[Persistent gestational trophoblastic disease following ectopic molar pregnancy]. / Persistiruyushchaya gestatsionnaya trofoblasticheskaya bolezn' posle polnogo puzyrnogo zanosa pri ektopicheskoi sheechnoi beremennosti.

A case of persistent gestational trophoblastic disease that developed after ectopic (cervical) pregnancy with complete hydatidiform mole (CHM) in a 56-year-old patient is presented. The diagnosis of CHM was made retrospectively based on immunohistochemical analysis of archival material using p57 and Ki67 antibodies. Observation shows the difficulty of objective diagnosis of hydatidiform mole in early pregnancy due to the lack of typical cystic transformation of the stroma of villi, focal proliferation of villous trophoblast. Application of the p57 marker for the differential diagnosis of CHM and other variants of cystic villi transformation may be especially important in cases of ectopic pregnancy, in which morphological changes in the chorion do not always correspond to the classical picture. The presence of ectopic pregnancy with CHM in a 56-year-old patient requires special attention of clinicians.

[Metastatic leiomyoma or synchronous lesion of the uteri corpus and vulva?] / Metastaziruiushchaia leiomioma ili sinkhronnoe porazhenie tela matki i vul'vy?

OBJECTIVE: To reveal the morphological characteristics of simultaneously diagnosed leiomyoma of the corpus uteri and vulva. SUBJECT AND METHODS: The paper describes a case of multiple uterine leiomyomas concurrent with vulvar leiomyoma in a 39-year-old patient with progressive tumor nodule growth over 2 years. Vulvar tumor was biopsied simultaneously with extirpation of the uterus; vulvar leiomyoma was removed six months later. Histological and immunohistochemical studies: such as hematoxylin and eosin staining, the expression of smooth muscle actin, desmin, and progesterone and estrogen receptors, S100, CD10, and determination of Ki-67 proliferation index, were conducted. RESULTS: The largest (14-cm) multiple tumor nodule in the corpus uteri had the structure of leiomyoma of uncertain malignant potential; the large (8-cm) vulvar tumor was a leiomyoma with hyalinosis. The immunohistochemical profile of uterine and vulvar leiomyoma (smooth muscle actin+, desmin+, progesterone+, estrogen+ receptors, CD117-, and Ki-67) was the same (1-3%). The vulvar leiomyoma was assumed to be a tumor of metastatic origin. CONCLUSION: Vulvar leiomyoma is rare; it can arise from smooth muscle tissue of various anatomical structures of the skin and soft tissues. The pathogenesis of the so-called metastatic leiomyoma is unclear; there are concepts of a metaplastic transformation of subcelomic mesenchyme and multifocal smooth muscle proliferation. The presented case demonstrates the synchronous development of uterine and vulvar leiomyoma.

[Features of the pathogenesis of the placenta growing in the scar after cesarean section]. / Osobennosti patogeneza vrastaniia platsenty v rubets posle kesareva secheniia.

OBJECTIVE: to investigate the structural and pathogenetic features of pathological placental attachment in the scar after cesarean section. MATERIAL AND METHODS: The investigators explored 12 uteri; 11 of which were removed with placentas at 9 to 38 weeks' gestation (one in the first trimester, three at 18-22 weeks, two at 32-35 weeks, and five at 37-38 weeks); one uterus was removed after an artificial abortion at 12 weeks' gestation in the scar, as well as the scars excised in the first trimester in non-developing (n=4) and progressive (n=2) pregnancies. For histological examination, fragments of the full-thickness uterine wall were taken from the placental bed in different areas. The sections were stained for fibrin with hematoxylin and eosin, van Gieson stain, and the Martius scarlet/blue (MSB) technique. Decidual tissue, trophoblast, vascular component, and smooth muscle tissue were identified by an immunohistochemical assay using antibodies to vimentin, pan-cytokeratin, vascular endothelium (СD31), and smooth muscle actin. RESULTS: In most cases, placental localization in the scar after cesarean section was accompanied by abnormal placental attachment: almost always placenta accreta, less frequently in combination with its ingrowth (placenta accreta/increta). The morphological substrate of placenta increta was a change in the content and ratio of normal histological components in the uterine wall, such as the mucosa, smooth muscle tissue, and vessels (the absence or thinning of decidual tissue and the myometrium, as well as its cicatricial changes). The structural criterion for placenta increta was necrosis of the walls of the large veins in the myometrium due to the replacement of their intermediate trophoblast and fibrin and to the destruction of vessel walls, leading to prolapse of the chorionic villi into the veins. CONCLUSION: In most cases, placental localization in the scar after cesarean section is accompanied by abnormal placental attachment: placenta accreta, less frequently in combination with its ingrowth (placenta accreta/increta).