Pancreatic carcinoma underlying a complex presentation in late pregnancy: a case report.

BACKGROUND: Gestational diabetes mellitus is strongly related to the risk of pancreatic cancer in pregnant women, but gestational diabetes can precede a diagnosis of pancreatic cancer by many years. Women with a history of gestational diabetes showed a relative risk of pancreatic cancer of 7.1. Pancreatic adenocarcinoma is one of the most common malignancies associated with thromboembolic events. A clinical study showed that thromboembolic events were detected in 36% of patients diagnosed as having pancreatic cancer. Studies showed that gestational diabetes mellitus could be one of the important risk factors for pancreatic cancer. CASE PRESENTATION: Gestational diabetes mellitus is associated with increased risk of breast and pancreatic cancer. This case report describes a 29-year-old Chinese woman who presented with: gestational diabetes mellitus; International Society on Thrombosis and Haemostasis criteria suggested disseminated intravascular coagulation with a score of 5; hemolysis, elevated liver enzymes, low platelet count syndrome; and pulmonary hypertension. After an intravenous injection of fibrinogen, she gave birth to a normal baby and following delivery, her blood pressure reached 180/110 mmHg. Laboratory analysis results showed elevated lactic dehydrogenase, decreased platelets and fibrinogen, and urine protein was positive. She was transfused with fresh frozen plasma, blood coagulation factor, and fibrinogen. Subsequently, she was transferred to a maternity intensive care unit, where magnesium sulfate seizure prophylaxis was continued for 24 hours to keep her magnesium level at a low therapeutic range. However, continuous oxygen therapy was needed to maintain her oxygenation. Further laboratory investigations revealed elevated carcinoembryonic antigen, carbohydrate antigen 19-9, and carbohydrate antigen 72-4. Positron emission tomography-computed tomography showed malignant carcinoma in the head of her pancreas with lymph node involvement along with bone, peritoneal, and left adrenal metastasis, as well as double lung lymphangitic carcinomatosis. CONCLUSION: A differential diagnosis of digestive system neoplasm should be considered when a pregnant patient presents with gestational diabetes mellitus and disseminated intravascular coagulation, where the disseminated intravascular coagulation has no specific cause and cannot be readily resolved.

MicroRNA-128a-induced apoptosis in HTR-8/SVneo trophoblast cells contributes to pre-eclampsia.

INTRODUCTION: Pre-eclampsia (PE) can endanger the survival of the mother and fetus. Currently, the pathogenesis of PE is not completely understood and no fundamental therapeutics are available. The present study was performed to determine the function of miR-128a in HTR-8/SVneo trophoblast cells and to ascertain its underlying role in the pathogenesis of PE. METHODS: We investigated the function of miR-128a in HTR-8/SVneo cells by overexpressing. We analyzed the apoptosis of HTR-8/SVneo cells by performing apoptosis assays and measured the loss of mitochondrial membrane potential (Δym), the generation of reactive oxygen species (ROS) and caspase activity. In addition, miR-128a target genes were predicted. RESULTS: Using computer-based programs, we identified Bax as a direct target of miR-128a. In the apoptosis assays of HTR-8/SVneo cells, miR-128a decreased the Δψm, depleted ATP levels and increased ROS generation, cytochrome c release as well as caspase activation. Further studies showed that miR-128a induced the apoptosis of HTR-8/SVneo cells by down-regulating Bax through the mitochondrial apoptosis pathway. CONCLUSIONS: miR-128a is an up-regulated miRNA in patient with PE. Our study demonstrated that the miR-128a-induced apoptosis of HTR-8/SVneo cells may contribute to PE and miR-128a may be a novel potential therapeutic target for PE.

Contribution of dysfunction of maternal hemodynamics to renal impairment in preeclampsia.

AIMS: To investigate the contribution of dysfunction of maternal hemodynamics to renal impairment in preeclampsia (PE). METHODS: Urinary protein excretion, serum creatinine, blood urea nitrogen, uric acid, and glomerular filtration rate were assessed in 571 pregnant women with PE in addition to and noninvasive hemodynamic monitoring. Patients were classified into two groups: PE with renal impairment (glomerular filtration rate <90 ml/min/1.73 m², n = 161) and PE with normal renal function (n = 410). Cut-off values for hemodynamic parameters were calculated using receiver-operating characteristic curve analysis. RESULTS: Maternal systolic function and cardiac output parameters were low and peripheral resistance was high in the PE renal impairment group. Cut-off values for the hemodynamic parameters, cardiac index, cardiac output, systemic vascular resistance index, and systemic vascular resistance were 2.85 l/min/m², 5.25 l/min, 3,014.5 dyn s cm⁻5 m² and 1,636.0 dyn s cm⁻5, respectively, according to receiver-operating characteristics curves. CONCLUSION: Renal impairment in PE is associated with reduced maternal cardiac output and increased peripheral resistance.

Screening for differential methylation status in human placenta in preeclampsia using a CpG island plus promoter microarray.

The development of preeclampsia (PE) seriously affects the health of the mother and the child, but the precise pathogenesis of PE remains elusive. The placenta is considered to play a key role and DNA methylation may be associated with altered placental development and function. The aim of this study was to perform a genome-wide analysis of the DNA methylation profile in placentas from pregnancies with severe preeclampsia. The authors analyzed normal and placental tissues with PE for aberrant DNA methylation using methylated DNA immunoprecipitation (MeDIP) and a human CpG island plus promoter microarray. The methylation status of identified candidate genes were validated by bisulfite sequencing PCR (BSP). Microarray analysis identified 296 genes that showed significantly aberrant DNA methylation in preeclampsia (PE). These genes were located more frequently in chromosome 1 (10.5%, P=0.005), chromosome 12 (8.1%, P=0.062) and chromosome 19 (7.4%, P=0.117). Functional analysis divided these genes into different functional networks. In addition, the methylation profile of six of these genes (CAPN2, EPHX2, ADORA2B, SOX7, CXCL1 and CDX1) in nine patients with PE was validated by BSP. This study demonstrated aberrant patterns of DNA methylation in PE, which may be involved in the pathophysiology of PE. Future work will assess the potential prognostic and therapeutic value for these findings in PE.