A new digital health tool for the telemonitoring of patients with scleroderma during iloprost administration: a feasibility and acceptability study.

OBJECTIVE: To assess the feasibility of a new device for telemonitoring vital parameters during iloprost infusion. MATERIALS AND METHODS: In a pilot study, patients with systemic sclerosis received iloprost infusion while being telemonitored with Umana T1 Heart Monitor, within the hospital, under the supervision of family/community nurses and rheumatologists. Patients were administered a questionnaire to obtain information on satisfaction, practicability, and compliance with the new monitoring device. RESULTS: Data recorded by the device for blood pressure, heart rate, and oximetry were concordant with those registered directly by nurses. Most patients found the device useful and thought it could be used at home, even while working. CONCLUSIONS: Umana Heart Monitor T1 could be a valuable aid in at-home iloprost therapy in patients with systemic sclerosis.

Thin-layer chromatography immunostaining in detecting anti-phospholipid antibodies in seronegative anti-phospholipid syndrome.

In clinical practice it is possible to find patients with clinical signs suggestive of anti-phospholipid syndrome (APS) who are persistently negative for the routinely used anti-phospholipid antibodies (aPL). Therefore, the term proposed for these cases was seronegative APS (SN-APS). We investigated the clinical usefulness of thin-layer chromatography (TLC) immunostaining in detecting serum aPL in patients presenting clinical features of SN-APS. Sera from 36 patients with SN-APS, 19 patients with APS, 18 patients with systemic lupus erythematosus (SLE), 20 anti-hepatitis C virus (HCV)-positive subjects and 32 healthy controls were examined for aPL using TLC immunostaining. Anti-ß(2) -glycoprotein-I, anti-annexin II, anti-annexin V and anti-prothrombin antibodies were tested by enzyme-linked immunosorbent assays (ELISA). Eahy926, a human-derived endothelial cell line, was incubated with immunoglobulin (Ig)G fraction from SN-APS patients and analysis of phospho-interleukin (IL)-1 receptor-associated kinase (IRAK) and phospho-nuclear factor (NF)-κB was performed by Western blot, vascular cell adhesion molecule 1 (VCAM-1) expression by cytofluorimetric analysis and supernatants tissue factor (TF) levels by ELISA. TLC immunostaining showed aPL in 58·3% of SN-APS patients: anti-cardiolipin in 47·2%, anti-lyso(bis)phosphatidic acid in 41·7% and anti-phosphatidylethanolamine in 30·5%. Six of 36 patients showed anti-annexin II. Incubation of Eahy926 cells with IgG from SN-APS induced IRAK phosphorylation, NF-κB activation, VCAM-1 surface expression and TF cell release. TLC immunostaining could identify the presence of aPL in patients with SN-APS. Moreover, the results suggest the proinflammatory and procoagulant effects in vitro of these antibodies.

Leishmania in SLE mimicking an exacerbation.

Systemic lupus erythematosus is a protean disease which may present manifestations that resemble other diseases posing serious problems of differential diagnosis. Visceral leishmaniasis is a parasitic infection, endemic in 88 countries, whose hallmarks may mimic a lupus flare. Fever, pancytopenia, splenomegaly, hypergammaglobulinemia, production of autoantibodies and complement consumption are some of the overlapping features between the two diseases. Thus, extra attention must be paid to patients with lupus who present with the mentioned symptoms. Diagnosis of visceral leishmaniasis relies on the detection of leishmania antibodies, on the presence of amastigotes in bone marrow aspirates, biopsies and cultures of the parasite. Treatment is based on the use of i.v. liposomal amphotericin B. The missed recognition of a leishmania infection in a lupus patient may lead to death, since both the omission of a specific anti-parasite treatment and the increase of the immunosuppressive therapy, in the conviction of a lupus flare, accelerate a fatal outcome. In this paper we present a case of visceral leishmaniasis occurring in a lupus patient. The clinical and laboratory features that overlap in the two diseases and the current literature on the topic were discussed.

Pregnancy, lupus and antiphospholipid syndrome (Hughes syndrome).

Autoimmune diseases (AD) occur frequently in women during their childbearing years and may influence pregnancy outcome and neonatal health. Patients with systemic lupus erythematosus (SLE) can experience a disease flare-up during pregnancy with potential negative effects on the product of conceptus, especially if the disease is active. Recurrent pregnancy loss is now considered as a treatable clinical condition associated with the presence of circulating antiphospholipid antibodies (aPL). The neonatal lupus syndromes (NLS), caused by the transplacental passage of maternal IgG anti-Ro/SS-A and anti-La/SS-B antibodies to the fetus, carry significant morbidity and mortality in case of cardiac manifestations. Immunosuppressive agents are often administered during pregnancy in order to control maternal disease and to ensure a better pregnancy outcome. Nowadays, owing to our increasing knowledge of the disease pathophysiological mechanisms and the development of combined medical-obstetric clinics, pregnancy outcome in patients with AD has notably improved.

[Advances in immunology and rheumatoid arthritis pathogenesis]. / La patogenesi dell'artrite reumatoide alla luce degli sviluppi delle conoscenze in immunologia.

The pathogenesis of Rheumatoid Arthritis (RA) is still largely unknown. From the seminal experimental studies, suggesting a multifactorial mechanism leaded by an antigen specific activation, the direct role of innate immunity in the disease progression has been recently emphasized. In the natural history of RA, characterized by the three phases of the induction, maintenance and tissue destruction, innate immunity seems to be the central player. On the other hands the recent advances about the molecules involved in the T lymphocyte activation, the T cell role in the mechanism of erosion, and the studies about chemokines in the homing and angiogenesis processes support the theory of an antigen specific activation of the adaptive immune system. Therefore, during RA, the pathogenesis of sinovitis and erosions comes from independent pathways involving either innate and adaptive immunity resulting in the final induction of the articular damage.