Cambios estructurales de la superficie dental erosionada pre y post tratamiento con bicarbonato de arginina y monofluorofosfato de sodio: estudio piloto / Structural changes of the eroded tooth surface before and after treatment with arginine bicarbonate and sodium monofluorophosphate: pilot study

La erosión dental se define como la pérdida patológica, crónica e indolora de los tejidos dentales, por la acción química de ácidos no producidos por la microflora bacteriana bucal. Los estadíos más avanzados pueden generar diferentes niveles de desgaste y producir hipersensibilidad destinaria. Objetivo: evaluar y describir los cambios estructurales de la superficie dental erosionada pre y post tratamiento con bicarbonato de arginina y monofluorofosfato de sodio, observados mediante microscopia electrónica de barrido (MEB). Materiales y Métodos: Se realizó un estudio piloto de tipo descriptivo, transversal y cuasi-experimental. Se seleccionó una muestra de cuatro pacientes, previo consentimiento informado; de manera aleatoria se le asignó el tratamiento luego de la primera cirugía, grupo 1 (bicarbonato de arginina) y grupo 2 (monofluorofosfato de sodio). Las exodoncias se realizaron en dos tiempos (tiempo 0 y post-tratamiento) para obtener los especímenes y ser evaluados con MEB. Resultados: Tras la evaluación realizada por MEB se observó que los segmentos de esmalte dental diagnosticados clínicamente con grado 1 de erosión, ya presentaban exposición de algunos túbulos dentinarios en la superficie evaluada. Luego de 14 días de tratamiento, se observó que ambas cremas dentales fueron capaces de sellar la entrada de los canalículos dentinarios; sin embargo, la crema dental con bicarbonato de arginina, formó una estructura mineralizada que se depositó sobre la superficie dental. Conclusión: ambos tratamientos fueron capaces de producir cambios estructurales en la superficie dental erosionada sellando la entrada de los túbulos dentinarios(AU)

Dental erosion is defined as the pathological, chronic and painless loss of dental tissues due to the chemical action of acids not produced by the oral bacterial microflora. The more advanced stages can generate different levels of wear and produce dentine hypersensitivity. Objective: to evaluate and describe the structural changes of the eroded dental surface before and after treatment with arginine bicarbonate and sodium monofluorophosphate, observed by scanning electron microscopy (SEM). Materials and Methods: A pilot study of descriptive, transversal and quasi-experimental type was carried out. A sample of four patients was selected, with prior informed consent; Randomly, he was assigned to the treatment after the first surgery, group 1 (arginine bicarbonate) and group 2 (sodium monofluorophosphate). Extractions were performed in two stages (time 0 and post-treatment) to obtain the specimens and be evaluated with SEM. Results: After the evaluation made by SEM, it was observed that dental enamel segments clinically diagnosed with erosion grade 1, already had exposure of some dentinal tubules in the evaluated surface. After 14 days of treatment, it was observed that both dental creams were able to seal the entrance of the dentinal canaliculi; however, the toothpaste with arginine bicarbonate, formed a mineralized structure that was deposited on the tooth surface. Conclusion: both treatments were able to produce structural changes in the eroded dental surface sealing the entrance of the dentinal tubules(AU)

IgE-mediated allergy to proton pump inhibitors with both delayed and immediate onset

Proton pump inhibitors (PPIs) are widely used for the treatment of gastrointestinal diseases. Incidence of drug hypersensitivity reactions (DHRs) to PPIs has been rising, presumably because of their increased consumption. Most DHR are IgE-mediated, with half of the reactions being anaphylactic. We describe the case of a Caucasian 50-year-old female patient referred to our allergy department after 2 episodes of anaphylaxis. The allergy work-up distinguished PPI as a cause of delayed onset (14 hours) and immediate onset (45 minutes) IgE-mediated DHR.

Muerte súbita asociada a hipersensibilidad tipo I en un equino pura sangre de carrera / Sudden death associated to type I hypersensitivity in a racing horse

El objetivo de este estudio fue reportar un caso de hipersensibilidad tipo I con muerte súbita en un equino Pura Sangre de Carrera en el Hipódromo “La Rinconada” Caracas, Venezuela. Se tomaron muestras de sangre y orina para estudios toxicológicos mediante la técnica de ELISA competitivo. Se le práctico la técnica de necropsia, fueron colectadas muestras de musculo, tejido pulmonar, hepático, renal, gástrico, esplénico, corazón y sistema nervioso central para estudio histopatológico, las muestras fueron procesados por los métodos convencionales histológicos. Los hallazgos de necropsia fueron flebitis severa en vena yugular derecha, con hematoma en el surco yugular. Edema severo de glotis, edema, congestión y hemorragia pulmonar. Hemorragia petequial subendocardica. Bazo esplenocontraido y con focos de necrosis de coagulación. Hidronefrosis aguda con hematuria. Hígado con patrón lobulillar acentuado. El resto de los órganos con evidente congestión y hemorragia. Los cortes histológicos evidenciaron edema, congestión y hemorragia pulmonar severa. Hemorragia subepicardica marcada. Edema subcapsular esplénico y necrosis centro-folicular. Degeneración hidropica tubular, necrosis tubular aguda. Necrosis de corteza renal. Los estudios toxicológicos permitieron la detección de furosemida y fenilbutazona en las muestras de sangre y orina. En conclusión se reporta un síndrome de hipersensibilidad tipo I asociado a la administración de un producto comercial a base de Vitamina E 80mg, Pangamato sódico (B15) 1 mg, Selenio Sódico 0.6 mg, Antioxidantes y Vehículos Solubles c.s.p. con colapso, shock y muerte aguda en un equino Pura Sangre de Carrera mediante un estudio multidisciplinario clínico, anatomopatologico y toxicológico.

The aim of this study was to report a case of type I hypersensitivity to sudden death in a Thoroughbred race horses at the Hippodrome “La Rinconada” Caracas, Venezuela. Samples of blood and urine for toxicology studies using competitive ELISA. He practiced the technique of necropsy, samples were collected from muscle, lung tissue, liver, kidney, stomach, spleen, heart and central nervous system for histopathological examination, samples were processed by conventional histological methods. Autopsy findings were severe phlebitis right jugular vein, with hematoma in the jugular groove. Severe edema of glottis edema, pulmonary congestion and hemorrhage. Subendocardial petechial hemorrhage. Esplenocontraido Spleen foci of necrosis and coagulation. Hydronephrosis with acute hematuria. Liver accentuated lobular pattern. The rest of the organs with obvious congestion and hemorrhage. The histological sections showed edema, severe pulmonary congestion and hemorrhage. Marked subepicardial hemorrhage. Edema and necrosis subcapsular splenic follicular center. Tubular hydropic degeneration, acute tubular necrosis. Necrosis of renal cortex. Toxicological studies allowed the detection of furosemide and phenylbutazone in samples of blood and urine. In conclusion we report type I hypersensitivity syndrome associated with the administration of a commercial product based Vitamin E 80mg, sodium pangamate (B15) 1 mg, 0.6 mg; Sodium Selenium, Soluble Antioxidants and Vehicle qs with collapse, shock and acute death in a race Thoroughbred horses by a multidisciplinary clinical, pathological and toxicological.

Functional changes of dendritic cells in hypersensivity reactions to amoxicillin

A better understanding of dendritic cell (DC) involvement in responses to haptenic drugs is needed, because it represents a possible approach to the development of an in vitro test, which could identify patients prone to drug allergies. There are two main DC subsets: plasmacytoid DC (pDC) and myeloid DC (mDC). β-lactams form hapten-carrier conjugates and may provide a suitable model to study DC behavior in drug allergy reactions. It has been demonstrated that drugs interact differently with DC in drug allergic and non-allergic patients, but there are no studies regarding these subsets. Our aim was to assess the functional changes of mDC and pDC harvested from an amoxicillin-hypersensitive 32-year-old woman who experienced a severe maculopapular exanthema as reflected in interleukin-6 (IL-6) production after stimulation with this drug and penicillin. We also aim to demonstrate, for the first time, the feasibility of this method for dendritic cell isolation followed by in vitro stimulation for studies of drug allergy physiopathology. DC were harvested using a double Percoll density gradient, which generates a basophil-depleted cell (BDC) suspension. Further, pDC were isolated by blood DC antigen 4-positive magnetic selection and gravity filtration through magnetized columns. After stimulation with amoxicillin, penicillin and positive and negative controls, IL-6 production was measured by ELISA. A positive dose-response curve for IL-6 after stimulation with amoxicillin and penicillin was observed for pDC, but not for mDC or BDC suspension. These preliminary results demonstrate the feasibility of this methodology to expand the knowledge of the effect of dendritic cell activation by drug allergens.

Tubercúlides: revisão sobre tema polêmico / Tuberculids: revision on controversial theme

Tubercúlides representam uma forma de reação de hipersensibilidade a antígenos bacterianos liberados de um foco de infecção distante. A maioria dos pacientes é caracterizada por apresentar PPD forte reator e evidência de passado de tuberculose pulmonar e(ou) contactante. O tratamento é baseado na terapia de dessensibilização com tuberculina, drogas antituberculosas e corticóides.

Tuberculids represent a form of hypersensitivity reaction to tuberculosis antigens released from a distant focus of infection. Most of patients are characterized by displaying a markedly positive Mantoux skin test and evidence of past tuberculosis infection or contacts of patient with tuberculosis. The treatment is based on tuberculin desensitizing therapy, antituberculous drugs and corticosteroids.