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Nephrology Dialysis Transplantation ; 37(SUPPL 3):i152-i153, 2022.
Article in English | EMBASE | ID: covidwho-1915685


BACKGROUND AND AIMS: Immunosuppressed patients are in general less likely to achieve a detectable antibody response to SARS-CoV-2 after the primary doses of vaccine administration. However, there are limited data for the effect of a third booster dose in this patient population, especially for those with vasculitides and renal involvement treated with rituximab (RTX). METHOD: We retrospectively assessed the antibody responses to SARS-CoV-2 vaccination, after completion of the primary vaccine series (two doses) and after the booster third dose, in patients with vasculitides and renal involvement. IgG antibodies to the spike protein S1 subunit of SARS-CoV-2 were measured using ELISA >1 month after completion of the primary vaccination series (two doses of Pfizer or AstraZeneca vaccines) and 15-30 days after the third booster dose (Pfizer, given 3-6 months after the second dose). RESULTS: We included 20 patients with vasculitis [AAV, n = 16 (80%), IgAV, n = 4 (20%)] and renal involvement. All patients received immunosuppressives, including RTX (80%), MMF/AZA (15%), cyclophosphamide (5%), while half of patients were on glucocorticoids. The seroconversion rate after the primary two doses (Pfizer n = 8/16, Astra-Zeneca n = 1/1) was 53%, which increased to 67% after the third booster dose (Pfizer, n = 12/18). Similarly, the median antibody titers increased from 451 U/mL [interquartile range (IQR) 81-10.845] after the second dose to 1016 U/mL (IQR: 64- 37.568) after the booster dose. Regarding patients treated with RTX, the respective response rates after the second and third dose were 58% and 62%. Seropositive patients after the third dose tended to have lower previous cumulative exposure to RTX compared with seronegative ones (4.55 versus 5.5 g, P = .62, respectively). No vaccine side effects or disease relapses were noted after the three vaccine doses. CONCLUSION: In our patient cohort with systemic vasculitis and renal involvement treated mainly with RTX, a third booster vaccine dose increased the seropositivity rate from 53% to 67%. Nevertheless, one-third of patients did not achieve seroconversion. Whether a fourth booster dose could benefit these patients is still unknown.

Rheumatology (United Kingdom) ; 61(SUPPL 1):i35-i36, 2022.
Article in English | EMBASE | ID: covidwho-1868366


Background/Aims Ultrasound (US) imaging has become established in clinical Rheumatology practice to aid diagnosis and monitoring of inflammatory arthritis (IA). We firstly wanted to explore the utility of US in the assessment for active synovitis in subjects with known IA, but clinically uncertain disease control. Secondly we set out to compare this with the diagnostic contribution of US in patients presenting with new inflammatory joint symptoms and uncertain clinical synovitis. Methods Two contemporaneous samples of subjects were selected from consecutive, pre-Covid, Rheumatology Consultant-delivered Ultrasound Clinic lists in our department: (i) subjects with known IA where clinical disease activity was uncertain, and (ii) subjects without know IA who had symptoms with inconclusive signs of suspected IA. Both grey scale and power Doppler US imaging was used to determine a sonographic conclusion of active IA being present, absent or equivocal. Treatment changes/ decisions were ascertained from the next available clinic letter to explore diagnostic consequences following US. Results (i) In the sample of subjects with known IA (n=30, mean age 53.9 years, 63% female, RA 76.7%, all on DMARDs [20% biologics]), 43.3%(n=13) had US evidence of active IA, and 50% of inactive IA (and the remainder reported as equivocal). At clinic review (n=30) only 6 of 13 subjects with active US IA had their DMARD treatment escalated (all within same DMARD) and 5 out of 15 subjects with inactive US IA their DMARD de-escalated. (ii) In the sample of subjects with suspected IA (n=30, mean age 51.5 years, 73% female): 16.7% (n=5) had US evidence of IA and 77.7% not (and remainder reported as equivocal). At the next clinic review seven patients were commenced on DMARDs: three patients with IA on US, and 4 without. Conclusion In our department, Rheumatology clinicians appear to be referring for diagnostic US in known IA from a situation approaching clinical equipoise which would suggest optimum referral practice. If we assume that this clinical equipoise also applies to the assessment and referral practice of new patients with arthralgia but uncertain clinical synovitis, our diagnostic sensitivity of US is approximately 16.7%, meaning: six patients with suspected IA need referral for US to identify one with sonographic IA. Irrespective of this, we observed that the sonographic diagnosis in known or suspected IA is commonly not followed by a concordant treatment decision, suggesting that the US diagnosis forms only part of the diagnostic 'jigsaw' decision process.