CHOICE international survey: Clusters of allergen immunotherapy prescription from French and Spanish cohorts.

Background: There is no description of the drivers of prescription for allergen immunotherapy (AIT) for respiratory allergic diseases. Methods: A prospective, multicentre, observational, non-interventional real-life study was performed in France and Spain for 20 months. Data were gathered using 2 different questionnaires, anonymously collected in an online platform. No names of AIT products were recorded. Multivariate analysis and unsupervised cluster analysis were performed. Results: One hundred and three physicians (50.5% from Spain and 49.5% from France) reported 1735 patients (433 in France and 1302 in Spain), 47.9% males, 64.8% adults with a mean age 26.2 years old. They suffered from allergic rhinitis (99%), allergic conjunctivitis (70.4%), allergic asthma (51.8%), atopic dermatitis (13.9%), and food allergy (9.9%). A clustering analysis based on 13 predefined relevant variables for AIT-prescription identified 5 different clusters, each of them including information regarding doctor's profile and patient demographics, baseline disease characteristics, and main AIT indication: 1) Looking at the future: focusing on asthma prevention (n = 355), 2) Efficacy after discontinuation of AIT (n = 293), 3) Fighting severe allergic disease (n = 322), 4) Looking at the present, facing current symptoms (n = 265) and 5) Doctor's own clinical experience (n = 500). Each one of these clusters have specific patients' and doctors' characteristics, representing distinctive AIT prescription drivers. Conclusion: Using data-driven analysis, we identified for the first time some reasons and patterns of AIT prescriptions in real-life clinical settings. There is no uniform indication for prescribing AIT, which varies amongst patients and doctors with multiple but specific drivers, taking into account several relevant parameters.

Adenoma de conductos biliares (hamartoma de glándulas peribiliares): la importancia de su adecuado reconocimiento / Bile duct adenoma (hamartoma of peribiliary glands): Importance of an adequate diagnosis

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Ablación de extrasistolia ventricular del tracto de salida ventricular derecho con sistema de cartografía sin contacto / Ablation of premature ventricular contractions originating in the right ventricular outflow tract using non-contact mapping

La extrasistolia ventricular originada en el tracto de salida de ventrículo derecho puede tener una respuesta pobre a fármacos y ser compleja de ablacionar mediante un sistema convencional con guía fluoroscópica debido a la dificultad en la inducibilidad. Describimos la ablación de extrasistolia ventricular de difícil inducibilidad originada en el tracto de salida de ventrículo derecho, mediante un sistema de cartografía sin contacto. Se realizó ablación de cinco focos extrasistólicos originados en tracto de salida de ventrículo derecho en una serie prospectiva de 4 pacientes. Los pacientes presentaban pobre calidad de vida y falta de respuesta a antiarrítmicos. Se realizó una media de tres aplicaciones de radiofrecuencia por foco, con un tiempo medio de aplicación de 113±15 s. Se obtuvo un 100% de éxito agudo y no hubo complicaciones. En un seguimiento medio de 30±16 meses, los pacientes se mantienen asintomáticos sin tratamiento farmacológico. El sistema de cartografía sin contacto permite una alta eficacia en la eliminación de extrasistolias ventriculares aisladas de difícil inducibilidad (AU)

Premature ventricular contractions originating in the right ventricular outflow tract may respond poorly to pharmacological treatment, and ablation using conventional fluoroscopically-guided systems may be complicated by the difficulty in inducing arrhythmias. We describe the use of a non-contact mapping system to ablate difficult-to-induce premature ventricular contractions originating in the right ventricular outflow tract. Five premature ventricular contractions sites in the right ventricular outflow tract were ablated in a prospective series of 4 patients. Patients had a poor quality of life and had not responded to antiarrhythmic drugs. A mean of 3 radiofrequency pulses per site was applied and mean application time was 113±15s. We achieved a 100% acute success rate and there were no complications. Patients were asymptomatic without drug therapy after a mean of 30±16 months of follow-up. The noncontact mapping system is highly effective in eliminating difficult to induce, isolated premature ventricular contractions (AU)

[Ablation of premature ventricular contractions originating in the right ventricular outflow tract using non-contact mapping]. / Ablación de extrasistolia ventricular del tracto de salida ventricular derecho con sistema de cartografía sin contacto.

Premature ventricular contractions originating in the right ventricular outflow tract may respond poorly to pharmacological treatment, and ablation using conventional fluoroscopically-guided systems may be complicated by the difficulty in inducing arrhythmias. We describe the use of a non-contact mapping system to ablate difficult-to-induce premature ventricular contractions originating in the right ventricular outflow tract. Five premature ventricular contractions sites in the right ventricular outflow tract were ablated in a prospective series of 4 patients. Patients had a poor quality of life and had not responded to antiarrhythmic drugs. A mean of 3 radiofrequency pulses per site was applied and mean application time was 113±15s. We achieved a 100% acute success rate and there were no complications. Patients were asymptomatic without drug therapy after a mean of 30±16 months of follow-up. The noncontact mapping system is highly effective in eliminating difficult to induce, isolated premature ventricular contractions.

Regulation of corticosterone production by vasopressin during water restriction and after drinking in rats.

Plasma vasopressin (VP) and corticosterone have each been shown to be rapidly suppressed after drinking in different models of osmotic stimulation in rats; however, no causal relationship between these responses has been investigated. Studies were performed to determine if plasma VP and corticosterone are reduced in parallel after drinking and if manipulation of plasma VP affects plasma, ACTH corticotropins and corticosterone in a model of water restriction. A strong correlation between changes in plasma VP and corticosterone, but not between plasma ACTH and corticosterone, was observed after drinking induced by 6 days of water restriction. Similarly, ingestion of isotonic saline resulted in a biphasic VP response that was paralleled by adrenal and plasma corticosterone, but not by plasma ACTH. Administration of an immunoneutralizing antibody directed against VP resulted in a rapid decrease in plasma corticosterone, but not ACTH, in water-restricted rats, but not in rats receiving water ad libitum. These data suggest that during dehydration, elevated plasma VP can stimulate the production of corticosterone by the adrenal, independently of ACTH. Moreover, they support the hypothesis that the decline in corticosterone after restriction-induced drinking is due, in part, to a decline in plasma VP.

Does whole body autoregulation mediate the hemodynamic responses to increased dietary salt in rats with clamped ANG II?

The present study was conducted to test the hypothesis that salt-dependent hypertension, in rats with an unresponsive renin-angiotensin system, is characterized by a "whole body autoregulation" hemodynamic profile. To test this hypothesis, rats were chronically instrumented to continuously measure cardiac output (CO) and arterial pressure (AP). A venous catheter was implanted for infusion of saline vehicle (Veh; n = 8) or treatment [enalapril (2 mg.kg-1.day-1) plus ANG II: ANG-NORM (5 ng.kg-1.min-1 ANG II, n = 8) or ANG-HI (10 ng.kg-1.min-1 ANG II, n = 9)] to pharmacologically clamp plasma ANG II. After a 10-day recovery period on a 0.1% NaCl diet, AP and CO were measured continuously for 5 days of control (0.1% NaCl), 7 days of high salt (4.0% NaCl), and 5 days of recovery (0.1% NaCl). Hemodynamics did not change in the Veh group at any time. AP increased by approximately 20 mmHg in the ANG-NORM and ANG-HI groups when NaCl was increased. Hypertension was mediated by an increase in CO of approximately 12% at steady state, with no change in total peripheral resistance (TPR) during the high salt period. AP returned to control levels when dietary sodium was decreased, mediated by a approximately 10% decrease in TPR, with CO remaining elevated. There was no difference in the hemodynamic responses to increased salt between the ANG-HI and ANG-NORM groups. We conclude that the whole body autoregulation hypothesis does not explain the hemodynamic profile of salt-dependent hypertension in rats with an unresponsive renin-angiotensin system.

Responsiveness vs. basal activity of plasma ANG II as a determinant of arterial pressure salt sensitivity.

Infusion of angiotensin II (ANG II) causes salt-sensitive hypertension. It is unclear whether this is due to the body's inability to suppress ANG II during increased salt intake or, rather, an elevated basal level of plasma ANG II itself. To distinguish between these mechanisms, Sprague-Dawley rats were instrumented with arterial and venous catheters for measurement of arterial pressure and infusion of drugs, respectively. The sensitivity of arterial pressure to salt was measured in four groups with the following treatments: 1) saline control (Con, n = 12); 2) administration of the angiotensin-converting enzyme inhibitor enalapril to block endogenous ANG II (ANG-Lo, n = 10); 3) administration of enalapril and 5 ng.kg(-1).min(-1) ANG II to clamp plasma ANG II at normal levels (ANG-Norm, n = 10); and 4) administration of enalapril and 20 ng.kg(-1).min(-1) ANG II to clamp ANG II at high levels (ANG-Hi, n = 10). Rats ingested a 0.4% NaCl diet for 3 days and then a 4.0% NaCl diet for 11 days. Arterial pressure of rats fed the 0.4% NaCl diet was lower in ANG-Lo (84 +/- 2 mmHg) compared with Con (101 +/- 3 mmHg) and ANG-Norm (98 +/- 4 mmHg) groups, whereas ANG-Hi rats were hypertensive (145 +/- 4 mmHg). Salt sensitivity was expressed as the change in arterial pressure divided by the change in sodium intake on the last day of the 4.0% NaCl diet. Salt sensitivity (in mmHg/meq Na) was lowest in Con rats (0.0 +/- 0.1) and progressed from ANG-Lo (0.8 +/- 0.2) to ANG-Norm (1.5 +/- 0.5) to ANG-Hi (3.5 +/- 0.5) rats. We conclude that the major determinant of salt sensitivity of arterial pressure is the basal level of plasma ANG II rather than the responsiveness of the renin-angiotensin system.