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The effect of different blossom thinners ammonium thiosulfate (ATS) (1%, 2%), Armothin (1.5%), Tergitol-TMN-6 (0.5%, 1%), applied on peach cv. Redhaven at 50–60% full bloom was evaluated in thinning experiments in south-west Slovenia. The photosynthesis inhibitor metamitron (0.05%) applied at 8 mm fruit diameter was evaluated as fruitlet thinner as well. Application of 2% ATS resulted in excessive thinning. The thinning effect of 1% ATS was also too strong in two out of three thinning experiments. The use of 0.05% metamitron did not cause any thinning effect on peach trees and gave similar results as the non-treated control. The effective fruit set reduction and increase of average fruit weight was achieved with 0.5% and 1% Tergitol application. In three-year experiment both Tergitol applications reduced fruit set toward hand thinned level, but the share of fruit from bigger size class was only once enhanced to the level of hand thinned trees. No sign of phytotoxicity was noticed on fruits in all thinner application treatments.

ObjectiveTo develop new antiphospholipid syndrome (APS) classification criteria with high specificity for use in observational studies and trials, jointly supported by the American College of Rheumatology (ACR) and EULAR.MethodsThis international multidisciplinary initiative included four phases: (1) Phase I, criteria generation by surveys and literature review; (2) Phase II, criteria reduction by modified Delphi and nominal group technique exercises; (3) Phase III, criteria definition, further reduction with the guidance of real-world patient scenarios, and weighting via consensus-based multicriteria decision analysis, and threshold identification; and (4) Phase IV, validation using independent adjudicators’ consensus as the gold standard.ResultsThe 2023 ACR/EULAR APS classification criteria include an entry criterion of at least one positive antiphospholipid antibody (aPL) test within 3 years of identification of an aPL-associated clinical criterion, followed by additive weighted criteria (score range 1–7 points each) clustered into six clinical domains (macrovascular venous thromboembolism, macrovascular arterial thrombosis, microvascular, obstetric, cardiac valve, and hematologic) and two laboratory domains (lupus anticoagulant functional coagulation assays, and solid-phase enzyme-linked immunosorbent assays for IgG/IgM anticardiolipin and/or IgG/IgM anti–β2-glycoprotein I antibodies). Patients accumulating at least three points each from the clinical and laboratory domains are classified as having APS. In the validation cohort, the new APS criteria vs the 2006 revised Sapporo classification criteria had a specificity of 99% vs 86%, and a sensitivity of 84% vs 99%.ConclusionThese new ACR/EULAR APS classification criteria were developed using rigorous methodology with multidisciplinary international input. Hierarchically clustered, weighted, and risk-stratified criteria reflect the current thinking about APS, providing high specificity and a strong foundation for future APS research.

Antiprothrombin antibodies can be measured by ELISA using either a prothrombin/phosphatidylserine complex (aPS/PT) or prothrombin alone (aPT) as antigen. We aimed to compare the clinical features of autoimmune patients with avidity of aPS/PT and determine the diagnostic efficiency of aPS/PT and aPT for assessing antiphospholipid syndrome (APS). aPS/PT were of low (n = 9), heterogeneous (n = 31) and high (n = 8) avidity out of 48 cases. None of the samples with low avidity were positive in aPT ELISA. Among patients with heterogeneous or high avidity aPS/PT, there was a significantly greater number of patients with APS as compared to patients with low avidity (38/39 vs. 7/9; p < 0.05). No SLE patients had high avidity antiprothrombin antibodies.

Autoantibodies against dsDNA are utilized for the diagnosis and prognosis of SLE as they are highly specific and correlate with disease activity/renal involvement. However, different detection methods are used in routine diagnostic laboratories. Farr radioimmunoassay (Farr-RIA) has been designated as the preferred method, since it provides very specific and at the same time quantitative results, enabling follow-up of level variations over time. Using intercalating fluorescent dsDNA dye would enable all the benefits of Farr-RIA without the radioactive material and organic solvents. To develop a modified fluorescent Farr method (Farr-FIA) and compare it to the classical Farr-RIA in regard to laboratory parameters, as well as clinical utility. Assays were tested on sera of 70 SLE patients, 78 other autoimmune patients, and 145 healthy blood donors. DNA for Farr-FIA was isolated from healthy donor, for Farr-RIA, 14C-labeled dsDNA from E. coli was used and mixed with sera in borate-buffered saline, followed by precipitation with saturated ammonium sulfate solution and centrifugation. The supernatant (S) was separated from the precipitate (P), and content of dsDNA was measured with PicoGreen (Invitrogen) in Farr-FIA or radioactive isotope in scintillation solution in Farr-RIA. The results were calculated as a ratio (P-S)/(P+S). Farr-FIA has a diagnostic sensitivity of 53% and diagnostic specificity of 100% (ROC AUC 0.781). Good correlation and agreement were shown between Farr-RIA and Farr-FIA. Also, there is good correlation between Farr-FIA and SLEDAI, comparable to that of Farr-RIA. Farr-FIA differs from Farr-RIA in the changed detection system yielding comparable results and thus could represent a nonradioactive replacement for Farr-RIA.

BackgroundIgA vasculitis (IgAV) is commonly marginalized disease in adults. Clinical data are scarce and mostly limited to patients with significant renal disease. Predictors of severity in acute adult IgAV are unknown.ObjectivesTo create a simple semi-quantitative score predicting the severity of adult IgAV and to aid the management of adult IgAV.MethodsWe performed a paper chart review of adult, histologically proven IgAV cases, diagnosed between 01.01.2010 and 31.12.2014 at our secondary/tertiary rheumatology center. The disease activity was assessed using BVAS-3. Predictors of severe disease were identified and an IgAV severity score (IgAVSS) was constructed.ResultsDuring the 60-month observation period, 129 new IgAV cases (58% male) were identified. The median (interquartile range (IQR), range) age was 64.2 (40.4–77.3, 18-92) years. Skin, gastrointestinal (GI), renal and joint involvement was present in 129 (purpura limited to lower limbs in 54.3% and generalized above waist in 45.7%), 48 (severe in 13), 65 (severe in 16) and 58 patients, respectively. Males and patients with generalized skin purpura had more severe disease (p=0.019 for male vs. female gender and p=0.0005 for generalized vs. limited purpura). Patients aged 45–75 years had more commonly severe GI and severe renal disease than younger (<45) or older (>75) ones (38.5% vs 31.6% vs 12.5% in case of severe GI disease and in 40.9% vs 9.5% vs 22.7% in case of severe renal disease respectively). The IgAVSS was constructed by assigning weights to patient age, gender and extent of purpura at presentation. It is a simple sum of the three domains (Table 1A). IgAVSS rendered good delineation between mild uneventful and severe IgAV when the cut off was set at ≥1.5 points. The difference in BVAS-3 between IgAVSS <1.5 and IgAVSS ≥1.5 was significant, p=0.003. (Table 1B).Table 1A. IgAVSSB. Performance of the IgAVSSCharacteristicIgAV scoreNo. of pts.GISevere GIRenalSevere renalArthritisBVASGenderMale1 point<1.568193294149 (3–14)Female0 points≥1.5 61291036121214 (6–19)PurpuraGeneralized1 pointP value–0.0290.0380.0780.02910.003Limited0 pointssevere GI – bloody diarrhea or ileus or surgical intervention; severe renal – acute renal failure or nephrotic syndromeAge<45 years0 points45–75 years0.5>75 yearsIgAVSS = gender + purpura + age. ConclusionsGender, patient age and extent of purpura predict the severity of adult IgAV. We propose a semi quantitative score the IgAVSS which is calculated based on clinical characteristics only as a decision making aid to the physician in a busy outpatient clinic setting to distinguish patients who might have a more severe disease requiring hospital management from those who can be managed on the outpatient basis.Disclosure of InterestNone declared

BackgroundChronic inflammation might be involved in the pathogenesis of different types of pulmonary hypertension (PH) [1]. Serum amyloid A (SAA) is an evolutionarily conserved, inflammatory protein expressed in the liver in a manner analogous to that of C-reactive protein (CRP). SAA is also expressed by several extrahepatic cells, including vascular smooth muscle, macrophages and endothelial cells in response to different stimuli, such as interleukin 6 (IL-6) [2]. Data on potential roles of SAA in PH are scarce. We recently reported that increased SAA is associated with pulmonary arterial hypertension (PAH) in patients with systemic sclerosis [3]. Furthermore, children with idiopathic PAH experiencing non-response to specific drugs and a worse prognosis, had significantly elevated SAA [4].ObjectivesTo check associations of SAA with CRP, IL-6 and noninvasive markers of disease severity in PH referral patients.MethodsSeventy five consecutive patients were evaluated in the PH out-patient clinic within one year. Serum SAA and CRP were measured by nephelometry and IL-6 by routine ELISA. Markers of PH severity were evaluated with serum troponin I (TnI), N-terminal pro-B-type natriuretic peptide (NTproBNP), tricuspid annular plane systolic excursion (TAPSE), cardiac index (CI) and systolic pulmonary arterial pressure (sPAP), as assessed by routine echocardiography, and the six minute walk test (6MWT) in the whole group of patients, as well as in subgroups of 60 patients with PAH specifically, group I (n=17) or IV (n=43) according to WHO classification.ResultsWithin the whole group of 75 PH patients (64% females, 36% males, mean age 63, range 29-89 years), we found significant correlations of SAA with CRP, diffusing capacity for CO, TnI (r=0.75, r=-0.36, r=0.23, respectively, all p<0.05) and NTproBNP (0.23, p=0.057). In the subgroup of patients with PAH type IV, SAA strongly correlated with CRP, IL-6, TnI, NTproBNP (r=0.93, r=0.53, r=0.91, r=0.90, respectively, all p<0.000), as well as with sPAP (r=0.39, p=0.03), while in patient subgroup PAH type I, SAA correlations were less strong. No significant correlations were found between SAA and CI, TAPSE or 6MWT, either in the whole patient group or in the subgroups.ConclusionsWe showed for the first time, that SAA is associated with markers of chronic inflammation and disease severity in unselected adult patients with PH. In subgroup PAH type IV, where increased SAA might indicate non-responsiveness to specific drugs and worse prognosis, this association is even stronger. These new findings are pending further evaluation.ReferencesKherbeck N, et al. Clin Rev Allergy Immunol. 2013; 44: 31-8.Eklund KK, et al. Crit Rev Immunol. 2012; 32: 335-48.Lakota K, et al. PLoS One. 2015 Jan 28;10(1):e0110820.Yeager ME, et al. Proteomics Clin Appl. 2012; 6:257-67.Disclosure of InterestNone declared

BackgroundIn early rheumatoid arthritis (RA), first assessment by a rheumatologist and/or initiation of disease-modifying anti-rheumatic drugs (DMARD) within 12 weeks of symptom onset are associated with a significant benefit in long-term disease outcome.1,2ObjectivesTo determine the proportion of patients with newly diagnosed RA in whom first rheumatology assessment and/or initiation of DMARD therapy was within the desired time frame.MethodsA retrospective chart review of adult patients diagnosed with RA during year 2014 and the first half of year 2015 was performed at our rheumatology department, which is a part of an integrated secondary/tertiary teaching hospital that provides rheumatology services for a population of more than 500.000 residents. Potential cases were identified by searching the electronic medical records for ICD-10 codes M05.* and M06.* Electronic and paper records of patients were then thoroughly reviewed. Dates were recorded for onset of inflammatory joint symptoms, referral to rheumatologist, initial assessment by a rheumatologist and initiation of DMARD therapy. The percentage of patients assessed by a rheumatologist and/or treated with a DMARD within 12 weeks of symptom onset and the median times for delay were then calculated.ResultsBetween 01.01.2014 and 30.06.2015, 188 new cases of RA were identified at our Department of Rheumatology. Of those, 153 (81.4%) were referred to our early interventional clinic. Within 12 weeks of symptom onset, 89 (47.3%) new RA patients were examined by a rheumatologist and 68 (36.2%) were started on DMARD therapy; the median time from symptom onset to consultation was 12.8 (IQR 4.9–27.7) weeks, median time from referral to consultation was 1 (IQR 1–3) day and median DMARD treatment delay was 16.1 (IQR 8.6–32.8) weeks.Table 1.Demographic data, clinical history, and delaysGender (female/male) (%)143/45 (76/24)Age, years (mean ± SD)62.4±15.4DAS28 3v (mean ± SD)5.3±1.3Patients fulfilling 2010 ACR/EULAR classification criteria for RA, # (%)177 (94.1)Time from symptom onset to first rheumatologist assessment, weeks (median)12.8 (IQR, 4.9–27.7)Time from referral to first rheumatologist assessment, weeks (median)0.14 (IQR, 0.14–0.43)Time from symptom onset to glucocorticoid initiation, weeks (median)13.0 (IQR, 5.8–27.2)Time from symptom onset to DMARD initiation, weeks (median)16.1 (IQR, 8.6–32.8)Legend: SD: standard deviation, IQR: interquartile range.Conclusions47% of new RA patients were assessed by a rheumatologist and 36% were treated with a DMARD within the recommended time frame of 12 weeks. Most of the treatment delay was due to the time elapsed between symptom onset and referral to a rheumatologist. These results substantiate the efficacy of our early interventional clinic in diagnosing and treating patients with early RA: despite the heavily protracted nationwide waiting times for first rheumatologist assessment and significantly (40%) lower number of rheumatologists per capita compared to European Union average, the percentage of timely treated patients was comparable to recent reports.ReferencesVan der Linden MPM, et al. Arthritis Rheum, 2010;62(12):3537–3546.Raza K, et al. Ann Rheum Dis, 2011;(70)10:1822–1825 [MT1].Disclosure of InterestNone declared

The pathogenicity of antibodies against beta 2-glycoprotein I (anti- beta 2GPI) depends on multiple factors such as subclass type, epitope binding and avidity. Due to their large heterogeneity, their impact on antiphospholipid syndrome (APS) onset is still not fully clarified. We studied the binding characteristics of IgG anti- beta 2GPI with known avidity from sera of 201 autoimmune patients (87 with APS, 67 with APS associated with systemic lupus erythematosus (SLE), 47 with only SLE) to six beta 2GPI peptides corresponding to amino acid clusters on domains I-II, II, III and III-IV by indirect ELISA and evaluated their association with clinical features of APS. Peptides A (LKTPRV; domain I-II), B (KDKATF; domain IV) and C (TLRVYK; domain III) were derived from a hexapeptide phage display library previously shown to react with pathogenic monoclonal anti- beta 2GPI. Peptides D (NGPANSK; domain III), E (YNPLWFV; domain II) and F (KMDGNHP; domain III-IV) represent surface amino acid clusters on beta 2GPI. The percentage of patients positive for peptides were observed as follows: 30.3 % for peptide D, 28.90 % for B, 25.9 % for C, 24.9 % for E, 24.4 % for F and 10.0 % for A. The anti-peptide antibodies in studied serum samples were predominantly of heterogeneous avidity, followed by law avidity anti-peptide antibodies, whereas only a few were of high avidity. Positive and negative correlations were found between several anti-peptide antibodies and the rate of thrombosis. Our results indicated diverse reactivity of IgG anti- beta 2GPI to different epitopes on beta 2GPI. Classification of IgG anti- beta 2GPI into subgroups regarding epitope specificity and avidity could represent an additional tool in understanding their pathogenicity in APS.

Issue Title: Special Issue: The 9th International Congress on Autoimmunity: Part II