BACKGROUND AND AIMS:Steatotic liver disease (SLD) is increasingly identified in pregnant populations. However, its associations with adverse pregnancy outcomes (APOs) in relation to specific trimesters remain unclear. This study aimed to evaluate the trimester-specific associations between SLD and APOs. METHODS:This study included 3806 pregnant women from Beijing Friendship Hospital. Hepatic ultrasonography was performed to assess SLD status during the first (T1) and third (T3) trimesters. Associations between SLD and APOs were assessed using logistic regression. RESULTS:The prevalence of SLD among pregnant women was 10.27%, varying across trimesters. Persistent SLD (present in both T1 and T3) demonstrated positive associations with overall APOs (OR = 1.728, 95% CI: 1.202-2.502, p = 0.003), including pregnancy-associated hypertension (OR = 1.742; 95% CI: 1.019-2.916; p = 0.038), preterm birth (OR = 2.552, 95% CI: 1.019-5.965, p = 0.037), and large-for-gestational-age neonates (OR = 1.762, 95% CI: 1.080-2.820, p = 0.020). T1 SLD (OR = 1.737, 95% CI: 1.128-2.700, p = 0.013) and persistent SLD (OR = 1.821, 95% CI: 1.282-2.600, p < 0.001) were both associated with a higher risk of caesarean section. Notably, T3 SLD was significantly associated with postpartum haemorrhage (OR = 2.154; 95% CI: 1.025-4.078; p = 0.028). A marginal association was observed between pregnancy-associated hypertension and T3 SLD (OR = 2.024; 95% CI: 0.965-3.876; p = 0.045). CONCLUSION:Persistent SLD in pregnancy is associated with an increased risk of APOs, trimester-specific assessment of SLD may facilitate risk stratification and inform clinical management. Further studies are warranted to evaluate whether lifestyle interventions can mitigate these risks.

OBJECTIVE:Wolfram Syndrome (WS) is a rare autosomal recessive neurodegenerative disorder caused by mutations in WFS1 or CISD2 (WFS2). We present a rare case report of pregnancy with WFS1 spectrum disorder (WFS1-SD) in our hospital and reviewed literature to provide the management of pregnancy in these patients through multi-disciplinary cooperation.CASE REPORT:A 31-year-old (gravida 6, para 1) woman with WFS1-SD conceived naturally. During the pregnancy, she adjusted insulin intermittently to control blood glucose and monitored intraocular pressure changes under the guidance of doctors without any complications. Cesarean section was delivered at 37+4 weeks of gestation due to breech position and uterine scar and the neonatal weight was 3200 g. Apgar score 10 at 1 min, 10 at 5-min and 10 at 10 min, respectively. This rare case had a good maternal and infant outcome under multidisciplinary management.CONCLUSION:WS is an extremely rare disease. Limited information is available on the impact and management of WS on maternal physiologic adaptation and fetal outcome. This case provide a guide for clinicians to raise awareness of this rare disease and strengthen the management of pregnancy in these patients.

Background: We retrospectively reviewed the data of three patients with intravenous leiomyomatosis (IVL), one of whom had intracardiac leiomyomatosis, and analyzed their clinical symptoms, preoperative assessment findings, operative approaches, and recurrence. Case presentation: The present study describes three cases of IVL extending into the inferior vena cava, even as far as the right atrium and ventricle, and discusses the imaging findings and differential diagnosis of this tumor entity. The three patients, two of whom were diagnosed during the first operation and one of whom had a giant pelvic mass, were surgically treated with complete tumor resection, hysterectomy, and bilateral salpingo-oophorectomy. The pathological examination findings were suggestive of IVL. The duration of time from the first myomectomy or hysterectomy to IVL occurrence ranged from 2 to 18 months. No signs of recurrence were observed during follow-up. Computed tomography and magnetic resonance imaging played a vital role in the diagnostic process and presurgical assessment. Conclusion: In clinical practice, IVL should be considered before surgery for a broad ligament myoma or giant pelvic mass. Surgery should always aim for complete tumor excision and include hysterectomy and bilateral salpingo-oophorectomy. Vascular reconstruction computed tomography is a good choice for diagnosis and follow-up.

BACKGROUND Intra-abdominal hemorrhage during pregnancy is a rare and dangerous complication of pregnancy. In this article, we report 4 cases of intra-abdominal hemorrhage during pregnancy, including the spontaneous rupture of uterine veins, spontaneous rupture of liver, rupture of external iliac vessel branch, and rupture of right renal hamartoma. CASE SUMMARY The clinical manifestations of three patients lacked specificity, and the localization of the bleeding was not clear prior to surgery. All 4 pregnant women were successfully treated, while only one full-term infant survived. CONCLUSION There are diverse causes of intra-abdominal hemorrhage during pregnancy in clinic, and it is clinically characterized by acute abdominal pain during pregnancy. Clear diagnosis before surgery is rather difficult. Early diagnosis, timely and appropriate treatment and surgery, and multidisciplinary cooperation are key to saving pregnant females' lives and improving the outcomes of perinatal infants.

Graft derived cell-free DNA was recently reported as a non-invasive biomarker to detect graft damage or rejection after liver transplantation. There are a number of methods for quantification of Gcf-DNA, including quantitative-PCR, digital droplet PCR and massively parallel sequencing (next generation sequencing). Here we present the NGS data and fragment size distribution of cell-free DNA in the plasma of patients with inborn errors of metabolism who underwent living-related liver transplantation. For more insights please see Analysis of fragment size distribution of cell-free DNA: a potential noninvasive marker to monitor graft damage in living-related liver transplantation for inborn errors of metabolism. [1].

Aims: This study aimed to evaluate the function and pathway of ATP-binding cassette transporter member A1 (ABCA1)-induced anti-inflammatory response in cells at the feto-maternal interface. Main methods: The primary amniotic mesenchymal cells (AMCs), chorion cells and decidual cells were isolated from placental membranes of women with uncomplicated pregnancies at full-term (not in labor) using enzymatic digestion. Flow cytometry was used to measure the purity of isolated cells. Immunofluorescence assay was performed to detect the location of ABCA1 and toll-like receptor 4 (TLR4). Reverse transcription PCR and western blotting analyses were used to examine ABCA1, TLR4 and inflammatory factor expression in primary cells. ELISA was used to detect cytokine secretions from the primary cells. Key findings: ABCA1 and TLR4 were mainly located in the cell nucleus and cytoplasm of feto-maternal interface cells. ABCA1 expression remained the highest in chorion cells, medium in decidual cells, and weakest in AMCs. Upregulated expression of ABCA1 decreased expression of TLR4 and the levels of pro-inflammatory factors, but increased cytoprotective factors in all cell types. In contrast, downregulated expression of ABCA1 increased the expression of TLR4 and pro-inflammatory factors, but decreased the levels of cytoprotective factors. Downregulated ABCA1 expression followed by decreased TLR4 expression using a small interference RNA (siRNA) induced reduction of interleukin (IL)-1 beta and tumor necrosis factor-alpha (TNF-alpha) in all cell types. Significance: ABCA1 at feto-maternal interface acts as an anti-inflammatory role by reducing the expression of TLR4 in uncomplicated pregnancies. ABCA1 might be a potential therapeutic target for preventing gestational diseases.

As the most effective treatment for end-stage renal diseases, renal transplantation can improve the quality of life of patients and prolong the survival time. However, during the prolonged survival time, malignancy has become one of the main causes of death of recipients, which vary geographically. Tumors in the digestive system and urothelial tumors have been highly reported in Asia. In general, the gynecological malignant tumors have been rarely reported, especially the endometrial carcinoma. Herein, a 63-year-old female renal transplant recipient diagnosed with endometrial carcinoma (15 years after transplantation) was reported. The patient had suffered irregular postmenopausal bleeding for a short time before hospitalization. She underwent abdominal hysterectomy, bilateral salpingo-oophorectomy, right pelvic lymphadenectomy, right para-aortic lymphadenectomy and omental excision. Postoperative pathology showed ovarian and pelvic lymph node metastasis and pathological stage IIIC. After six courses of chemotherapy with paclitaxel 270 mg + carboplatin 500 mg, the patient’s renal function was normal. During the third cycle of chemotherapy, the patient suffered a third-degree bone marrow suppression and returned to normal soon when treated with the recombinant human granulocyte stimulating factor. In conclusion, early screening of gynecologic tumors is important for female patients after renal transplantation, which has a positive significance for the prognosis improvement.

Graft-derived-cell-free DNA (Gcf-DNA) in plasma is a promising biomarker to monitor graft-rejection after liver transplantation (LTx). However, current methods of measuring Gcf-DNA have several limitations including high cost, long turnaround-time and the need to request donor's genetic information. In this study, eleven patients diagnosed with different inborn errors of metabolism (IEMs) who required living-related LTx were enrolled in order to establish a potentially useful noninvasive method to monitor graft damage. Circulating cell-free DNA (cfDNA) was extracted from plasma specimens serially collected at specific time points (day 0, day 1, day 7, day 14, day 30, day 60) after LTx. The distribution of Gcf-DNA fragment sizes was measured using sequencing read lengths and quantified by using Y-chromosome capture methodology in seven sex-mismatched recipients. In the analysis of fragment size distribution, we observed Gcf-DNA exhibited smaller fragment sizes than the recipient-cfDNA. Based on this phenomenon, two fragment sizes (105-145 bp, 160-170 bp) of the cfDNA pool were extracted to enrich Gcf-DNA. Accordingly, the ratio of short fragments to long fragments (S/L-Frag) in cfDNA was calculated. A high S/L-Frag ratio pointed towards an early trend of graft injury when compared to two routine liver function enzymes (ALT and AST) and Gcf-DNA, and it significantly correlated with ALT (P < 0.0001) and AST (P < 0.0001) during full-blown rejection. In conclusion, we established the Gcf-DNA size profile in patients who have undergone living-related LTx and established a potential biomarker to monitor graft function after LTx.

ABCA1 is expressed in placental trophoblasts, such that when the expression level of ABCA1 changes, the function of trophoblasts dramatically changes. However, the mechanism by which ABCA1 affects the function of trophoblast cells remains unclear. Here, we used biochemical and transcriptomic to uncover the potential mechanism of the effect of ABCA1 on trophoblast function. HTR8/SVneo cells were either treated with the agonist T0901317 or transfected with siRNA to regulate ABCA1 expression levels. A human gene expression microarray was used to analyze the expression spectrum of ABCA1. Microarray results were confirmed by Western blotting and RT-PCR. Immunofluorescence allowed detection of the cellular localization of ABCA1, CCL8, CXCL10, CXCL11, and S1PR1 in HTR8/SVneo cells. Co-immunoprecipitation was used to test interactions among these proteins. Concomitant with an increase in ABCA1 expression, S1PR1 expression increased, whereas expression of CCL8, CXCL10, and CXCL11 decreased significantly; opposite effects were observed with a decrease in ABCA1 expression. Thus, changes in ABCA1 expression may lead to changes in downstream gene expression. Whereas the interaction between ABCA1 and S1PR1 was direct, interactions among ABCA1 and CCL8, CXCL10, and CXCL11 were indirect. We propose that, in conjunction with S1PR1, ABCA1 regulates expression levels of CCL8, CXCL10, and CXCL11; this may lead to changes in the immune function of trophoblastic cells. Thus, we suspect that the effect of ABCA1 on trophoblast function may involve many biological processes, molecular function changes, and the activation of multiple signaling pathways.

AIMS:To study the potential impact of ABCA1 on the function of the placenta.MAIN METHODS:Trophoblasts and macrophages were isolated from the placenta with enzymatic digestion; Immunofluorescence assay was used to detect the location of ABCA1 in cells; RT-PCR and Western-blot were used to detect the expression of ABCA1; The cholesterol efflux assays of primary trophoblasts was detected by Amplex Red cholesterol assay kit (Invitrogen);Inflammatory factor secretion from primary macrophages was detected by Elisa.KEY FINDINGS:ABCA1 was mainly located on trophoblast membranes. Decreased ABCA1 expression in trophoblasts reduced the cholesterol efflux of trophoblasts (P<0.01). while increased ABCA1 expression in trophoblasts reduced the cholesterol efflux of trophoblasts (P<0.05). ABCA1 was uniformly expressed on the cell membrane, cytoplasm, and nucleus of macrophages. Decreased ABCA1 expression in macrophages, increased inflammatory factors but reduced IL-10 (P<0.01). While increased ABCA1 expression in macrophages, reduced inflammatory factors but increased IL-10 (P<0.01).SIGNIFICANCE:ABCA1 may be a potential target for the prevention of gestation diseases.

Objective. Abnormal expression of ABCA1 and ABCG1 in the placenta can elicit lipid metabolism disorder and adverse pregnancy outcomes. However, whether it is associated with preterm delivery remains unclear. Our present study aimed to evaluate the relationship between abnormal expression of ABCA1 or ABCG1 and preterm delivery. Methods. Maternal blood and placental tissues from women with spontaneous deliveries (SPD), iatrogenic deliveries (IPD), and term deliveries (TD) were collected. The lipid content and expression of ABCA1 and ABCG1 were subsequently measured. Results. Compared with IPD and TD groups, the HDL, TD, LDL, and TC levels were lower in the maternal blood but higher (except TC) in the cord blood of the SPD group. The extracellular lipid content in the placentas of the SPD group was also notably lower relative to the IPD and TD groups. Moreover, the protein and mRNA expressions of ABCA1 in the placentas of the SPD group were significantly higher compared with the IPD and TD groups; however, there was no obvious difference among the three groups in the protein and mRNA expressions of ABCG1. Conclusions. Abnormal expression of ABCA1 may be associated with the dysregulation of placental lipid metabolism and the occurrence or development of SPD.

Spontaneous preterm delivery (SPTD) with gestational age between 28 and 37 complete weeks was reported to have a genetic predisposition in lipids metabolism. This study aimed to investigate the association between the lipid levels and gene polymorphisms of ABCA1 (rs2422493), APOE (rs7412) and HMGCR (rs12916) in Chinese pregnant women with SPTD. A case-control study was conducted at the baseline randomization in 200 SPTD and 178 healthy full term delivery (FTD) women. Maternal blood lipids were detected close to delivery of fetus in SPTD group and in FTD group with gestational age-matched. Cord blood lipids were detected after delivery in two groups. Three genotypes both in maternal and cord blood were determined by real time PCR. The results showed that the levels of total cholesterol (TCHO), triglyceride (TG), high density lipoprotein (HDL), and low-density lipoprotein cholesterol (LDL) in the maternal blood in the SPTD group were significantly lower than those in the FTD group, while the levels of TCHO, HDL, and LDL in the cord blood in the SPTD group were significantly higher than those in the FTD group. In the SPTD subjects, the levels of TG and LDL in the maternal blood were associated with different genotypes of HMGCR gene rs12916 loci. These results indicate that abnormal lipid metabolism may exist in SPTD women and the premature fetus and the HMGCR gene may be a susceptible gene for SPTD.