Case report
Figure 2 Days of illness and corresponding admissions, C reactive protein and treatment given. NSAID, non-steroid anti-inflammatory drug.
Broad-spectrum antibiotic treatment (piperacillin/tazobactam) was immediately administered intravenously at the second admis- sion, and this treatment was continued until synovial fluid culture came out negative. Treatment for reactive arthritis was also initi- ated at the first day of admission. This treatment consisted of the non-steroid anti-inflammatory drug (NSAID) ibuprofen 400mg orally three times a day and prednisolone 25mg orally once daily. As presented in figure 2, the anti-inflammatory drugs had a signif- icant effect on the CRP levels, and the patient improved clinically. After 5days, the patient had recovered and was able to walk again, and he was discharged from hospital. Prednisolone was given for 6days, and the patient still takes ibuprofen at the time of writing this report. OUTCOME AND FOLLOW-UP By January 2021, 4months after COVID-19 symptom debut, the patient has completely recovered from both COVID-19 and reac- tive arthritis. He has returned to work and reports that he is feeling well. DISCUSSION Reactive arthritis is a well-known complication after an infection. Often, it is related to infections in other body compartments with a mucosal entry such as the urogenital ( Chlamydia ) and digestive ( Campylobacter , Salmonella and Shigella ) systems. Individuals with the HLA-B27 allele or with a family history of spondyloarthritis apparently have an increased risk of developing reactive arthritis. 2 Since the emergence of COVID-19, only a few cases of post- COVID-19 reactive arthritis have been published. 6–9 There seems to be some common traits in these case reports. Joint inflam- mation and elevated CRP appeared approximately 1 week after COVID-19 symptoms had dissolved. Age span in the other cases was 47–73 years, and all cases involved were men. All cases were affected in the lower extremities including the knees, 6 9 ankle 7 and metatarsophalangeal and interphalangeal joints. 8 However, one case also had involvement of the wrist and shoulder. Recommended first-choice treatment for reactive arthritis caused by other pathogens is NSAIDs and glucocorticoids. If these agents are insufficient, disease-modifying antirheumatic drugs may be attempted. In our case and two of the previ- ously reported cases, 7 8 NSAID and glucocorticoid therapy was successful. One patient received etoricoxib and intra-articular
of polynuclear cells and a minor part of mononuclear cells were detected. There were no crystals when viewed in polarised microscope. Both synovial fluid and blood cultures were nega- tive. SARS-CoV-2 PCR was not performed on joint fluid. To investigate the presence of other rheumatological diseases, we measured rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies—both were within normal range. Also, the patient was HLA-B27 negative. Other negative analyses were HIV testing, antinuclear antibodies, antimyeloperoxidase antibodies, antiproteinase 3 antibodies and antibodies against the glomerular basal membrane. DIFFERENTIAL DIAGNOSIS At the second admission, the patient presented with inflamed joints shortly after a viral infection. As other viruses are well known to cause reactive arthritis, we immediately suspected this diagnosis from the anamnesis. There are no validated diagnostic criteria or definitive laboratory tests for reactive arthritis. The diagnosis is based on a clinical assessment following the exclu- sion of other differential diagnoses. 2 Swollen inflamed joints are also seen in septic arthritis, but this condition most often presents as monarthritis. 3 Before giving antibiotic therapy, we aspirated synovial joint fluid. We intended to perform a synovial fluid leucocyte count because this may give a hint to the cause of the inflammation. Unfortunately, as mentioned above, the vial sent for analysis was lost. Synovial fluid and blood cultures were negative, and we thus ruled out septic arthritis. Rheumatoid arthritis (RA) may also cause sterile inflamed joints; nevertheless, several aspects made this diagnosis less likely. Our patient had not previously experienced swollen joints, and we found it unlikely that such an autoimmune disease would be revealed shortly after treatment with dexamethasone (see the Treatment section). The serological tests for RF and anti-CCP were both negative. The patient had involvement of one knee and both ankles. In RA, the typical sites of joint involvement at disease onset are the smaller joints in the hands and feet with a symmetrical pattern, although the condition may present differ- ently. Finally, a large proportion of patients with RA have family members who are also affected; in this case, there was no history of autoimmune diseases in the family. Altogether, we did not find that the patient had RA. TREATMENT Initially, the patient presented with classic COVID-19 symptoms requiring oxygen therapy. Blood saturation was satisfactory at 95% by high-flow oxygen (up to 60L/min and 88% oxygen), and mechanical ventilation was avoided. At first day of admis- sion, we initiated antiviral therapy with 200 mg intravenous remdesivir followed by 100 mg daily for a total of 5 days. 4 The patient also received 6 mg intravenous dexamethasone for 10 days 5 in line with Danish and most international guidelines at this particular time of the pandemic.
Learning points
► ► Reactive arthritis may occur after COVID-19. ► ► Clinical and laboratory presentation of reactive arthritis triggered by COVID-19 resembles reactive arthritis due to other pathogens. ► ► Non-steroid anti-inflammatory drugs and prednisolone have successfully been used for treatment.
Hønge BL, et al . BMJ Case Rep 2021; 14 :e241375. doi:10.1136/bcr-2020-241375
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