RESUMEN
HELLP, a syndrome characterised by haemolysis, elevated liver enzymes and low platelets, a variant of pre-eclampsia/eclampsia, is a multisystemic disorder with an incidence of up to 0.9% in all pregnancies and occurs in about one-quarter of pre-eclamptic patients. Most obstetricians presume that HELLP derives from an autoimmune reaction, leading to a materno- fetal imbalance, with accompanying aggregation of platelets, endothelial malfunction along with inborn errors of fatty acid oxidative metabolism. HELLP is characterised by high mortality and morbidity rates, leading to possibly life-threatening complications regarding both the mother and the fetus. Delivery is indicated if HELLP syndrome occurs after 34 gestational weeks or the fetal and/or maternal conditions deteriorate. Vaginal delivery is preferable. Standard corticosteroid treatment is of uncertain clinical value in maternal HELLP syndrome. Future observations and research results may shed more light on improving our understanding of the aspects of HELLP syndrome.
Asunto(s)
Síndrome HELLP/diagnóstico , Síndrome HELLP/etiología , Síndrome HELLP/terapia , Diagnóstico Diferencial , Femenino , Síndrome HELLP/epidemiología , Humanos , Recién Nacido , Enfermedades del Recién Nacido/etiología , EmbarazoRESUMEN
Irritable bowel syndrome (IBS) is considered to be a physical disorder that mainly affects the bowel and is clinically characterized by lower abdominal pain or discomfort, diarrhea, constipation (or alternating diarrhea/constipation), gas, bloating, and nausea. According to recent studies, it appears that there is an association with increased prolactin levels in patients suffering from IBS. We report a rare case of regression of IBS symptoms (constipation type) in a 16-year-old female adolescent after receiving cabergoline for treating hyperprolactinemia due to pituitary macroadenoma. Our hypothesis is that increased prolactin levels, for instance due to a pituitary adenoma, may suppress prolactin-releasing peptide release and lead to a reverse feedback interaction, consequently resulting in oversecretion of cholecystokinin, inducing the development of IBS.