ABSTRACT
Los agonistas GLP-1 presentan como efectos secundarios más frecuentes las náuseas y vómitos que son de carácter leves y moderados, siendo transitorios y dosis dependiente sin necesidad de suspender el fármaco en la mayoría de casos. Estos efectos ocurren más frecuentemente con exenatide y raramente con liraglutide, sin conocer un caso clínico de tal severidad y sobre todo precocidad. Se describe una mujer de 55 años caucasiana con diabetes mellitus tipo 2 de larga evolución asociadas que presentó cuadro de dolor abdominal, náuseas, vómitos incoercibles e hiperlipasemia de aparición súbita tras la primera dosis de titulación de liraglutide, completando solo 2 dosis en 48 horas, consultando en urgencias donde se apreció fracaso renal agudo y descompensación hiperosmolar que requirió su ingreso en unidad de cuidados intensivos. Al emplear la escala de probabilidad de reacción a fármaco de Naranjo obtenemos dicha reacción como probable, sin encontrar otras alternativas justificables clinicamente.
The most frequent side effects seen with GLP-1 agonists are mild and moderate nausea and vomiting, which are typically transient and dose-dependent, in most cases not requiring discontinuation of the drug. These effects occur most frequently with exenatide, and rarely with liraglutide; no clinical cases with such a severity -and especially with such an early occurrence- had been previously reported. The case herein described is that of a 55-year-old Caucasian female with a long-standing Type 2 diabetes mellitus, who presented with sudden abdominal pain, nausea, relentless vomiting an increased lipase serum levels after the first dosage of liraglutide, after completing only 2 dosages in 48 hours. The patient was seen at the emergency room, where she was diagnosed acute renal failure and hyperosmolar decompensation that required admission at the intensive care unit. According to Naranjo’s odds scale, the reaction was considered to be likely related to the drug; no other alternatives were considered to be clinically justified.
ABSTRACT
Celiac disease (CD), with a 1 percent worldwide prevalence, is an enteropathy caused by an autoimmune reaction to gluten in genetically susceptible individuals, which codify for histocompatibility molecules HLA DQ-2/DQ-8. From the anatomical point of view, CD is characterized by intestinal villous atrophy, crypt hyperplasia, intraepithelial lymphocytosis (IELs) and leukocyte infiltration of the lamina propriety. Patients achieve a complete clinical and endoscopic remission with a gluten free diet. However, symptoms and anatomical alterations recur when this protein is reintroduced in the diet. The pathogenic mechanisms in this disease are not yet well understood, but it is clear that genetic, environmental and immunological factors play a role. The latter are the focus of this review, since this is the only autoimmune disease whose precipitating factor for immunological tissue damage is known.