Placental damages in preeclampsia - from ultrasound images to histopathological findings.

Preeclampsia is a unique pregnancy-related disease that affects 5-7% pregnancies worldwide. Placental architecture is modified in PE and eclampsia. Placental morphology and cellular arrangement are important for oxygen delivery from the mother to the fetus. Fetal growth and well-being after 20 weeks of gestation are dependent upon successful placental development. This, in turn, is achieved by an enhanced maternal blood supply to the placenta (normal uterine artery Doppler) and growth/ differentiation of the gas-exchanging placental villi. Conversely, pregnancy with severe placental insufficiency exhibits abnormalities both in uterine artery and in umbilical artery Doppler, and results in adverse perinatal outcome. The evaluation of placental functioning is possible nowadays through ultrasound examinations. Sonographic images associated with placental lesions include cystic areas, heterogeneous appearance of the placental mass, and thick or thin placentas. Sonographic evidence of destructive placental lesions is defined as the evolution of irregular cystic spaces with echogenic borders - the echogenic cystic lesions. Histological examinations of placenta may confirm these antepartum observations. Decidual vasculopathy and accelerated villous maturity are considered indicative of uteroplacental vascular insufficiency. Perivillous fibrin deposition and intervillous fibrin are considered indicative of intervillous coagulation. Detailed sonographic evaluation of the placenta and histopathological confirmation after birth are used to identify lesions associated with preeclampsia, intrauterine growth restriction and adverse short and long-term perinatal outcome, but the presence of cystic images in the placenta is not uniformly associated with adverse perinatal outcome. Combining Doppler studies with placental texture studies may lead to satisfactory results.

[Hereditary pancreatitis]. / Pancreatita ereditara.

We present the cases of three brothers (a woman and two men) with recurrent attacks of necrotic acute pancreatitis that were treated in our clinic. Two of them have diabetes mellitus controlled through insulin treatment. All patients have presented the first episode of acute pancreatitis around age of 35. We have observed a high level of serum triglyceride at admission, without evidence of lipid disorder. In addition we couldn't identify other causes of these episodes of acute pancreatitis (biliary stones, alcohol, trauma, drugs, lipid disorders). During the last year two members of this family presented recurrent attacks of abdominal pain without any biochemical or imaging signs of acute pancreatitis.