disorders.


Pain


Similarly, pain in a variety of forms is present in most patients with long COVID with estimates in patient-driven surveys of up to 90%; myalgia is reported in 70% and joint pain in 55%. Much of the pain in the setting of long COVID falls under the umbrella of chronic overlapping pain conditions, which include conditions such as fibromyalgia, tension headache, irritable bowel syndrome, low back pain, temporomandibular disorders, and bladder pain syndromes. Investigations describing musculoskeletal pain reveal a wide range in prevalence with some estimates suggesting joint pains and muscle aches in 50% to 70% of respondents. Unfortunately, the vast majority is lacking granular details such as the results of standardized musculoskeletal examinations or the use of imaging modalities to define the pathologic nature. Inflammatory arthritis as a consequence of COVID-19 has only been anecdotally reported. The constellation of musculoskeletal pain and multiple overlapping pain disorders in a predominantly female population with chronic fatigability, sleep disorders and neurocognitive complaints is highly reminiscent of and consistent with fibromyalgia. There is currently a rich debate evolving in the rheumatologic literature as to whether long COVID could be equated with fibromyalgia. , Several groups have asserted that fibromyalgia and long COVID are closely linked. , Of urgent need for clarification is whether patients with long COVID with the clinical picture of fibromyalgia have PEM as there have been no detailed studies of PEM in fibromyalgia to date. Clarifying these relationships between COVID-19 and fibromyalgia particularly regarding the presence and significance of PEM has immediate practical implications as to what type of rehabilitation and exercise programs should be prescribed and which should be avoided.


Neurocognitive Dysfunction


Since the beginning of the pandemic, there have been reports of patients describing lingering problems with neurocognition, commonly describing impairment of memory and concentration and often referred to as “brain fog.” , , There have been numerous studies documenting varying aspects of this neurocognitive impairment that have led to differing viewpoints on prevalence, severity, relationship to neuropsychiatric comorbidity and lasting impact. In terms of neurocognitive function, patients with long COVID frequently display loss of short-term memory, episodic memory loss, and greater decline in vigilance with time on task. , In terms of its severity and lasting impact, the literature has been mixed with numerous studies suggesting that the neurocognitive deficits are mild and reversible while for others it can be debilitating. , Some studies suggest that cognitive decline described during the pandemic may not be directly attributable to COVID-19; these studies are supported by observations from surveys suggesting an overall decline in cognitive as well as physical health in the general population independent of the effects of COVID-19. Other studies have supported a greater degree of concern regarding the causal role of SARS-CoV-2 in neurocognitive health as supported by a range of findings including subtle but reproducible changes in MRI, and in a recent large community study of 800,000 adults, a 3 point loss of intelligence quotient compared to uninfected control participants.


Dysautonomia


In recent years, dysautonomia, a family of disorders attributed to dysfunction of the autonomic nervous system with frequent clinical manifestations such as postural orthostatic tachycardia syndrome and small fiber neuropathy among others has become increasingly well recognized in a variety of settings including ME/CFS, fibromyalgia, hypermobility syndromes, and long COVID. , When present, it can be profoundly disabling and requires a coordinated care effort for appropriate management as discussed in a later section.


Miscellaneous Symptoms


Virtually every system can be potentially affected by long COVID with other prominent complaints including breathlessness, cough, gastrointestinal symptoms similar to irritable bowel syndrome, reproductive system disorders including menstrual alterations, sexual dysfunction, and others. , , Interestingly anosmia and ageusia, which were relatively common complications in the early experience of long COVID, are only rarely reported since the onset of the Omicron era in late 2022.


Relationships among long COVID, myalgic encephalomyelitis/chronic fatigue syndrome, and fibromyalgia


It is both interesting and important to note that there are strong similarities between the core symptoms most frequently encountered in long COVID and in those most strongly associated with both ME/CFS and fibromyalgia. , ME/CFS is a chronic multisystem disease that affects millions of people worldwide but until the mid-1980s was largely ignored. , Even then, with the growing body of research on the disorder, patients with this condition were often marginalized, and the legitimacy of the disorder was under constant question. One of the shared features of both ME/CFS and long COVID is that general screening laboratory studies are often completely normal, further contributing to the skepticism of the reality of a disorder that has disabled so many patients. The core features of ME/CFS—fatigue with PEM, varying presence of pain, nonrefreshing sleep, dysautonomia, and evidence of immune dysregulation—bear strong similarities to the phenotype of long COVID; this has recently been elegantly reviewed. Determinations of exactly how many patients suffering with long COVID meet diagnostic criteria for ME/CFS are inexact. Studies citing frequency of both diagnoses are subject to numerous forms of bias but a recent review has cited a range of 13% to 45%, which in some clinics may reach 50% or more. In our opinion, most of the studies are limited by selection bias as many are taken from referral clinics that generally see the worst cases of long COVID. Regardless, given the high prevalence of COVID-19 infection in the United States, even a few percent meeting the case definition of ME/CFS could equal 1 million or more patients suffering from this devastating condition. In the NIH-sponsored RECOVER trial, the presence of PEM was a strong discriminate between fatigability in the COVID-19 experienced versus the control population. Additional parallels between these disorders include perturbations of autonomic nervous system and energy metabolism. Importantly, the NIH has recently published an in-depth deep phenotyping of postinfectious ME/CFS describing numerous abnormalities across multiple organ systems including evidence suggesting chronic antigenic stimulation as well as neurophysiologic and metabolic defects. Additional studies using similar methodology in patients with long COVID are eagerly awaited.


Similar to ME/CFS, fibromyalgia is a disorder characterized by widespread pain, fatigability, sleep disturbances, and intercurrent mood disorders, which also has a very strong resemblance to long COVID. , Other features of fibromyalgia with strong parallels to both long COVID and ME/CFS are its overexpression in female individuals in association with the immune dysregulatory disorders. Another similarity with ME/CFS is that the disease and patients who suffer both conditions have often been marginalized as having an illness that is, in some way, psychosomatic. It should be noted that like ME/CFS and long COVID, fibromyalgia is also characterized by having normal screening laboratory studies. Within the rheumatology literature, there is currently an active debate as to whether long COVID and fibromyalgia are the same condition. To answer this, it will be necessary to further explore the biologic interrelationship between fibromyalgia and ME/CFS. , Not surprisingly, there is evidence for a strong overlap between these 2 conditions because in several case definitions for ME/CFS, pain is a prerequisite finding.


Diagnosis and management: general principles of management


The role of rheumatologists in diagnosis and management of long COVID generally occurs in 1 of 2 settings. The first is when patients with chronic rheumatic diseases develop long COVID, and the second is when patients with rheumatic, immunologic, and/or inflammatory long COVID symptoms are referred to rheumatology for further diagnosis and/or treatment. There are no approved therapies for long COVID, thus treatment guidelines are largely derived from expert opinion and consensus guidelines. Patients with long COVID, once diagnosed, frequently feel unempowered to manage their condition because there is often reluctance for clinicians to take ownership of this disease. Furthermore, both clinicians and patients are often surrounded by a tumult of often-contradicting perspectives on long COVID including whether it is real or in some way imagined as well as advocacy from numerous groups for a myriad of therapeutics that lack efficacy data and have uncertain risk–benefit profiles. We believe that the treatment of long COVID should begin with empathic communication with the patient, which validates and destigmatizes the diagnosis and limits uncertainty. We also strive, in addition to assessing the patient’s chief complaints, to identify the patient’s chief concerns regarding the overall illness, which are often disparate from mere physical complaints and may belie underlying psychosocial distress. Counseling on the prognosis of long COVID is challenging but, in general, most studies have shown gradual improvement over time. The majority, but clearly not all, patients recover to some degree; some patients, generally less than 5%, may fail to improve at all. A number of variables have been linked to delayed improvement including female gender and intercurrent mood disorders. In our experience, patients with severe PEM fitting the ME/CFS phenotype, which is often complicated by dysautonomia, clearly have the worst prognoses. Collectively, the overall clinical approach to the treatment of long COVID is to focus on symptom management, functional goals, and improvement in quality of life.


Diagnosis and intake


From the clinical perspective, a guiding principle is that not all patients with post-COVID symptoms have long COVID and, especially given the lack of diagnostic biomarkers or even current classification or diagnostic criteria, a vigorous diagnostic workup is indicated. Numerous biomarkers have been described as abnormal in the setting of long COVID, including a variety of immunologic tests such as cytokine levels, blood cortisol and adrenocorticotropic hormone levels, elevated titers of certain antiviral antibodies, as well as other studies, but such testing at present lacks utility in clinical decision-making, and we do not generally endorse it. Similar to the commonplace occurrence (for the rheumatologist) of evaluating patients with positive antinuclear antibodies and nonspecific subjective symptomatology, the presence of such antibodies in patients who have recovered from COVID-19 has limited positive predictive value in establishing this diagnosis as tests such as the antinuclear antibody (ANA) are found in increased prevalence in patients who have recovered from COVID-19 with or without post-COVID sequela. , , Following diagnosis and given the broad array of symptoms associated with long COVID, triaging these complaints is critical to making a therapeutic plan. We generally ask the patient to focus on the top 3 symptoms that are most bothersome to them and which they believe are interfering most with their quality of life. Such a prioritization of chief complaints is vital to develop a care plan. Accordingly, given that the general laboratory screening of patients with long COVID is typically normal, we strongly advocate the use of baseline patient-reported outcomes that reflect general physical health, fatigue, pain, sleep, and mental health. Scales such as the patient reported outcomes measurement information system (PROMIS) Global Health items have been used successfully in the long COVID setting as part of routine clinical care.


Treatment of specific symptoms


Fatigue


Fatigue is of paramount importance in long COVID as it is generally the most frequent and dominant complaint among patients. In the absence of any approved therapies for long COVID, the approach to fatigue must be guided by experience derived from other conditions including fibromyalgia and ME/CFS. Central to the management of fatigue in long COVID is physical rehabilitation; pivotal in the assessment of fatigue is determining whether the patient has PEM. Unfortunately, there are no high-efficiency diagnostic tests for PEM. A careful history should be taken to determine whether physical or cognitive stress that was previously well tolerated now leads to the exacerbation or new onset of symptoms within 24 to 72 hours after the activity. In the absence of PEM, most patients should still receive individualized physical rehabilitation based on their history and capacity for physical activity. The precise role of exercise in patients with long COVID has been controversial; fears of inducing PEM have been widely publicized and discussed. However, recent data suggest that most patients tolerate a broad range of intensity within the exercise prescription. , In our experience, the majority of patients with long COVID may potentially benefit from a variety of integrative medical techniques such as mind–body exercises (eg, tai chi, Qigong, and yoga) that have been demonstrated to be effective in fibromyalgia as adjuncts to the treatment of fatigue. For patients at the extreme end of fatigue whose clinical features are consistent with ME/CFS, a rehabilitation program based on the principles of pacing is advised. Pacing, a form of rehabilitation that emphasizes energy conservation, was pioneered for the management of patients with ME/CFS and has recently been introduced as part of the management of symptoms of long COVID. Evaluation of PEM is not generally part of a rheumatologic evaluation, and the prevalence of PEM in inflammatory and noninflammatory rheumatic diseases has yet to be described. There are now guidelines from both the American College of Rheumatology and european allaince of associations for rheumatology (EULAR) with exercise recommendations for patients with inflammatory and noninflammatory rheumatic diseases, which we believe are applicable for the majority of patients with long COVID but without severe PEM. We believe that patients with long COVID with the phenotype of ME/CFS should be referred to physical medicine specialists familiar with the principles of rehabilitation of the disorder. ,


Pain


As previously discussed, pain is common in patients with long COVID but unfortunately the musculoskeletal component has generally been poorly described. While inflammatory arthritis is extremely rare, noninflammatory pain in soft tissues and joints is extremely common. In general, our approach is consistent with the Department of Veterans Administration recommendations on treating “chronic multisystem illness”; we agree with the leading principle, which recommends against the long-term use of opioid medications in the management of such disorders. Similarly, we agree with the general principles of treating nociplastic pain with a variety of nonpharmacologic therapies such as cognitive behavioral therapy, meditation, yoga, tai chi, Qigong, and acupuncture/acupressure. As with all somatic complaints, treatment of intercurrent mood issues such as anxiety, stress, and depression is essential.


Other Symptoms


As previously discussed, patients with long COVID may have numerous other symptoms besides pain and fatigue, which are beyond the scope of this review to discuss. If other nonpain, nonfatigue symptoms (such as headache, breathlessness, chest pain, or other symptoms) are of high concern to the patient, referral to specialty care is generally indicated. Again, it cannot be emphasized enough that ruling out other diagnoses is critically important. It must be kept in mind that pathologically based sequela of COVID-19 are common, including thrombotic, endocrine, and other disorders. Finally, one of the most pressing and complex symptoms encountered in long COVID clinics is that of dysautonomia, which is commonly seen in patients with the most severe forms of fatigue with phenotypic features of ME/CFS. Patients with suspicious symptoms (eg, tachycardia, dizziness, chest pains, syncope, or near-syncope) for such should be referred for formal tilt table testing and cardiac monitoring and treated by specialists knowledgeable in this disorder. Unfortunately, most clinics specializing in these disorders are currently overwhelmed with long waiting periods.


Experimental Therapies and Prevention


While there are no currently approved drugs for long COVID, there are an increasing number of therapeutic agents now entering clinical trials including a number sponsored by the NIH. As of May 2024, there are 484 studies under the heading of long COVID listed on clinicaltrials.gov , the majority of which are therapeutic trials.


Summary


The field of long COVID is rapidly changing and poses a major challenge to a number of stakeholders: caregivers, the health care industry, the pharmaceutical industry, health insurance, the federal government, and especially the patients suffering from it. Rheumatologists need to remain knowledgeable about long COVID, at the minimum for the benefits of their own patients who may be concerned or who have developed this syndrome and need assessment and care. Furthermore, many of the clinical features of long COVID are well within the sphere of rheumatology, and some clinicians may wish to engage in care of such patients. Importantly, long COVID poses a variety of research questions regarding the role of immune dysregulation, inflammation, and possibly autoimmunity.


Clinics care points








  • There exist multiple proposed definitions for syndromic long COVID that define the syndrome as the persistence or development of medically unexplained symptoms for anywhere from 4 to 12 weeks after infection.



  • While laboratory workup in patients with long COVID is typically normal/negative, it is important for other potential causes for long COVID patients’ symptoms to be evaluated for and ruled out.



  • Many patients with long COVID have features of ME/CFS, fibromyalgia, or both.



  • There are currently no approved treatments for long COVID; however, for most patients with prominent pain and fatigue, many nonpharmacologic interventions can be helpful.



  • Expansion of clinical trials of mechanistically based therapeutics is urgently needed.


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May 20, 2025 | Posted by in RHEUMATOLOGY | Comments Off on Long COVID for the Rheumatologist

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