Evidence for anti-inflammatory effects of firocoxib administered to mares with experimentally induced placentitis.

PROBLEM: Minimal evidence exists supporting therapeutic selections for equine placentitis. The goal of this study was to characterize the anti-inflammatory effects of firocoxib when administered to mares with placentitis. METHODS: Mares (gestation D270-300) were assigned to: INFECT (n = 6; placentitis, no treatment), FIRO (n = 6; placentitis, firocoxib, 0.1 mg/kg, PO, daily), and NORM (n = 6; no infection/treatment). Allantoic fluid (8 hours, 24 hours, birth) and amniotic fluid (birth) were collected from mares after infection. Concentrations of IL-1ß, IL-6, TNF-α, IL-10, PGF2α , and PGE2 in fluids were measured by ELISA. mRNA expression of IL-1ß, IL-6, TNF-α, IL-8, IL-10, matrix metalloproteinases (MMPs) -1, 3, and 9 in fetal membranes/fetuses was quantified using real-time PCR. RESULTS: Allantoic TNF-α concentrations were lowest in FIRO at 8 hours and 24 hours post-infection; IL-6 concentrations were lower in FIRO than NORM at 8 hours, lower in FIRO than INFECT at 24 hours post-inoculation, and lower in NORM than FIRO or INFECT at birth. Marginal mean allantoic IL-ß and IL-10 concentrations were lower in FIRO and NORM than INFECT. Amniotic fluid cytokines were lowest in NORM with all measurements in that group being below the limit of detection. Allantoic PGF2α concentrations were lower in FIRO and INFECT than NORM at 8 hours post-inoculation, and lower in FIRO than INFECT or NORM at 24 hours post-inoculation. Allantoic PGE2 concentrations were lower in FIRO than INFECT. Amniotic PGF2α and PGE2 concentrations were lower in NORM than INFECT. In fetal membranes, group differences with respect to IL-1ß, IL-6, IL-8, and MMP1 were dependent on tissue type. CONCLUSIONS: Data suggest a suppressive effect of firocoxib administration on cytokine and prostaglandin production in mares with placentitis.

Effect of edaravone on pregnant mice and their developing fetuses subjected to placental ischemia.

Growing evidence indicates that reduced uterine perfusion pressure (RUPP) triggers the cascade of events leading to preeclampsia. Edaravone is a powerful free radical scavenger used for the treatment of ischemia/reperfusion diseases due to its anti-oxidative stress and anti-inflammatory properties. Here we investigate the effect of edaravone (3 mg/kg) on different maternal and fetal outcomes of RUPP-induced placental ischemia mice model. RUPP surgery was performed on gestation day (GD) 13 followed by edaravone injection from GD14 to GD18, sacrifice day. The results showed that edaravone injection significantly decreased the maternal blood pressure (113.2 ± 2.3 mmHg) compared with RUPP group (131.5 ± 1.9 mmHg). Edaravone increased fetal survival rate (75.4%) compared with RUPP group (54.4%), increased fetal length, weights, and feto-placental ratio (7.2 and 5.7 for RUPP and RUPP-Edaravone groups, respectively) compared with RUPP group. In addition, RUPP resulted in many fetal morphological abnormalities as well as severe delayed ossification, however edaravone decreased the morphological abnormalities and increased the ossification of the fetal endoskeleton. Edaravone improved the histopathological structure of the maternal kidney and heart as well as decreased the elevated blood urea and creatinine levels (31.5 ± 0.15 mg/dl (RUPP), 25.6 ± 0.1 mg/dl (RUPP+edaravone) for urea and 5.4 ± 0.1 mg/dl (RUPP), 3.5 ± 0.1 mg/dl (RUPP+edaravone) for creatinine) and decreased cleaved caspase-3 expression in the maternal kidney. In conclusion, this study demonstrated that our RUPP mice model recapitulated preeclampsia symptoms and edaravone injection ameliorated most of these abnormalities suggesting its effectiveness and potential application in preeclampsia treatment regimes.

IFPA meeting 2018 workshop report II: Abnormally invasive placenta; inflammation and infection; preeclampsia; gestational trophoblastic disease and drug delivery.

Workshops are an important part of the IFPA annual meeting as they allow for discussion of specialized topics. At IFPA meeting 2018 there were nine themed workshops, five of which are summarised in this report. These workshops discussed new perspectives and knowledge in the following areas of research: 1) preeclampsia; 2) abnormally invasive placenta; 3) placental infection; 4) gestational trophoblastic disease; 4) drug delivery to treat placental dysfunction.

Coexistence of Kasabach-Merritt Syndrome and placental chorioangioma in a premature infant.

Kasabach-Merritt syndrome is a rare life-threatening clinical presentation in neonatal period. it is characterized by giant hemangioma and serious thrombocytopenia. The diagnostic criteria include: 1) hemangiomas on skin, 2) thrombocytopenia or coagulopathy, 3) hemangioma on internal organs diagnosed by ultrasonography, computed tomography or magnetic resonance imaging, and 4) excluding reasons, such as idiopathic thrombocytopenic purpura or hypersplenism.Placental chorioangiomas are the most widespread non-trophoblastic benign tumor-like lesions of placenta. The clinical signs are associated with tumor size. Chorioangiomas larger than 4-5 cm may lead to various maternal and fetal complications.Here, a female premature infant was diagnosed with placental chorioangioma and liver hemangioma during antenatal period. She developed heart failure secondary to non-immune hydrops fetalis in the neonatal period. The atypical giant hemangioma and coagulopathy suggested the diagnosis of Kasabach-Merritt syndrome. The macroscopic and histopathological examination of the placenta confirmed the diagnosis of chorioangioma. The patient died due to purpura fulminans despite the treatment with prednisolone and propranolol that was started on the second day of life. We are presenting this rare case where placental chorioangioma leading to non-immune hydrops fetalis co-existed with Kasabach-Merritt syndrome.

Intraplacental choriocarcinoma coexisting with fetomaternal hemorrhage: Case report, chemotherapy management, and literature review.

RATIONALE: Near-term intraplacental choriocarcinoma (IC) coexisting with massive fetomaternal hemorrhage (FMH) is rare, and its clinical course is poorly understood. Here, we report a new case from our hospital, with detailed discussion and literature review. PATIENT CONCERNS: A 21-year-old Chinese female at 35 weeks gestation was admitted to our hospital due to reduced fetal movement. Near-term IC coexisting with massive FMH was diagnosed after delivery. INTERVENTION: The mother and infant were followed 3 months after delivery. Beta-human chorionic gonadotropin (ß-HCG), pathological examination of the placenta, and computed tomography scans were performed for the mother and ß-HCG was performed for the infant. OUTCOMES: The mother's ß-HCG serum level increased from 31,280 IU/L (6 days postdelivery) to 192,070 IU/L (49 days postdelivery), and then steadily fell to 42,468 IU/L (3 months postdelivery) without chemotherapy. The mother died from metastasis and cerebral hemorrhage. The infant survived and his ß-HCG serum level fell to within the normal range without chemotherapy. LESSONS: FMH associated with near-term IC is a rare disease. Measurement of maternal ß-HCG may therefore represent a useful parameter when IC is a possible differential diagnosis. A pathological examination of the placenta should be performed in all cases of FMH to better identify cases of IC. Future research should aim to develop methods of identifying which patients with IC should receive chemotherapy, whether we should use single- or multiagent chemotherapies, and whether there is a positive correlation between chemotherapy regimen and ß-HCG serum levels.

HIV antiretroviral exposure in pregnancy induces detrimental placenta vascular changes that are rescued by progesterone supplementation.

Adverse birth outcomes are common in HIV-positive pregnant women receiving combination antiretroviral therapy (cART), especially when cART is initiated in early pregnancy. The mechanisms remain poorly understood. Using a mouse model we demonstrate that protease inhibitor based-cART exposure beginning on day 1 of pregnancy was associated with a pro-angiogenic/pro-branching shift in the placenta driven by lower Flt-1 levels and higher Gcm-1 expression. Micro-CT imaging revealed an increase in the number of arterioles in cART-treated placentas, which correlated with fetal growth restriction. Delaying initiation of cART, or supplementing cART-treated mice with progesterone, prevented the pro-angiogenic/pro-branching shift and the associated placenta vascular changes. In agreement with our mouse findings, we observed an increase in the number of terminal-villi capillaries in placentas from HIV-positive cART-exposed women compared to HIV-negative controls. Capillary number was inversely correlated to maternal progesterone levels. Our study provides evidence that cART exposure during pregnancy influences placenta vascular formation that may in turn contribute to fetal growth restriction. Our findings highlight the need for closer investigation of the placenta in HIV-positive pregnancies, particularly for pregnancies exposed to cART from conception, and suggest that progesterone supplementation could be investigated as a possible intervention to improve placenta function in HIV-positive pregnant women.

Estradiol cypionate aided treatment for experimentally induced ascending placentitis in mares.

The overall goal of this study was to assess the efficacy of various therapeutic combinations of estradiol cypionate (ECP, a long-acting estrogen) and altrenogest (ALT, a long-acting progestin) in addition to basic treatment for placentitis with trimethoprim-sulfamethoxazole (TMS) and flunixin meglumine (FM). Specific outcomes measured in this experiment were (i) time from induction of bacterial placentitis to delivery, and foal parameters (high-risk, survival, and birth weight); and (ii) serum steroid concentrations (progesterone, 17α-hydroxyprogesterone, 17ß-estradiol, and cortisol) in response to treatment. Pregnant mares (∼300 days gestation, n = 46) were randomly assigned into healthy mares (control group, CONT, n = 8) and mares with experimentally induced ascending placentitis (n = 38). Placentitis was induced via intracervical inoculation of Streptococcus equi subspecies zooepidemicus. Thereafter, placentitis induced mares were randomly assigned into: (1) basic treatment, TMS+FM (n = 8); (2) basic treatment with ALT supplementation, TMS+FM+ALT (n = 8); (3) basic treatment with ECP supplementation, TMS+FM+ECP (n = 6); (4) basic treatment with ALT and ECP supplementation TMS+FM+ALT+ECP (n = 6); and (5) no treatment (INOC, n = 10). Treatments were started 48 h after bacterial inoculation and carried out for ten consecutive days. Blood samples were collected daily, and mares were assessed for signs of placentitis until the mare delivered, or for ten consecutive days after onset of treatment. Steroids were analyzed via RIA. Continuous data were analyzed by ANOVA, and categorical data analyzed by Fisher's exact test. Significance was set at p < 0.05. Foal survival at parturition and seven days post-delivery were similar across treated groups (66.7-100%), and to the CONT group. Similar to CONT group, mares in the TMS+FM+ECP group had no high-risk foals while mares in the other groups had higher incidences (50-75%) (p < 0.05). The inclusion of ECP in the treatments resulted in foals with body weight similar to CONT group (p > 0.05). There were no group effects or time by group interactions on concentrations of steroids assessed herein (p > 0.05). In conclusion, in addition to basic treatment TMS+FM, mares with experimentally induced ascending placentitis benefited from ECP supplementation. Conversely, ALT did not appear to make a difference in outcomes. The immunoassays used for measurements of steroid concentrations did not appear useful to assess treatment response.

Luteolin Inhibits Proliferation and Induces Apoptosis of Human Placental Choriocarcinoma Cells by Blocking the PI3K/AKT Pathway and Regulating Sterol Regulatory Element Binding Protein Activity.

Luteolin is a natural compound known for its anticancer effects on various human cancers by regulating signal transduction cascades. However, the effects of luteolin on human placental choriocarcinoma are not known. Results of the present study revealed that luteolin decreased viability of JAR and JEG-3 cells, which are valuable placental models, in a dose-dependent manner, and it induced apoptosis and loss of mitochondrial membrane potential in JAR and JEG-3 cells. The results also suggested that the PI3K/AKT pathway was inhibited by luteolin treatment of JAR and JEG-3 cells in a dose- and time-dependent manner. Next, we established effects of luteolin in the presence of pharmacological inhibitors of PI3K/AKT, ERK1/2 MAPK, and mTOR on proliferation of JAR and JEG-3 cells. In addition, these inhibitors were used to verify phosphorylation of AKT, GSK3beta, and ERK1/2 and to confirm mechanisms regulated by luteolin in JAR and JEG-3 cells. We also determined levels of SREBP1 and SREBP2 expression to investigate regulatory functions of luteolin in lipid metabolism in JAR and JEG-3 cells. Expression levels of both SREBP1 and SREBP2 mRNAs were significantly reduced, but only SREBP1 protein was influenced by luteolin. We compared viability of JAR and JEG-3 cells in response to luteolin alone or in combination with other chemotherapeutic drugs (etoposide, cisplatin, and paclitaxel) and found that luteolin has synergistic effects with the conventional chemotherapeutic drugs as an anticancer agent. Collectively, these results showed that luteolin plays an important role in the treatment of human choriocarcinoma cells by inhibiting the PI3K/AKT/mTOR/SREBP cascade and expression of lipogenic genes.

Molecular Mechanisms of Preeclampsia.

Preeclampsia is a pregnancy-specific disease characterized by new onset hypertension and proteinuria after 20 wk of gestation. It is a leading cause of maternal and fetal morbidity and mortality worldwide. Exciting discoveries in the last decade have contributed to a better understanding of the molecular basis of this disease. Epidemiological, experimental, and therapeutic studies from several laboratories have provided compelling evidence that an antiangiogenic state owing to alterations in circulating angiogenic factors leads to preeclampsia. In this review, we highlight the role of key circulating antiangiogenic factors as pathogenic biomarkers and in the development of novel therapies for preeclampsia.

Vitamin D3 inhibits lipopolysaccharide-induced placental inflammation through reinforcing interaction between vitamin D receptor and nuclear factor kappa B p65 subunit.

It is increasingly recognized that vitamin D3 (VitD3) has an anti-inflammatory activity. The present study investigated the effects of maternal VitD3 supplementation during pregnancy on LPS-induced placental inflammation and fetal intrauterine growth restriction (IUGR). All pregnant mice except controls were intraperitoneally injected with LPS (100 µg/kg) daily from gestational day (GD)15-17. In VitD3 + LPS group, pregnant mice were orally administered with VitD3 (25 µg/kg) before LPS injection. As expected, maternal LPS exposure caused placental inflammation and fetal IUGR. Interestingly, pretreatment with VitD3 repressed placental inflammation and protected against LPS-induced fetal IUGR. Further analysis showed that pretreatment with VitD3, which activated placental vitamin D receptor (VDR) signaling, specifically suppressed LPS-induced activation of nuclear factor kappa B (NF-κB) and significantly blocked nuclear translocation of NF-κB p65 subunit in trophoblast gaint cells of the labyrinth layer. Conversely, LPS, which activated placental NF-κB signaling, suppressed placental VDR activation and its target gene expression. Moreover, VitD3 reinforced physical interaction between placental VDR and NF-κB p65 subunit. The further study demonstrates that VitD3 inhibits placental NF-κB signaling in VDR-dependent manner. These results provide a mechanistic explanation for VitD3-mediated anti-inflammatory activity. Overall, the present study provides evidence for roles of VDR as a key regulator of placental inflammation.

Early detection of placental inflammation by MRI enabling protection by clinically relevant IL-1Ra administration.

OBJECTIVE: We studied whether magnetic resonance imaging (MRI) could be used to detect placental inflammation before the detection of irreversible tissue damage. Next, we tested whether this early detection would enable the administration of treatment (ie, interleukin-1 receptor antagonist [IL-1Ra]) in a realistic clinical time after diagnosis. STUDY DESIGN: Pregnant rats were injected intraperitoneally with lipopolysaccharide with/without delayed IL-1Ra. MRI was performed at different time after the injection, and placentas were collected for comparison. Placental inflammation was assessed by determination of the levels of inflammatory cytokines. RESULTS: Placental inflammation was detected by MRI as early as 3 hours after maternal administration of lipopolysaccharide, concomitantly to IL-1ß up-regulation. This was observed before any tissue damage, which appeared only at 24 hours after the administration of lipopolysaccharide. Delayed IL-1Ra administration (after MRI diagnosis) protected the placenta, as seen by the preserved tissue integrity and limited macrophages infiltration in the placental parenchyma. CONCLUSION: These findings established a noninvasive diagnostic method for early in utero detection of placental inflammation that would allow the administration of placentoprotective intervention within a clinically relevant delay after diagnosis.

Ascending placentitis in the mare: an update.

CONTENTS: Ascending placentitis is a common cause of premature birth, abortion and delivery of compromised, ill foals. Recent experimental models have investigated diagnostic procedures and treatment strategies in an attempt to improve live foal rate. Diagnostics such as transrectal and transabdominal ultrasonography are used to evaluate foetal well-being and placental separation, while measurement of plasma progestins or oestrogen identifies a stressed or hypoxic foetus. Treatment is directed at stopping spread of infection, maintaining uterine quiescence and blocking production of pro-inflammatory cytokines. It must be instituted early if a pregnancy is to be saved. Treatments include antibiotics, tocolytics and immunomodulators. Prompt, aggressive treatment with antibiotics has improved foal viability in experimental models of placentitis.

[A rare case of placental chorioangioma associated with neonatal disseminated hemangiomatosis]. / Association rare d'un choriangiome et d'une hémangiomatose néonatale diffuse.

Placental chorioangioma is a benign vascular tumor. Lesions larger than 4 cm may cause fetal and maternal complications. Its association with disseminated neonatal hemangiomatosis is rarely described. We report a case of a large chorioangioma associated with an hydrops foetalis and disseminated neonatal hemangiomatosis. The relationship between placental chorioangioma and hemangioma is briefly discussed.

Intraplacental choriocarcinoma in a term placenta with both maternal and infantile metastases: a case report and review of the literature.

BACKGROUND: Intraplacental choriocarcinoma is rare, and usually results in maternal metastasis at the time of diagnosis. Intraplacental choriocarcinoma involves both mother and infant is extremely rare. There was only one case report of intraplacental choriocarcinoma with confirmed metastases involving both the mother and the infant. CASE: We describe a second case of intraplacental choriocarcinoma in a term placenta with both maternal and infantile metastases. Grossly, the primary lesion of the placenta resembled an old infarct. Microscopically, clusters of malignant trophoblasts arose from residual normal chorionic villi and infiltrated into the intervillous spaces. Both the mother and the infant received chemotherapy and were alive without disease after one year's follow-up. CONCLUSION: The optimal treatment for intraplacental choriocarcinoma is controversial. However, aggressive chemotherapy is suggested for patients with metastatic disease.

Placental site trophoblastic tumor: an overview.

OBJECTIVE: To analyze 15 consecutive cases of placental site trophoblastic tumor seen in a single reference institution for gestational trophoblastic disease, San Gerardo Hospital, Monza, Italy. STUDY DESIGN: Consecutive patients affected by placental site trophoblastic tumors were selected from our computerized database. RESULTS: There were 15 patients with placental site trophoblastic tumor, with a median age of 35 years. The antecedent pregnancy was a term one in 6 cases (40%), a miscarriage in 4 cases (27%), a termination in 2 cases (13%) and a molar abortion in 2 cases (13%). In 1 case the previous pregnancy was unrecognized. The median interval from the last pregnancy was 12 months, and the presenting symptom in 11 cases was vaginal bleeding, in 2 cases amenorrhea, in 1case a nephrotic syndrome and in 1 case, presenting with metastatic disease, hemoptysis. Six patients were treated using neoadjuvant chemotherapy with etoposide/methotrexate/actinomycin-etoposide/ vincristine (EMA-CO) followed in 5 of 6 (83%) cases by hysterectomy. One patient had only medical treatment with EMA-CO because of a strong desire for or childbearing and had a complete response; after 15 months she was free from disease. The last 9 patients underwent surgery as the first therapy. Among these patients 1 had presented with metastatic pulmonary disease and underwent chemotherapy, with complete disappearance of the pulmonary lesions. Two of these 9 patients had a relapse; the mirst patient had a pelvic and bladder relapse, and 14 months after multiple chemotherapy and surgery, she died. The second had a suburethral relapse 2 months after initial surgery; after chemotherapy and surgery she was well and free of disease. CONCLUSION: Our experience suggests that the role of chemotherapy may be reconsidered not only for metastatic disease but als of or uterine disease when choosing conservative management in young, fertile patients who desire childbearing. Chemotherapy may play an important role in avoiding relapse or early metastases even in patients who underwent hysterectomy as primary treatment.

Ultrasound diagnosis of severe thrombotic placental damage in the second trimester: an observational study.

OBJECTIVES: To screen women with uteroplacental insufficiency between 18 and 26 weeks' gestation for sonographic evidence of destructive placental lesions, to observe the effect of low molecular-weight heparin (LMWH) in these cases, and to compare the outcome with similar but untreated controls. METHODS: We screened 180 women at high risk for placental damage using 16-week maternal serum screening (alpha-fetoprotein and human chorionic gonadotropin), placental shape and texture, and uterine artery Doppler waveforms at the 18-20-week level II examination. Serial gray-scale examinations of placental texture were performed at 22, 24 and 26 weeks. LMWH was offered to women with ultrasound evidence of destructive placental lesions in the absence of intrauterine growth restriction and/or pre-eclampsia. RESULTS: We prospectively identified six women (3.3%) with abnormal maternal serum screening and uterine artery Doppler in whom abnormal placental texture (echogenic cystic lesions) suggestive of destructive lesions in the placental parenchyma was found either at the 18-20-week ultrasound examination (n = 4), or by 26 weeks of gestation (n = 2). All six received LMWH and had live births (gestational age at delivery, 33-37 weeks; birth weight, 1000-3200 g). A further 14 women were referred with similar multiparameter evidence of placental damage at or after 26 weeks, outside the screening study. All had significant fetal growth restriction and were therefore not offered heparin. In 9/14 cases there was a perinatal death. Ischemic and/or thrombotic placental pathology was confirmed in each case, but no maternal thrombophilia disorders were identified in the 20 women. CONCLUSIONS: Integrated biochemical and ultrasound testing of placental function at 16-20 weeks of gestation, followed by serial placental gray-scale ultrasound, may be an effective method of identifying a subset of pregnancies at high risk of adverse pregnancy outcome due to destructive lesions in the placental parenchyma. This strategy of identifying thrombo-occlusive placental lesions before the development of pregnancy complications may prove useful in the design of trials to study the effectiveness of LMWH in the prevention of clinical complications resulting from thrombo-occlusive placental disease.

Placental site trophoblastic tumor.

Placental site trophoblastic tumor (PSTT) is an uncommon form of gestational trophoblastic disease (GTD) with variable spectrum of clinical behavior. PSTT can occur after a normal pregnancy, spontaneous abortion, termination of pregnancy, ectopic pregnancy or molar pregnancy. Surgery is the primary treatment. Chemotherapy has an established role in loco-regionally advanced and metastatic disease. Many studies indicate that mitotic index is an important prognostic indicator. This article reviews the literature on this rare disease.

Alcoholization: the choice of intrauterine treatment for chorioangioma.

Chorioangioma is a vascular tumor of the placenta. Most are small and asymptomatic, whereas the large tumors are clinically significant and often associated with polyhydramnios and fetal heart failure. To prevent fetal loss from these complications, many interventions have been proposed, including intrauterine transfusion in anemic cases and fetoscopic surgery to ablate the feeding vessels. The case presented herein had large chorioangiomas, 8 and 4cm in diameter, associated with polyhydramnios and early signs of hydrops fetalis, diagnosed at 27 weeks gestation. After extensive counseling, we performed alcohol ablation of the feeding vessel of the larger tumor. Signs of fetal heart failure and hydrops fetalis disappeared dramatically. The pregnancy was extended for 2 weeks, followed by premature rupture of the membranes and spontaneous labor at 32 weeks gestation and a surviving female baby, weighing 1360g, was delivered uneventfully. This preliminary experience suggests that alcoholization may be one of the best choices for this condition due to its high efficacy, simplicity, safety and very low cost. To our knowledge, this is the first report using alcoholization for the treatment of hydrops fetalis secondary to chorioangioma.

Prevalencia de la infección transplacentaria por Trypanosoma cruzi en el Hospital de Calama, II Región - Chile / Prevalence of the transplacentary infection for Trypanosoma cruzi in the Calama Hospital, II Region - Chile

Desde 1997, INCOSUR ha propuesto incorporar a las actividades de control, los programas que realicen los diversos países para intervenir la transmisión transplacentaria del Trypanosoma cruzi. El presente estudio tuvo como propósito conocer, diagnosticar y tratar los casos de enfermedad de Chagas congénita en la II Región de Chile, para lo que se estudiaron los 1.987 partos producidos en un año cronológico en uno de sus hospitales más importantes. De los 1.987, 45 casos resultaron positivos (2,4 por cento) para la infección por el T. cruzi y la transmisión transplacentaria se produjo en 5 niños (11 por cento). Todos los niños fueron asintomáticos al nacer, se trataron médicamente con Nifurtimox y al cabo de un año todos presentaron cura serológica y parasitológica la cual fué corroborada durante 2 años de seguimiento. El estudio epidemiológico de los casos índices permitió detectar otros 8 niños infectados, los cuales también fueron tratados, obteniéndose una cura serológica y parasitológica en 50 por cento de los casos a los dos años de control. De acuerdo a los resultados se recomienda la implementación de un programa de intervención de la infección transplacentaria por Trypanosoma cruzi en las áreas de endemia chagásica de Chile.

Conservative management of placental polyp with oral administration of methotrexate.

Surgical treatment is usually selected for placental polyp accompanied by massive bleeding but patients wishing to conserve their fecundity require conservative management. A 35-year old nullipara was diagnosed as having placental polyp on the basis of typical episodes, and detection of placental polypeptide hormones and blood flow by Doppler ultrasonography and dynamic magnetic resonance imaging. Oral administration of methotrexate (2.5 mg, three times a day for 5 days) was repeated for three cycles because surgical treatment was rejected. Serum human placental lactogen, blood flow and the polyp disappeared sequentially following chemotherapy. This report thus advocates considering conservative management for placental polyp.