Adult intussusceptions induced by a terminal ileum diverticulum: a case report.

We herein report a case of adult intussusceptions induced by a terminal ileum diverticulum. Histological examination confirmed a terminal ileum diverticulum full of feces, and it was considered an infiltrated region. The clinical characteristics of previously reported adult intussusceptions are also discussed, including jejunoileal diverticulum and surgical management.

Single-incision laparoscopic surgery for a small-intestinal gastrointestinal stromal tumor: report of a case.

Our report concerns a 64-year-old man with a small-intestinal gastrointestinal stromal tumor (GIST), which was successfully treated with single-incision laparoscopic surgery (SILS). Small-bowel endoscopy detected a submucosal tumor located approximately 10 cm from the ligament of Treitz in the wall of the proximal jejunum. Contrast-enhanced computed tomography revealed a tumor (diameter, 4 cm) containing high- and low-density areas in the proximal jejunum. On 18F-fluorodeoxyglucose (FDG) positron-emission tomography (PET), the tumor demonstrated intense FDG uptake (maximum standard uptake value, 3.82), whereas it displayed high signal intensity on diffusion-weighted magnetic resonance images. No metastatic lesions were observed. The patient was diagnosed with a jejunal GIST. Wedge resection of the jejunum was performed using the SILS procedure. The tumor was histopathologically diagnosed as a low-grade malignant GIST. SILS is a useful resection technique for small-intestinal GIST.

Laparoscopy-assisted resection of ileocecal intussusception caused by ileal pedunculated lipoma.

We report on a case of ileal lipoma that prolapsed into the ascending colon and was resected by laparoscopy-assisted surgery. A 31-year-old male Japanese patient was admitted to our hospital because of hematochezia and anemia. Colonoscopy revealed a pedunculated polyp arising from the ileum. The surface was covered with slightly edematous mucosa. Abdominal computed tomography showed a low-density mass in the ascending colon. A diagnosis of pedunculated ileal lipoma with intussusception was made, and laparoscopy-assisted surgery was performed. The intussusception was reducted by resection of the lipoma. The surgical specimen was a 40 × 30 × 25 mm round tumor with a long stalk 11 cm in length. Microscopic examination of the specimen revealed ileal lipoma. Laparoscopic surgery is recommended for benign tumors of the small intestine because it is minimally invasive.

Treatment of hyperinsulinemic hypoglycemia due to diffuse nesidioblastosis in adults: a case report.

An 82-year-old man was admitted to our hospital with a complaint of hypoglycemic syncope in the early morning. Insulinoma was suspected, but an abdominal CT showed no mass. Abdominal angiography showed a slight stain fed from the splenic artery. Arterial stimulation and venous sampling (ASVS) showed an abnormal insulin response only from the splenic artery. Under a provisional diagnosis of insulinoma, surgical treatment was undertaken. Although no pancreatic masses were palpable, we performed a distal pancreatectomy. Subsequently, a pathological examination revealed diffuse nesidioblastosis. Reported cases of diffuse nesidioblastosis have had common clinical features: postprandial hyperinsulinemic hypoglycemia, no abnormal findings in radiological examinations, and the presence of the ductulo-insular complex on histological examination. Surgical resection is recommended, but the extent of surgery is controversial. Our case had some clinical features of insulinoma but was diagnosed as diffuse nesidioblastosis according to histopathologic criteria. Because ASVS showed that the pancreatic body and tail had a lesion producing insulin abnormally, we performed a distal pancreatectomy to cure the hypoglycemia. Clinically, it is very difficult to distinguish diffuse nesidioblastosis from insulinoma. When we treat hyperinsulinemic hypoglycemia, ASVS can be an essential examination to decide the extent of pancreatectomy.

Lack of activated Smad2 in transforming growth factor-beta signaling is an unfavorable prognostic factor in patients with esophageal squamous cell carcinoma.

BACKGROUND AND OBJECTIVES: Transforming growth factor-beta (TGF-beta) regulates cell growth in various cells, and inactivation of the TGF-beta-signaling pathway contributes to tumor progression. In this study, we investigated the expression of Smad2 and Smad3, which are specific intracellular mediators of TGF-beta signaling. We also examined the relationship between the expression levels of activated Smad2 by TGF-beta and clinicopathologic characteristics of patients with esophageal squamous cell carcinoma (SCC). METHODS: Immunohistochemical staining with anti-phosphorylated Smad2 (P-Smad2) polyclonal antibody, anti-Smad2 monoclonal antibody, and anti-Smad3 polyclonal antibody was performed on surgical specimens obtained from 80 patients with esophageal SCC. RESULTS: Our data indicated that a low level of P-Smad2, as detected immunohistologically, correlated with lymph node metastasis (P = 0.0002), distant metastasis (P = 0.0338), pathologic stage (P = 0.0093), and poor survival rate (P = 0.0246). All patients without positive Smad2 immunostaining were included among those without positive P-Smad2 immunostaining. There was no significant correlation between expression of Smad2 or Smad3 and clinicopathologic characteristics. CONCLUSIONS: We demonstrated that a lack of Smad2-P appears to be correlated with tumor development and poor prognosis in patients with esophageal SCC.

Idiopathic omental bleeding: report of a case.

We report a case of idiopathic omental bleeding in a 27-year-old man who was brought to our hospital after the sudden development of intermittent abdominal pain, nausea, and fainting. Computed tomography showed intra-abdominal fluid and emergency laparotomy revealed a hemorrhagic mass in the omental bursa, which was excised. The patient was successfully treated and a diagnosis of idiopathic omental bleeding was made.

Prognostic value of the expression of Smad6 and Smad7, as inhibitory Smads of the TGF-beta superfamily, in esophageal squamous cell carcinoma.

BACKGROUND: The transforming growth factor beta (TGF-beta) superfamily regulates cell growth in various cells. Previous studies have shown that altered expression of TGF-beta receptors, Smad2 and Smad4, as mediators of TGF-beta superfamily signaling, contributes to tumor progression in esophageal squamous cell carcinoma (SCC). The expression of Smad6 and Smad7 as negative regulators was examined, to investigate the further effects of TGF-B superfamily signaling. MATERIALS AND METHODS: Immunohistochemical staining with anti-Smad6 and anti-Smad7 polyclonal antibodies was performed on surgical specimens obtained from 115 patients with esophageal SCC. RESULTS: The expression of Smad6 and Smad7 was inversely correlated with depth of invasion in the early stages (p = 0.0003 and p = 0.0173, respectively). Moreover, there was a significant correlation between the expression of Smad6 and Smad7, and poor survival rate (p = 0.0078 and p = 0.0207, respectively). CONCLUSION: Smad6 and Smad7 expression affects the progression of early lesions of esophageal SCC and indicates a poor prognosis.

Reduced expression of transforming growth factor-beta receptors is an unfavorable prognostic factor in human esophageal squamous cell carcinoma.

Transforming growth factor-beta (TGF-beta) inhibits epithelial cell proliferation. Inactivation of the TGF-beta signaling pathway is thought to play a role in tumorigenesis. Our purpose was to clarify the correlation between TGF-beta receptors or TGF-beta 1 expression and the clinicopathologic characteristics of patients with esophageal squamous cell carcinoma (SCC). Immunohistochemical staining for TGF-beta type I receptor (TGF-beta R-I), TGF-beta R-II and TGF-beta 1 was performed on surgical specimens obtained from 80 patients with esophageal SCC. Preoperative plasma TGF-beta1 levels were measured and correlated with pathologic features and clinical outcomes. Expression of TGF-beta R-I and TGF-beta R-II was reduced in 43 (53.8%) and 23 (28.8%) specimens, respectively. TGF-beta 1 was overexpressed in 29 (36.3%). Reduced expression of TGF-beta R-I and TGF-beta R-II showed a significant association with depth of invasion (p = 0.0015 and p = 0.0012), lymph node metastasis (p = 0.0309 and p = 0.0059) and pathologic stage (p = 0.0103 and p = 0.0401). Overexpression of TGF-beta 1 had a significant association with depth of invasion only (p = 0.0335). Reduced expression of TGF-beta R-I and TGF-beta R-II was correlated with cancer-specific survival (p = 0.0324 and p = 0.0243). The mean preoperative plasma TGF-beta 1 level was 10.5 +/- 0.8 ng/ml in patients with esophageal carcinoma and was significantly higher compared to healthy controls (p < 0.01). We demonstrate that reduced expression of TGF-beta receptors in esophageal SCC appears to be correlated with depth of invasion, lymph node metastasis, pathologic stage and poor prognosis. TGF-beta receptor expression may play a key role in the progression of this cancer.

Decreased Smad4 expression in the transforming growth factor-beta signaling pathway during progression of esophageal squamous cell carcinoma.

BACKGROUND: Transforming growth factor-beta (TGF-beta) has antiproliferative effects in various cells, and inactivation of the TGF-beta signaling pathway contributes to tumor progression or development. Smad4, a tumor suppressor gene, is a central mediator in the signaling pathways of the TGF-beta superfamily. This study was undertaken to clarify the correlation between Smad4 expression and the clinicopathologic characteristics of patients with esophageal squamous cell carcinoma (SCC). The authors also investigated the expression of components of the TGF-beta signaling pathway in seven established cell lines derived from esophageal SCC. METHODS: Immunohistochemistry for Smad4 using monoclonal anti-Smad4 antibody was performed on surgical specimens obtained from 80 patients with esophageal SCC. In seven cell lines, the authors examined the expression of components of the TGF-beta signaling pathway using Western and Northern blot analyses. RESULTS: There was a significant inverse correlation between Smad4 expression and both depth of invasion (P = 0.0008) and pathologic stage (P = 0.0079). The expression of Smad4 proteins could be detected in five of seven cell lines. The expression of TGF-beta type II receptor protein was decreased in two of seven cell lines, and the expression of both Smad2 and Smad3 proteins was decreased in only one cell line. The level of expression of Smad4 mRNA did not differ dramatically between cell lines and was not correlated with the quantity of Smad4 protein. CONCLUSIONS: In this study, the expression of Smad4 protein appeared to be correlated with the depth of invasion of esophageal SCC. The loss of Smad4 expression was not regulated at the level of transcription.