ABSTRACT
Between november 1994 and september 1995, there were 4 cases of premature infants in our Neonatal Intensive Care Unit (NICU) who developed gastrointestinal perforation and bleeding due to peptic ulcer and 3 died of this complication. In the first case, the neonate developed pneumoperitonium when weaning from the ventilator and was submitted to the operation with clinical diagnosis of Necrotizing Enterocolitis. Surprisingly, during the procedure, a perforated gastric ulcer was disclosed. Ever since, this NICU is aware of this diagnosis and try to better identify the possible risks factors. Asphyxia, prematurity, stress and situations where low gastrointestinal flow (asphyxia, exchange transfusion, pneumothorax, hemodynamic shock, cardiac arrest) were observed in almost every case. Treatment with dexamethasone or aminophilline was used in 3 of 4 cases and this potential serious side effect should be considered in all babies treated with steroids. The association of ranitidine (2 mg/kg 12/12 h) could not prevent the perforation in cases 1 and 3. Better understanding of physiopathology of the ulcer in this period of life and a effective preventable drug is still lacking.
Subject(s)
Peptic Ulcer Perforation/etiology , Stomach Ulcer/complications , Fatal Outcome , Female , Humans , Infant, Newborn , Intensive Care Units, Neonatal , Male , Peptic Ulcer Perforation/diagnosis , Risk Factors , Stomach Ulcer/diagnosis , Stomach Ulcer/etiologyABSTRACT
CRF, a hypothalamic neurohormone, has been shown to be present in several tissues outside the brain. During pregnancy, both fetal (placental trophoblast, chorion, and amnion) and maternal (decidua) intrauterine tissues contain immunoreactive CRF. A paracrine/autocrine role of CRF as a regulator of hormonogenesis in human placenta and decidua has been suggested. The expression of CRF mRNA in human decidua was demonstrated in the present study by Northern blot analysis and was found to be higher in specimens collected at term than in those collected during the first and second trimesters of gestation. Furthermore, the presence of CRF was detected immunocytochemically in cultured decidual cells isolated from term decidua as well as in endometrial stromal cells decidualized in vitro by treatment with a mixture of medroxyprogesterone acetate, estradiol, and relaxin. These results indicate that human decidua is an intrauterine extrahypothalamic source of CRF in the maternal compartment and offer new tools to explore the in vitro decidualization processes and the regulation of CRF release from decidual cells.