佐田友 藍

74歳、女性。検診で便潜血検査陽性を指摘され当院を受診し、大腸内視鏡検査を施行した。挿入時にS状結腸の伸展を認め、挿入に2人の医師が関与した。盲腸までの挿入時間は43分であった。全大腸を観察し特に異常は認められなかった。検査後4日目に心窩部痛が出現し、10日目に下腹部痛が出現したため近医を受診。単純CTで骨盤内に腹水貯留を認めたため、精査加療目的に当科紹介となった。来院時、循環動態は安定しており、下腹部に軽度の自発痛および圧痛を認めた。腹部造影CTで脾周囲を中心に、肝表面、骨盤内に液体貯留を認め、脾臓下極の被膜損傷による腹腔内出血と診断した。循環動態は安定しており、モニタリングを行いながら保存的に経過を観察する方針とした。入院4日目の造影CTで腹腔内出血の増悪はなく、入院21日目に退院となった。大腸内視鏡検査後の脾損傷は、遅発性に出現することがあり、稀ではあるが留意すべき検査後合併症の一つである。(著者抄録)

A 41-year-old woman presented with a positive fecal occult blood test. Colonoscopy showed a 20mm, elastic, hard lesion at the appendiceal orifice. Abdominal computed tomography revealed a protruding lesion in the intestine. Laparoscopic ileocecal resection was performed. Histological examination showed endometrial glands in the muscularis propria, consistent with appendiceal endometriosis. We report a patient with appendiceal endometriosis with intussusception.

症例は41歳女性,便潜血検査陽性のため行われた大腸内視鏡検査で,虫垂開口部に径20mmの正常粘膜に覆われた弾性,硬の隆起性病変を認めた.腹部CTでは腸管内腔に突出した隆起性病変として描出され,粘膜下腫瘍の術前診断で腹腔鏡下回盲部切除術を行った.術中観察では虫垂は盲腸内に反転しており虫垂重積を疑う所見であった.病理組織学的検査では,割面で虫垂粘膜の内反を認め,筋層内には円柱状の細胞からなる腺管が内膜様間質を伴って散見され,虫垂子宮内膜症に矛盾しない所見であった.虫垂子宮内膜症を原因とした虫垂重積症は稀であるが,特徴的な内視鏡所見を把握することで,盲腸切除などの縮小手術を施行できる可能性がある.(著者抄録)

Intestinal ischemia/reperfusion (I/R) injury is a life-threatening complication that leads to inflammation and remote organ damage. The NLRP3 inflammasome regulates the caspase-1-dependent release of IL-1β, an early mediator of inflammation after I/R injury. In this study, we investigated the role of the NLRP3 inflammasome in mice with intestinal I/R injury. Deficiency of NLRP3, ASC, caspase-1/11, or IL-1β prolonged survival after intestinal I/R injury, but neither NLRP3 nor caspase-1/11 deficiency affected intestinal inflammation. Intestinal I/R injury caused acute lung injury (ALI) characterized by inflammation, reactive oxygen species generation, and vascular permeability, which was markedly improved by NLRP3 deficiency. Bone marrow chimeric experiments showed that NLRP3 in non-bone marrow-derived cells was the main contributor to development of intestinal I/R-induced ALI. The NLRP3 inflammasome in lung vascular endothelial cells is thought to be important to lung vascular permeability. Using mass spectrometry, we identified intestinal I/R-derived lipid mediators that enhanced NLRP3 inflammasome activation in lung vascular endothelial cells. Finally, we confirmed that serum levels of these lipid mediators were elevated in patients with intestinal ischemia. To our knowledge, these findings provide new insights into the mechanism underlying intestinal I/R-induced ALI and suggest that endothelial NLRP3 inflammasome-driven IL-1β is a novel potential target for treating and preventing this disorder.

BACKGROUND: Goblet cell carcinoid (GCC) is a neuroendocrine tumor usually found in the appendix. GCCs exhibit characteristic findings with mixed endocrine-exocrine features such as staining positive for neuroendocrine markers and producing mucin. The primary GCC of the rectum is exceedingly rare. CASE PRESENTATION: A 77-year-old Japanese male presented with hematochezia. Anal tenderness and a hard mass in the anal canal were found on the digital rectal examination, and colonoscopy was performed. Colonoscopy showed an irregularly shaped mass in the anal canal. Biopsy showed mixed features including adenocarcinoma in situ, well-differentiated adenocarcinoma, and mucinous carcinoma with invasive proliferation. No metastatic lesions were found on the computed tomography scan. Pelvic magnetic resonance imaging scan showed extramural growth of a tumor on the ventral side of the rectum without invasion to the prostate. Laparoscopic abdominoperineal resection was performed. The final diagnosis was well-differentiated adenocarcinoma in the mucosa and goblet cell carcinoid from the submucosa to the adventitia of the rectum. The patient was discharged from the hospital on postoperative day 16. Six months after resection, a computed tomography scan revealed multiple metastatic lesions in the liver. Several chemotherapy regimens were given, and the patient has stable disease 27 months after surgery. CONCLUSION: We present a patient with rectal GCC with metachronous liver metastases. Since GCC grows intramurally and is biologically aggressive compared to typical carcinoid lesions, the disease is usually diagnosed at an advanced stage. The development of optimal adjuvant chemotherapy is needed for those patients.

BACKGROUND: Intestinal ischemia/reperfusion (I/R) injury is a life-threatening complication that leads to inflammation and remote organ damage. However, the underlying mechanism is not yet fully understood. Toll-like receptor 5 (TLR5) is highly expressed in mucosa and recognizes flagellin, the main component of the bacterial flagella. Here, we investigated the role of TLR5 in inflammation and tissue damage after intestinal I/R injury using TLR5-deficient mice. METHODS AND RESULTS: Intestinal levels of TLR5 mRNA and flagellin protein were elevated in wild-type mice subjected to intestinal I/R. Although TLR5 deficiency had no effect on intestinal flagellin levels, it significantly attenuated intestinal injury and inflammatory responses after intestinal I/R. TLR5 deficiency also markedly improved survival in mice after intestinal I/R injury. In wild-type mice, intestinal I/R injury induced remote organ damage, particularly in the lung, which was attenuated by TLR5 deficiency. Furthermore, TLR5 deficiency prevented lung inflammatory responses and vascular permeability after intestinal I/R injury. CONCLUSION: These findings demonstrate a novel role of TLR5 and provide new insights into the mechanism underlying inflammation and tissue damage after intestinal I/R injury.