Management of Acute Superior Mesenteric Artery Occlusion by Thrombolytic Therapy

Acute occlusion of the superior mesenteric artery (SMA) causes extensive bowel necrosis, resulting in a poor prognosis with an extremely high mortality rate. An 82-year-old woman was admitted to our hospital with the complaint of abdominal pain. She was diagnosed as having acute SMA occlusion by enhanced CT. Five hours from onset, the first thrombolytic therapy with urokinase was performed, but failed to complete thrombolysis and recanalization of peripheral blood flow. An exploratory laparotomy following the first thrombolytic therapy showed a mild ischemic change in the affected intestine and mesentery, but no sign of necrosis. After the laparotomy, local thrombolytic therapy with angiographic evaluation of blood flow at 24, 36 and 48 h from the first thrombolysis was performed. As a result, the residual thrombus disappeared and all branches of the SMA became well visualized. The patient was discharged well without a second-look operation or major bowel resection. Sequential intermittent thrombolytic therapy with meticulous angiographic evaluation of blood flow is effective for early-stage acute SMA occlusion

Attenuated response to liver injury in moesin-deficient mice: Impaired stellate cell migration and decreased fibrosis

AbstractHepatic stellate cells (HSCs) respond to injury with a coordinated set of events (termed activation), which includes migration and upregulation of matrix protein production. Cell migration requires an intact actin cytoskeleton that is linked to the plasma membrane by ezrin–radixin–moesin (ERM) proteins. We have previously found that the linker protein in HSCs is exclusively moesin. Here, we describe HSC migration and fibrogenesis in moesin-deficient mice. We developed an acute liver injury model that involved focal thermal denaturation and common bile duct ligation. HSC migration and collagen deposition were assessed by immunohistology and quantitative real-time PCR. Activated HSCs were isolated from wild-type or moesin-deficient mice for direct examination of migration. Activated HSCs from wild-type mice were positive for moesin. Migration of moesin-deficient HSCs was significantly reduced. In a culture assay, 22.1% of normal HSCs migrated across a filter in 36h. In contrast, only 1.3% of activated moesin-deficient HSCs migrated. Collagen deposition around the injury area similarly was reduced in moesin-deficient liver. The linker protein moesin is essential for HSC activation and migration in response to injury. Fibrogenesis is coupled to migration and reduced in moesin-deficient mice. Agents that target moesin may be beneficial for chronic progressive fibrosis

Incidentally Discovered Adenocarcinoma in situ of the Appendix in a Young Woman

Primary appendiceal adenocarcinoma is an infrequent disease. This report presents a rare case of incidentally discovered carcinoma in situ of the appendix. A 35-year-old parturient female simultaneously underwent appendectomy and oophorectomy due to an ovarian abscess that adhered to the appendix during cesarean section. Although her excised appendix showed no apparent tumorous lesion, histopathological examination revealed carcinoma in situ in the excised appendix. She underwent additional right hemicolectomy a few days later due to the possibility of a positive surgical margin. Histopathological examination detected no malignant cells in the resected specimen. She was discharged without any complications and has since remained healthy. Appendiceal adenocarcinoma is generally considered to be difficult to diagnose during the early stage because it seldom shows any specific findings. This results in a poor prognosis. Histopathological examination is not always conducted for appendices resected during other surgery. However, the current study suggests that a careful routine histopathological examination of excised appendix, as well as careful preoperative examination and detailed intraperitoneal inspection during surgery, is indeed important to detect occult appendiceal tumors

Surgical treatment of hepatocellular carcinoma with severe intratumoral arterioportal shunt

We report a case of hepatocellular carcinoma (HCC) that caused a severe arterioportal shunt (APS). A 49-year-old man was admitted to hospital due to esophagogastric variceal hemorrhage and HCC, and underwent endoscopic variceal ligation (EVL) and endoscopic injection sclerotherapy (EIS). He was then referred to our hospital. Abdominal computed tomography revealed a low-density lesion in the posterior segment of the liver and an intratumoral APS, which caused portal hypertension. Although the patient underwent EVL, EIS, Hassab’s operation, and transcatheter arterial embolization for APS, he vomited blood due to rupture of esophagogastric varices. Right hepatectomy was performed for the treatment of HCC and APS, although the indocyanine green retention value at 15 min after intravenous injection was poor (30%). The patient’s postoperative course was uneventful. Eventually, APS disappeared and the esophagogastric varices improved

Efficacy of Goshajinkigan for Oxaliplatin-Induced Peripheral Neuropathy in Colorectal Cancer Patients

Objective. To evaluate the efficacy of Goshajinkigan for oxaliplatin-induced peripheral neuropathy in colorectal cancer patients. Patients. Colorectal cancer patients () who received ≥4 weeks of Goshajinkigan for oxaliplatin-induced peripheral neuropathy during chemotherapy at Kyoto Prefectural University of Medicine were (Goshajinkigan group) compared to 44 patients who had not received Goshajinkigan during the same period (non-Goshajinkigan group). Main Outcome Measures. The effect of Goshajinkigan was graded as curative, effective, stabilizing, or deleterious. The relationships between the grade of peripheral neuropathy and the dose of oxaliplatin in the Goshajinkigan and non-Goshajinkigan groups were evaluated. Results. The effect of Goshajinkigan on peripheral neuropathy in the Goshajinkigan group was curative, effective, stabilizing, and deleterious in 3.4, 20.7, 69.0, and 6.9% of patients, compared to the effect in the non-Goshajinkigan group (4.5, 15.9, 45.5, and 34.1%). The ratio of deleterious effects was significantly different between these two groups (). A Kaplan-Meier analysis in relation to the cumulative dose of oxaliplatin showed that the incidence of grade 3 peripheral neuropathy tended to be less in the Goshajinkigan group (). There were no significant differences in time to treatment failure and severe adverse events between these two groups. Conclusions. Goshajinkigan prevented exacerbation of oxaliplatin-induced peripheral neuropathy. This trial is registered with UMIN00000995