RESUMO
BACKGROUND: In this prospective cohort study, we examined the utility of elastography to evaluate the fetus and placenta. PATIENTS AND METHODS: Pregnant women in their third trimester of pregnancy, by which time the placenta has formed, were included in this study. A total of 111 women underwent ultrasound examinations, including elastography. Elastographic evaluation was performed using two protocols. First, the placental index (PI) was measured, which quantitatively assesses the hardness of tissue. Second, regions of interest (ROI) were categorized into 3-step scores according to the frequency of the blue area (hardness of placental tissue score [HT score]), which is a qualitative method. After delivery, 40 of the 111 placentas were pathologically examined. RESULTS: The average PI was 44.3 (± 29.4) in the in utero SGA group, which was significantly higher than that in the normal group (8.8 (± 10.0); p < 0.01) during pregnancy. There was a significant correlation between the PI and z score for estimated fetal weight (EFW) (r = -0.55; p < 0.01). Moreover, a significant positive correlation was observed between the PI and the z score of birth weight (r = -0.39; p < 0.01). Pathological ischemia findings of the placenta were identified in 67% of the HT score 3 group, representing 6 of the 9 patients, and in 20% of the HT score 1 group, representing only 3 of the 15 patients. CONCLUSIONS: Placental hardness, as determined by elastography, correlates with both lower estimated fetal body weight and birth weight. These results suggest that ultrasound elastography in the placenta may be an additional marker of intrauterine fetal well-being.
RESUMO
A 62-year-old man with a complaint of back pain lasting 2 months was admitted. He also presented a huge abdominal tumor. Diagnostic imaging showed metastatic tumors in the liver, lumbar vertebrae and bilateral lung. An ultrasound-guided needle biopsy revealed a lung tumor containing melanic tissue. Subsequently, there was an evident elevation in uric acid, phosphoric acid, potassium and lactate dehydrogenase concentrations in serum. Continuous hemodiafiltration and administration of rasburicase was initiated following the diagnosis of tumor lysis syndrome (TLS). However, he died on the fourth day owing to arrhythmia. An autopsy revealed metastatic deposits in the liver, lung, spine, ribs, and lymph nodes along the biliary system. Microscopic examinations revealed massive necrosis of normal hepatocytes and tumor cells with disseminated tumor thrombi in the portal system. The catastrophic progression of TLS appears to be influenced by a persistent portal blood flow deficiency by portal tumor thrombus in this case.
RESUMO
Mutations of the methyl CpG binding protein 2 (MeCP2) gene are a major cause of Rett syndrome. To investigate whether the expression of this gene was related to JC virus (JCV) infection, we examined brains of four progressive multifocal leukoencephalopathy (PML) patients. JCV infection was confirmed by immunohistochemical labeling with antibodies against JCV VP1, agnoprotein and large T antigen. MeCP2 expression was examined by immunohistochemistry using a specific polyclonal antibody against MeCP2. In normal brains and uninfected cortices of PML brains, MeCP2 expression was observed in the nuclei of neurons, but not observed in glial and endothelial cell nuclei. However, in PML brains intense immunolabeling was observed in abnormally enlarged glial nuclei of JCV-infected cells. Double immunolabeling using antibodies against large T antigen (visualized as blue) and MeCP2 (visualised as red) revealed dark red JCV-infected nuclei, which confirmed that the JCV infected nuclei expressed MeCP2. We conclude that MeCP2 is highly expressed in the JCV-infected nuclei of PML brain and these results may provide a new insight into the mechanism which regulates the MeCP2 expression in glial cells by the infection of JCV.
