Tag: long Covid

COVID-19 and Chronic Fatigue Syndrome: An Endocrine Perspective

Abstract:

Patients recovering from COVID-19 may have persistent debilitating symptoms requiring long term support through individually tailored cardiopulmonary and psychological rehabilitation programs. Clinicians need to be aware about the likely long-term complications and their diagnostic assessments to help identify any occult problems requiring additional help. Endocrinological evaluations should be considered as part of the armamentarium in the management of such individuals with diligent cognizance about the involvement of the hypothalamo-pituitary-adrenal (HPA) axis, adrenals, and thyroid.

Source: Bansal R, Gubbi S, Koch CA. COVID-19 and Chronic Fatigue Syndrome: An Endocrine Perspective. J Clin Transl Endocrinol. 2021 Dec 3:100284. doi: 10.1016/j.jcte.2021.100284. Epub ahead of print. PMID: 34877261; PMCID: PMC8641402. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8641402/ (Full text)

Chronic fatigue syndrome against the background of the COVID-19 pandemic

Abstract:

The more we learn about the new coronavirus infection, the more we understand that we will feel the echoes of the pandemic for many years, and those who have successfully endured the acute phase of COVID-19 may face the consequences of the infection. One of the most frequent manifestations will be the development of chronic fatigue syndrome (CFS) after COVID-19. This article discusses the possible causes of the development of CFS, as well as possible ways of its treatment and prevention.

Source: Nikitina AJ, Levin OS. Sindrom khronicheskoi ustalosti na fone pandemii COVID-19 [Chronic fatigue syndrome against the background of the COVID-19 pandemic]. Zh Nevrol Psikhiatr Im S S Korsakova. 2021;121(10. Vyp. 2):92-98. Russian. doi: 10.17116/jnevro202112110292. PMID: 34870921. https://pubmed.ncbi.nlm.nih.gov/34870921/  [in English, Russian]

Case Report: Neutralization of Autoantibodies Targeting G-Protein-Coupled Receptors Improves Capillary Impairment and Fatigue Symptoms After COVID-19 Infection

Abstract:

Clinical features of Coronavirus disease 2019 (COVID-19) are caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Acute infection management is a substantial healthcare issue, and the development of long-Covid syndrome (LCS) is extremely challenging for patients and physicians. It is associated with a variety of characteristics as impaired capillary microcirculation, chronic fatigue syndrome (CFS), proinflammatory cytokines, and functional autoantibodies targeting G-protein-coupled receptors (GPCR-AAbs). Here, we present a case report of successful healing of LCS with BC 007 (Berlin Cures, Berlin, Germany), a DNA aptamer drug with a high affinity to GPCR-AAbs that neutralizes these AAbs.

A patient with a documented history of glaucoma, recovered from mild COVID-19, but still suffered from CFS, loss of taste, and impaired capillary microcirculation in the macula and peripapillary region. He was positively tested for various targeting GPCR-AAbs. Within 48 h after a single BC 007 treatment, GPCR-AAbs were functionally inactivated and remained inactive during the observation period of 4 weeks. This observation was accompanied by constant improvement of the fatigue symptoms of the patient, taste, and retinal capillary microcirculation. Therefore, the removal of GPCR-AAb might ameliorate the characteristics of the LCD, such as capillary impairment, loss of taste, and CFS.

Source: Hohberger B, Harrer T, Mardin C, Kruse F, Hoffmanns J, Rogge L, Heltmann F, Moritz M, Szewczykowski C, Schottenhamml J, Kräter M, Bergua A, Zenkel M, Gießl A, Schlötzer-Schrehardt U, Lämmer R, Herrmann M, Haberland A, Göttel P, Müller J, Wallukat G. Case Report: Neutralization of Autoantibodies Targeting G-Protein-Coupled Receptors Improves Capillary Impairment and Fatigue Symptoms After COVID-19 Infection. Front Med (Lausanne). 2021 Nov 18;8:754667. doi: 10.3389/fmed.2021.754667. PMID: 34869451; PMCID: PMC8637609. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8637609/ (Full text)

Post-COVID-19 Tachycardia Syndrome: A Distinct Phenotype of Post-Acute COVID-19 Syndrome

Abstract:

In this paper we highlight the presence of tachycardia in post-acute COVID-19 syndrome by introducing a new label for this phenomenon—post-COVID-19 tachycardia syndrome—and argue that this constitutes a phenotype or sub-syndrome in post-acute COVID-19 syndrome. We also discuss epidemiology, putative mechanisms, treatment options, and future research directions in this novel clinical syndrome.

Source: Ståhlberg M, Reistam U, Fedorowski A, et al. Post-COVID-19 Tachycardia Syndrome: A Distinct Phenotype of Post-Acute COVID-19 Syndrome [published online ahead of print, 2021 Aug 11]. Am J Med. 2021;S0002-9343(21)00472-1. doi:10.1016/j.amjmed.2021.07.004  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8356730/ (Full text)

Use of Cardiopulmonary Stress Testing for Patients With Unexplained Dyspnea Post-Coronavirus Disease

Abstract:

Objectives: The authors used cardiopulmonary exercise testing (CPET) to define unexplained dyspnea in patients with post-acute sequelae of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection (PASC). We assessed participants for criteria to diagnose myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Background: Approximately 20% of patients who recover from coronavirus disease (COVID) remain symptomatic. This syndrome is named PASC. Its etiology is unclear. Dyspnea is a frequent symptom.

Methods: The authors performed CPET and symptom assessment for ME/CFS in 41 patients with PASC 8.9 ± 3.3 months after COVID. All patients had normal pulmonary function tests, chest X-ray, and chest computed tomography scans. Peak oxygen consumption (peak VO2), slope of minute ventilation to CO2 production (VE/VCO2 slope), and end tidal pressure of CO2 (PetCO2) were measured. Ventilatory patterns were reviewed with dysfunctional breathing defined as rapid erratic breathing.

Results: Eighteen men and 23 women (average age: 45 ± 13 years) were studied. Left ventricular ejection fraction was 59% ± 9%. Peak VO2 averaged 20.3 ± 7 mL/kg/min (77% ± 21% predicted VO2). VE/VCO2 slope was 30 ± 7. PetCO2 at rest was 33.5 ± 4.5 mm Hg. Twenty-four patients (58.5%) had a peak VO2 <80% predicted. All patients with peak VO2 <80% had a circulatory limitation to exercise. Fifteen of 17 patients with normal peak VO2 had ventilatory abnormalities including peak respiratory rate >55 (n = 3) or dysfunctional breathing (n = 12). For the whole cohort, 88% of patients (n = 36) had ventilatory abnormalities with dysfunctional breathing (n = 26), increased VE/VCO2 (n = 17), and/or hypocapnia PetCO2 <35 (n = 25). Nineteen patients (46%) met criteria for ME/CFS.

Conclusions: Circulatory impairment, abnormal ventilatory pattern, and ME/CFS are common in patients with PASC. The dysfunctional breathing, resting hypocapnia, and ME/CFS may contribute to symptoms. CPET is a valuable tool to assess these patients.

Source: Mancini DM, Brunjes DL, Lala A, Trivieri MG, Contreras JP, Natelson BH. Use of Cardiopulmonary Stress Testing for Patients With Unexplained Dyspnea Post-Coronavirus Disease. JACC Heart Fail. 2021 Dec;9(12):927-937. doi: 10.1016/j.jchf.2021.10.002. PMID: 34857177.  https://pubmed.ncbi.nlm.nih.gov/34857177/

Skeletal muscle alterations in patients with acute Covid-19 and post-acute sequelae of Covid-19

Abstract:

Background and methods: Skeletal muscle-related symptoms are common in both acute Covid-19 and Post-Acute Sequelae of Covid-19 (PASC). In this narrative review, we discuss cellular and molecular pathways that are affected, and consider these in regard to skeletal muscle involvement in other conditions, such as acute respiratory distress syndrome, critical illness myopathy and post-viral fatigue syndrome.
Results: Patients with severe Covid-19 and PASC suffer from skeletal muscle weakness and exercise intolerance. Histological sections present muscle fiber atrophy, metabolic alterations, and immune cell infiltration. Contributing factors to weakness and fatigue in patients with severe Covid-19 include systemic inflammation, disuse, hypoxemia, and malnutrition. These factors also contribute to post-ICU syndrome and ICU-acquired weakness, and likely explain a substantial part of Covid-19-acquired weakness. The skeletal muscle weakness and exercise intolerance associated with PASC are more obscure and different factors likely contribute. Direct SARS-CoV-2 viral infiltration into skeletal muscle or an aberrant immune system likely contribute. Similarities between skeletal muscle alterations in PASC and chronic fatigue syndrome deserve further study.
Conclusion: Both SARS-CoV-2 specific factors and generic consequences of acute disease likely underlie the observed skeletal muscle alterations in both acute Covid 19 and PASC.
Source: Soares, M., Eggelbusch, M., Naddaf, E., Gerrits, K., van der Schaaf, M., van den Borst, B., Wiersinga, W. J., et al. Skeletal muscle alterations in patients with acute Covid-19 and post-acute sequelae of Covid-19. Journal of Cachexia, Sarcopenia and Muscle. https://doi.org/10.17863/CAM.78509 https://www.repository.cam.ac.uk/handle/1810/331064

Post COVID-19 Syndrome in Patients with Asymptomatic/Mild Form

Abstract:

Post COVID-19 Syndrome (PCS) is a complex of various symptoms developing a month or more after the acute phase of the disease. The cases of PCS development among patients with asymptomatic/mild forms are frequently reported; however, the pathogenesis of PCS in this group of patients is still not completely clear. The publications about COVID-19 which were published in online databases from December 2019 to September 2021 are analyzed in this review. According to the analysis, PCS develops on average in 30-60% of patients, mainly among women. Fatigue, shortness of breath, cough, and anosmia were reported as the most common symptoms. The possible association between the described PCS symptoms and brain damage was revealed.

We assume the possibility of an alternative course of COVID-19, which develops in genetically predisposed individuals with a stronger immune response, in which it predominantly affects the cells of the nervous system, possibly with the presence of an autoimmune component, which might have similarity with chronic fatigue syndrome or autoimmune disautonomia. Thus, the gender (female) and the presence of anosmia during an asymptomatic or mild course of the disease can be predictive factors for the development of PCS, which can be caused by autoimmune damage to neurons, glia, and cerebral vessels.

Source: Malkova A, Kudryavtsev I, Starshinova A, Kudlay D, Zinchenko Y, Glushkova A, Yablonskiy P, Shoenfeld Y. Post COVID-19 Syndrome in Patients with Asymptomatic/Mild Form. Pathogens. 2021 Oct 30;10(11):1408. doi: 10.3390/pathogens10111408. PMID: 34832564. https://pubmed.ncbi.nlm.nih.gov/34832564/

Addressing the Long COVID Crisis: Integrative Health and Long COVID

Abstract:

While COVID-19 has killed millions of people globally, its lasting effects on the health and well-being of entire populations are just becoming clear. As many as 30% of those diagnosed with COVID-19 report continuing health-related problems, regardless of the severity of the initial infection. Given the infection rate in the world, that translates to between 5.4 and 17.9 million globally; about 700 000 in the US. The syndrome goes by many names; here we call it “long COVID.” Patients experience a wide range of symptoms, including serious organ system effects such as pulmonary fibrosis, myocarditis, new diabetes diagnoses, stroke, and other cerebrovascular events. They also experience ongoing pain, fatigue, and cognitive dysfunction. We suggest here that these patients require an integrative health approach, one that combines traditional medical management, non-pharmacological approaches, and behavior and lifestyle changes. Such an approach has been shown to be beneficial in other chronic illnesses such as fibromyalgia, chronic fatigue syndrome, and post-Lyme disease.

Source: Roth A, Chan PS, Jonas W. Addressing the Long COVID Crisis: Integrative Health and Long COVID. Glob Adv Health Med. 2021 Nov 16;10:21649561211056597. doi: 10.1177/21649561211056597. PMID: 34820152; PMCID: PMC8606968. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8606968/  (Full text)

Missteps in Creating a Long Haul COVID Case Definition

Excerpt:

Millions of individuals who have not recovered from the COVID virus are now dealing with a host of symptoms that are challenging our health care system. Many are experiencing significant problems in being recognized by health care workers as a real disorder, as for many of them, there are no biological markers of persistent illness. Just as with ME/CFS, we need to be sure that long haul COVID patients are not victimized first by the pandemic and then by the health care skepticism of their significant symptoms. We have the conceptual and theoretical grounding to develop clinical and research case definitions for those with persisting COVID symptoms. Patients must be instrumentally involved in all such efforts as failure to do so will only further delegitimize their condition.

Read the rest of this article HERE.

Source: Leonard Jason, Ph.D. and Vernita Perkins, PhD. Missteps in Creating a Long Haul COVID Case Definition. Psychology Today. Posted November 22, 2021

Post-COVID syndrome: the aftershock of SARS-CoV-2

Introduction:

Significant time has passed since the coronavirus disease of 2019 (COVID-19) pandemic outbreak, which led to severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection in hundreds of millions of individuals all around the globe. Accumulation evidence along the pandemic raised an association between the SARS-CoV-2 and autoimmunity (1). SARS-CoV-2 infected patients have a high presence of various autoantibodies (1). Moreover, numerous cases of new-onset of autoimmune-related disorders had been documented following the infection, including both organ-specific and systemic autoimmune diseases (1).

Recent studies focused on analyzing recovered COVID-19 patients demonstrate a broad spectrum of persistent and systemic symptoms, which had got the novel terms of “post-COVID syndrome”, “long COVID” and “chronic COVID-19” (2). This new disorder had led to the understanding that the absence of SARS-CoV-2 following COVID-19 does not necessarily mean full recovery (2).

Studies conducted follow-ups on COVID-19 patients indicate that 50-80% of symptomatic COVID-19 patients who recovered report non-specific symptoms, most commonly fatigue, headache, dyspnea, anosmia, and memory complaint (3–5). An Italian study that examined patients after a mean of 60 days from the first COVID-19 symptom on-set had found only 12.6% of the patients completely recovered; 55% had three or more symptoms, and worsened quality of life was observed among 44% of patients (3). Intriguingly, a systematic review and meta-analysis reported more than 50 possible long-term effects of the SAR-CoV-2 infection (6). The chronic phase of COVID-19 is also presented in objective findings; for example, a study conducted in Germany had found that 78% of recently recovered symptomatic COVID-19 patients had at least one chronic symptom; the most common abnormality was myocardial inflammation (60%) (4).

In this issue of the journal, Bertin D et al. documented a case of post-COVID syndrome with a one-year follow-up. This case describes persistent anti-cardiolipin IgG autoantibodies and eosinopenia with ongoing neurologic symptoms, demonstrating the long-term disease course of COVID-19 in many patients. Anti-cardiolipin autoantibodies and eosinopenia were defined as independent factors associated with COVID-19 severity, indicating their active involvement in the progression of the disease (7,8). Additional studies that included follow-up on recovered COVID-19 patients describe similar findings: patients report respiratory, neurologic, and non-specific symptoms, accompanied by the presents of autoantibodies (6). Interestingly, in a one-year prospective cohort study, neurocognitive symptoms frequency were found significantly higher in patients with ANA titer of ≥1:160 in comparison to <1:160 at 12 months post–COVID-19 symptom onset (9). It should be emphasized that the development of autoantibodies, which appears to be common following symptomatic SARS-CoV-2 infection, could act as the preclinical stage of many autoimmune diseases. Thus, the long-term autoimmune implications of SARS-CoV-2 could be severe.

Involvement of the autonomic nervous system dysfunction in post-COVID syndrome

Many viruses are well known to contribute to autoimmunity in genetically pre dispositioned individuals, such as those with human leukocyte antigen B27 (10). SARS-CoV-2 had been associated with numerous autoantibodies (1); some are believed to be the basis of the severe forms of COVID-19 (11). Furthermore, these autoantibodies, along with others, could lead to the multi-organ involvement of post-COVID syndrome, which manifests as broad and unspecific symptoms (6). Autoantibodies against the autonomic nervous system compounds are believed to be an incremental part of the post-COVID syndrome etiology. A study that included post-COVID syndrome patients had unidentified in all the subjects between 2 and 7 different functionally active autoantibodies that acted as receptor agonists, such as β2-adrenoceptor, α1-adrenoceptor, and angiotensin II receptor type 1 receptor (12). Functionally active autoantibodies such as those were present in several neurological and cardiac disorders, which might clarify the onset of neurological and cardiovascular symptoms of the post-COVID syndrome (12).

Post-COVID patients commonly have a clinical presentation similar to the encephalomyelitis/chronic fatigue syndrome (ME/CFS): severe fatigue, sleep disorders, cognition impairments, and different manifestations of autonomic dysfunction exacerbated in physical exercise (6,13–15). ME/CFS has an autoimmune etiology, which can be demonstrated by high titers of autoantibodies against autonomic receptors, such as beta-adrenergic and muscarinic receptors (16,17). These autoantibodies, similar to those found in patients with post-COVID symptoms, lead to unspecific symptoms due to autonomic nervous system dysregulation. In addition to ME/CFS, many features of the post-COVID syndrome are shared with fibromyalgia patients. It had been shown that 189/616 (30.7%) of COVID-19 recovered patients satisfied the American College of Rheumatology criteria for fibromyalgia, 43.4% of which were men (18).

Therapeutic options and vaccination

ME/CFS and fibromyalgia have solid evidence of dysregulated immune involvement (16,17,19). Moreover, current studies suggest that immunosuppression, such as monoclonal anti-CD20 antibody and cyclophosphamide, may benefit patients suffering from ME/CFS (20,21). Such immunosuppressive therapeutic options can assist in the depletion of B cells, thus reducing the functionally active autoantibodies linked to autonomic dysfunction. Beneficial effects had also been demonstrated by the use of anti-ß2 adrenergic receptor-binding immunoadsorption (22). It should be emphasized that such treatment can diminish other pathogenic antibodies that the medical community had not yet recognized. Due to the possible involvement of autoantibodies against the autonomic nervous system in the post-COVID syndrome, similar immunosuppressive options in these patients may be effective, thereby should be investigated.

Most individuals infected by SARS-CoV-2 are asymptomatic or experience mild symptoms (23,24). While the frequency of post-COVID syndrome in such individuals is still uncertain, it seems to be much lower than in symptomatic patients (9). Thus, avoiding COVID-19 with SARS-CoV-2 vaccination could prominently assist in preventing long-term symptoms of COVID-19, lower the prevalence of post-COVID syndrome and help overcome the pandemic. Nonetheless, even with the ongoing heist mass vaccination programs, the COVID-19 pandemic will leave its mark.

Conclusion

Due to the accumulating evidence of persistent post-infectious symptoms reported by numerous recovered patients, the focus of the medical and research communities might need to start shifting focus from the acute phase of COVID-19 to the chronic manifestations of the SARS-CoV-2 infection, referred to as by “post-COVID syndrome”. Post-COVID syndrome presents as non-specific symptoms, most commonly fatigue, headache, dyspnea, anosmia, and memory complaint, which is suspiciously similar to the infection-induced myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and fibromyalgia (15,18). As current studies suggest an involvement of immune-related dysfunction in the development of post-COVID syndrome, immunosuppressive therapeutic options could be beneficial in parallel to heist SARS-CoV-2 vaccination of the population (15,20,21).

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Article Info

Publication History

Accepted: November 9, 2021
Received: November 9, 2021

Publication stage

In Press Journal Pre-Proof

Identification

DOI: https://doi.org/10.1016/j.ijid.2021.11.020

Copyright

© 2021 The Author(s). Published by Elsevier Ltd on behalf of International Society for Infectious Diseases.