Acute hospitalization in a cohort of patients with systemic sclerosis: a 10-year retrospective cohort study.

This study aimed at analysing the causes and predictors of acute hospitalization and mortality in a cohort of SSc. Retrospective analysis of all acute hospital admissions of SSc patients fulfilling the 2013 EULAR/ACR Classification Criteria, from a single-centre cohort of 95 patients, between 2010 and 2020. The total number of SSc patients registered in our hospital, in this period, was 123. Clinical data were collected from medical files of our institution and from the National Healthcare Registry platform. 53 patients needed acute hospitalization, in a total of 164 admissions. The most frequent causes for admission were: infectious diseases [27%; 70% due to pneumoniae, of which 74% had SSc-associated interstitial lung disease (ILD)], cardiac disease (16.5%), peripheral vascular disease [12.8%; all due to digital ulcers], pulmonary hypertension (PH) (9.8%) and ILD (9.1%). There was an increase in admissions due to cardiac disease over the 10 years of follow-up, and a decrease of ILD over the last 5 years. Fourteen patients died (in-hospital mortality of 9%) mainly due to pneumoniae (36%), heart failure (21%), neoplastic diseases (21%), PH (14%) and ILD (7%). From all the admissions due to infection 70.5% were under immunosuppression at the time of the hospitalization. The frequency of acute admissions superior to 1 was associated with infection (OR 2.29, 95%CI 1.11-4.71). There were several factors associated with both acute admissions and mortality, including: gender, race, digital ulcers, cardiac dysfunction, ILD and PH. Infection was the principal cause of acute hospitalization and mortality, mainly due to pneumoniae. Although a high percentage of those had ILD, it has been decreasing in the last years in our cohort, as a direct cause of hospital admission and mortality, possibly reflecting the advances in its management.

Evaluating SARS-CoV-2 Seroconversion Following Relieve of Confinement Measures.

Seroprevalence studies are crucial both for estimating the prevalence of SARS-CoV-2 exposure and to provide a measure for the efficiency of the confinement measures. Portuguese universities were closed on March 16th 2020, when Portugal only registered 62 SARS-CoV-2 infection cases per million. We have validated a SARS-CoV-2 ELISA assay to a stabilized full-length spike protein using 216 pre-pandemic and 19 molecularly diagnosed SARS-CoV-2 positive individual's samples. At NOVA University of Lisbon, presential work was partially resumed on May 25th with staggered schedules. From June 15th to 30th, 3-4 weeks after the easing of confinement measures, we screened 1,636 collaborators of NOVA university of Lisbon for the presence of SARS-CoV-2 spike specific IgA and IgG antibodies. We found that spike-specific IgG in 50 of 1,636 participants (3.0%), none of which had anti-spike IgA antibodies. As participants self-reported as asymptomatic or paucisymptomatic, our study also provides a measurement of the prevalence of asymptomatic/paucisymptomatic SARS-CoV-2 infections. Our study suggests that essential workers have a 2-fold increase in viral exposure, when compared to non-essential workers that observed confinement. Additional serological surveys in different population subgroups will paint a broader picture of the effect of the confinement measures in the broader community.

Nailfold Videocapillaroscopy Changes Are Associated With the Presence and Severity of Systemic Sclerosis-Related Interstitial Lung Disease.

OBJECTIVE: The aim of this study was to evaluate the association of nailfold videocapillaroscopy (NVC) changes and the presence and severity of interstitial lung disease (ILD) in systemic sclerosis. METHODS: This was a cross-sectional analysis of 48 systemic sclerosis patients (21 patients with ILD). The NVC characteristics considered were capillary organization, capillary loss (CL), avascular areas, enlarged and giant capillaries, hemorrhages, abnormally shaped capillaries, edema, and intermittent flux.We analyzed the association between NVC findings and (1) presence and extension of ILD and (2) percent predicted of forced vital capacity (FVC) and the carbon monoxide diffusing capacity (DLCO). RESULTS: Capillary loss and avascular areas showed a significant association with the presence of ILD (odds ratio, 18.57; 95% confidence interval [CI], 2.17-158.72 [p = 0.008]; and odds ratio, 4.64; 95% CI, 1.35-15.91 [p = 0.015], respectively). Receiver operating characteristic (ROC) curve analysis confirmed the association between CL and ILD (area under the ROC curve, 90.1%; 95% CI, 81.8-91.4). Avascular areas and CL were associated with a worse pulmonary function (FVC -18.1% [p = 0.034], DLCO -14.0% [p = 0.013]; and FVC -15.3% [p = 0.086], DLCO -12.3% [p = 0.049], respectively). No association was found between other NVC findings and ILD or lung function. CONCLUSIONS: Capillary loss and avascular area showed a significant association with the presence of ILD, supported by ROC curve analysis. These results may reinforce a prognostic role for NVC and a physiopathology mechanism for ILD based on vascular damage.

Atherosclerosis, oxidative stress and auto-antibodies in systemic lupus erythematosus and primary antiphospholipid syndrome.

Overwhelming evidence spanning three decades has consistently shown that coronary artery disease is a major cause of morbidity and mortality in Systemic Lupus Erythematosus. Traditionally this was explained by abnormalities of the lipid profile induced by prolonged steroid treatment. Subsequently, antiphospholipid antibodies were presented as an additional cardiovascular risk factor. Recently, antibodies towards high-density lipoprotein and antiapolipoprotein A-I have been identified. These, together with anti-beta2 glycoprotein-1, interfere with the major antioxidant defence of patients with SLE and with primary antiphospholiqid syndrome exposing them to the atherogenic potential of enhanced oxidative stress. The present review discusses how the latter auto-antibodies, together with abnormalities of their target lipid auto-antigens, could enhance the risk of atherosclerosis in SLE and APS.