Large gastric intramural hematoma mimicking a visceral artery aneurysm: a case report.

BACKGROUND: Gastric hematoma is a rare disorder. Here we report a case of a large gastric intramural hematoma mimicking an impending rupture of a visceral artery aneurysm. CASE PRESENTATION: A 60-year-old Japanese woman complained of left flank pain. Computed tomography with intravenously administered contrast agent showed a solid mass of 5 × 5 × 8 centimeter in the left middle abdominal quadrant. On completion of computed tomography, the working diagnosis was an impending rupture of an aneurysm located in a branch of the superior mesenteric artery. Transcatheter arterial embolization was performed, but angiography of the superior mesenteric artery and the inferior mesenteric artery did not indicate extravasation of the contrast agent and we did not observe any aneurysmal structure. We decided to perform surgery. The operational findings revealed that the mass was a gastric intramural hematoma. CONCLUSION: On encountering an intra-abdominal mass found to be attached to a gastric wall, a gastric intramural hematoma should be considered.

No-touch pylorus-resecting pancreatoduodenectomy can reduce postoperative complications even in low volume center.

PURPOSES: Pancreatoduodenectomy (PD) was performed for 6 periampullary cancer patients by using methods verified by quality randomized controlled trials (RCT) in a low-volume center (LVC). The purpose of this study was to verify the clinical results. METHODS: No-touch pylorus-resecting pancreatoduodenectomy (PrPD), antecolic gastrojejunostomy, pancreatico-jejunostomy with a lost stent tube to the main pancreatic duct, and early removal of a prophylactic drain were performed. RESULTS: The drain could be removed 4 days after operation, and no pancreatic fistula was observed in all cases. Solid food could be started on POD4 after removing the drain. Furthermore, postoperative systemic chemotherapy could be started earlier. CONCLUSION: Although we have only a few PD cases a year in our institution, PD can be conducted safely without complications by using the methods verified by quality RCTs.

Huge retroperitoneal dedifferentiated liposarcoma presented as acute pancreatitis: report of a case.

A 74-year-old male with abdominal pain was admitted to the emergency room in our hospital. The high value of serum amylase was shown in his blood test. The postcontrast computed tomography (CT) showed the huge retroperitoneal tumor with a thin-walled mass occupying most of the part of the right retroperitoneal space. The tumor spread into the soft tissues around the pancreas; as a result, the duodenum was compressed and the pancreas was displaced to the right side. The irregular pancreatic outline, obliterated peripancreatic fatty tissue and fluid in the left anterior pararenal space were revealed, so acute pancreatitis was diagnosed. The diagnostic biopsy of retroperitoneal tumor was done, and the pathological findings of retroperitoneal mass revealed dedifferentiated liposarcoma. The medical treatment against acute pancreatitis was performed firstly. After the patient recovered from that, the surgical resection of the tumor with the right kidney and right adrenal gland was completed successfully. The patient remained well, without any evidence of recurrence three months after surgery. However, the histology showed dedifferentiated liposarcoma; therefore, postoperative regular examination is necessary.

Lateral abdominal wall hematoma as a rare complication after carotid artery stenting: a case report.

Abdominal wall hematoma is a rare and life-threatening complication after carotid artery stenting (CAS), but it can occur when activated clotting time is prolonged. We report a right lateral abdominal wall hematoma caused by rupture of the superficial circumflex iliac artery after CAS in a 72-year-old man with severe stenosis of the origin of the right internal carotid artery. We performed CAS for the targeted lesion while activated clotting time exceeded 300 seconds. After 2 hours, he complained of right lateral abdominal pain. Abdominal computed tomography revealed an extensive hematoma in the right lateral abdominal wall. Activated clotting time was 180 seconds at this point. Seven hours later, he developed hypotension and hemoglobin level dropped to 11.3 g/dl. Subsequent computed tomography showed enlargement of the hematoma. Emergent selective angiography of the external iliac artery revealed active bleeding from the right superficial circumflex iliac artery. Transcatheter arterial embolization with Gelfoam and microcoils was performed successfully. With more CAS procedures being performed, it is important for endovascular surgeons and radiologists to consider the possibility of abdominal wall hematoma in this situation.

Protective effect of FK506 and thromboxane synthase inhibitor on ischemia-reperfusion injury in non-heart-beating donor in rat orthotopic liver transplantation.

The study investigated the possibility of pharmacologically modulating hepatic allograft function from non-heart-beating donors (NHBDs) using male Lewis rats. The donors were divided into 4 groups: Group 1 in which the vehicle was administered, Group 2 in which FK506 (tacrolimus; a powerful immunosuppressive agent) was administered, Group 3 in which OKY046 (a specific thromboxane synthetase inhibitor) was administered and Group 4 in which FK506 and OKY046 were administered. The recipients received orthotopic liver transplantation. The survival rates differed significantly between the recipients that had received liver transplantation from Groups 1 and 4. The serum liver enzyme and inflammatory cytokine concentrations of the recipients which had received liver transplantation from Groups 2, 3 and 4 were significantly lower than those of the recipients that had received liver transplantation from Group 1. Although there was no significant difference, all parameters were better in the recipients that had received transplantation from Group 4 than those that had received transplantation from Groups 2 and 3. The action mechanisms of FK506 and OKY046 are completely different. Therefore, concomitant use of FK506 and OKY046 might have additive effects on liver transplantation from NHBDs. In conclusion, we demonstrated that pretreatment of NHBDs using FK506 and OKY046 ameliorated graft viability.

Heat shock protein 70 induction in hepatocytes after right portal vein embolization.

BACKGROUND/AIMS: Preoperative right portal vein embolization enhances remnant liver function following massive hepatectomy. Several studies have reported an increase in the volume of the left hepatic lobe after right portal vein embolization, but little information exists regarding heat shock protein induction in hepatocytes after right portal vein embolization. The objective of this study is to determine whether heat shock protein is induced in hepatocytes after right portal vein embolization in patients who underwent extended right hepatic lobectomy. METHODOLOGY: Four patients with gallbladder cancer and one patient with intrahepatic cholangiocellular carcinoma who underwent extended right hepatic lobectomy combined with caudate lobectomy and resection of the extrahepatic bile duct after right portal vein embolization were enrolled in this study. Operation was performed 21-36 days after right portal vein embolization. At operation, small liver specimens were taken immediately after laparotomy from both the right anterior segment (embolized lobe) and lower part of the left medial segment (non-embolized lobe) and heat shock protein 70 was induction in these specimens was measured by Western blotting. RESULTS: Heat shock protein 70 was induced in the left lobe relative to the right lobe in four patients, three of whom had an uneventful postoperative course. CONCLUSIONS: This paper is the first report to show the induction of heat shock protein 70 in the non-embolized hepatic lobe after right portal vein embolization in the clinical cases.

Effects of aging and calorie restriction of Fischer 344 rats on hepatocellular response to proliferative signals.

It is well established that the proliferative potential of the liver declines with aging. Epidermal growth factor (EGF)-stimulated DNA synthesis is reduced in hepatocytes from aged rats relative to young rats, and this reduction correlates with diminished activation of the extracellular signal-regulated kinase (ERK) pathway and lower phosphorylation of the EGF receptor on residue Y1173. Calorie restriction (CR) can increase rodent life span and retard many age-associated declines in physiologic function, but its influence on cell proliferation is unknown. Here, we investigated the effects of long-term CR on proliferation of hepatocytes derived from young and aged rats following in vitro stimulation with either low-dose hydrogen peroxide or EGF. CR reduced the proliferative response of hepatocytes derived from young hosts, but long-term CR was associated with enhanced proliferation in aged cells relative to that of ad libitum (AL)-fed animals. ERK activation mirrored the effects of CR on proliferation, in that young CR cells exhibited lower ERK activation than young AL cells, but old CR cells showed higher ERK activation than old AL cells. Finally, a decline in EGF receptor phosphorylation on Y1173, which normally occurs with aging, was absent in cells of old hosts maintained on long-term CR, supporting the view that alterations in this early signaling event underlie the age-related decline in proliferative potential in rat hepatocytes.

Expression of the pro-apoptotic gene gadd153/chop is elevated in liver with aging and sensitizes cells to oxidant injury.

Aging is generally accompanied by reduced tolerance to oxidative stress and altered responsiveness to proliferative signals. We have shown that hepatocytes derived from aged rats (24-26 months) exhibit greater sensitivity to H(2)O(2) treatment and reduced proliferation following epidermal growth factor (EGF) treatment than cells of young adult rats (5-6 months). Here we examined the effects of aging and calorie restriction (CR) on expression of the oxidative stress-inducible and pro-apoptotic gene gadd153 (chop) in these hepatocytes, and we investigated its influence on sensitivity to oxidants. We show that aging was associated with elevated expression of gadd153, both basally and in response to H(2)O(2) treatment. CR, which attenuates age-associated declines in stress tolerance, prevented the age-related increase in gadd153 expression. EGF treatment also resulted in gadd153 induction in old cells. This effect was absent in young cells and in old cells of CR rats. gadd153 induction by EGF was reactive oxygen species-dependent and correlated with heightened sensitivity to subsequent H(2)O(2) treatment, suggesting that elevated Gadd153 contributes to the greater sensitivity of EGF-pretreated old cells to oxidative stress. Additional support for this hypothesis was provided by experiments with Rat1 fibroblasts in which conditional expression of Gadd153 conferred increased sensitivity to H(2)O(2). We propose a model whereby the diminished ability of old hepatocytes to overcome an EGF-triggered reactive oxygen species load leads to induction of the proapoptotic gene gadd153, which, in turn, sensitizes the cells to oxidant injury. Our findings point to gadd153 expression levels as an important factor in liver aging.

Age-related decline in cellular response to oxidative stress: links to growth factor signaling pathways with common defects.

Accumulation of oxidative damage is believed to be a major contributor to the decline in physiologic function that characterizes mammalian aging, and recent studies suggest that how well you respond to acute oxidative stress is an important factor in determining longevity. Oxidant injury elicits a wide spectrum of responses ranging from proliferation to cell death. The particular outcome observed largely reflects the severity of the stress encountered and the relative degree of activation of various signal transduction pathways aimed at enhancing survival or inducing cell death. Herein we examine the relationship between pathways important in supporting cell survival in response to oxidant injury and those involved in regulating proliferation. We review evidence indicating that [Curr. Opin. Cell Biol. 10 (1998) 248] common pathways are indeed involved in regulating these responses, and [Physiol. Rev. 82 (2002) 47] alterations in shared signaling events likely account for the age-related decline in the ability of cells to respond to both proliferative signals and oxidant stimuli.

Loss in oxidative stress tolerance with aging linked to reduced extracellular signal-regulated kinase and Akt kinase activities.

Oxidative stress is believed to be an important factor in the development of age-related diseases, and studies in lower organisms have established links between oxidative stress tolerance and longevity. We have hypothesized that aging is associated with a reduced ability to mount acute host defenses to oxidant injury, which increases the vulnerability of aged cells to stress. We tested this hypothesis by using primary hepatocytes from young (4-6 months) and aged (24-26 months) rats. Old hepatocytes were more sensitive to H2O2-induced apoptosis than were young cells. Lower survival is associated with reduced activations of extracellular signal-regulated kinase (ERK) and Akt kinase, both of which protect against oxidant injury. That reduced ERK and Akt activities contribute to lower survival of aged cells was supported by additional findings. First, pharmacologic inhibition of ERK and Akt activation in young cells markedly increased their sensitivity to H2O2. Second, caloric restriction, which increases rodent life span and delays the onset of many age-related declines in physiologic function, prevented loss in ERK and Akt activation by H2O2 and enhanced survival of old hepatocytes to levels similar to those of young cells. Strategies aimed at boosting these host responses to acute oxidant injury could have significant anti-aging benefits.