study of two alternative cooling systems of a mold insert used in die casting process of light alloy components

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FRI0191 CRANIAL-LIMITED AND LARGE-VESSEL GIANT CELL ARTERITIS: PRESENTING FEATURES AND OUTCOME

Background:Giant cell arteritis (GCA) comprises two main phenotypes: cranial (C) and large-vessel (LV) disease1. A full baseline steroid-free vascular imaging evaluation is required to properly diagnose LV involvement2Objectives:To compare presenting and prognostic features of LV-GCA and C-GCA patients after an adequate vascular imaging evaluation at baselineMethods:Data from GCA patients followed-up at our Institution were retrospectively collected. Only patients who underwent large-vessel imaging (PET, CTA, MRA) at disease onset or within 1 week after steroid introduction were included. Patients with evidence of LV involvement were classified as LV-GCA. Differences between LV-GCA and C-GCA patients regarding presenting features, treatment, prognosis were evaluated. Non-parametric tests were usedResults:In our cohort, we identified 161/280 patients who underwent LV-imaging study at baseline. Of these, 100 (62.1%) had signs of LV inflammation. Table 1 compares demographic features, diagnostic delay, pre-existing comorbidities and complementary treatment between the 2 groups. Table 2 compares disease features at diagnosis. Mean follow-up was similar between LV- and C-GCA patients (31.8±31.8 vs 27.8±29.1 months; 70% vs 73.8% followed-up ≥12 months). Corrected cumulative prednisone dose (CCPD, grams/months) was equivalent (LV, 0.67±0.57; C, 0.87±1.37; p=0.871). A DMARD was added in 73% of LV- and in 55.7% of C-GCA patients (p=0.027), but, notably, it was introduced at baseline in 52% of LV- vs 23.5% of C-GCA patients (p=0.006). CCPD was equivalent even considering only patients who did not receive DMARDs (LV, 0.92±0.81; C, 0.94±1.18; p=0.522). Frequency of relapses was not significantly different (LV, 51%; C, 57.3%, p=0.515), even when considering only DMARD-receiving patients (LV, 36.1%; C, 38.2%, p=0.833). Aortic aneurysms incidence at 5 years was similar (LV, 17.3%; C, 15.7%; p=0.826). Rate of metabolic and infective complications was similar, in terms of arterial hypertension (LV, 3%; C, 0%, p=0.286), diabetes (2% vs 0%, p=0.524), osteoporotic fractures (7% vs 5%, p=0.742), severe infections (3% vs 3.3%, p=1)Table 1.Demographic features, diagnostic delay, pre-existing comorbidities, and complementary treatment at baseline in LV and C-GCA patientsLV imaging +n=100 (%)LV imaging-n=61 (%)p-valueAge (years)73.2 ± 8.976 ± 8.80.018Sex (female)65 (65)40 (65)1Diagnostic delay (months)3.5 ± 4.62.3 ± 4.90.001Pre-existing comorbidities- CAD3 (3)7 (11.5)0.043- Diabetes4 (4)6 (9.8)0.181- Dyslipidemia17 (17)17 (27.9)0.114- Hypertension42 (42)34 (55.7)0.105- Stroke3 (3)3 (5)0.674- Cancer20 (20)6 (9.8)0.122Ongoing complementary treatment- Antiplatelet18 (18)15 (25)0.322- Anticoagulant1 (1)6 (9.8)0.012- Statin14 (14)14 (23)0.198Table 2.Diseases features at onset in LV and C-GCA patientsLV imaging +n=100 (%)LV imaging-n=61 (%)p-valueTemporal biopsy positive17/31 (55)9(43)0.573Symptoms- Headache65 (65)52 (85)0.006- Jaw claudication22 (22)20 (32.8)0.142- Scalp tenderness31 (31)26 (42.6)0.174- Ocular symptoms14 (14)20 (32.8)0.006- Ischemic optic neuropathy7 (7)17 (27.9)<0.001- Stroke3 (3)0 (0)0.290- Polymyalgia rheumatica42 (42)31 (50.8)0.328- Fever44 (44)12 (19.7)0.002- Fatigue72 (72)21 (34.4)<0.001- Weight loss37 (37)7 (11.5)<0.001- Cough10 (10)1 (1.6)0.053Laboratory findings, mean- C-reactive protein, mg/L80.8 ± 60.865.7 ± 58.20.057- Erythrocyte sedimentation rate76.8 ± 3071.5 ± 270.360- Hemoglobin, g/dL11.4 ± 1.512 ± 1.60.007- Platelet count389.4 ± 116.6366.8 ± 125.20.758Conclusion:LV-GCA patients are younger and suffer of a greater diagnostic delay. Although a greater systemic inflammation seems to be a feature of LV-GCA patients, the vascular prognosis is similar to C-GCA patients, who, conversely, have a greater incidence of ocular complicationsReferences:[1]Dejaco C, et al. Nat Rev Rheumatol (2017)[2]Kermani T, et al. Rheumatology (2019)Disclosure of Interests:Alessandro Tomelleri: None declared, Corrado Campochiaro Speakers bureau: Novartis, Pfizer, Roche, GSK, SOBI, Silvia Sartorelli: None declared, Nicola Farina: None declared, Elena Baldissera Speakers bureau: Novartis, Pfizer, Roche, Alpha Sigma, Sanofi, Lorenzo Dagna Grant/research support from: Abbvie, BMS, Celgene, Janssen, MSD, Mundipharma Pharmaceuticals, Novartis, Pfizer, Roche, SG, SOBI, Consultant of: Abbvie, Amgen, Biogen, BMS, Celltrion, Novartis, Pfizer, Roche, SG, and SOB

FRI0506 EFFICACY AND SAFETY OF CANAKINUMAB IN ADULT-ONSET STILL'S DISEASE: A SINGLE-CENTER REAL-LIFE EXPERIENCE

Background:The pro-inflammatory cytokine interleukin (IL)-1 has a central role in the pathogenesis of adult-onset Still's disease (AOSD), a rare auto-inflammatory condition. Anakinra, has been for years the cornerstone of IL-1-blocking therapy in AOSD. More recently, the monoclonal antibody canakinumab, a new agent blocking IL-1, has become availableObjectives:To describe our real-life experience with CNK in a cohort of AOSD patients from a single Italian CenterMethods:AOSD patients diagnosed according to Yamaguchi's criteria followed-up at our Autoinflammatory Unit and treated with CNK for at least 3 months were included. Demographic features, disease characteristics, reasons for CNK introduction, concomitant therapies, variation in systemic steroids dose, adverse events, and response to treatment were retrospectively evaluated. Non-parametric tests were used for statistical comparisonResults:13 patients (5 women; median age 49 years, range 21-74), treated with subcutaneous CNK 4 mg/kg 4-weekly, were identified. Median disease duration before CNK introduction was 12 (6-240) months. After CNK introduction, 2 patients were followed-up for 18 months, 3 for 12 months, 6 for 6 months, 2 for 3 months. CNK was introduced as first-line biologic DMARD in 6 patients. The other 7 patients had been already treated with at least one other bDMARD, for a total of 15 treatment courses (7, anakinra, ANK; 4, tocilizumab; 4, TNF-inhibitors), with a median bDMARD therapy duration of 8 (4-178) months. Previous bDMARDs had been interrupted because of inefficacy (8 cases) or adverse events (AE, 7 cases); of the 7 ANK-treated patients, therapy interruption was due to inefficacy in 3 cases. At CNK introduction, 11 patients were on systemic steroid therapy, prednisone (PDN) equivalent dose 15 (5-80) mg, and 10 were concomitantly receiving a conventional DMARD (7, methotrexate; 2, colchicine; 1, cyclosporine-A).Graphic 1summarizes main clinical features at CNK introduction. After CNK start, a striking and rapid clinical response was observed, as demonstrated by a substantial decrease of modified Pouchot score and a normalization of acute phase reactants after only 3 months (see Table 1 for details). CNK showed also a significant steroid-sparing effect: median PDN dose was reduced to 7.5 (2.5-12.5) mg at month 3 and 5 (0-7.5) mg at month 6; PDN was stopped in 3 patients (1 at month 3, 1 at month 6, 1 at month 12) due to optimal disease control. CNK was temporarily held-off in 3 patients (zoster reactivation, 1; prostatitis, 1; mild leukopenia, 1). We observed no case of primary inefficacyTable 1.Disease activity and blood tests at canakinumab introduction and during follow-upDaily prednisone dosemgBaseline(n=13)3 months(n=13)6 months(n=11)12 months(n=5)18 months(n=2)Pouchot score15 (5-80)7.5 (2.5-12.5)5 (0-7.5)5 (0-7.5)2.5VAS pain3 (2-5)1 (0-2)0 (0-1)00Erythrocyte sedimentation ratemm/h7 (2-10)3 (1-8)2 (1-4)1 (1-2)1C-reactive proteinmg/L42 (8-120)21 (2-69)13 (2-55)14 (2-41)11Ferritinng/mL20.8 (3-180)3.1 (0.5-22.5)1.6 (0.5-8.4)1 (0.3-6.3)0.5Hemoglobing/dL379.5 (161-914)282 (82-552)215 (34-464)177 (77-401)19913.1 (9.4-15.7)13.2 (10.7-15.3)13.8 (11.5-15.5)13.9 (11.3-14.3)13.5Figure 1.Graphic 1 Main clinical features at canakinumab introductionConclusion:Our real-life data confirm that CNK is highly effective and safe in AOSD treatment and has significant steroid-sparing effects. CNK showed its efficacy both as first-line therapy and after other bDMARDs failure, also in patients who have previously failed IL-1 inhibition through ANKReferences:[1] Cavalli G, et al. Treating rheumatological diseases and co-morbidities with interleukin-1 blocking therapies. Rheumatology (2015)[2] Cavalli G, et al. Efficacy of Canakinumab as First-Line Biologic Agent in Adult-Onset Still's Disease. Arthritis Res Ther (2019)Disclosure of Interests:Alessandro Tomelleri: None declared, Corrado Campochiaro Speakers bureau: Novartis, Pfizer, Roche, GSK, SOBI, Giacomo De Luca Speakers bureau: SOBI, Novartis, Celgene, Pfizer, MSD, Nicola Farina: None declared, Elena Baldissera Speakers bureau: Novartis, Pfizer, Roche, Alpha Sigma, Sanofi, Giulio Cavalli Speakers bureau: SOBI, Novartis, Pfizer, Lorenzo Dagna Grant/research support from: Abbvie, BMS, Celgene, Janssen, MSD, Mundipharma Pharmaceuticals, Novartis, Pfizer, Roche, SG, SOBI, Consultant of: Abbvie, Amgen, Biogen, BMS, Celltrion, Novartis, Pfizer, Roche, SG, and SOB

Herbário das pastagens naturais: 41 anos de história.

Resumo

Fibra em Gramíneas Forrageiras Tropicais.

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