BREAKING! News-COVID-19: Italian Researchers Report First European Documented Case Of SARS-CoV-2 Induced Arthritis In A COVID-19 Patient
Source: News-COVID-19 Oct 07, 2020 4 years, 2 months, 2 weeks, 21 hours, 17 minutes ago
News-COVID-19: Italian researchers from the University Hospital In Torino report of the first European documented case of viral induced arthritis in a 58 year patient who was infected with the SARS-CoV0-2 coronavirus that causes the COVID-19 disease.
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Arthralgia is a symptom in which there are joint pains and such a viral induced arthritis if common in most viral infections.
The case report was published in the journal: Lancet Rheumatology
https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913(20)30348-9/fulltext#%20
Roughly about 15% of patients with COVID-19 present with arthralgia at some point, but not much is known about the nature or presentation of such rheumatic manifestations of this infection.
It is well-known that most viral infections are associated with acute joint inflammation and pain, including single joint involvement with viruses such as the hepatitis B virus, hepatitis C virus, parvovirus, Epstein-Barr virus, and HIV.
Zika and Chikungunya viruses are also commonly associated with post-viral arthralgia.
In reality, about one percent of all cases of acute inflammatory arthritis have a preceding viral infection history. As a result, even though challenging to trace, such a history should be sought in all such patients with inflammation of multiple joints and of sudden onset.
It has been reported that especially in women and older patients; rheumatoid arthritis is present at a higher prevalence in association with circulating viral respiratory infections.
Hence suggests that these infections present an environmental risk factor for this condition.
Already it is known is now that the SARS-CoV-2 virus binds to the host cell receptor, the angiotensin-converting enzyme-2 (ACE-2), to gain entry to and infect the host cell. The virus is then detected by Toll-like receptor-7 (TLR7) via several fragments of the viral genome.
The TLR7 receptor is found not only within immunological cells but very strongly in the lung and bronchial tissue. This leads to early recognition of the virus in the very tissue that is most susceptible to it and which harbors the initial infection.
The subsequent result is the activation of other cellular signaling pathways such as c-Jun N-terminal kinase and NF- κB signaling which in turns, leads to the secretion of cytokines such as the pro-inflammatory IL-6 and IL-12p40.
Hence this scenario makes it plausible that COVID-19 patients might have features of systemic inflammation, including viral arthritis.
The research study is aimed at assessing the role of this SARS-CoV-2 coronavirus in the etiology of inflammatory arthritis.
A key method in the confirmation of this diagnosis is serologic testing.
Interestingly however, in viral arthritis, cross-reactive autoantibodies such as the rheumatoid factor (RF) or antinuclear antibody (ANA) which are involved in the pathogenesis could yield a low-titer false-positive test for COVID-19.
Hence besides serological te
sting, the epidemiology of the disease, along with the clinical characteristics, must be analyzed to arrive at such a diagnosis.
Importantly some of the determining features of viral arthritis include arthritis of more than one joint, either symmetric or asymmetric, which responds well to non-steroidal anti-inflammatory drugs (NSAIDs); early onset of arthritis within the first weeks of COVID-19 symptom onset; and the self-limited nature of the illness.
This case report discusses arthritis in a 58-year-old white woman with COVID-19 of less than severe intensity. She was treated with paracetamol. The first test for COVID-19 was at 25 days from the onset of infection when she reported joint pain, fever, cough, and nausea, along with disturbances of taste and diarrhea. She had a nasal swab taken for testing by reverse transcriptase-polmerase chain reaction (RT PCR).
This patient then had inflammation of an ankle joint, and further laboratory tests showed a small rise in the inflammatory marker CRP, a drop in the lymphocyte count to near the lower limit of normal and normal liver and kidney function.
The female patient was tested for numerous autoantibodies, including ANA, anti-extractable nuclear antigen, anti-ds-DNA, RF, and anti-CCP antibodies, all of which were negative. HLA-B27 was performed to rule out other genetic predispositions to inflammation of the joints and spinal column.
A detailed ultrasound examination showed thickening of the synovial membrane of the ankle, with inflammation of the Achilles tendon. Other tendons were not obviously inflamed. The patient was then treated with the NSAID ibuprofen. This produced significant alleviation of pain and inflammation.
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Interestingly at 30 days from the first symptom, the nasal swab was negative for SARS-CoV-2, as was a second swab at 7 days from the first. By this time, her symptoms had resolved.
Even though the joint pain went down, the ultrasound repeat examination continued to show evidence of inflammation, specifically synovitis. The patient was still in follow up for joint surveillance.
This was the first document case of viral induced arthritis by the SARS-CoV-2 coronavirus in a COVID-19 patient in Europe. There have been other such documented cases in China and in Thailand and doctors elsewhere including in the United States are reporting of more such emerging cases.
https://pubmed.ncbi.nlm.nih.gov/32109013/
and
https://pubmed.ncbi.nlm.nih.gov/32222804/
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