359 e-Letters

  • Correspondence to 'Impact of the COVID-19 pandemic on morbidity and mortality in patients with inflammatory joint diseases and in the general population: a nationwide Swedish cohort study' by Bower et al.

    Article type: Letter to the Editor

    Correspondence to 'Impact of the COVID-19 pandemic on morbidity and mortality in patients with inflammatory joint diseases and in the general population: a nationwide Swedish cohort study' by Bower et al.

    Pei-En Kao1, I-Kuan Wu1, Jung Chi Chiang1, Amy Ker1, James Cheng-Chung Wei, MD, PhD.2,3,4
    1 School of Medicine, Chung Shan Medical University
    2 Department of Allergy, Immunology & Rheumatology, Chung Shan Medical University Hospital
    3 Institute of Medicine, College of Medicine, Chung Shan Medical University
    4 Graduate Institute of Integrated Medicine, China Medical University, Taichung, Taiwan.

    Correspondence author:
    James Cheng-Chung Wei, MD, PhD.
    No. 110, Sec. 1, Jianguo N. Rd., South District, Taichung City 40201, Taiwan. (TEL)+
    886 4 24739595 #34718.
    E-mail: jccwei@gmail.com

    Conflicts of interest: None to declare

    Funding acknowledgement: Not applicable.

    Total word count: 311 words, table: 0

    With great interest, we read the article of Bower et al investigating whether patients with inflammatory joint disease (IJDs) is associated with the different all-cause mortality and COVID-19-related outcomes.1 However, some points need to be discussed.
    First and foremost, we notice that there are other unmeasured factors such as occupation and smoking s...

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  • Rujittika Mungmunpuntipantip and Viroj Wiwanitkit Response

    We thank Mungmunpuntipantip and Wiwanitkit for their response and comments on our manuscript and their local experience. Of note, the serologies of the cohort we presented were tested repeatedly during the hospitalization, not only at admission. Also, for reference, the days from symptom onset to ICU admission are presented in Table 3 of the manuscript".

  • COVID-19, autoantibody and clinical outcome

    COVID-19, autoantibody and clinical outcome
    Rujittika Mungmunpuntipantip1,Viroj Wiwanitkit2
    1.Private Academic Consultant, Bangkok Thailand
    2. Dr DY Patil University, Pune, India
    Rujittika Mungmunpuntipantip
    Private Academic Consultant, Bangkok Thailand
    Email: rujittika@gmail.com

    Dear Editor, we would like to share ideas and experience on “Anticardiolipin and other antiphospholipid antibodies in critically ill COVID-19 positive and negative patients [1].” Trahtemberg et al. concluded that “Positive APLA serology was associated with more severe disease regardless of COVID-19 status [1].” In the study, the laboratory data on the day of admission are referred to. In individual patient, the period of illness before admission might be different and whether this period affects affect clinical outcome or not is an interesting question. In COVID-19, the development of COVID-19 is reported and the rate of positive autoimmunity is different in different reports [2]. In our settings, positive autoantibody is detectable after complete recovery from COVID -19 among patients with history of previously autoantibody negative. Hence, it might be difficult to interpret the clinical association of positive autoantibody at first admission.

    Conflict of interest

    1. Trahtemberg U, Rottapel R, Dos Santos CC, Slutsky AS, Baker A, Fritzler MJ. Anticardi...

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  • Correspondence on "Factors associated with COVID-19–related death in people with rheumatic diseases: results from the COVID-19 Global Rheumatology Alliance physician-reported registry"

    Strangfeld et al (1) recently reported on the association between death of patients affected by inflammatory rheumatic diseases and COVID-19 and a series of factors, the most notable of which were advanced age, specific comorbid conditions, and, surprisingly, sulfasalazine. This finding differed from those for other drugs in the overall model and in all the subgroups, with an odds ratio that was only exceeded by
    that of rituximab. However, the finding only applied to those with a current or previous history of smoking.
    While we should not attribute causality to the association between sulfasalazine and COVID-19–related death, and despite the limitations arising from selection bias due to the voluntary nature of the registry in the study under discussion, we need to find an explanation for this association, especially given the coincidence with another series discussed by Strangefeld et al (1), where COVID-19 was more severe in patients treated with sulfasalazine or its metabolite 5-ASA for inflammatory bowel disease.
    In their attempt to provide an explanation for their findings, the authors state that the choice of sulfasalazine over other DMARDs in groups of patients who are affected by more comorbid conditions and are therefore more likely to die is a confounding factor. However, this does not explain the findings in the series of patients with inflammatory bowel disease the authors themselves comment on.
    We believe there may be a reason for this...

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  • Correspondence on “New EULAR/ACR 2019 SLE Classification Criteria: defining ominosity in SLE” by Whittall Garcia et al

    We read with interest the study by Whittall Garcia and colleagues (1) which reports on the ominosity associated with an EULAR/ACR-2019 SLE classification score of 20 or greater.

    While the correlation of score and disease severity is interesting, they do not report any association with health-related quality of life. We applied the EULAR/ ACR-2019 criteria to a cross-sectional cohort of 103 patients with SLE (92.2% female) with a mean [SD] age and disease duration of 44.8 [12.8] years and 12.9 [10] years respectively, which have previously been described.(2, 3) Of these patients, 37 (36%) had a EULAR/ ACR-2019 score of ≥20; defining ‘high ominosity’. The SF-36 physical and mental components score were calculated, and normalised against the UK population. The mean [SD] physical and mental summary scores were reduced in this cohort (31.6 [16.0] and 45.3 [10.5], respectively). We found no difference in either score between those who scored ≥20 and those who scored <20, in the physical components score (OR 1.0, CI 0.98-1.04, p=0.67) and mental components score (OR 1.0, CI 0.95-1.04, p=0.85). This suggests that even though some patients may have a ‘less severe’ disease trajectory and fewer number of manifestations at baseline, their quality of life may, nevertheless, be impaired. We postulate that this may be related to the ‘illness identity’ associated with being diagnosed with a rare chronic health condition, and concern over the clinical consequences of this diseas...

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  • is it too early for patients with asymptomatic hyperuricemia recommended to control serum uric acid at 5-6 mg/dL?

    Dear Editor:
    In a recently published article in Ann Rheum Dis, Dr Ruriko Koto et al [1] performed a retrospective study to report the potential benefits of serum uric acid levels (sUA) control for preventing gout flare in subjects with asymptomatic hyperuricaemia. This topic is very meaningful because the current guidelines vary from country to country [2-4]. The study found that the occurrence of gout flare in asymptomatic hyperuricaemia and gout tended to be lower for patients who were prescribed ULT and achieved sUA ≤6.0 mg/dL than for controls. I appreciate the authors for designing such an excellent article, but I still want to make the following perspectives.
    Firstly, I don’t see any data about how many end-point events can be covered by the claims database? In other words, whether all patients with gout flare will fill out an insurance claim form? As we know, most of the drugs used to treat gout flare are over-the-counter drugs. For some patients with gout flare, they may choose to purchase drugs for treatment without being recorded in the claims database. It may result in missing some end-points for not combining the pharmacy data.
    Secondly, the authors only used two points of sUA to define the sUA control using annual medical check-ups data, which may cause misclassification for grouping because sUA is affected by many factors, such as a high-purine diet. Using multiple consecutive sUA testing data to define sUA control may obtain more accurate g...

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  • Anti-nuclear antibodies for SLE classification versus diagnosis: titer-specific likelihood ratios to the rescue. Response to Aringer M et al. Ann Rheum Dis. 2021 Feb 10:annrheumdis-2020-219373

    Anti-nuclear antibodies for SLE classification versus diagnosis: titer-specific likelihood ratios to the rescue. Response to Aringer M, Brinks R, Dörner T, et al. European League Against Rheumatism (EULAR)/American College of Rheumatology (ACR) SLE classification criteria item performance. Ann Rheum Dis. 2021 Feb 10:annrheumdis-2020-219373.

    Antinuclear antibodies (ANA) are important laboratory markers for the diagnosis and classification of systemic lupus erythematosus (SLE). In the 2019 European League Against Rheumatism (EULAR)/American College of Rheumatology (ACR) classification criteria for SLE, ANA with titer ≥1:80 are an entry criterion [1].
    Even though ANA 1:80 are highly sensitive for SLE, they have a low specificity. This has recently been reinforced by Aringer et al. [2] who analyzed the performance of the individual items included in the 2019 EULAR/ACR classification criteria for SLE on a large group of SLE patients (n=1197) and non-SLE disease controls (n=1074), including patients with other connective tissue diseases (two-thirds of the controls). In this study, ANA with titer ≥1:80 were highly sensitive (99.5%), but only 19.4% specific for SLE [2]. As ANA are an entry criterion for the 2019 EULAR/ACR classification criteria, the low specificity of ANA for SLE does not affect the specificity of the 2019 SLE classification criteria. An important item that conferred specificity to the 2019 SLE classification was the attribution rule [2]. The a...

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  • SARS-CoV-2 vaccine : a trigger of rheumatoid arthritis ?


    We read with great interest the letter from M. Barbhaiya et al. on systemic rheumatic disease flares after SARS-Cov-2 vaccination.[1] Whether COVID-19 vaccines could trigger rheumatoid arthritis remains unclear. To date, only few cases have been reported on this topic.[2,3]

    We report the case of a 44-year-old man, working as a teacher, without medical history or treatment, who had arthralgia affecting the hands and feet without joint swelling since early 2020. There was no clinical synovitis and the joint ultrasound showed doppler positive bursitis of the 3rd bilateral interdigital space. Acute phase reactant (C-reactive protein and sedimentation rate) were in the normal range, rheumatoid factors and antinuclear antibodies were negative unlike anti-CCP (48 UI/ L, uppper limit of normal [ULN] 3UI/L). X-rays of the hands and forefoots were normal. Treatment with hydroxychloroquine 200 mg twice a day was started in November 2020 associated with corticosteroid injections in each bursitis with a good improvement at three months.

    In early May 2021, the patient received a first injection of the anti SARS-CoV-2 BNT162b2 vaccine (BioNTech-Pfizer). A week later, he reported a flare of rheumatoid arthritis (RA) with pain and synovitis of 2 proximal interphalangeal joints and the right wrist, and pain in both shoulders with morning stiffness. DAS28-CRP was 4.2, DAS28-ESR 3.7. No skin rash was observed. Treatment with methotrexate at a dose of 20 mg/week subcu...

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  • A closer look at the enthesis using ultrasound

    We read the editorial by Filippucci et al., entitled "Ultrasound definition of enthesitis in spondyloarthritis and psoriatic arthritis: arrival or starting point?" with great interest. The authors eloquently discuss the challenges with the existing scoring methods and propose solutions (1). We would like to raise additional points that we believe are necessary to improve the assessment of enthesitis using ultrasound.

    Before the introduction of ultrasound to the field, enthesitis was determined as present or absent, based on the physical exam. Therefore, only prevalence could be compared between patient groups. Ultrasound allows precise phenotyping of the entheseal changes. The ability to accurately characterize anatomical changes within the entheseal soft tissue and on the surface of the bone, detect abnormal vascularisation and further categorize the two opposite bony changes (erosion vs new bone formation) brought a different perspective on the understanding of enthesitis. Despite some similarities between psoriatic arthritis (PsA) and other spondyloarthritis (SpA) subtypes, clear distinctions also exist (2). From the enthesitis perspective, patients with PsA have larger enthesophytes (bony spurs) at the entheseal insertions than ankylosing spondylitis (AS), despite similar levels of sonographic inflammation (3). Supporting that observation, psoriasis is shown to be an independent risk factor for enthesophytes with Axial SpA (4). Similar findings have lo...

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  • Could discontinuing JAKi’s in the event of SARS-CoV-2 infection be harmful?

    Sparks et al. (1) are to be congratulated on an important and timely study. They found that the use of JAKi was associated with worse outcome of Covid-19 infection, and they interpret this as a harmful effect of the treatment in that particular setting. But this question deserves further consideration. Assuming that the observation is correct, what could the mechanism be? As the authors correctly point out, some JAKis did show benefits for patients with severe Covid-19 infection (2, 3). We therefore propose an alternative explanation of the observed data.

    Some guidance documents (4,5), and certainly medical practice traditions, frequently have patients discontinue immunomodulatory treatments when a potentially severe infection is diagnosed, and it seems safe to assume that the vast majority of patients in the study did, in fact, stop their treatment when they became aware of the infection. While this would of course apply to all antirheumatic therapies, there are important differences in the impact this might have. Biologicals have half-lives in the order of weeks, and the effect of stopping the treatment is therefore limited in the acute setting. For MTX, pharmacodynamic aspects also lead to a long latency in the impact of discontinuing the drug. In contrast, JAKi have short half-lives and discontinuing the treatment will almost immediately lead to the re-activation of the relevant signaling pathways.

    We therefore propose, as an alternative possible explan...

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