I did some research. It turns out I am suffering from Covid Myositis. Random Joint pain . It will last for about 30 days
Wonderful
Myositis as a rare manifestation of COVID-19 is only recently being reported. This review examines the current literature on COVID-19-induced myositis focusing on etiopathogenesis, clinical presentations, diagnostic practices, and therapeutic challenges with immunosuppression, and the difficulties experienced by rheumatologists in established myositis in the COVID-19 era.
Recent Findings
COVID-19 is associated with a viral myositis attributable to direct myocyte invasion or induction of autoimmunity. COVID-19-induced myositis may be varied in presentation, from typical dermatomyositis to rhabdomyolysis, and a paraspinal affliction with back pain. It may or may not present with acute exponential elevations of enzyme markers such as creatine kinase (CK). Virus-mediated muscle inflammation is attributed to ACE2 (angiotensin-converting enzyme) receptor–mediated direct entry and affliction of muscle fibers, leading on to innate and adaptive immune activation. A greater recognition of the stark similarity between anti-MDA5-positive myositis with COVID-19 has thrown researchers into the alley of exploration — finding common etiopathogenic basis as well as therapeutic strategies. For patients with established myositis, chronic care was disrupted during the pandemic with several logistic challenges and treatment dilemmas leading to high flare rates. Teleconsultation bridged the gap while ushering in an era of patient-led care with the digital transition to tools of remote disease assessment.
Summary
COVID-19 has brought along greater insight into unique manifestations of COVID-19-related myositis, ranging from direct virus-induced muscle disease to triggered autoimmunity and other etiopathogenic links to explore. A remarkable shift in the means of delivering chronic care has led patients and caregivers worldwide to embrace a virtual shift with teleconsultation and opened doorways to a new era of patient-led care.
Keywords: COVID-19, Myositis, Idiopathic inflammatory myopathy, Rhabdomyolysis, Dermatomyositis, Myasthenia, Telemedicine, Tele-triage, Immunopathogenesis
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Introduction
The ongoing Coronavirus disease 2 pandemic (COVID-19) has brought several interesting observations to the fore, ranging from virus-induced muscle disease to a possibility of virus-triggered inflammation in patients with long-standing chronic autoimmune diseases [
1,
2]. The initial pandemic period left physicians grappling with the uncertainty of the course of COVID-19 in patients with severe and disabling rheumatic diseases, in particular the idiopathic inflammatory myopathies (IIM) [
3•]. Moreover, extended lockdowns in various parts of the world hampered mobility and access to care for most patients [
4••].
COVID-19 is a multisystem disease that presents with a plethora of manifestations involving the lungs, liver, kidneys, and gastrointestinal tract, among others. Emerging evidence suggests that the acute inflammatory response and production of autoantibodies contribute to morbidity observed in COVID-19 [
5]. Lasting effects are observed in some individuals at 6 months or even longer after recovery. While fever, cough, and sore throat have been the most reported symptoms associated with the disease, published case reports have recently started to describe more atypical and rarer presentations of infection with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). It is apparent now that the musculoskeletal system is not spared either [
6] with musculoskeletal manifestations of COVID-19 ranging from a mild elevation of creatine kinase (CK) with mild or no weakness to severe rhabdomyolysis.
This review aims to examine current knowledge available on COVID-19-related myositis, including but not limited to the presentation, diagnostic challenges, currently proposed disease mechanisms, and management. Furthermore, we discuss the complexity of administering immunosuppressive treatment in diagnosed cases of IIM, who may be at risk for contracting COVID-19. We also explore the effect of the pandemic on the management of the idiopathic inflammatory myopathies (IIM) and the proposed directions for care of these debilitating disorders in the future.
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Muscle Involvement in COVID-19
Alongside the typical respiratory manifestations like cough, fever, and sore throat, proximal muscle weakness is increasingly being reported as a manifestation causing significant morbidity in occasional COVID-19 patients. Myalgia is reported extensively in the literature as a common musculoskeletal manifestation of COVID-19 infection, presenting in nearly half of all COVID-19-infected patients. COVID-19-related myositis and consequently rhabdomyolysis are other reported manifestations, albeit relatively rare [
7,
8]. By July 2020, a single case of COVID-19-related myositis had been reported in the literature [
9]. Since then, several case reports and series reporting a virus-induced myositis attributed to COVID-19 disease have been published. The muscle involvement may vary from an asymptomatic elevation of CK to severe rhabdomyolysis.
Acute Viral Myositis
Nearly 23 patient cases of myositis attributable to COVID-19 have been described so far. COVID-19-induced myositis may vary in presentation, ranging from frank muscle weakness to typical dermatomyositis replete with classic rashes, or mere back pain with muscle disease on MRI. Most patients test positive for COVID-19 on initial presentation with most reported being males aged 33–87. Noteworthily, COVID–19 may or may not present with acute exponential elevations of enzyme markers such as CK, and muscle enzymes may not necessarily have a direct bearing on prognosis.
Rhabdomyolysis
Rhabdomyolysis is one of the rare and severe complications of COVID-19 infection which can be an initial presentation in some cases [
10,
11]. In such cases, patients present with typical COVID-19 symptoms such as fever, cough, myalgia, and shortness of breath as well as manifest acute lower limb–dominant symmetric muscle weakness and subsequently go on to develop rhabdomyolysis associated with elevated CK levels. A study reported a peak CK value as high as 33,000 U/L [
12•]. In this setting, they may present with frank muscle weakness, which is profound, proximal, lower limb–dominant, acute, and symmetric. At times, the patients are critically ill and requiring ventilatory support. The only manifestation of rhabdomyolysis in these may be myoglobinuria (dark urine) and acute kidney injury (AKI) needing hemodialysis with raised CK >5000 IU/L [
13•,
14•,
15•]. Rhabdomyolysis can be fatal, with casualties reported in nearly 45% (4 of 9 reported) of those with this presentation over a short follow-up duration (Table
(Table1).1). Among all reported cases (n = 23) of COVID-19-related myositis so far, 21.7% (n = 5) succumbed to the illness of which 80% (n=4) had rhabdomyolysis.
