Policlinica Metropolitana

Transcatheter aortic valve implantation (TAVI) is a minimally invasive option for severe aortic stenosis (AS). The Crea Aortic Valve (CAV) is a new self-expanding transcatheter aortic valve implant that has been successfully tested in preclinical studies. We aimed to assess the technical success, device performance, and early safety of the CAV System in a first-in-human study for the device in patients with severe AS. We prospectively evaluated the CAV using the Valve Academic Research Consortium (VARC)-3 criteria in three high-risk patients with severe AS. A computed tomography angiography and transthoracic echocardiographic (TTE) assessment were carried out, which was followed by TAVI according to standard protocol. TTE was performed before and after the procedure, before discharge, and at the 1- and 6-month clinical follow-ups to monitor the aortic valve area, the maximum velocity (Vmax), the mean (MG) and peak pressure gradients, and paravalvular leak (PVL). The CAV was successfully implanted, using the cusp-overlap technique for patient 1 and the coplanar view for patients 2 and 3, with good usability of the delivery system for optimal positioning, reduction of the Vmax to <2 m/s and MG to <10 mmHg, and trivial PVL. An atrioventricular block necessitating a permanent pacemaker occurred in one patient. There was no incidence of stroke, heart failure, or renal failure at 6 months of follow-up. The CAV was implanted with success, and the system performed as intended as per VARC-3 criteria. The device should be evaluated in a larger clinical study for further efficacy and safety data.

MiRNAs are a class of non-coding RNAs acting as gene expression regulators by modulating the lifespan of messenger RNA. Commonly referred to as the most frequent leukemia in the Western world, chronic lymphocytic leukemia (CLL) is a lymphoproliferative malignancy characterized by clonal expansion of CD19, CD23, and CD5-positive mature B-cells. While this pathology is regarded as less aggressive and has a variety of treatment options, the cause of its clinical heterogeneity is not yet understood. Moreover, the prognostic markers and treatment recommendations based on predictive markers are limited. This review aims to investigate some miRNAs that are dysregulated and possibly involved in CLL pathogenesis as a starting point for the proposal of new prognostic and predictive markers and, as more agents targeting miRNA expression become available, their potential role as therapeutic targets.

BackgroundSystemic lupus erythematosus (SLE) SLE often mimics the symptoms of other diseases, and the interval between symptom onset and diagnosis remains long in these patients.ObjectivesTo examine the variables associated with a delay to diagnosis and their impact in damage accrual and mortality in patients with SLE.MethodsGLADEL a multi-ethnic, multi-national Latin-American SLE inception cohort was studied. Patients were recruited based on the physicians’ diagnosis but 97% fulfilled the ACR criteria. Delay to diagnosis was defined as ≥6 months from the first ACR criterion to SLE diagnosis. Socio-demographic, clinical/laboratory, disease activity, damage and mortality were compared using descriptive statistical tests. Multivariable Cox regression (HR) model with damage accrual and mortality as the end points were performed.ResultsOf the 1437 included in this analysis, the median delay to diagnosis was 5.9 months (Q1-Q3 2.4–16.1) and 721 (50.2%) had ≥6 months delay in SLE diagnosis. Patients with delay in diagnosis were more frequently of female gender, older age at diagnosis, mestizo ethnicity and without medical insurance. The characteristics of patients according to delay in diagnosis are depicted in Table 1. Delay to diagnosis did not impact on disease outcome: damage accrual [HR 1.21 (IC 95% 0.78-1.88; p=0.39)] and mortality [HR 1.30, CI 95% 0.84-2.01; p= 0.24)], after adjusting for age at SLE diagnosis, gender, ethnicity and socioeconomic status.ConclusionIn the GLADEL cohort, delay to diagnosis was associated to sex, age, thrombosis, sicca syndrome, cutaneous and neurological involvement. Furthermore, delay to diagnosis had no apparent negative impact on disease outcome (damage accrual and mortality). Early referral when there are suspicious clinical manifestations of SLE is crucial to reduce the diagnostic delay.Table 1.Comparison between the two patient groups in relation at the time to SLE diagnosis.VariableTime to SLE Diagnosis< 6 months (n=716)≥ 6 months (n=721)p valueAge at diagnosis, years(median, IQR)25.6 (16.2)30.4 (15.6)<0.001Follow-up time, months(median, IQR)54(44.1)53(48.6)0.302Female, n %628 (87.7)662 (91.8)0.010Ethnicity, n %MestizoAfrican Latin AmericansCaucasian306 (42.7)116 (16.2)294 (41.1)339 (47.0)70 (9.71)312 (43.3)0.001Education level, years, n%0-7 years8-12 years>12 years216 (30.2)329 (45.9)171 (23.9)237 (32.9)320 (44.4)164 (22.7)0.541Have medical insurance*(13), n%606 (84.6)573 (79.5)0.020Socioeconomic status, n%LowMiddleHigh436 (61.2)204 (28.7)72 (10.1)437 (60.6)208 (28.8)76 (10.6)0.955Clinical manifestations§, n%Malar rashDiscoid lupusPhotosensitivityOral ulcersArthritis/ ArthralgiaPleuritisPericarditisPsychosis/ seizuresHematological disorderProteinuria/ cylindruriaFeverLymphadenopathyLivedo reticularisRaynaud’s phenomenonSicca syndromeCardiac tamponadeVascular thrombosisStroke (ischemic)Pulmonary involvementPeritoneal serositis376 (52.5)70 (9.8)327 (45.7)239 (33.4)611 (85.3)124 (17.3)92 (12.9)39 (5.5)372 (52.0)254 (35.5)403 (56.3)97 (13.6)32 (4.5)125 (17.5)21 (2.9)6 (0.8)14 (2.0)4 (0.6)24 (3.4)9 (1.3)186 (25.8)72 (10.0)379 (52.6)226 (31.4)634 (87.9)104 (14.4)61 (8.5)60 (8.3)403 (55.9)202 (28.0)303 (42.0)67 (9.3)52 (7.2)190 (26.4)52 (7.2)0 (0.0)28 (3.9)12 (1.7)14 (1.9)1 (0.1)0.9000.8940.0090.4090.1480.1330.0070.0310.1340.002<0.0010.0110.027<0.0010.0020.0140.0300.0460.0960.011Hypocomplementemia§, n%487 (68.0)385 (53.4)<0.001Antiphospholipid antibodies§, n%363 (50.7)375 (52)0.795SLEDAI† at diagnosis, median (RIQ)*(257)12.0 (10.0)9.0 (9.0)<0.001SDI at the last visit‡ ≥ 1494 (69.0)484 (67.1)0.448Death during follow-up, n%39 (5.5)45 (6.2)0.521SD (standard deviation); IQR (Interquartile range); § Before SLE diagnosis; † Systemic Lupus Erythematosus Disease Activity Index; ‡ SDI (Systemic Lupus International Collaborating Clinics) Damage Index;*(Missing data)REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

BackgroundSystemic Lupus Erythematosus (SLE) patients experience frequent hospitalizations; lupus flares and infections have been shown to be the two most common causes.ObjectivesThe aim of this study is to describe the main causes and predictors of first hospitalizations due to disease activity and infections in SLE patients.MethodsSLE patients from GLADEL, a multi-ethnic, multi-national Latin-American (LA) cohort were studied. The first hospitalization during these patients’ follow-up due to either infection and/or SLE disease activity was examined. Baseline sociodemographic, clinical, damage (SDI) and treatments were evaluated as possible predictors. First, descriptive analyses were performed. Predictors of infection or SLE disease activity associated hospitalization were identified using univariate and multivariate logistic.ResultsA total of 1341 patients were included; 1201 (89.6%) were female. Their median interquartile range (IQR) age at diagnosis was 27 (20-37) years and their median IQR follow up time 27.5 (4.7-62.2) months. 456 (34.9%) patients were hospitalized; 344 (75.4%), 85 (18.6%) and 27 (5.9%) were hospitalized for disease activity, infections, or both, respectively, as depicted in Graph 1. In the multivariable analysis, arthritis was associated with hospitalizations due to infection. Serositis, disease activity and damage were associated with hospitalizations due to disease activity. Older age, higher socioeconomic status and antimalarial use were found to be protective, as depicted in table 1.Figure 1.Table 1.Univariable and multivariable logistic regression analysis of predictors of hospitalization due to disease activity and infections in patients with SLEINFECTIONSUnivariable OR (95% CI)p valueMultivariable OR (95% CI)p valueACTIVITYUnivariable OR (95% CI)p valueMultivariable OR (95% CI)p valueGender, Female1.14 (0.54-2.41)0.73Gender, Female0.89 (0.60-1.32)0.56Age at diagnosis1.00 (0.98-1.02)0.78Age at diagnosis0.98 (0.97-0.99)<0.0010.98 (0.97-0.99)0.02EthnicityCaucasiansMestizoALAOthersRef.1.47 (0.90-2.38)0.84 (0.36-1.95)2.34 (0.86-6.39)0.16EthnicityCaucasiansMestizoALAOthersRef.1.26 (0.96-1.65)1.51 (1.02-2.23)1.13 (0.55-2.31)0.16Socioeconomic statusHighMediumLow0.60 (0.25-1.42)0.63 (0.37-1.07)Ref.0.16Socioeconomic statusHighMediumLow0.24 (0.13-0.44)0.75 (0.57-0.98)Ref.<.00010.32 (0.17-0.61)0.89 (0.65-1.22)Ref.0.002SDI*b1.11 (0.93-1.33)0.25SDI ab1.52 (1.37-1.70)<.00011.33 (1.18-1.50)<.0001SLEDAI*1.02 (0.99-1.04)0.20SLEDAI a1.07 (1.05-1.09)<.00011.05 (1.03-1.07)<.0001Arthritis1.90 (0.99-3.64)0.051.93 (1.01-3.72)0.05Arthritis0.83 (0.62-1.11)0.21Serositis1.27 (0.78-2.07)0.34Serositis1.62 (1.23-2.14)<0.0011.40 (1.02-1.92)0.04Renal1.38 (0.89-2.15)0.15Renal2.31 (1.79-2.96)<.0001Anti-dsDNA1.38 (0.76-2.52)0.29Anti-dsDNA1.40 (1.01-1.94)0.04Antimalarial use1.35 (0.86-2.12)0.19Antimalarial use0.52 (0.39-0.70)<.00010.71 (0.51-0.98)0.04PrednisonecNone<7.5mg/d7.5-15mg/d15-60mg/d≥60mg/dRef.1.56 (0.36-6.86)1.44 (0.62-3.32)2.07 (1.22-3.52)1.84 (0.97-3.49)0.08PrednisonecNone<7.5mg/d7.5-15mg/d15-60mg/d≥60mg/dRef.0.76 (0.30-1.90)0.86 (0.53-1.38)0.84 (0.61-1.16)0.89 (0.60-1.31)0.79ALA: African Latin American; LDAS: Low disease activity; SLEDAI: Systemic Lupus Erythematosus Disease Activity Index; SDI: Systemic Lupus International Collaborating Clinics/American College of Rheumatology Disease Index, * At cohort entry, aAt diagnosis, bIncrease on per 1 unit, c highest doseConclusionIn this large LA lupus cohort, one third of the patients had at least one hospitalization; of them, were due to SLE disease activity. Our findings call attention for controlling disease activity and preventing damage using antimalarials early in the disease course disease to prevent the first hospitalization.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsRosana Quintana: None declared, Romina Nieto: None declared, Rosa Serrano Morales: None declared, Manuel F. Ugarte-Gil: None declared, Guillermina B. Harvey: None declared, Daniel Wojdyla: None declared, Jose A. Gómez-Puerta: None declared, Mercedes García: None declared, Luis Catoggio: None declared, Veronica Saurit: None declared, Cristina Drenkard: None declared, Nílzio da Silva: None declared, Fernando Cavalcanti: None declared, Eduardo Borba: None declared, Emília Sato: None declared, Oscar Neira: None declared, loreto massardo: None declared, Gloria Vásquez: None declared, Luis Alonso González: None declared, Marlene Guibert-Toledano: None declared, Luis Humberto Silveira Torre: None declared, Ignacio Garcia-De La Torre: None declared, MARIA JOSEFINA SAUZA DEL POZO: None declared, Rosa Chacon: None declared, Graciela S Alarcon: None declared, Ashley Orillion Employee of: Janssen Pharmaceutical Companies of Johnson & Johnson, Spring House, PA, USA, Urbano Sbarigia Employee of: Janssen Pharmaceutica NV, Beerse, BE, Federico Zazzetti Employee of: Janssen Pharmaceutical Companies of Johnson & Johnson, Horsham, PA, USA, Bernardo Pons-Estel: None declared, Guillermo Pons-Estel: None declared.

Se analizó un resultado con alteración cromosómica tomado de una base de datos conformada por un total de 4755 muestras de líquido amniótico extraídos mediante amniocentesis con indicación de su médico tratante, riesgo sérico y edad materna avanzada. En este reporte se presenta la detección de un mosaico de trisomía 21 en líquido amniótico, mediante la técnica de Banda G donde se analizaron 20 metafases. Los resultados obtenidos documentan una composición cromosómica 47, XY+21 y 46, XY con una relación 9:11 respecto a las metafases analizadas, confirmándose así el diagnostico del Síndrome de Down secundario a mosaico.

Esophageal intramural pseudodiverticulosis is an uncommon esophageal benign disease. The typical finding during endoscopy is the presence of numerous pinhead-sized outpouchings along the esophageal wall. We reported a case of food bolus impaction secondary to esophageal intramural pseudodiverticulosis. A 67-year-old man presented with sudden-onset dysphagia. Multiple tiny orifices were revealed during upper endoscopy. In addition, there were an impacted food bolus and an esophageal web. The patient was treated with balloon dilatation and proton pump inhibitors. As a result the symptoms disappeared completely. Esophageal intramural pseudodiverticulosis is a rare cause of food bolus impaction and its treatment is directed towards the underlying associated conditions as well as the resolution of complications.