ABSTRACT
La duodenitis eosinofílica tiene una prevalencia entre 5,1 a 8,2 por 100000 personas. Se desconocen los mecanismos moleculares subyacentes de la enfermedad, pero la hipersensibilidad (alergias estacionales y alimentarias) juega un papel importante en su patogénesis, la predisposición alérgica se encuentra en el 25-35% de los casos. El diagnóstico incluye manifestaciones clínicas, hallazgos imagenológicos y evidencia histológica de infiltración eosinofílica >20 eosinófilos por campo de alto poder. Realizamos un informe de caso clínico y revisión de literatura. Hombre de 25 años con vitíligo que consulta a urgencias refiriendo síntomas de dispepsia, vómitos y dolor abdominal de máxima intensidad, en el examen médico se localiza dolor abdominal superior, con paraclínicos normales excepto un recuento de eosinófilos >2000 células/ul, la ecografía abdominal fue normal, la endoscopia superior reveló pangastritis eritematosa y duodenitis con pliegues rígidos y engrosados, la colonoscopia mostró hemorroides grado I. Coproscópico seriado negativo para parásitos, IgE total, IgA e IgG en rango normal, se reportó IgG positivo a Toxoplasma gondii, perfil de autoinmunidad negativo. En los siguientes 4 días aumenta el dolor abdominal y el recuento de eosinófilos, con endoscopia control y tomografía abdomino-pélvica contrastada que muestran duodeno edematizado con reflujo biliar severo, reporte histopatológico con duodenitis crónica atrófica y con pruebas para alergenos alimentarios positivo a cereales (centeno, soja, cebada), Manihot esculenta, plátano verde, tomate, leche de vaca, naranja y piña. Se indicó dieta restrictiva e inhibidor de la bomba de protones (pantoprazol), control ambulatorio a los 45 días de resolución de los síntomas con recuento de eosinófilos en sangre normal. Se presenta un caso de duodenitis eosinofílica relacionada con alergia alimentaria con mecanismos IgE independientes en un varón joven con vitíligo, que debutó con cuadro clínico inusual de dolor visceral agudo y reflujo biliar, que se resolvió con dieta de eliminación y pantoprazol sin uso de corticoides.
Background: Eosinophilic duodenitis has a prevalence of 5.1 to 8.2 per 100000 persons. The underlying molecular mechanisms are unknown, but hypersensitivity (seasonal and food allergies, asthma, eczema) response plays a major role in its pathogenesis, allergic predisposition can be found up-to 25-35% of cases. The diagnosis includes clinical manifestation, imaging findings and histological evidence of eosinophilic infiltration >20 eosinophils per high-power field. This is a clinical case report. a 25-years old man with vitiligo consult to emergency department referring dyspepsia symptoms, vomiting and abdominal pain of maximal intensity, in the medical exam upper abdominal pain was found, blood laboratories were unremarkable except a high net eosinophil-count >2000 cells/ul, abdominal ultrasound were normal, upper endoscopy revealed duodenitis with rigid and thickened folds, colonoscopy show hemorrhoids grade I. Coproscopy exam was negative for parasites, total IgE, IgA and IgG were in normal range, a positive IgG to Toxoplasma gondii was reported, autoimmunity panel was negative. In the following 4 days the abdominal pain and eosinophils count increase, a new abdomin-pelvic tomography was done showing thickened duodenum with a new endoscopy showing marked edema in duodenum with severe biliary reflux with biopsies describing an atrophic chronic duodenitis. Allergy tests -skin prick and patch tests- were done resulting positive to cereals (rye, soy, barley), Manihot esculenta, green banana, tomato, cow milk, orange and pineapple. A restrictive diet and protons pump inhibitor was indicated, ambulatory control at 45 days after show symptoms resolution with a normal blood eosinophils count. Here is reported a case of eosinophilic duodenitis related to food allergy in a young man with vitiligo debuting with an unusual clinical presentation of acute visceral pain and biliary reflux which resolved with elimination diet and pantoprazole without use of corticoids, with both, IgE and non-IgE mechanisms playing important roles explaining food sensitization.
ABSTRACT
BACKGROUND: Eosinophilic duodenitis has a prevalence of 5.1 to 8.2 per 100000 persons. The underlying molecular mechanisms are unknown, but hypersensitivity (seasonal and food allergies, asthma, eczema) response plays a major role in its pathogenesis, allergic predisposition can be found up-to 25-35% of cases. The diagnosis includes clinical manifestation, imaging findings and histological evidence of eosinophilic infiltration >20 eosinophils per high-power field. This is a clinical case report. a 25-years old man with vitiligo consult to emergency department referring dyspepsia symptoms, vomiting and abdominal pain of maximal intensity, in the medical exam upper abdominal pain was found, blood laboratories were unremarkable except a high net eosinophil-count >2000 cells/ul, abdominal ultrasound were normal, upper endoscopy revealed duodenitis with rigid and thickened folds, colonoscopy show hemorrhoids grade I. Coproscopy exam was negative for parasites, total IgE, IgA and IgG were in normal range, a positive IgG to Toxoplasma gondii was reported, autoimmunity panel was negative. In the following 4 days the abdominal pain and eosinophils count increase, a new abdomin-pelvic tomography was done showing thickened duodenum with a new endoscopy showing marked edema in duodenum with severe biliary reflux with biopsies describing an atrophic chronic duodenitis. Allergy tests -skin prick and patch tests- were done resulting positive to cereals (rye, soy, barley), Manihot esculenta, green banana, tomato, cow milk, orange and pineapple. A restrictive diet and protons pump inhibitor was indicated, ambulatory control at 45 days after show symptoms resolution with a normal blood eosinophils count. Here is reported a case of eosinophilic duodenitis related to food allergy in a young man with vitiligo debuting with an unusual clinical presentation of acute visceral pain and biliary reflux which resolved with elimination diet and pantoprazole without use of corticoids, with both, IgE and non-IgE mechanisms playing important roles explaining food sensitization.