Multiple esophageal hematomas with oozing observed and successfully treated after transcatheter mitral valve edge-to-edge repair procedure.

Although previously reported as relatively rare, esophageal hematoma can likely develop in patients on anticoagulants or those with underlying hemorrhagic disorders. From April 2018 to December 2018, among 36 patients who received transcatheter mitral valve edge-to-edge repair (TMVr) at our hospital, seven (19.4%), who were suspected of having digestive tract hemorrhage evidenced by blood stains on a probe extracted after transesophageal echocardiography, underwent esophagogastroduodenoscopy. Esophageal hematomas were noted in all patients, and endoscopic hemostasis was performed in two cases. Depending on their form, hematomas were noted on the submucosa and the epithelium of the shallow esophageal layer. Esophageal hematomas caused by transesophageal echocardiography for TMVr are not rare, and clinicians should be aware of it.

Giant cavernous hepatic hemangioma shrunk by use of sorafenib.

Here we report a case of a 76-year-old man with a giant cavernous hepatic hemangioma of more than 20 cm in diameter. Since the hepatic hemangioma was actually growing and might possibly rupture and he complained of abdominal symptoms, we decided to perform interventional therapy. First we performed transcatheter arterial embolization (TAE) of the hepatic arteries. However, since this was not sufficiently effective, we added sorafenib (600 mg/day). As a result, the tumor shrank with symptomatic improvement. Subsequently, an adverse event occurred, and we suspended the sorafenib therapy. Then, the tumor began to grow, and we resumed administering sorafenib at 400 mg/day. The tumor shrank again, and we continued the sorafenib therapy thereafter. The tumor shrinkage, although possibly induced by the effect of TAE, is considered primarily due to the effect of treatment with sorafenib, because (1) TAE did not sufficiently reduce the blood supply to the inside of the tumor; (2) other tumors shrank in the area not targeted by TAE; and (3) the tumor grew during suspension of sorafenib therapy and shrank again after resuming the treatment.

[A case of anorectal malignant melanoma appearing 1 year after endoscopic mucosal resection of a rectal adenocarcinoma].

We present a case of a 61-year-old woman who underwent endoscopic mucosal resection (EMR) for early-stage colorectal cancer. However, because the condition of the horizontal margin of the resected tumor was unknown, she further underwent local transanal excision. Lower gastrointestinal endoscopy performed 1 year later showed protruding lesions both on the scar tissue and in the vicinity. Biopsy revealed malignant melanoma. She then underwent laparoscopic abdominoperineal resection and colostomy. This was an extremely rare case of adenocarcinoma complicated by malignant melanoma after resection.

A reduced COX-2 expression and a reduced number of pericryptal myofibroblasts are associated with depressed adenoma of the colon.

The histogenesis of depressed adenoma of the colon has not been sufficiently investigated. Pericryptal myofibroblasts are stromal cells expressing smooth muscle actin, and are involved in the differentiation and multiplication of epithelial cells in the colonic epithelium. COX-2 has been reported to be involved in the development of colon adenoma. We studied the histogenesis of depressed adenoma of the colon by examining the relationship between the presence of pericryptal myofibroblasts and COX-2 expression. Twenty-one depressed adenomas of the colon that had been resected endoscopically between June 1998 and May 2003 (mild-moderate atypia; mean diameter, 6.7 mm) and 23 elevated adenomas that had been resected endoscopically in 2003 (mild-moderate atypia; mean diameter, 11.7 mm), were studied. We performed immunohistochemical staining using alpha-smooth muscle actin antibody to detect pericryptal myofibroblasts. We also performed immunohistochemical staining for Cox-2. Eighteen (78.3%) of the 23 elevated adenomas and six (28.6%) of the 21 depressed adenomas were positive for pericryptal myofibroblasts immunohistochemically, showing a significant difference (P<0.001). Seventeen elevated adenomas (73.9%) and eight depressed adenomas (38.1%) were positive for COX-2 expression (P=0.016). COX-2 expression was detected in the stroma, and the sites of COX-2 expression coincided with the sites of pericryptal myofibroblasts. The histogenesis of depressed adenomas differs from that of elevated adenomas. Our results suggest that a low number of pericryptal myofibroblasts and a low COX-2 expression are associated with depressed adenomas.

Relationship between molecular markers and endoscopic findings in laterally spreading tumors.

BACKGROUND AND AIM: Characteristic clinicopathological features of laterally spreading tumors (LSTs) have been reported by endoscopists; however, only a few studies have been conducted on the biological features. These studies were not fully associated with the endoscopic findings of LSTs. The aim of this study was to estimate the biological features of each type of endoscopic finding of LST using two molecular markers, matrix metalloproteinase-7 (MMP-7) and beta-catenin. METHODS: Expression of the molecular markers and the endoscopic findings were compared in 22 LSTs and 14 subpedunculated polyps. MMP-7 and beta-catenin were immunostained. Three types of representative endoscopic findings of LST were defined as segments in LSTs. They were 15 granular segments, seven large nodular segments, and seven flat segments that corresponded to the area composed of aggregates of similar size granules, large nodules of diameter more than 10 mm, and a flat surface with no granule, respectively. RESULTS: Expression of MMP-7 and coexpression of MMP-7 and beta-catenin were higher in large nodular segments than in granular segments (P < 0.0167). Among the three types of segments, flat segments showed the highest expression densities of beta-catenin accumulated in the nucleus. Large nodular segments and subpedunculated polyps showed similar expression patterns for the molecular markers. CONCLUSIONS: This study provides new and important information on the relationship between the molecular markers and endoscopic findings of LSTs.

Study on the colonoscopic features of GVHD enteritis that developed after hematopoietic stem cell transplantation.

BACKGROUND/AIMS: Graft-versus-host disease (GVHD) enteritis is a frequent gastrointestinal complication following hematopoietic stem cell transplantation (HSCT). The diagnosis of GVHD enteritis was made if apoptotic bodies in crypt epithelium were observed in a biopsy specimen(s). However, there is no standardized protocol as to what colonoscopic findings to use as a guide, and from which segment of the colon and how many biopsy specimens should be obtained. Our aim was to develop a colonoscopic protocol for detection of GVHD enteritis. METHODOLOGY: This retrospective study included 19 patients who had refractory watery diarrhea beyond day 20 after HSCT and underwent colonoscopic examination. Four to nine colonoscopic biopsy specimens were obtained from various regions of the colon in each patient. Fifteen of the 19 patients were diagnosed with GVHD enteritis. RESULTS: In the 15 patients with GVHD enteritis, colonoscopy revealed non-specific findings such as edema, redness, and erosions. Apoptotic bodies were found in one biopsy specimen in 7 patients, 2 biopsy specimens in 5 patients, and 3 or more biopsy specimens in 3 patients. Apoptotic bodies were found in the distal colon (descending colon or sigmoid colon or rectum) in 8 patients, and in the proximal to transverse colon in the remaining 7 patients. Apoptotic bodies were most frequently detected in colonoscopic biopsy specimens of erosions and aphthous lesions. CONCLUSIONS: When patients who have undergone HSCT develop refractory diarrhea, many biopsy specimens from the entire colon should be obtained on colonoscopic examination for histopathologic detection of GVHD enteritis.

Clinical significance of measuring blood coagulation factor XIIIA regularly and continuously in patients with Crohn's disease.

BACKGROUND: The aim of the present paper was to determine the mechanism by which the level of coagulation factor XIIIA declines during the active phase of Crohn's disease. METHODS: The relationship between the activity of Crohn's disease and factor XIIIA was observed in 31 patients with Crohn's disease prospectively. The relationship between factor XIIIA and thrombin-antithrombin III complex (TAT), factor XIIIA expressed on the surface of peripheral monocytes, was also evaluated. RESULTS: During the first year, there were 11 patients with Crohn's disease in the active phase and 20 patients who remained in remission. The average of the lowest level of factor XIIIA among the patients in the active phase was 60.1%. The average of the lowest level of factor XIIIA in patients who remained in remission was 78.1% (P = 0.049). Among the 20 patients who remained in remission for 1 year, eight patients had factor XIIIA levels below 70%. Six of them required surgical enterectomies, on average 2 years and 1 month later. However, none of the 12 patients who remained in remission for 1 year and who never had factor XIIIA levels <70% had a surgical enterectomy during follow up of 4 years and 6 months (P = 0.002). The decline of factor XIIIA was not due to increased consumption secondary to blood coagulation (TAT), nor was it due to a decline in the function of monocytes that produce factor XIIIA. CONCLUSION: Factor XIIIA declines during the active phase of Crohn's disease because it might be consumed in the repair of injured tissue.