Pregnancy is a thrombogenic condition in both antenatal and postpartum periods. Venous thromboembolism (VTE) is a common cause of morbidity, and the cause of maternal death in such situations is pulmonary embolism. There are several risk factors for thrombotic phenomena in pregnancy both acquired and hereditary. Accurate diagnosis of deep vein thrombosis (DVT) and its treatment are very important to prevent life-threatening pulmonary embolism. Among the diagnostic techniques, compression ultrasound is the mainstay for DVT diagnosis, whereas computed tomographic pulmonary angiography (CTPA) is for pulmonary embolism. Anticoagulants play a major role in therapy. They are used both in the active stage of thromboembolism and also in thromboprophylaxis in the postpartum period. Different types of heparins are available, which can be tailored to the individual requirements. During therapy they need monitoring to prevent hemorrhagic complications. Oral anticoagulants cannot be given in pregnancy as a general rule because of their teratogenicity, though they can be used in the postpartum period. Thrombolysis is can be taken up in selected cases in the acute situations. A very prolonged treatment of anticoagulants and compression stockings are needed in patients with past history of VTE. The most convenient drug regimen for prophylaxis is once-daily weight-adjusted low-molecular-weight heparin (LMWH). The goal of this article is to facilitate the recognition of thromboembolic disorders in pregnancy and different regimens in their management during antenatal, intrapartum, and postpartum periods. A few interesting and rare cases from the author’s experience are also presented at the end.
Background:
Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with the onset or first recognition during pregnancy and is the most common metabolic complication of pregnancy. Significant maternal and fetal complications can result from undiagnosed or inadequately treated GDM. Aim: To investigate the difference in the expression of the CD-68 marker in the Hofbauer cells (HCs) and their distribution within the villi in the placentas of diabetic and non-diabetic mothers.
Materials and Methods:
Sixty placentas were included in the study, 30 as controls and 30 from mothers with diagnosed GDM as cases. Full-thickness cross sections of placentas were obtained. Tissue processing was done, followed by haematoxylin and eosin (H&E). A study of CD68 markers (placental macrophages) was done using standard protocols of immunohistochemistry.
Statistical Analysis:
Frequencies and percentages of Hofbauer cells (HCs) found in case and control placental tissue were calculated. Student’s t-test was used to compare two groups using SPSS 13.0 software. When P is 0.0001, differences were considered statistically significant.
Results and Conclusion:
We studied the distribution and number of fetal macrophages (CD68+) in diabetic and non-diabetic placentas. The immunostained CD68+ cell count was identified to be significantly higher in the GDM placenta. In relation to fetal blood vessels in the villus stroma of the GDM placenta in comparison to control, CD68+ cells were found more frequently. This study shows a significant increase in the number of Hofbauer cells in the placenta of mothers with GDM in comparison to control (P < 0.0001). An increase in macrophages in these placentae might be related to the protective mechanism against inflammation. Further studies are required to investigate the mechanism in detail.
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