Uterine Vascular Lesions

Vascular lesions of the uterus are rare; most reported in the literature are arteriovenous malformations (AVMs). Uterine AVMs can be congenital or acquired. In recent years, there has been an increasing number of reports of acquired vascular lesions of the uterus following pregnancy, abortion, cesarean delivery, and curettage. It can be seen from these reports that there is confusion concerning the terminology of uterine vascular lesions. There is also a lack of diagnostic criteria and management guidelines, which has led to an increased number of unnecessary invasive procedures (eg, angiography, uterine artery embolization, hysterectomy for abnormal vaginal bleeding). This article familiarizes readers with various vascular lesions of the uterus and their management.Key words: Uterine arteriovenous malformations, Uterine hemangioma, Placental chorioangioma, Uterine arteriovenous fistula, Uterine pseudoaneurysm, Acquired AVMVascular lesions of the uterus are very rare; most reported in the literature are arteriovenous malformations (AVMs). Uterine vascular malformations can be congenital or acquired. Recently, there has been a rise in the number of reported cases following pregnancy, abortion, and curettage. Many of these studies report spontaneous resolution of vascular lesions during follow-up; in addition, there is an increasing trend toward use of uterine artery embolization (UAE) to treat these lesions. In many of the reported studies, the diagnosis of uterine vascular malformation was made as early as the second day after a delivery or an abortion. In a study by Timmerman and colleagues,¹ out of 30 cases reported as uterine AVM based on Doppler study, only 3 were true AVMs. Rufener and associates² conducted a sonologic evaluation of postpartum and postabortion uterine vascular lesions that were reported as AVMs; the study revealed that, on pathologic examination, none turned out to be AVMs. Thus, we observe that there is confusion with regard to the terminology of vascular lesions such as uterine AVM, vascular malformation, arteriovenous fistula (AVF), and non-AVM vascular abnormalities of the uterus. The term malformation, however, is generally used to describe defects in the structure of an organ or region of the body resulting from an intrinsically abnormal process of development. Therefore, spontaneous resolution of a malformation in a short period of time is unlikely. An investigation by Mulliken and Glowacki,³ published in 1982, provided the groundwork for a proper identification of vascular lesions. Vascular tumors grow by cellular (mainly endothelial) hyperplasia: the very common hemangioma is, in reality, a benign vascular tumor. In contrast, vascular malformations have a quiescent endothelium and are considered to be localized defects of vascular morphogenesis, likely caused by dysfunction in pathways regulating embryogenesis and vasculogenesis. Therefore, the terms vascular abnormality or vascular lesion seem to best describe hypervascular areas within the uterus seen on color Doppler ultrasound, unless they are proven to be an AVM by angiography or pathologic examination. Many of these vascular lesions are increasingly being managed by UAE. Although there have been various reports of successful pregnancy following UAE, there have also been reports of ectopic pregnancy following UAE.⁴It is important to correctly identify various vascular lesions in the uterus to avoid unnecessary invasive intervention. This article aims to familiarize the reader with various vascular lesions of the uterus and their management.Uterine AVM is a rare condition, and the true incidence is not yet known. A study by O’Brien and associates⁵ showed an incidence of AVM of 4.5% in 464 pelvic sonographic examinations performed for pelvic bleeding. AVM has been described in patients between 18 and 72 years of age, and may be congenital or acquired pathologic conditions.⁶ The congenital form is very rare and is the result of a defect in embryonic vascular differentiation or a premature arrest in the development of the capillary plexus leading to multiple abnormal connections between arteries and veins.⁷ These congenital AVMs often penetrate the surrounding tissue and can cause an elaborate collateral vascular network. Furthermore, these congenital lesions can grow as pregnancy progresses.⁸The International Society for the Study of Vascular Anomalies classification system divides vascular anomalies into two primary biologic categories: (1) vasoproliferative or vascular neoplasms and (2) vascular malformations. The major distinction between the two categories is whether there is increased endothelial cell turnover, which is ultimately determined by the identification of mitoses seen on histopathology. Vasoproliferative neoplasms have increased endothelial cell turnover (ie, they proliferate and undergo mitosis) because they are neoplasms. Vascular malformations do not have increased endothelial cell turnover; rather, they are structural abnormalities of the capillary, venous, lymphatic, and arterial system, and can be congenital or acquired.     

Detection of reactive oxygen species (ROS) and apoptosis in human fragmented embryos

In human in-vitro fertilization (IVF)-embryo transfer, the in-vitro culture environment differs from in-vivo conditions in that the oxygen concentration is higher, and in such conditions the mouse embryos show a higher concentration of reactive oxygen species (ROS) in simple culture media. ROS are believed to cause damage to cell membranes and DNA fragmentation in somatic cells. This study was conducted to ascertain the level of H2O2 concentration within embryos and the morphological features of cell damage induced by H2O2. A total of 62 human oocytes and embryos (31 fragmented, 15 non-fragmented embryos, 16 unfertilized oocytes) was obtained from the IVF-embryo transfer programme. The relative intensity of H2O2 concentrations within embryos was measured using 2',7'-dichlorodihydrofluorescein diacetate by Quanti cell 500 fluorescence imaging and DNA fragmentation was observed with transmission electron microscopy and an in-situ apoptosis detection kit. The H2O2 concentrations were significantly higher in fragmented embryos (72.21 +/- 9.62, mean +/- SEM) compared to non-fragmented embryos (31.30 +/- 3.50, P < 0.05) and unfertilized oocytes (30.75 +/- 2.67, P < 0.05). Apoptosis was observed only in fragmented embryos, and was absent in non-fragmented embryos. Electron microscopic findings confirmed apoptotic bodies and cytoplasmic condensation in the fragmented blastomeres. We conclude that there is a direct relationship between increased H2O2 concentration and apoptosis, and that further studies should be undertaken to confirm these findings.      

Hyperprolactinemia disrupts neuroendocrine responses of male rats to female conspecifics

An increase in plasma luteinizing hormone levels which occurs in the male rat in response to the presence of a receptive female was associated with increased norepinephrine metabolism in several regions of the hypothalamus and reduced norepinephrine metabolism in preoptic area and olfactory bulbs. Hyperprolactinemia induced by grafting three anterior pituitary glands beneath the kidney capsule blocked female-induced changes in norepinephrine metabolism and attenuated the increase in luteinizing hormone release. These results suggest that endocrine and behavioral responses of male rats to the presence of a female are mediated by changes in catecholamine metabolism in several brain regions. The ability of hyperprolactinemia to induce deficits in male sexual behavior may be due to the blockade of these CNS responses to exteroceptive stimuli originating from the female.     

Primary leiomyosarcoma of inferior vena cava: Case report

An intramural venous leiomyosarcoma is a rare, malignant tumour arising from the smooth muscle cells of the vessel wall and the inferior vena cava (IVC) is the most common location. The middle part of IVC is most often affected, often involving the kidneys. There is a strong prediction for women. Clinical symptoms depend upon the size and location of the tumour. Diagnosis is often not made until advanced stage, as the symptoms are non-specific and they present late in the disease course.     

Lack of association between ACE and bradykinin B2 receptor gene polymorphisms and ACE inhibitor-induced coughing in hypertensive Koreans

Background & Objective:  Angiotensin converting enzyme (ACE) inhibitors are used widely in therapy for hypertension, congestive heart failure and myocardial infarction. However, coughing, one of their major adverse effects limits their use. It is documented that Asians are more liable to coughing than Europeans. The aim of this study was to investigate genetic polymorphism involved in ACE inhibitor-induced coughing.
Methods:  We monitored hypertensive subjects ( n  = 110) treated with ACE inhibitors, and tested for any associations between ACE inhibitor-induced coughing and polymorphisms in the genes for ACE and the bradykinin B2 receptor, which are suspected to be related to coughing.
Results & Discussion:  We found no significant differences between the groups with coughing and without coughing in the frequency of ACE I/D (Insertion/Deletion) polymorphisms. One single nucleotide polymorphism was discovered in the promoter (−58T/C) and, one in intron-exon junction upsteam of exon 2 (−59C/A), of the bradykinin B2 receptor gene. However, no significant correlation was found between those genotypes or allele distributions and ACE inhibitor-induced coughing.
Conclusion:  We found no significant links between polymorphisms of the ACE gene or bradykinin B2 receptor gene with ACE inhibitor-induced coughing in hypertensive Koreans. But, the topic remains controversial and requires more study.