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Defective pericyte recruitment of villous stromal vessels as the possible etiologic cause of hydropic change in complete hydatidiform mole.

ABSTRACT: The pathogenetic mechanism underlying the hydropic change in complete hydatidiform moles (CHMs) is poorly understood. A growing body of data suggests that pericytes play a role in vascular maturation. Since maturation of villous stromal vessels in CHMs is markedly impaired at early stages, we postulated that a defect in pericytes around stromal vessels in chorionic villi might cause vascular immaturity and subsequent hydropic change. To investigate this, we examined several markers of pericytes, namely, ?-smooth muscle actin (?-SMA), platelet-derived growth factor receptor-? (PDGFR-?), and desmin, in 61 normally developing placentas and 41 CHMs with gestational ages of 4-12 weeks. The ultrastructure of villous stromal vessels was also examined. Mature blood vessels from normal placentas show patent vascular lumens and formed hematopoietic components in the villous stroma. ?-SMA and PDGFR-? expression in the villous stroma gradually increased and extended from the chorionic plate to peripheral villous branches. The labeled cells formed a reticular network in the villous stroma and, after week 7, encircled villous stromal vessels. In comparison, ?-SMA and PDGFR-? expression in the villous stroma and stromal vessels of CHMs was significantly lower (p<0.05). Ultrastructurally, endothelial cells in villous stromal vessels in normal placentas were consistently attached by pericytes after week 7 when the vessels formed distinct lumen, whereas the villous stromal vessels in CHMs consisted of linear chains of endothelial cells, often disclosing primitive clefts without hematopoietic cells inside, and neither pericytes nor basal lamina surrounded the endothelial cells at any gestational age studied. This suggests that pericytes recruitment around villous stromal vessels is defective in CHMs and links to the persistent vascular immaturity of the villous stroma in CHMs, which in turns leads to hydropic villi.

SUBMITTER: Kim KR

PROVIDER: S-EPMC4388658 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Defective pericyte recruitment of villous stromal vessels as the possible etiologic cause of hydropic change in complete hydatidiform mole.

Kim Kyu Rae KR Sung Chang Ohk CO Kwon Tae Jeong TJ Lee JungBok J Robboy Stanley J SJ

PloS one 20150407 4

The pathogenetic mechanism underlying the hydropic change in complete hydatidiform moles (CHMs) is poorly understood. A growing body of data suggests that pericytes play a role in vascular maturation. Since maturation of villous stromal vessels in CHMs is markedly impaired at early stages, we postulated that a defect in pericytes around stromal vessels in chorionic villi might cause vascular immaturity and subsequent hydropic change. To investigate this, we examined several markers of pericytes, ...[more]

PMID: 25849742

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Project description:BackgroundHydatidiform mole (HM), also called a molar pregnancy, is characterised by an overgrowth of foetal chorionic tissue within the uterus. HMs may be partial (PM) or complete (CM) depending on their gross appearance, histopathology and karyotype. PMs usually have a triploid karyotype, derived from maternal and paternal origins, whereas CMs are diploid and have paternal origins only. Most women with HM can be cured by evacuation of retained products of conception (ERPC) and their fertility preserved. However, in some women the growth persists and develops into gestational trophoblastic neoplasia (GTN), a malignant form of the disease that requires treatment with chemotherapy. CMs have a higher rate of malignant transformation than PMs. It may be possible to reduce the risk of GTN in women with HM by administering prophylactic chemotherapy (P-Chem). However, P-Chem given before or after evacuation of HM to prevent malignant sequelae remains controversial, as the risks and benefits of this practice are unclear.ObjectivesTo systematically review the evidence for the effectiveness and safety of P-Chem to prevent GTN in women with a molar pregnancy.Search methodsWe performed electronic searches in the Cochrane Gynaecological Cancer Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL, Issue 2, 2012), MEDLINE (1946 to February week 4, 2012) and EMBASE (1980 to week 9, 2012). The search strategy was developed using free text and medical subject headings (MESH). We handsearched reference lists of relevant literature to identify additional studies.Selection criteriaWe included randomised controlled trials (RCTs) of P-Chem for HM.Data collection and analysisTwo review authors independently assessed studies for inclusion in the review and extracted data using a specifically designed data collection form. Meta-analyses were performed by pooling data from individual trials using RevMan 5.1 software.Main resultsWe included three RCTs with a combined total of 613 participants. One study compared prophylactic dactinomycin to no prophylaxis (60 participants); the other two studies compared prophylactic methotrexate to no prophylaxis (420 and 133 participants). All participants were diagnosed with CMs. We considered the latter two studies to be of poor methodological quality.P-Chem reduced the risk of GTN occurring in women following a CM (3 studies, 550 participants; RR 0.37; 95% confidence interval (CI) 0.24 to 0.57; I(2) = 0%; P < 0.00001), However, owing to the poor quality of two of the included studies, we performed sensitivity analyses excluding these two studies. This left only one small study of high-risk women to contribute data for this primary outcome (59 participants; RR 0.28; 95% CI 0.10 to 0.73; P = 0.01), therefore we consider this evidence to be of a low quality.The time to diagnosis was longer in the P-Chem group than the control group (2 studies, 33 participants; mean difference (MD) 28.72; 95% CI 13.19 to 44.24; P = 0.0003) and the P-Chem group required more courses to cure subsequent GTN (1 poor-quality study, 14 participants; MD 1.10; 95% CI 0.52 to 1.68; P = 0.0002). We consider this evidence to be of a low to very low quality for similar reasons to those listed above.There were insufficient data to perform meta-analyses for toxicity, overall survival, drug resistance and reproductive outcomes.Authors' conclusionsP-Chem may reduce the risk of progression to GTN in women with CMs who are at a high risk of malignant transformation; however, current evidence in favour of P-Chem is limited by the poor methodological quality and small size of the included studies. As P-Chem may increase drug resistance, delay treatment of GTN and expose women unnecessarily to toxic side effects, this practice cannot currently be recommended.

Dataset Information

Defective pericyte recruitment of villous stromal vessels as the possible etiologic cause of hydropic change in complete hydatidiform mole.

Publications

Defective pericyte recruitment of villous stromal vessels as the possible etiologic cause of hydropic change in complete hydatidiform mole.

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