Since the global coronavirus disease 2019 (COVID-19) pandemic began, findings indicate that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) might induce autoimmune disorders. Thrombotic thrombocytopenic purpura (TTP) is a devastating disease if not emergently treated. It presents with severe thrombocytopenia, microangiopathic hemolytic anemia, and neurologic findings with or without renal insufficiency. The antibody-mediated reduced activity of the disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) induces the accumulation of ultrahigh-molecular-weight multimers of von Willebrand factor, leading to platelet aggregation and thrombosis. TTP can be an unusual presentation of COVID-19 disease mediated by the virus-induced immune response. We report a case of a healthy young patient presenting with the classic TTP pentad a few days after a diagnosis of COVID-19 confirmed by a positive SARS-CoV-2 RT-PCR test. The patient was initially treated with high-dose methylprednisolone and fresh frozen plasma until she was transferred to a tertiary care facility and plasma exchange was available. She evolved with a malignant ischemic vascular accident and was declared brain-dead 24 hours after the first plasma exchange section.

Background:Patients with psoriatic arthritis (PsA) experience substantial functional impairment, which impacts on health-related quality of life.1Evidence from randomized clinical trials (RCTs) suggests better patient-reported functional outcomes when lower disease activity is achieved.2,3,4Objectives:To evaluate the impact of achieving DAPSA remission (REM) or low disease activity (LDA) on long term function measured by HAQ-DI. To verify predictors of achieving a minimum clinically important difference (MCID) in HAQ-DI (≤ -0.35).Methods:This is a longitudinal analysis of a real-life retrospective cohort. Inclusion criteria were adult patients fulfilling CASPAR criteria for PsA with at least 4 years of follow-up in the PsA Clinic. Demographic and clinical data were extracted from electronic medical records. Comparison of HAQ-DI variation between patients with DAPSA REM/LDA and those with moderate/high disease activity was performed using generalized estimating equation (GEE), adjusted by Bonferroni test. Correlation between HAQ-DI and DAPSA was analyzed by Spearman correlation method. A multivariate hierarchical regression model was applied in order to evaluate predictors of achieving a MCID in HAQ-DI scores.Results:Seventy-three patients were included in the analysis, of which 58.9% were female, with a median (25/75th) of 8 (3-15) years since PsA diagnosis and a mean follow up time of 6.2±1.2 years. In total, 37% of patients (N=27) presented a MCID in HAQ-DI during the follow-up. Function measured by HAQ-DI was determined by PsA disease activity measured by DAPSA (interaction test: p <0.0001) (Figure 1). A moderate and statistically significant correlation between ΔDAPSA and ΔHAQ-DI was observed (rs= 0.60; p<0.001) (Figure 2), demonstrating that a decrease in PsA disease activity was associated to improvement in function. Only patients in DAPSA REM demonstrated a constant declining in HAQ-DI scores during the 6 years of follow-up (Figure 1). White ethnicity and older age at baseline were predictors for not achieving MCID in HAQ-DI (RR 0.33 95% CI 0.16-0.67, p=0.002 and RR 0.96 95% CI 0.93-0.98, p<0.0001, respectively), while higher scores of HAQ-DI at baseline were predictors of achieving a MCID (RR 1.71 95%CI 1.12-2.60, p=0.013).Figure 1.Variation in HAQ-DI according to PsA disease activity measured by DAPSAFigure 2.Correlation between changes in PsA disease activity (ΔDAPSA) and changes in functional indices (ΔHAQ-DI) over three years of follow-upConclusion:In PsA, patients who maintained DAPSA REM/LDA over time had better long term functional outcomes. Higher HAQ-DI scores at baseline, non-white ethnicity and younger age were predictors for achieving a clinical significant improvement in HAQ-DI.References:[1]Mease P et al. Semin Arthritis Rheum. 2018 Dec;48(3):436-448.[2]Coates, LC et al. The Lancet. 2015 Dec; 386, 19-26.[3]Aletaha D et al. Ann Rheum Dis. 2017;76(2):418-421.[4]Kavanaugh A et al. Annals rheum Dis 2014; 73: 1689-94.Median HAQ-DIFollow-up in yearsDisclosure of Interests:Larissa Vargas Cruz: None declared, Júlia Boechat Farani: None declared, Júlia Rabello Costa: None declared, Franciele Menegat: None declared, João Victor Andrade Águas: None declared, Bruna Ruschel: None declared, Andrese Aline Gasparin: None declared, Claiton Brenol: None declared, Charles Kohem Grant/research support from: This work was sponsored by the regional society of rheumatology (Sociedade de Reumatologia do Rio Grande do Sul)., Penelope Palominos Grant/research support from: This work was sponsored by the regional society of rheumatology (Sociedade de Reumatologia do Rio Grande do Sul).