Platypnoea-orthodeoxia syndrome (POS) is a rare disorder and its pathophysiology has puzzled clinicians for years. Few cases of POS are described in COVID-19 patients in the literature, with a high variability of conditions related to the syndrome.  In this article, we report the case of a patient admitted to our hospital for SARS-CoV-2 interstitial pneumonia, who developed POS during the hospitalization.

Background/Purpose Anti-carbamylated protein antibodies (anti-CarP) were detected in a large cohort of patients with Systemic Lupus Erythematosus (SLE) in correlation with erosive arthritis but not with disease activity indexes. In animal models, T-cells may be activated by carbamylated epitopes playing a role in the development of arthritis. The imbalance between circulating regulatory (Treg) and CD28-effector T-cells was described in active SLE patients, explaining its involvement in disease's pathogenesis. Actually, no data are available about the possible correlation with these T-cell subpopulations and anti-CarP levels in SLE. Methods Eight SLE patients with a median (10th-90th percentile) SLEDAI-2K=0 (0-4), anti-dsDNA levels=34.1 (15.6-427.4) UI/ml (nv<7), SDI=1 (0-1.3) were enrolled. Serum anti-CarP levels were evaluated using a home-made ELISA (nv<340 AU/ml) and peripheral blood T cell immunophenotyping was done using Flow Cytometry (Beckman Coulter). Treg were defined as CD4+CD127lowCD25high T-cells. Results Enrolled patients showed levels of anti-CarP=189.38 (93.5-341.1) AU/ml, Treg=2.2 (% of CD4+), CD4+CD28-=7.7 (4.8-22.5) (% of CD4+) and CD8+CD28-=30.3 (17.2-35.6) (% of CD8+). Analyzing possible correlations among different T-cell subtypes and anti-CarP levels, a significant inverse correlation was found between these autoantibodies and CD4 +CD28-T cells (r=-0.8, p<0.01; Spearman rank correlation). No correlations were found between autoantibodies and other T-cell subpopulations or disease activity/damage indexes. Conclusions In a small cohort of patients with serologically active SLE, anti-CarP autoantibodies were found as negatively correlated to circulating CD4+CD28-T-cells, which were described in association with disease damage, independently of age, gender, disease duration and activity. This suggest a potential role of anti-CarP as marker of SLE with a minor extent of T-cell activation and, consequently, with a possible better prognosis.

Background/Purpose Anti-carbamylated protein antibodies (anti-CarP) have been described not only in Rheumatoid arthritis but in other systemic autoimmune diseases. Recently, they have been reported in different cohorts of Systemic Lupus Erythematosus (SLE) with a prevalence of 9-28% 1-4 in patients selected with arthritis/arthralgias. Anti-CarP have been proposed as a marker of erosive arthritis in SLE. 4 The aim was to assess the prevalence of anti-CarP in SLE patients from a single center cohort and their association to clinical and laboratory data. Methods Serum anti-CarP levels were evaluated using a homemade ELISA (nv<340 AU/ml). Clinical data were obtained from clinical charts. Results Complete clinical and serological data were available for 314 consecutive patients: 85 (27%) positive and 229 (73%) negative. No association was found among CarP+ and arthritis/arthralgias. CarP+ patients presented an earlier disease onset compared with CarP-(mean 28±11vs32±14.7, p=0.001), a trend towards a higher prevalence of xerophtalmia (36% vs 26.5%, p=0.075;OR:1.62,95%CI:0.95-2.75) and extractable nuclear antigen positivity (67% vs 54%,p=0.064; OR:1.65,95%CI:0.97-2.8). Interestingly, patients anti-CarP+ less frequently experienced class IV glomerulonephritis (12%vs 21.8%,p=0.05;OR:0.53,95%CI:0.26-1.08). Fifty-six patients evaluated were treated with anti-Blys therapy and longitudinally sera were available (T0,T6,T12). At baseline anti-CarP were positive in 10 (17.8%) and titre significantly decreased at T6 (p=0.006) and T12 (p=0.01). Negative seroconversion was observed in 7/10 sera. Conclusions The prevalence of anti-CarP antibodies found in our unselected cohort is in line with to what previously reported. In our hands, anti-CarP antibodies seems to identify a less severe form of SLE, with less kidney involvement and probably in overlap with Sjogren disease. Further studies are needed in order to be able to identify a possible role for this autoantibody.