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The objectives of the ‘Task Force on Catastrophic Antiphospholipid Syndrome (APS) and Non-criteria APS Manifestations’ were to assess the clinical utility of the international consensus statement on classification criteria and treatment guidelines for the catastrophic APS, to identify and grade the studies that analyze the relationship between the antiphospholipid antibodies and the non-criteria APS manifestations, and to present the current evidence regarding the accuracy of these non-criteria APS manifestations for the detection of patients with APS. This article summarizes the studies analyzed on thrombocytopenia and skin manifestations, and presents the recommendations elaborated by the Task Force after this analysis.

The objectives of the ‘Task Force on Catastrophic Antiphospholipid Syndrome (APS) and Non-criteria APS Manifestations’ were to assess the clinical utility of the international consensus statement on classification criteria and treatment guidelines for the catastrophic APS, to identify and grade the studies that analyse the relationship between the antiphospholipid antibodies and the non-criteria APS manifestations and to present the current evidence regarding the accuracy of these non-criteria APS manifestations for the detection of patients with APS. This article summarizes the studies analysed on the catastrophic APS, APS nephropathy and heart valve lesions, and presents the recommendations elaborated by the Task Force after this analysis.

Pathogenic antiphospholipid antibodies (aPL) are the driving factors of recurrent pregnancy loss and thrombosis that characterize antiphospholipid syndrome (APS). Current evidence indicates that aPL induce a procoagulant phenotype in the vasculature and abnormal cellular proliferation and differentiation in placental tissues to cause the typical clinical features; however, the molecular mechanisms underlying these processes remain incompletely understood. Inflammation serves as a necessary link between the observed procoagulant phenotype and actual thrombus development and is an important mediator of the placental injury in APS patients. However, the underlying mechanisms for these events have also not been fully elucidated. In this review, we will outline the available data that give us our current understanding of the pathophysiology of APS, especially as it relates to the development of thromboembolic and obstetric pathological phenomena in these patients. We will also describe the intracellular signaling pathways activated by aPL in various cellular subtypes and outline the current evidence linking these pathways to clinical phenotypes. Finally, we will discuss the implications of distinct molecular patterns defining clinical phenotypes of APS patients.

Excessive fluoride exposure during enamel development is a major risk factor for dental fluorosis, particularly in populations relying on groundwater sources with naturally elevated fluoride concentrations. Rural regions with limited access to centralized water systems may present heterogeneous exposure patterns influenced by environmental and socioeconomic factors. This study aimed to evaluate fluoride concentration in drinking water and the prevalence of dental fluorosis in schoolchildren from La Rioja, Argentina. A cross-sectional ecological study was conducted including 469 schoolchildren aged 6-12 years from San Blas de los Sauces and Arauco. Only children born and continuously residing in the study area were included. Dental fluorosis was assessed using the Thylstrup and Fejerskov (T-F) index by calibrated examiners (Kappa > 0.8). Fluoride concentration was determined in 82 georeferenced groundwater samples using an ion-selective electrode. Spatial analysis included Moran's I and Local Indicators of Spatial Association (LISA). Associations between fluorosis severity and locality were evaluated using chi-square tests with Monte Carlo simulation. The overall prevalence of dental fluorosis was 46.3% (95% CI: 40.8-49.9), with moderate fluorosis as the most frequent category. A significant association between locality and fluorosis severity was observed (  < 0.0001; Cramér's V = 0.23), with marked spatial heterogeneity. Fluoride concentrations varied across localities, with several exceeding the 1.5 mg/L threshold. Spatial analysis revealed significant clustering of high fluoride concentrations (Moran's I = 0.16;  = 0.006) and localized hotspots. Although areas with higher fluoride concentrations and higher fluorosis severity were spatial overlapped, this was therefore interpreted as a descriptive pattern of co-occurrence, not as evidence of causality. A high prevalence of dental fluorosis with significant spatial variability was identified in the study area. The absence of a direct association between fluoride levels and fluorosis severity suggests a complex exposure pattern influenced by multiple factors. The integration of epidemiological, environmental, and spatial data provides a useful framework for identifying high-risk areas and supporting targeted public health interventions in regions with decentralized water systems.

Background. Primary pneumonia and metastatic pulmonary infection have become more common in patients with invasive community-acquired Staphylococcus aureus disease at Texas Children's Hospital (TCH; Houston). Methods. In this study, we sought to describe pulmonary involvement in children with community-acquired S. aureus invasive infection and to determine whether the presence of genes encoding Panton-Valentine leukocidin (PVL) (luk-S-PV and luk-F-PV) and collagen adhesin (cna) is correlated with pulmonary manifestations. Patients with invasive staphylococcal infections admitted to TCH between 1 August 2001 and 30 June 2004 were studied. Chest imaging and postmortem examination reports were reviewed. Isolates were tested for the presence of genes encoding PVL and collagen adhesin by PCR. Results. A total of 47 of 70 patients with community-acquired methicillin-resistant S. aureus (MRSA) infection had abnormal pulmonary imaging findings, compared with 12 of 43 patients with community-acquired methicillin-susceptible S. aureus (MSSA) infection (P < .001). Pneumonia and/or empyema, in addition to septic emboli, were the most common findings. Metastatic pulmonary disease occurred more frequently among patients with osteomyelitis. Severe necrotizing pneumonia was present in 3 children coinfected with influenza and parainfluenza virus. The presence of genes encoding PVL was investigated in 67 MRSA and 36 MSSA isolates. Abnormal chest imaging findings were observed for 51 of 80 patients with PVL-positive isolates, compared with 2 of 23 patients with PVL-negative isolates (P < .001). Only 2 isolates (both of which were MSSA) from patients with abnormal chest radiograph findings carried cna. PVL remained independently associated with abnormal chest imaging findings in patients with secondary pneumonia in a multivariate analysis (P = .03). Conclusions. Pulmonary involvement is commonly observed in patients with invasive community-acquired S. aureus infections. Community-acquired MRSA may cause primary community-acquired pneumonia, as well as metastatic pulmonary disease. The presence of genes encoding PVL is highly associated with pulmonary involvement by S. aureus.

Background: Osteonecrosis is common in systemic lupus erythematosus (SLE) and often disabling. The role of glucocorticoids in its development is well known. Objective: To explore other possible risk factors for osteonecrosis in SLE. Methods: A nested matched case–control study undertaken in the context of a large, longitudinal, multiethnic lupus cohort (LUMINA), currently formed of 571 SLE patients meeting American College of Rheumatology criteria. All those developing symptomatic osteonecrosis after the diagnosis of SLE were considered cases. Two controls matched for age, disease duration, ethnicity, and centre were selected for each case. Cases and controls were compared by univariable analyses using selected variables. Variables with p<0.10 and those thought clinically relevant were entered into conditional logistic regression models including either the average dose or the highest dose of glucocorticoids, with osteonecrosis as the dependent variable. Results: 32 cases were identified and 59 matched controls selected (in five cases only one control could be found). By univariable analyses, both groups were largely comparable for socioeconomic-demographic, clinical, and laboratory variables. Cases were less exposed to hydroxychloroquine (as assessed by the percentage of exposure time) (p = 0.026), used higher doses of glucocorticoids (average and highest doses) (p = 0.011 and 0.001, respectively), and received cytotoxic drugs more often (p = 0.015). In the multivariable analyses only cytotoxic drug use (both models) and the highest dose of glucocorticoids remained associated with the occurrence of osteonecrosis. Conclusions: Cytotoxic drug use is a risk factor for the development of symptomatic osteonecrosis in SLE patients, along with glucocorticoids. No definite protective factors were identified.

Activation of the complement cascade is an important mechanism for antiphospholipid antibody-mediated thrombosis. We examined the effects of rEV576 (coversin), a recombinant protein inhibitor of complement factor 5 activation, on antiphospholipid antibody-mediated tissue factor up-regulation and thrombosis. Groups of C57BL/6J mice (n = 5) received either IgG from a patient with antiphospholipid syndrome (APS) or control IgG from normal human serum (NHS). Each of these groups of mice had IgG administration preceded by either rEV576, or phosphate buffer control. For each of the four treatment groups, the size of induced thrombus, tissue factor activity in carotid homogenates, anticardiolipin and anti-β2glycoprotein I (anti-β2GPI) levels were measured 72 h after the first injection. Mice treated with IgG-APS had significantly higher titers of anticardiolipin antibodies and anti-β2GPI at thrombus induction compared with those treated with IgG-NHS. The IgG-APS/phosphate buffer treatment induced significantly larger thrombi and tissue factor activity compared with other groups. Mice treated with IgG-APS/rEV576 had significantly smaller thrombi and reduced tissue factor activity than those treated with IgG-APS/phosphate buffer. The data confirm involvement of complement activation in antiphospholipid antibody-mediated thrombogenesis and suggest that complement inhibition might ameliorate this effect.

Objective: We sought to determine the effect of hydroxychloroquine therapy on the levels proinflammatory/prothrombotic markers and disease activity scores in patients with systemic lupus erythematosus (SLE) in a multiethnic, multi-center cohort (LUMINA). Methods: Plasma/serum samples from SLE patients (n = 35) were evaluated at baseline and after hydroxychloroquine treatment. Disease activity was assessed using SLAM-R scores. Interferon (IFN)-α2, interleukin (IL)-1β, IL-6, IL-8, inducible protein (IP)-10, monocyte chemotactic protein-1, tumor necrosis factor (TNF)-α and soluble CD40 ligand (sCD40L) levels were determined by a multiplex immunoassay. Anticardiolipin antibodies were evaluated using ELISA assays. Thirty-two frequency-matched plasma/serum samples from healthy donors were used as controls. Results: Levels of IL-6, IP-10, sCD40L, IFN-α and TNF-α were significantly elevated in SLE patients versus controls. There was a positive but moderate correlation between SLAM-R scores at baseline and levels of IFN-α (p = 0.0546). Hydroxychloroquine therapy resulted in a significant decrease in SLAM-R scores (p = 0.0157), and the decrease in SLAM-R after hydroxychloroquine therapy strongly correlated with decreases in IFN-α (p = 0.0087). Conclusions: Hydroxychloroquine therapy resulted in significant clinical improvement in SLE patients, which strongly correlated with reductions in IFN-α levels. This indicates an important role for the inhibition of endogenous TLR activation in the action of hydroxychloroquine in SLE and provides additional evidence for the importance of type I interferons in the pathogenesis of SLE. This study underscores the use of hydroxychloroquine in the treatment of SLE.

The ESR International Forum at the ECR 2021 discussed effects of artificial intelligence on the future of radiology and the need for increased visibility of radiologists. The participating societies were invited to submit written reports detailing the current situation in their country or region. The European Society of Radiology (ESR) established the ESR International Forum in order to discuss hot topics in the profession of radiology with non-European radiological partner societies. At the ESR International Forum 2021, different strategies, initiatives and ideas were presented with regard to radiology community’s response to the changes caused by the emerging AI technology.

Background. Methicillin-resistant Staphylococcus aureus (MRSA) isolates are increasingly frequent causes of skin and soft-tissue infections or invasive infections in many communities. Methods. Prospective surveillance for community-acquired S. aureus infections at Texas Children's Hospital was initiated on 1 August 2001. Infections meeting the definition of community-acquired were identified. Demographic and clinical data were collected. Antibiotic susceptibilities, including inducible resistance to macrolide, lincosamide, and streptogramin B (${\\rm MLS}_{{\\rm B}}$), were determined in the clinical microbiology laboratory with the methodology of the NCCLS. All data were entered into a computer database. Data were analyzed by χ² tests. Results. From 1 August 2001 to 31 July 2004, the percentage of community-acquired S. aureus isolates that were methicillin resistant increased from 71.5% (551 of 771 isolates) in year 1 to 76.4% (1193 of 1562 isolates) in year 3 (P = .008). The number of both community-acquired MRSA (CA-MSRA) isolates and community-acquired methicillin-susceptible S. aureus (CA-MSSA) isolates increased yearly, but the rate of increase was greater for the CA-MRSA isolates. Among the CA-MRSA isolates, 2542 (95.6%) were obtained from children with skin and soft-tissue infections, and 117 (4.4%) were obtained from children with invasive infections. Overall, 62% of children with CA-MRSA isolates and 53% of children with CA-MSSA isolates were admitted to the hospital (P = .0001). The rate of clindamycin resistance increased significantly for both CA-MRSA isolates (P = .003) and CA-MSSA isolates (P = .00003) over the 3 years.${\\rm MLS}_{{\\rm B}}$inducible resistance was found in 27 (44%) of 62 clindamycin-resistant CA-MSSA isolates, compared with 6 (4.5%) of 132 clindamycin-resistant CA-MRSA isolates (P < .000001). Conclusions. CA-MRSA isolates account for an increasing percentage and number of infections at Texas Children's Hospital. Clindamycin resistance increased among community-acquired S. aureus isolates. Community surveillance of community-acquired S. aureus infections is critical to determine the appropriate empiric antibiotic treatment for either local or invasive infections.