Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: A subsequent pregnancy after uterine artery embolization (UAE) raises several concerns, one of which is placenta accreta spectrum (PAS). Placenta previa is the strongest risk factor for PAS, which is most likely to occur in the lower uterine segment. PAS without placenta previa (i.e., uterine body PAS) is considered relatively rare. CASE PRESENTATION: A 35-year-old woman, gravida 2 para 1, had undergone UAE for postpartum hemorrhage due to uterine atony after vaginal delivery in her previous pregnancy. She developed placenta previa during her subsequent pregnancy and was therefore evaluated for PAS in the lower uterine segment. On the basis of examination findings, we considered PAS to be unlikely. During cesarean section, we found that the placenta was not detached from the uterine body, and the patient was determined to have uterine body PAS. Ultimately, a hysterectomy was performed. CONCLUSIONS: PAS can occur in a subsequent pregnancy after UAE. When a subsequent pregnancy after UAE is accompanied by placenta previa, it is important to maintain a high index of suspicion of uterine body PAS without being misled by the presence of placenta previa.

DOI： 10.1186/s12884-022-05031-0

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Language：English   Publisher：(一社)日本癌学会  

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Language：English  

DOI： 10.1016/j.ejogrb.2022.05.018

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Language：English   Publishing type：Research paper (scientific journal)  

It has become evident that somatic mutations in cancer-associated genes accumulate in the normal endometrium, but spatiotemporal understanding of the evolution and expansion of mutant clones is limited. To elucidate the timing and mechanism of the clonal expansion of somatic mutations in cancer-associated genes in the normal endometrium, we sequence 1311 endometrial glands from 37 women. By collecting endometrial glands from different parts of the endometrium, we show that multiple glands with the same somatic mutations occupy substantial areas of the endometrium. We demonstrate that "rhizome structures", in which the basal glands run horizontally along the muscular layer and multiple vertical glands rise from the basal gland, originate from the same ancestral clone. Moreover, mutant clones detected in the vertical glands diversify by acquiring additional mutations. These results suggest that clonal expansions through the rhizome structures are involved in the mechanism by which mutant clones extend their territories. Furthermore, we show clonal expansions and copy neutral loss-of-heterozygosity events occur early in life, suggesting such events can be tolerated many years in the normal endometrium. Our results of the evolutionary dynamics of mutant clones in the human endometrium will lead to a better understanding of the mechanisms of endometrial regeneration during the menstrual cycle and the development of therapies for the prevention and treatment of endometrium-related diseases.

DOI： 10.1038/s41467-022-28568-2

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Language：English   Publishing type：Research paper (scientific journal)  

Patient-derived cells and xenografts retain the biological characteristics of clinical cancers and are instrumental in gaining a better understanding of the chemoresistance of cancer cells. Here, we have established a panel of patient-derived spheroids from clinical materials of ovarian cancer. Systematic evaluation using therapeutic agents indicated that sensitivity to platinum-based compounds significantly varied among the spheroids. To understand the molecular basis of drug sensitivity, we performed integrative analyses combining chemoresistance data and gene expression profiling of the ovarian cancer patient-derived spheroids. Correlation analyses revealed that cisplatin resistance was significantly associated with elevated levels of glucose-6-phosphate dehydrogenase (G6PD) and glutathione-producing redox enzymes. Accordingly, cisplatin-resistant spheroids established in vitro showed elevated levels of G6PD and active glutathione. Moreover, treatment with a G6PD inhibitor in combination with cisplatin suppressed spheroid proliferation in vitro and largely eradicated peritoneal metastasis in mouse xenograft models. Furthermore, G6PD expression was elevated during carcinogenesis and associated with poor prognosis. Thus, the combination of gene expression data and chemosensitivity revealed the essential roles of G6PD-driven redox metabolism in cisplatin resistance, underscoring the significance of an integrative approach using patient-derived cells.

DOI： 10.1016/j.canlet.2021.08.018

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Language：English   Publishing type：Research paper (scientific journal)  

KRAS is the most frequently mutated in ovarian endometriosis. However, it is unclear whether the KRAS mutant allele's mRNA is expressed and plays a biological role in ovarian endometriosis. Here, we performed mutation-specific RNA in situ hybridization to evaluate mutant allele expression of KRAS p.G12V, the most frequently detected mutation in ovarian endometriosis in our previous study, in formalin-fixed paraffin-embedded tissue (FFPE) samples of ovarian endometriosis, cancer cell lines, and ovarian cancers. First, we verified that mutant or wild-type allele of KRAS were expressed in all 5 cancer cell lines and 9 ovarian cancer cases corresponding to the mutation status. Next, we applied this assay to 26 ovarian endometriosis cases, and observed mutant allele expression of KRAS p.G12V in 10 cases. Mutant or wild-type allele of KRAS were expressed in line with mutation status in 12 available endometriosis cases for which KRAS gene sequence was determined. Comparison of clinical features between ovarian endometriosis with KRAS p.G12V mutant allele expression and with KRAS wild-type showed that KRAS p.G12V mutant allele expression was significantly associated with inflammation in ovarian endometriosis. Finally, we assessed the spatial distribution of KRAS mutant allele expression in 5 endometriosis cases by performing multiregional sampling. Intratumor heterogeneity of KRAS mutant allele expression was observed in two endometriosis cases, whereas the spatial distribution of KRAS p.G12V mutation signals were diffuse and homogenous in ovarian cancer. In conclusion, evaluation of oncogene mutant expression will be useful for clarifying the biological significance of oncogene mutations in benign tumors.

DOI： 10.1111/cas.14871

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Language：English   Publishing type：Research paper (scientific journal)  

The fundamental morphology of the endometrial glands is not sufficiently understood by 2D observation because these glands have complicated winding and branching patterns. To construct a large picture of the endometrial gland structure, we performed tissue-clearing-based 3D imaging of human uterine endometrial tissue. Our 3D immunohistochemistry and layer analyses revealed that the endometrial glands form a plexus network in the stratum basalis and expand horizontally along the muscular layer, similar to the rhizome of grass. We then extended our method to assess the 3D morphology of tissue affected by adenomyosis, a representative "endometrium-related disease," and observed its 3D morphological features, including the direct invasion of endometrial glands into the myometrium and an ant colony-like network of ectopic endometrial glands within the myometrium. Thus, further understanding of the morphology of the human endometrium based on 3D analysis will lead to the identification of the pathogenesis of endometrium-related diseases.

DOI： 10.1016/j.isci.2021.102258

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Language：English   Publishing type：Research paper (scientific journal)  

Advanced-stage gynecologic cancer remains a life-threatening disease. Here, we present a protocol for establishment of stable in vitro 3D spheroid cells derived from human uterine endometrial and ovarian cancer tissues. The tumor-derived spheroid cells have cancer stem cell-related characteristics, including tumorigenesis, and can be used for biological and biochemical analyses and drug efficacy assays. Because these cells possess the biological characteristics of original human tumors, spheroid cells and spheroid-derived xenografts will have applications in personalized medicine in the future. For complete details on the use and execution of this protocol, please refer to Ishiguro et al. (2016) and Mori et al. (2019).

DOI： 10.1016/j.xpro.2021.100354

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Language：English   Publishing type：Research paper (scientific journal)  

Cancer stem-like cells (CSCs) induce drug resistance and recurrence of tumors when they experience DNA replication stress. However, the mechanisms underlying DNA replication stress in CSCs and its compensation remain unclear. Here, we demonstrate that upregulated c-Myc expression induces stronger DNA replication stress in patient-derived breast CSCs than in differentiated cancer cells. Our results suggest critical roles for mini-chromosome maintenance protein 10 (MCM10), a firing (activating) factor of DNA replication origins, to compensate for DNA replication stress in CSCs. MCM10 expression is upregulated in CSCs and is maintained by c-Myc. c-Myc-dependent collisions between RNA transcription and DNA replication machinery may occur in nuclei, thereby causing DNA replication stress. MCM10 may activate dormant replication origins close to these collisions to ensure the progression of replication. Moreover, patient-derived breast CSCs were found to be dependent on MCM10 for their maintenance, even after enrichment for CSCs that were resistant to paclitaxel, the standard chemotherapeutic agent. Further, MCM10 depletion decreased the growth of cancer cells, but not of normal cells. Thus, MCM10 may robustly compensate for DNA replication stress and facilitate genome duplication in cancer cells in the S-phase, which is more pronounced in CSCs. Overall, we provide a preclinical rationale to target the c-Myc-MCM10 axis for preventing drug resistance and recurrence of tumors.

DOI： 10.1111/cas.14776

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Language：English   Publishing type：Research paper (scientific journal)  

Cancer stem cells (CSCs) reside in a supportive niche, constituting a microenvironment comprised of adjacent stromal cells, vessels, and extracellular matrix. The ability of CSCs to participate in the development of endothelium constitutes an important characteristic that directly contributes to the general understanding of the mechanisms of tumorigenesis and tumor metastasis. The purpose of this work is to establish a reproducible methodology to investigate the tumor-initiation capability of ovarian cancer stem cells (OCSCs). Herein, we examined the neovascularization mechanism between endothelial cells and OCSCs along with the morphological changes of endothelial cells using the in vitro co-culture model NICO-1. This protocol allows visualization of the neovascularization step surrounding the OCSCs in a time course manner. The technique can provide insight regarding the angiogenetic properties of OCSCs in tumor metastasis.

DOI： 10.3791/61751

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Language：English   Publisher：(一社)日本癌学会  

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Language：English   Publishing type：Research paper (scientific journal)  

ARID1A loss-of-function mutation accompanied by a loss of ARID1A protein expression is considered one of the most important driver events in endometriosis-associated ovarian cancer. Although our recent genomic study clarified that ARID1A loss-of-function mutations were detected in 13% of ovarian endometriosis, an association between the ARID1A mutation status and ARID1A protein expression in ovarian endometriosis remains unclear. We performed immunohistochemical staining for ARID1A in 78 ovarian endometriosis samples and 99 clear cell carcinoma samples. We revealed that not only 70 endometriosis samples without ARID1A mutations but also eight endometriosis samples with ARID1A loss-of-function mutations retained ARID1A protein expression. On the other hand, most of clear cell carcinomas with ARID1A loss-of-function mutations showed a loss of ARID1A protein expression. In particular, clear cell carcinoma samples which harbor multiple ARID1A loss-of-function mutations or both a single ARID1A loss-of-function mutation and ARID1A allelic imbalance lost ARID1A protein expression. However, ARID1A protein expression was retained in seven clear cell carcinomas with ARID1A loss-of-function mutations. These results suggest that a single ARID1A loss-of-function mutation is insufficient for ARID1A loss in ovarian endometriosis and some clear cell carcinoma. Further driver events may be needed for the malignant transformation of ovarian endometriosis with ARID1A loss-of-function mutations.

DOI： 10.1038/s41598-020-71273-7

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Language：English   Publishing type：Research paper (scientific journal)  

Uterine endometrial cancer is associated with poor survival outcomes in patients with advanced-stage disease. Here, we developed a three-dimensional cell cultivation method of endometrioid cancer stem-like cells with high aldehyde dehydrogenase (ALDH) activity from clinical specimens. ALDH inhibition synergized with paclitaxel to block cancer proliferation. In the clinical setting, high ALDH1A1 expression was associated with poor survival. A high level of ALDH correlated with an increase of glucose uptake, activation of the glycolytic pathway, and elevation of glucose transporter 1 (GLUT1). Blockade of GLUT1 inhibited characteristics of cancer stem cells. Similarly to ALDH inhibition, GLUT1 inhibition synergized with paclitaxel to block endometrial cancer proliferation. Our data indicated that ALDH-dependent GLUT1 activation and the resulting glycolytic activation are of clinical importance for both prognostic evaluation and therapeutic decision-making in endometrial cancer patients. In addition, the synergistic effects of taxane compounds and ALDH or GLUT1 inhibitors may serve as a new clinical treatment option for endometrial cancer.

DOI： 10.1016/j.stemcr.2019.08.015

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Language：English   Publishing type：Research paper (scientific journal)  

We explored the frequency of germline and somatic mutations in homologous recombination (HR)-associated genes in major histological types of ovarian cancer. We performed targeted sequencing to assess germline and somatic mutations of 16 HR-associated genes and 4 mismatch repair (MMR) genes among 207 ovarian cancer patients (50 high-grade serous carcinomas (HGSC), 99 clear cell carcinomas (CCC), 39 endometrioid carcinomas (EC), 13 mucinous carcinomas (MC), and 6 low-grade serous carcinomas (LGSC)). Germline or somatic mutations of HR-associated genes were detected in 44% of HGSC, 28% of CCC, 23% of EC, 16% of MC, and 17% of LGSC patients. The profile of HR-associated gene mutations was remarkably different among each histological type. Germline BRCA1/2 mutations were frequently detected in HGSC and were rarely observed in CCC, EC, and MC patients. ATM somatic mutation was more frequently detected in CCC (9%) and EC patients (18%) than in HGSC patients (4%). There was a positive correlation between MMR gene mutations and HR-associated gene mutations (p = 0.0072). Our findings might be useful in selection of ovarian cancer patients that should be treated with PARP inhibitors.

DOI： 10.1038/s41598-019-54116-y

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Language：English   Publisher：(一社)日本癌学会  

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Language：English   Publishing type：Doctoral thesis  

DOI： 10.1111/cas.13196

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Language：English   Publishing type：Research paper (scientific journal)  

Endometriosis is characterized by ectopic endometrial-like epithelium and stroma, of which molecular characteristics remain to be fully elucidated. We sequenced 107 ovarian endometriotic and 82 normal uterine endometrial epithelium samples isolated by laser microdissection. In both endometriotic and normal epithelium samples, numerous somatic mutations were identified within genes frequently mutated in endometriosis-associated ovarian cancers. KRAS is frequently mutated in endometriotic epithelium, with a higher mutant allele frequency (MAF) accompanied by arm-level allelic imbalances. Analyses of MAF, combined with multiregional sequencing, illuminated spatiotemporal evolution of the endometriosis and uterine endometrium genomes. We sequenced 109 single endometrial glands and found that each gland carried distinct cancer-associated mutations, demonstrating the heterogeneity of the genomic architecture of endometrial epithelium. Remarkable increases in MAF of mutations in cancer-associated genes in endometriotic epithelium suggest retrograde flow of endometrial cells already harboring cancer-associated mutations, with selective advantages at ectopic sites, leading to the development of endometriosis.

DOI： 10.1016/j.celrep.2018.07.037

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Language：English   Publishing type：Research paper (scientific journal)  

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We previously found that therapeutic targetable fusions are detected across various cancers. To identify therapeutic targetable fusion in uterine cervical cancer, for which no effective gene targeted therapy has yet been clinically applied, we analyzed RNA sequencing data from 306 cervical cancer samples. We detected 445 high confidence fusion transcripts and identified four samples that harbored FGFR3-TACC3 fusion as an attractive therapeutic target. The frequency of FGFR3-TACC3-fusion-positive cervical cancer is also 1.9% (2/103) in an independent cohort. Continuous expression of the FGFR3-TACC3 fusion transcript and protein induced anchorage-independent growth in the cervical epithelial cell line established from the ectocervix (Ect1/E6E7) but not in that from endocervix (End1/E6E7). Injection of FGFR3-TACC3 fusion-transfected-Ect1/E6E7 cells subcutaneously into NOG mice generated squamous cell carcinoma xenograft tumors, suggesting the association between FGFR3-TACC3 fusion and squamous cell carcinogenesis. Transfection of a FGFR3-TACC3 fusion transcript into four cervical cancer cell lines (SiHa, ME180, HeLa, and Ca Ski) induced activation of the MAPK pathway and enhancement of cell proliferation. Transcriptome analysis of the FGFR3-TACC3 fusion-transfected cell lines revealed that an IL8-triggered inflammatory response was increased, via activation of FGFR3-MAPK signaling. Continuous expression of FGFR3-TACC3 fusion led to activation of the PI3K-AKT pathway only in the two cell lines that harbored PIK3CA mutations. Sensitivity to the FGFR inhibitor, BGJ398, was found to depend on PIK3CA mutation status. Dual inhibition of both FGFR and AKT showed an obvious synergistic effect in cell lines that harbor mutant PIK3CA. Additionally, TACC3 inhibitor, KHS101, suppressed FGFR3-TACC3 fusion protein expression and showed antitumor effect against FGFR3-TACC3 fusion-transfected cell lines. FGFR3-TACC3 fusion-positive cancer has frequent genetic alterations of the PI3K/AKT pathway and selection of appropriate treatment based on PI3K/AKT pathway status should be required.

DOI： 10.1038/s41389-017-0018-2

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Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1111/cas.13196

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Language：English   Publishing type：Research paper (scientific journal)  

Recently, many types of in vitro 3-D culture systems have been developed to recapitulate the in vivo growth conditions of cancer. The cancer 3-D culture methods aim to preserve the biological characteristics of original tumors better than conventional 2-D monolayer cultures, and include tumor-derived organoids, tumor-derived spheroids, organotypic multicellular spheroids, and multicellular tumor spheroids. The 3-D culture methods differ in terms of cancer cell sources, protocols for cell handling, and the required time intervals. Tumor-derived spheroids are unique because they are purposed for the enrichment of cancer stem cells (CSCs) or cells with stem cell-related characteristics. These spheroids are grown as floating spheres and have been used as surrogate systems to evaluate the CSC-related characteristics of solid tumors in vitro. Because eradication of CSCs is likely to be of clinical importance due to their association with the malignant nature of cancer cells, such as tumorigenicity or chemoresistance, the investigation of tumor-derived spheroids may provide invaluable clues to fight against cancer. Spheroid cultures have been established from cancers including glioma, breast, colon, ovary, and prostate cancers, and their biological and biochemical characteristics have been investigated by many research groups. In addition to the investigation of CSCs, tumor-derived spheroids may prove to be instrumental for a high-throughput screening platform or for the cultivation of CSC-related tumor cells found in the circulation or body fluids.

DOI： 10.1111/cas.13155

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Language：Japanese   Publisher：(株)ニュー・サイエンス社  

卵巣がんの早期診断は一般に困難な事、また進行再発卵巣がんに対する有効な治療法に乏しい事より、新たな治療法の構築は卵巣がん患者の予後改善をめざす上で喫緊の課題である。卵巣がんの典型的な臨床像は、がん幹細胞の存在を強く示唆しており、従って卵巣がん幹細胞を標的とした治療法の開発が強く望まれる。これまでの研究で、普遍的な卵巣がん幹細胞マーカーは明らかになってはいないものの、CD44、CD133、ALDH等が有力な候補として報告されている。これまでに同定された卵巣がん幹細胞を標的とした治療法としては、機能的ながん幹細胞マーカーや、生存に必須なシグナル経路を標的とした阻害剤の使用が検討されているが、その現況について概説したい。(著者抄録)

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Language：English   Publishing type：Research paper (scientific journal)  

Recent advances in RNA-sequencing technology have enabled the discovery of gene fusion transcripts in the transcriptome of cancer cells. However, it remains difficult to differentiate the therapeutically targetable fusions from passenger events. We have analyzed RNA-sequencing data and DNA copy number data from 25 endometrial cancer cell lines to identify potential therapeutically targetable fusion transcripts, and have identified 124 high-confidence fusion transcripts, of which 69% are associated with gene amplifications. As targetable fusion candidates, we focused on three in-frame kinase fusion transcripts that retain a kinase domain (CPQ-PRKDC, CAPZA2-MET, and VGLL4-PRKG1). We detected only CPQ-PRKDC fusion transcript in three of 122 primary endometrial cancer tissues. Cell proliferation of the fusion-positive cell line was inhibited by knocking down the expression of wild-type PRKDC but not by blocking the CPQ-PRKDC fusion transcript expression. Quantitative real-time RT-PCR demonstrated that the expression of the CPQ-PRKDC fusion transcript was significantly lower than that of wild-type PRKDC, corresponding to a low transcript allele fraction of this fusion, based on RNA-sequencing read counts. In endometrial cancers, the CPQ-PRKDC fusion transcript may be a passenger aberration related to gene amplification. Our findings suggest that transcript allele fraction is a useful predictor to find bona-fide therapeutic-targetable fusion transcripts.

DOI： 10.1038/srep18657

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Language：Japanese   Publisher：新潟産科婦人科学会  

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Language：Japanese   Publisher：(一社)日本癌治療学会  

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Language：Japanese   Publisher：(一社)日本癌治療学会  

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Language：Japanese   Publisher：新潟産科婦人科学会  

巨大な子宮頸部筋腫を合併した38歳初産婦が妊娠18週で子宮内胎児死亡となり、経腟的処置は困難であることから流産手術として帝王切開術を選択し、また妊孕性を温存するため子宮筋腫核出術を同時に施行した。そのさい出血軽減対策として内腸骨動脈バルーン塞栓術とバソプレシン局注を併施することで、輸血せずに手術を完遂できた。妊孕性は温存され、3年後に生児を得た。

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Language：Japanese   Publisher：新潟産科婦人科学会  

妊娠中の子宮破裂は母児ともに重篤な状態を招きやすい病態であるが、特徴的な臨床所見や徴候について明確な知見がなく、早期診断が困難である。今回、当院で過去15年間に子宮破裂と診断された5症例について臨床所見と母児の転帰を中心に検討した。臨床的背景として、4例が高齢妊娠、うち1例は多産婦であった。特徴的な臨床所見として、陣痛とは異なる腹痛を3例、分娩前の異常出血を2例に認めた。子宮収縮の特徴的な所見として、陣痛減弱を1例に認め、他の1例に子宮頻収縮を認めた。母体の転帰として、輸血を要したものが3例あり、うち1例は出血コントロールが困難で子宮全摘術を施行された。児の転帰は、長期予後を調査しえた4例すべてが転帰良好であった。

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Language：English   Publishing type：Research paper, summary (international conference)   Publisher：WILEY  

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Authorship：Lead author   Language：Japanese   Publisher：新潟産科婦人科学会  

32歳。自然妊娠の1絨毛膜2羊膜双胎で、妊娠17週時に前医で双胎間輸血症候群(TTTS)と診断され、胎児鏡下吻合血管レーザー焼灼術を施行された。羊水除去も同時に行われ、TTTSを離脱した。帰省分娩を希望し、妊娠20週に当院を初診した。外来で慎重に経過をみていたところ、妊娠25週に胎児超音波検査で第2児(元供血児)に先天性上部消化管閉鎖症を疑わせる腸管拡張を認めた。第2児には発育不全も認め、入院管理を開始した。羊水量は両児とも正常範囲で推移していたが、妊娠34週2日の心拍数モニターで第2児の心拍が確認できず、超音波検査により子宮内胎児死亡と診断した。死因として、臍帯潰瘍部の臍帯血管破綻による失血死が疑われた。

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Language：Japanese   Publisher：(株)東京医学社  

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Language：Japanese   Publisher：(株)東京医学社  

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Language：Japanese   Publisher：(株)自然科学社  

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Language：Japanese   Publisher：(株)自然科学社  

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Language：English   Publisher：日本癌学会  

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Language：English   Publishing type：Research paper, summary (international conference)   Publisher：AMER ASSOC CANCER RESEARCH  

DOI： 10.1158/1538-7445.AM2017-529

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Language：English   Publishing type：Research paper, summary (international conference)   Publisher：AMER ASSOC CANCER RESEARCH  

DOI： 10.1158/1538-7445.AM2016-1504

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Language：Japanese   Publisher：鶴岡市立荘内病院  

山形県庄内地域は他地域へのアクセスが悪いという地理的な不利を乗り越えるべく、庄内地方の病院に勤務する医師を対象とした腹腔鏡下手術のトレーニングセミナーを開催した。他地域より招いた講師とその補助者を除く当地域からの参加者は15名で、その内訳は婦人科5名、外科7名、臨床研修医3名であった。これまでに同様のセミナー参加経験のない医師の参加が多く、今後トレーニングを開始し続けていく意思が芽生えたようであった。今後も同様の形式でのセミナー継続意見が多くみられた。このセミナーを今後も開催するにあたっては、参加者間での交流を深め、複数診療科の医師が集まることを生かしていくことが望まれる。(著者抄録)

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Language：Japanese   Publisher：新潟産科婦人科学会  

2011年4月〜2014年2月に婦人科良性疾患に対して腹腔鏡下手術が行われた症例数と開腹手術が行われた症例数を年度別に集計し、腹腔鏡下手術が全手術に占める割合を算出するとともに、腹腔鏡下手術群と開腹手術群で「手術時間」「出血量」「術後1日目のCRP」「手術合併症」などを比較検討した。結果、腹腔鏡下手術が占める割合は、2011年度が61%、2012年度56%、2013年度69%であった。開腹手術施行群との比較では「出血量」「CRP」が低値であったが、腹腔鏡下手術での合併症発生率は全国平均に比べて少し高かったことから、今後さらなる技術向上を図る必要があると考えられた。

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Language：Japanese   Publisher：(一社)日本産科婦人科内視鏡学会  

2003〜2011年に初期子宮体癌に対し腹腔鏡下根治術(LAVH、LH、TLH)を施行した44例を対象に、3名の術者による手術時間、出血量、摘出リンパ節数を比較し、更に開腹手術移行例、合併症、予後も調査した。術者の経験年数は術者A:24年、術者B:22年、術者C:18年で、術者Bは日本産科婦人科内視鏡学会技術認定医・日本婦人科腫瘍専門医の資格を有していた。3名の術者(A・B・C)により各11例、19例、14例の手術が行われた。有意差があったのは手術時間で、術者B、A、Cの順に短かった。多重比較検定では術者B、Cの間に有意差を認めた。術者間差を年次別にみると、腹腔鏡手術開始初期の2003〜2007年に認めていた有意差は、2008〜2011年には認めなかった。開腹手術移行例は3例であった。重篤な術中・術後合併症は認めず、術後に漿膜性腺癌IB期の1例に腟断端再発を認めたため再手術を行った。術後観察期間12〜108ヵ月(中央値46ヵ月)で、全例が生存中である。

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Language：Japanese   Publisher：新潟産科婦人科学会  

症例は30歳女性で、前医より重複子宮を指摘されていたところ、右側子宮に自然妊娠成立し経過は良好であった。妊娠36週6日に少量の性器出血と下腹部痛が認められたため当科入院となり経過観察としていたが、妊娠37週0日に常位胎盤早期剥離の疑いで緊急帝王切開となった。術中、左側の子宮はやや小さく左付属器は完全に欠損しているのを認め、右側の子宮は胎盤の一部に血腫と軽症の常位胎盤早期剥離が認められたものの、横切開にて女児を娩出した。術後4日目に強い左下腹部痛が生じ、経腟超音波検査で子宮頸部左側に傍頸部嚢胞を疑う腫瘤が認められたが、術後5日目に陣痛様の痛みと共に血液塊が排出され下腹部痛は改善した。その後のMRI検査で左傍頸部嚢胞を認め、更に左右の子宮頸部との間、左子宮頸部と嚢胞との間に交通が認められた。病理検査により排出物は脱落膜であることを認め、分娩後に非妊娠子宮の脱落膜が左傍頸部嚢胞へ貯留し子宮間の交通部分を閉塞したため左下腹部痛が生じ、交通部分を通じて脱落膜が自然排出したことにより症状が軽快したと考えられた。経過は良好で、術後10日目に退院となった。

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Language：Japanese   Publisher：新潟産科婦人科学会  

症例は26歳女性で、妊娠39週1日で正常経腟分娩後、胎盤娩出の際に軽度の臍帯牽引を行ったところ、胎盤が腟内に見える位置まで下降したため用手的に把持して娩出した。その後異常出血は認めなかったが、子宮底は通常より低くかつ硬く触れ、更に間欠的に子宮内より出血を認め、双手圧迫、子宮収縮剤投与を行った。しかし会陰裂傷縫合後、意識レベルJCSI-2に低下し、出血量約1000ml、血圧65/48mmHg、脈拍153/分となり、産科危機的出血と判断し開腹手術となった。開腹したところ子宮底部が子宮円索を伴い噴火口状に消失しているのを認め不全子宮内反症の所見であったため、経腟的に子宮内に内診指を挿入し子宮底部中心を上方に押し上げ整復した。更に双手圧迫、冷罨法、オキシトシン点滴静注、濃厚赤血球8単位、新鮮凍結血漿(FFP)10単位、ATIII製剤1500単位の投与を行ったところ、子宮収縮は良好となった。術後、FFP8単位、血小板濃厚液25単位を輸血し、抗DIC製剤として遺伝子組み換え型ヒトトロンボモジュリン製剤を投与したところDICを離脱し、その後再燃なく術後10日目に母児共に退院となった。

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Language：Japanese   Publisher：新潟産科婦人科学会  

37歳(2妊0産)。子宮頸癌Ib1期に対する腹式広汎子宮頸部摘出術(RT)を受け、併せて非吸収糸で2重の頸管縫縮術が行われた。術後4年に体外受精、凍結胚盤胞移植にて妊娠した。妊娠21週5日に発熱、感冒症状を来したのを契機に入院管理となった。入院後は分娩まで塩酸リトドリンを投与し、NSTにて連日のモニターを行った。また、腟鏡診や経腟エコーを頻回行い、連日腟洗浄を行った。妊娠は概ね良好に継続し、妊娠37週1日目に選択的帝王切開術を行い、3154gの男児を娩出した。術後経過は良好で、術後7日目に母児共に退院し、術後1ヵ月(RT後4年10ヵ月)現在、子宮頸癌の再発は認めない。

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Language：Japanese   Publisher：長岡赤十字病院  

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Language：Japanese   Publisher：長岡赤十字病院  

70歳男性。患者は腹痛を主訴に著者らの施設へ救急外来受診し、身体所見および検査所見より急性膵炎と診断された。ICU入院後、胃管挿入をはじめ中心静脈ライン確保の上、輸液、FOYなどの投与が開始されたが重症化し、膵動注療法、持続血液濾過透析を含めた積極的治療を行うも入院3日目に死亡となった。剖検所見では急性出血性壊死性膵炎に加え、肺、心、腎などの遠隔臓器にも変性、壊死が認められ、多臓器不全症候群(MODS)の状態であった。また、末梢血中にはSRA陽性単球、マクロファージを多数みられ、高サイトカイン血症、全身性炎症反応症候群の状態であることが明らかとなった。尚、本症例の現病歴を再考すると、入院の2〜3ヵ月前にも腹痛発作を起こしており、その時、すでに膵炎によって引き起こされるpriming phaseが発生していたことが推測され、そこに再度膵炎の活性化が生じ、MODSを起こし、死に至ったものと考えられた。

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