Background:Inflammatory myopathies (IM) are a group of rare diseases that involve muscle inflammation. Several types are defined with a wide range of different manifestations and prognosis.Objectives:Describe the characteristics of the cohort of patients with IM in a tertiary hospital, in order to identify their demographic and clinical characteristics and try to find a correlation between them.Methods:Retrospective observational study of patients with IM: dermatomyositis (DM), polymyositis, antisynthetase syndrome (ASS), necrotizing autoimmune myopathy and overlap syndrome (OS). Clinical, biological, neurophysio and histopathological data were collected. Statistical analysis was performed using SPSS 23 IBM®.Results:28 patients were included with a follow-up of 10.9 ± 9.8 years (y). According to the 2017 EULAR / ACR criteria for IM, 89.2% were classified as definitive MI, with an average score of 12.1 ± 3.2. Age at diagnosis 47.3 ± 17.7y; ratio 1.3; 78.6% Caucasian, 10.7% Asian and 10.7% Latino. 39.3% had DM, 3.6% hypomyopathic and 3.6% amyopathic DM, 28.6% OS and 17.9% ASS. Lung involvement was the most prevalent extramuscular manifestation (67.9%). Systemic sclerosis was the most frequent overlapping autoimmune disease (AD) (21.4%) and 2 patients (7.1%) overlapped more than 1 AD. In Table 1 are detailed the clinical characteristics of the patients, and in Figures 1 and 2, the autoantibody (aa) profile and treatments used. The incidence of neoplasm was 10.7% 10.3 ± 9.6y after the diagnosis of myopathy (3 breast neoplasms, 1 colon and 1 cutaneous lymphoma), and of them, 66.7% had two synchronous neoplasms. No neoplasms were observed in the 2 anti-TIF1-γ+ patients. The subtype of IM in these patients was 1 OS anti-RNP+, 1 DM anti-PL-12+ and 1 ASS anti-OJ+. 17.9% smoked and 21.4% had taken statins at some point, without it being related to the start of the myopathic clinic. A capillaroscopy was performed in 67.9%, being pathological in 63.1%The positivity of anti-RNP (p=0.01) and steroid bolus (p=0.039) were correlated with a more severe disease, defined as a summation index composed of a series of manifestations (pulmonary hypertension (PH), ischemic heart disease, venous/arterial thrombosis, myo/pericarditis, interstitial lung disease (ILD), severe infections, neoplasms or hospitalizations). Other statistically significant correlations between aa and clinical manifestations are detailed in Table 3, among which the anti-RNP+ with myopericarditis stands out. No correlation was found between the findings on capillaroscopy and the type of IM.Conclusion:The most frequent subtype of IM was DM. 10.3% of the patients presented a neoplasm, all with different subtypes of myopathy and aa. The presence of anti-RNP+ correlated with greater severity of the disease and myopericarditis. Likewise, significant differences were found between the subtypes of aa and certain clinical manifestations. There is no correlation between findings on capillaroscopy and the type of IM.Table 1.Clinical characteristics.Clinical manifestationsFrequency %PresentationAcute40.7Subacute22.2Insidious37Muscular Weakness82.1Muscle Enzymes Elevation85.7Muscle Pain67.9Joint Manifestations (Mf)67.9Systemic Mf67.9Digestive Mf46.4Raynaud’s Syndrome (RS)53.6Sclerodactyly32Digital ulcers (DU)25Calcinosis10.7ILD67.9Nonspecific Interstitial Pneumonia63.2Usual Interstitial Pneumonia15.8Organizing Pneumonia10.5Lymphocytic Interstitial Pneumonia5.3Undefined Pattern5.3PH10.7Serious Infections17.9Figure 1.Aa.Figure 2.Treatment.Table 2.Correlations between clinical manifestations and aa.ManifestationsAutoantibodiesp valueDUAnti-MDA50.005SclerodactylyAnti-RNP0.011PericarditisAnti-RNP0.000MyocarditisAnti-RNP0.005DiabetesAnti-RNP0.027RSAnti-PM/Scl0.033CalcinosisAnti-PM/Scl0.027Flexion ContracturesAnti-PM/Scl0.027ArrhythmiasAnti-PL-120.001Disclosure of Interests:Irene Carrión Barberà Grant/research support from: I received a grant from the Spanish Rheumatology Foundation (FER) and laboratories KERN PHARMA for a brief stay abroad., Ana Pros Simón: None declared, Tarek Carlos Salman Monte: None declared, Manel Ciria: None declared, Francisco Vílchez-Oya: None declared, Selene Labrada: None declared, Toni Meraz: None declared, Jordi Monfort: None declared
Background:Systemic lupus erythematosus (SLE) is an autoimmune multisystemic disease with a wide variety of clinical manifestations, being one of them serositis, which includes pericarditis, pleuritis and peritonitis [1]. Incidence of serositis ranges between 11-54% [2].Objectives:To determine the prevalence of serositis in patients (pt) with SLE attended at the outpatient Lupus Unit and identify factors that could be used as predictors of this manifestation.Methods:Retrospective case-control study. 297 medical records of SLE pt were reviewed: 28 pt were diagnosed with serositis (cases) and were age- and sex-matched with 2 controls with SLE without serositis. Differences between cases and controls were analyzed as well as factors associated with serositis.Results:Patient’s characteristics are described in Table 1. The prevalence of serositis in our cohort was 9.42%. The difference between the prevalence of serositis in men and women was statistically higher in men, 30% vs 7.9% (p=0.001, CI 95%: 1.7%-42.4%). Serositis was diagnosed at an age of 41 ±14 years (y) and in 40.7% it was the first symptom. Time from SLE diagnosis to serositis was 4±5.3 y. 10 pt had recurrences: 6 had 2, and 4 had 3. Incidence of pericarditis and pleuritis was 78.6% and 82.1% respectively. 2 pt suffered from pericardial tamponade. Mean prednisone dose received during the serositis was 44.6±26.6mg. At the moment of serositis 100% were ANA+, 85.7% antidsDNA+, 80% CrithidiaDNA+, 57.9% antiRo60+, 52.6% antiRo52+, 15.9% antiLa+, 47.4% antiRNP+, 21.1% antiSm+, and 77.8% had low C3.When looking for serositis-associated factors we only found association with antidsDNA measured by Crithidia (p=0.016) and different measures of glucocorticosteroids (GC), having cases needed higher doses than controls (Table 1). Those with serositis had significantly received more mycophenolic acid (p=0.021) and marginally, more belimumab (p=0.056).Table 1.Comparison between groups of adverse maternal-fetal outcome.VARIABLESCASES (28)CONTROLS (54)p-value Female22 (33.3%)44 (66.7%)0.775 Male6 (37.5%)10 (62.5%) Caucasian20 (32.8%)41 (67.2%)0.693 Hispanic American7 (38.9%)11 (61.1%) Others1(33.3%)2 (66.6%)Arthritis22 (38.6%)35 (61.4%)0.219Leukopenia17 (34.0%)33 (66.0%)1.000Lymphopenia25 (33.8%)49 (66.2%)1.000Thrombocytopenia5 (20.8%)19 (79.2%)0.128Nephritis8 (50.0%)8 (50.0%)0.152Raynaud’s phenomenon6 (42.9%)8 (57.1%)0.263Haemolytic anaemia3 (42.9%)4 (57.1%)0.686Antinuclear antibodies28 (34.6%)53 (65.4%)1.000AntidsDNA23 (37.7%)38 (62.3%)0.295AntiSm9 (42.9%)12 (57.1%)0.425AntiRo5210 (41.7%)14 (58.3%)0.444AntiRo6013 (37.1%)22 (62.9%)0.645AntiRNP14 (43.8%)18 (56.3%)0.159CrithidiaDNA19 (47.5%)21 (52.5%)0.016Low C321 (39.6%)32 (60.4%)0.224Low C413 (38.2%)21 (61.8%)0.637Low CH5013 (39.4%)20 (60.6%)0.480SLICC*0.54 (±0.9)0.49 (±1.1)0.717SLEDAI*3.1 (±3.1)2.98 (±3.2) 0.844CorticosteroidsEver27 (38.6%)43 (61.4%)0,051Pulses ever9 (60.0%)6 (40.0%)0.033Maximum prednisone dose ever:<10mg18 (85.7%)3 (14.3%)0.00310-29mg14 (87.5%)2 (12.5%)30-60mg11 (45.8%)13 (54.2%)>60mg8 (47.1%)9 (52.9%)Conclusion:The prevalence of serositis was 9.42%. Serositis is significantly more frequent in SLE men than in women: almost ⅓ will develop serositis, so we need greater awareness of serositis in SLE men.CrithidiaDNA+ was identified as an associated factor of serositis. Furthermore, pt with serositis significantly received more pulses of GC and a higher maximum dose throughout the disease, which could imply a more aggressive form of SLE than in those without serositis. No correlation was found between serositis and any other characteristic.References:[1]Hochberg MC. Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 1997;40:1725[2]Ryu S, Fu W, Petri MA: Associates and predictors of pleurisy or pericarditis in SLE. Lupus. Science. 2017, 4(1):e000221.Disclosure of Interests:None declared
BackgroundIt has been postulated that AGES could have a relevant role as inducers in the chronic inflammatory pathway present in various diseases1; among them, in immune-mediated diseases such as SLE, as well as that its concentration could be related to some parameters of the disease such as activity 2 or accumulated damage 3, showing studies discrepant results to date.ObjectivesTo describe correlations between the concentrations of AGEs measured by cutaneous autofluorescence and various parameters related to the disease in a population of SLE patients.MethodsAGE concentrations were measured by skin autofluorescence (Age Reader Mu Connect from Diagnoptics Technologies BV) in 66 SLE Caucasian patients and correlations with demographic and clinical data were analyzed, after adjusting for age, smoking and corticosteroids as possible confounding factors, according to previous data. Previous validation studies have shown that skin autofluorescence is strongly related to AGE levels in skin biopsies4. The indices were analyzed both as quantitative and categorized variables according to previously established categories or to medians/tertiles/quartiles depending on the distribution of the variable in our population.ResultsTable 1 shows some descriptive characteristics of our cohort. There were clinically and statistically significant differences in the values of AGEs according to the patient’s SLEDAI and SLICC. Specifically, it was observed that AGEs’ values in the population with severe activity according to SLEDAI was 0.61 (95% CI 0.85-2.046; p=0.045) points > than in those in remission (p=0.045); as well as AGEs‘ values in patients with SLICC ≥1 was 1.23 (95% CI 0.49-1.98; p=0.030) points > than in the group without cumulative damage. In all the models, the values of AGEs increased significantly with age, smoking and current treatment with corticosteroids, except for the model including the SLICC variable. Interactions in said model were explored, and it was observed that the concentration of AGES depended on the interaction between the value of SLICC and the intake of corticosteroids, so that differences were only observed between SLICC groups in those who took corticosteroids.Table 1.Descriptive characteristics of the cohort. c: categorized.AverageSD%Age5415BMI25.364.68SmokerNo68.2Yes31.8AGEs2.60.7Disease duration (years)1611DAS282.221.16cDAS28remission71.2low9.1moderate15.2high4.5SLEDAI54cSLEDAIremission21.2low16.7moderate51.5high10.6SLICC11cSLICC00.0148.5>130.3321.2FACIT Fatigue Scale1810Patient global assessment (PGA)3.02.4cPGA0-131.82-328.8>339.4Physician global assessment1.71.3cPhysician global assessment0-147.0>153.0Visual Analogue Scale (VAS)3.13.1cVAS034.81-430.3>434.8Health Assessment Questionnaire (HAQ)0.5270.551cHAQ033.30-0.7536.4>0.7530.3CorticoidsYes27.3No72.7ConclusionA correlation with elevated values of AGEs was observed in those SLE patients with higher scores in the indexes of activity (SLEDAI) and damage accrual (SLICC). The fact that the differences in SLICC are only observed in those patients treated with corticosteroids suggests that, maybe, only the accumulated damage related to taking corticosteroids could be mediated by AGEs.References[1]Medzhitov R. Origin and physiological roles of inflammation. Nature 2008;454:428–435.[2]Vytášek R, Šedová L, Vilím V. Increased concentration of two different advanced glycation end-products detected by enzyme immunoassays with new monoclonal antibodies in sera of patients with rheumatoid arthritis. BMC Musculoskelet Disord 2010;11:83.[3]leeuw K de, Graaff R, Vries R de, Dullaart RP, Smit AJ, Kallenberg CG, Bijl M. Accumulation of advanced glycation endproducts in patients with systemic lupus erythematosus. Rheumatology 2007;46:1551–1556.[4]Meerwaldt R, Links T, Graaff R, Thorpe SR, Baynes JW, Hartog J, Gans R, Smit A. Simple noninvasive measurement of skin autofluorescence. Ann N Y Acad Sci 2005;1043:290-298.Disclosure of InterestsNone declared
Background:Tocilizumab (TCZ) is a recombinant humanized, anti-human monoclonal antibody of the immunoglobulin G1ksubclass directed against soluble and membrane-bound interleukin 6 receptors (IL-6R) [1].Interleukin-6 (IL-6) has a pleiotropic effect on inflammation, immune response, and hematopoiesis. When it was first identified, it was named as B-cell-stimulating factor 2 (BSF-2) according to its ability to induce immunoglobulin production in Epstein-Barr virus-transformed B-cell lines or in Staphylococcus aureus Cowan 1-stimulated B cells [2-4].Nowadays, it is known that IL-6 controls the survival, population expansion and maturation of B cells and plasmablasts. In that way, the regulation of Blimp-1 by STAT3 is linked to antibody secretion and is associated with long-lived plasma cells that produce large amounts of immunoglobulin. Furthermore, the ability of IL-6 to promote humoral immunity has been linked to its effects on follicular helper T cells where they promote B cell proliferation and immunoglobulin class switching [5].Objectives:Hypogammaglobulinaemia is a known complication of some immunosuppressive drugs, not previously described in patients who received therapy with monoclonal antibody against the IL-6R. We aimed to analyzed the prevalence of hypogammaglobulinaemia in our series of patients treated with tocilizumab after a carefully diagnostic workup which ruled out other causes and analyzed whether is associated with a higher risk of infection.Methods:We conducted a retrospective review from 2010 to 2019 of forty-two patients affected with a rheumatic disease and treated with TCZ at our centre. In those patients in whom we had no record of immunoglobulin levels, we determined them in the blood analysis performed by usual clinical practice.Results:42 patients were identified, from whom 38 had rheumatoid arthritis. A 31% had immunoglobulin levels prior to starting treatment with TCZ but no one had hypogammaglobulinaemia. 2 patients were excluded due to their underlying disease could justify the IgG level abnormalities. During the treatment’s follow-up, we identified that a 30% of the patients (12/40) had hypogammaglobulinaemia. Of those patients in whom immunoglobulin levels had been determined prior to starting treatment with TCZ, a 36.3% of them (4/11) developed hypogammaglobulinaemia during the follow-up. From the series, we observed a statistical significance tendency (p=0.0057) for infection risk in those patients with hypogammaglobulinaemia in contrast to those with normal IgG level (41.5% vs 14.3%, respectively).Conclusion:Secondary hypogammaglobulinaemia may occurs in patients receiving anti-IL6 agents such as tocilizumab and this could be associated with an increasing infection risk. The prevalence is not precisely known, in part because measurement of IgG prior to or during the treatment has not been a standard of care. No medical data have been previously disclosed about this possible adverse effect of anti-interleukin-6 agents. Nevertheless, ideally randomized trials are needed to assess this initial hypothesis.References:[1]Sheppard M, Laskou F, Stapleton PP, Hadavi S, Dasgupta B. Tocilizumab (Actemra). Hum Vaccin Immunother. 2017;13(9):1972–1988.[2]Tanaka T, Kishimoto T. The biology and medical implications of interleukin-6. Cancer Immunol Res. 2014;2(4):288–294.[3]Tanaka T, Narazaki M, Kishimoto T. IL-6 in inflammation, immunity, and disease. Cold Spring Harb Perspect Biol. 2014;6(10):a016295. Published 2014 Sep 4.[4]Kishimoto T. Interleukin-6: discovery of a pleiotropic cytokine. Arthritis Res Ther. 2006;8 Suppl 2(Suppl 2):S2.[5]Hunter CA, Jones SA. IL-6 as a keystone cytokine in health and disease [published correction appears in Nat Immunol. 2017 Oct 18;18(11):1271]. Nat Immunol. 2015;16(5):448–457.Disclosure of Interests:Francisco Vílchez-Oya: None declared, Ana Pros: None declared, Irene Carrión Barberà Grant/research support from: I received a grant from the Spanish Rheumatology Foundation (FER) and laboratories KERN PHARMA for a brief stay abroad., Juan Antonio Meraz Ostiz: None declared, Tarek Carlos Salman Monte: None declared, Carolina Perez-Garcia: None declared
Increased posterior tibial slope (PTS), medial tibial plateau slope (MTPS) and lateral tibial plateau slope (LTPS) have been proposed as potential risk factors for anterior cruciate ligament (ACL) tear. However, prior literature is inconclusive. The primary goal of the study was to investigate the relationship of MTPS, LTPS and PTS with ACL tears. The secondary goal was to determine whether injury mechanisms, age, gender, tobacco, obesity, extreme PTS (>12˚) or previous injuries are risk factors in ACL tears. Three groups were identified: a study group of patients with ACL injury; a second group diagnosed with meniscal injury; and a third group of non-injured patients. Demographic data was collected. MTPS and LTPS were measured in MRI and PTS in lateral radiographs by two blinded observers. Data was analyzed using SPSS. 416 patients were included in the study. MTPS ranged from 0˚ to 14˚ (average value 5.66 ± 2.98), LTSA 0˚ to 16˚ (5.69 ± 3.5) and PTS 0˚ to 17˚ (6.75 ± 3.18). Neither MTPS, LTPS nor PTS revealed increased risk of ACL tears related with higher slopes, although high MTPS showed a decreased risk. However, when comparing traumatic groups, extreme PTS was associated with LCA tear, but no differences were found when comparing non-traumatic groups. This could mean that the importance of extreme angles in the LCA rupture may be restricted to traumatic mechanisms. Previous ACL tear was identified as a risk factor to ACL tear; increased age and a traumatic mechanism were associated with a lower risk.
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