Cardiovascular complications of systemic lupus erythematosus: impact of risk factors and therapeutic efficacy-a tertiary centre experience in an Appalachian state.

Objectives: Cardiovascular complications became a notable cause of morbidity and mortality in patients with lupus as therapeutic advancements became more efficient at managing other complications. The Appalachian community in Kentucky has a higher prevalence of traditional cardiovascular risk factors, predisposing them to cardiovascular events. Namely, the mean body mass index of the members of the Kentucky Appalachian community was reported at 33 kg/m and 94.

Churg-Strauss vasculitis presenting with steroid-responsive left ventricular cardiac mass.

A 35-year-old black Saudi man, with a known case of bronchial asthma and allergic rhinitis since childhood, presented with joint pain and swelling, orthopnoea, paroxysmal nocturnal dyspnoea and lower extremity oedema. On examination, we found jugular venous distension, bilateral basal crepitation, wheezing and diffuse synovitis. Investigations were notable for peripheral blood eosinophilia, pericardial effusion and elongated structure in the left ventricular outflow tract on echocardiography, mediastinal and hilar lymphadenopathy and right upper lobe infiltrate on high-resolution CT scan.

Intercellular Interactions as Regulators of NETosis.

Neutrophil extracellular traps (NETs) are chromatin-derived webs extruded from neutrophils in response to either infection or sterile stimulation with chemicals, cytokines, or microbial products. The vast majority of studies have characterized NET release (also called NETosis) in pure neutrophil cultures . The situation is surely more complex as neutrophils constantly sample not only pathogens and soluble mediators but also signals from cellular partners, including platelets and endothelial cells.

Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome.

Objectives: Patients with antiphospholipid syndrome (APS) are at risk for subclinical endothelial injury, as well as accelerated atherosclerosis. In the related disease systemic lupus erythematosus, there is a well-established defect in circulating endothelial progenitors, which leads to an accrual of endothelial damage over time. This defect has been at least partially attributed to exaggerated expression of type I interferons (IFNs).

Treatment of catastrophic antiphospholipid syndrome.

Purpose Of Review: Catastrophic antiphospholipid syndrome (CAPS) is a severe manifestation of antiphospholipid syndrome (APS). Although affecting only 1% of patients with APS, the condition is frequently fatal if not recognized and treated early. Here, we will review the current approach to diagnosis and treatment of CAPS.

Do neutrophil extracellular traps contribute to the heightened risk of thrombosis in inflammatory diseases?

Thrombotic events, both arterial and venous, are a major health concern worldwide. Further, autoimmune diseases, such as systemic lupus erythematosus, anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, and antiphospholipid syndrome, predispose to thrombosis, and thereby push the risk for these morbid events even higher. In recent years, neutrophils have been identified as important players in both arterial and venous thrombosis.

Systemic lupus erythematosus complicated by diffuse alveolar haemorrhage: risk factors, therapy and survival.

Objectives: While diffuse alveolar haemorrhage (DAH) is recognised as a life-threatening complication of systemic lupus erythematosus (SLE), little is known about its risk factors and response to treatment. We describe 22 cases of DAH in a US lupus cohort of approximately 1000 patients, and compare them to 66 controls from the same outpatient cohort.

Methods: We captured variables pertaining to diagnoses of SLE and secondary antiphospholipid syndrome (APS), and analysed them by univariate testing.

Unusual aetiology of isolated lower motor neuron facial palsy: systemic lupus erythematosus presenting with cranial nerve palsy and nephritis.

A 20-year-old woman presented with common cold symptoms was found to have a left-sided facial droop. On examination, peripheral facial nerve palsy was confirmed. Subsequent testing showed nephrotic range proteinuria and positive serologies including antinuclear antibody and anti-smith antibody.