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Keisho Kataoka

Publications and source records attributed to Keisho Kataoka.

At least 19 recordsLinked to original sources
PubMed2006

Consensus of primary care in acute pancreatitis in Japan.

The incidence of acute pancreatitis in Japan is increasing and ranges from 187 to 347 cases per million populations. Case fatality was 0.2% for mild to moderate, and 9.0% for severe acute pancreatitis in Japan in 2003. Experts in pancreatitis in Japan made this document focusing on the practical aspects in the early management of patients with acute pancreatitis. The correct diagnosis of acute pancreatitis and severity stratification should be made in all patients using the criteria for the diagnosis of acute pancreatitis and the multifactor scoring system proposed by the Research Committee of Intractable Diseases of the Pancreas as early as possible. All patients diagnosed with acute pancreatitis should be managed in the hospital. Monitoring of blood pressure, pulse and respiratory rate, body temperature, hourly urinary volume, and blood oxygen saturation level is essential in the management of such patients. Early vigorous intravenous hydration is of foremost importance to stabilize circulatory dynamics. Adequate pain relief with opiates is also important. In severe acute pancreatitis, prophylactic intravenous administration of antibiotics at an early stage is recommended. Administration of protease inhibitors should be initiated as soon as the diagnosis of acute pancreatitis is confirmed. A combination of enteral feeding with parenteral nutrition from early stage is recommended if there are no clear signs and symptoms of ileus and gastrointestinal bleeding. Patients with severe acute pancreatitis should be transferred to ICU as early as possible to perform special measures such as continuous regional arterial infusion of protease inhibitors and antibiotics, and continuous hemodiafiltration. The Japanese Government covers medical care expense for severe acute pancreatitis as one of the projects of Research on Measures for Intractable Diseases.

Acute Disease↗
PubMed2006

Effects of the cholecystokinin A receptor antagonist loxiglumide on the proliferation and cell cycle time of pancreatic acinar cells in rats.

OBJECTIVES: Prior studies have indicated that endogenous or exogenous cholecystokinin (CCK) induces transient acinar cell proliferation at about 24 hours after its stimulation. The aims of the present study were to determine the time point when the administration of the CCK-A-receptor antagonist loxiglumide had its maximal suppressive effect on the proliferation of pancreatic acinar cells and to investigate the effects of loxiglumide on the cell cycle time of pancreatic acinar cells during transient acinar cell proliferation induced by endogenous or exogenous CCK. METHODS: Eight-week-old Wistar rats were divided into the following groups: preadministration of loxiglumide (40 mg/kg) intravenously at 120, 60, and 0 minutes before endogenous CCK stimulation induced by a single oral administration of camostat (50 mg/kg) or exogenous CCK stimulation by a subcutaneous injection of CCK-8 (6 g/kg body weight). For the controls, intravenous saline was used instead of loxiglumide (n = 7 in each group). The proliferative activity of pancreatic acinar cells at 24 hours after CCK stimulation and the cell cycle time of these proliferating pancreatic acinar cells were studied using an immunohistochemical technique. RESULTS: The most significant suppression of the proliferation of the acinar cells was observed in those groups which received loxiglumide 60 minutes before CCK stimulation (P < 0.016), but preadministration of loxiglumide had no effect on the cell cycle time of the proliferating acinar cells (not significant). CONCLUSION: CCK antagonist loxiglumide is expected as an excellent clinical applicable agent for acute pancreatitis. Previous researches suggest that CCK is an aggravating factor during the acute phase of acute pancreatitis, but CCK may be a healing factor during the recovery period. From the results of the present study, it can be said that the excess chronic administration of CCK antagonists during the acute phase of acute pancreatitis may prevent any regrowth of pancreatic cells during the healing period of acute pancreatitis.

Animals↗
PubMed2006

[A case of pancreatic intraductal papillary-mucinous carcinoma with penetration to the stomach and splenic abscess].

We report the case of an 80-year-old man given a diagnosis of pancreatic intraductal papillary-mucinous carcinoma (IPMC) and early gastric cancer. He refused surgery, therefore endoscopic mucosal resection (EMR) for gastric cancer and careful observation were performed. Penetration of the IPMC to the stomach was observed 3 months later. Ten months after the initial diagnosis, he was found to have a splenic abscess and was subsequently treated by antibiotics and percutaneous drainage, and a fistula between the IPMC and the splenic abscess was observed. We suppose IPMC penetration to the spleen and bacterial transmission from the stomach through the fistula caused the splenic abscess. While IPMC is recognized as a low-grade malignancy, some cases of invasive carcinoma with fistulation to adjacent organs have been reported. To the best of our knowledge, this is the first case of IPMC associated with splenic abscess due to pancreatosplenic fistula.

Abdominal Abscess↗
PubMed2005

Endoscopic resection for the diagnosis of visceral Kaposi's sarcoma.

Kaposi's sarcoma is an uncommon neoplasm that occasionally involves the gastrointestinal tract in immunosuppressed individuals. Infection with human herpes virus 8 is known to be necessary for developing all forms of Kaposi's sarcoma. We report a renal transplant recipient who developed visceral Kaposi's sarcoma 18 months after the transplantation. In Oriental countries, the incidence of Kaposi's sarcoma is extremely low, and this is the first case of Kaposi's sarcoma arising from a transplant recipient in Japan. Standard forceps biopsies of the gastric lesions failed to make the correct diagnosis. However, endoscopic resection successfully led to the correct diagnosis of Kaposi's sarcoma and herpes simplex virus 8 infection as well. This is the first report of a patient with visceral Kaposi's sarcoma who underwent endoscopic resection that reliably confirmed histological diagnosis and the viral genome at the same time.

Endoscopy, Digestive System↗
PubMed2004

Solid pseudopapillary tumor as a possible cause of acute pancreatitis.

CONTEXT: Acute pancreatitis is not commonly seen in the first presentation of pancreatic neoplasms. Solid pseudopapillary tumor as a cause of acute pancreatitis has not yet been reported. This is the first report of acute pancreatitis resulting from solid pseudopapillary tumor. CASE REPORT: We report the case of a 21-year-old female who presented with a sudden onset of severe abdominal pain associated with elevated serum pancreatic enzyme concentration. The initial diagnosis was acute pancreatitis. However, subsequent ultrasonography and computed tomography showed an abdominal mass in the tail of the pancreas, retroperitoneal fluid and left pleural effusion. There was scarce pain relief even with large doses of analgesics. A distal pancreatectomy was then performed and a final diagnosis of solid pseudopapillary tumor was made histologically. The surrounding pancreatic tissue was characterized as hemorrhagic edematous pancreatitis. CONCLUSIONS: Solid pseudopapillary tumor is generally known as a slow-growing pancreatic neoplasm with few, if any, symptoms. However, solid pseudopapillary tumors should be kept in mind as a possible cause of acute pancreatitis, especially in cases of non-alcoholic young women having an acute pancreatitis attack.

Acute Disease↗
PubMed2004

Detection of BCL2-IGH rearrangement on paraffin-embedded tissue sections obtained from a small submucosal tumor of the rectum in a patient with recurrent follicular lymphoma.

A 59-year-old woman was admitted to our hospital because of recurrent follicular lymphoma (FL). Colonoscopic examination revealed a rectal submucosal tumor (SMT) without any erosions and ulcers. In this patient, it was difficult to distinguish non-Hodgkin's lymphoma (NHL) invasion from other disorders of the colon including carcinoid tumor merely based on endoscopic findings. Histopathologic and immunohistochemical studies on biopsy specimens showed an infiltration of atypical lymphocytes that were positive for CD20 and BCL2 but negative for UCHL-1. Fluorescence in situ hybridization on paraffin-embedded tissue sections (T-FISH) identified a translocation of BCL2 with IGH gene. Based on these findings, the tumor was defined as an invasion of FL. T-FISH method is useful for the detection of a monoclonality of atypical lymphocytes in an SMT of the gastrointestinal tract, and particularly for the detection of chromosomal translocations specific to lymphoma subtypes.

Biopsy↗
PubMed2004

Lack of evidence for leukocyte maternal microchimerism in primary biliary cirrhosis.

AIM: It is reasonable to assume that microchimerism could also be involved in the induction of primary biliary cirrhosis (PBC). However, previous reports investigated only fetus-microchimerism in women patients. Maternal microchimerism has not been investigated until now. The current study aimed to clear either maternal microchimerism was involved in the pathogenesis of PBC or not. METHODS: We used fluorescence in situ hybridization on paraffin-embedded tissue (We called "Tissue-FISH".) to determine whether maternal cells infiltrated in male patients who were diagnosed as having PBC. Tissue-FISH was performed by using both X and Y specific probes on the biopsy liver sample of 3 male PBC patients. RESULTS: Infiltrating lymphocytes demonstrated both X and Y signals in all 3 male patients. CONCLUSION: Maternal microchimerism dose not play a significant role in PBC. PBC may not relate to fetus and maternal microchimerism.

Chimera↗
PubMed2004

Increased QT dispersion in patients with alcoholic pancreatitis.

OBJECTIVES: Increased dispersion of the QT interval has been proposed to be a novel marker for increased risk of ventricular arrhythmia and sudden cardiac death. This study examined whether QT dispersion is affected in patients with alcoholic pancreatitis. METHODS: We measured the QT interval, corrected QT interval, activation recovery interval, activation time, recovery time, and their respective dispersions in 3 age- and gender-matched groups: patients with alcoholic pancreatitis [age, 58.9 +/- 11.8 years; male/female (M/F), 33/3], patients with alcohol dependence (age, 59.3 +/- 8.9 years; M/F, 33/4), and a healthy control group (age, 55.8 +/- 8.8 years; M/F, 33/3). RESULTS: The QT dispersions in patients with alcoholic pancreatitis (62.4 +/- 19.9 milliseconds; P < 0.001) or alcohol dependence (58.2 +/- 19.6 milliseconds; P < 0.001) were significantly greater than in the control group (41.4 +/- 13.3 milliseconds). Similarly, the corrected QT dispersions in patients with alcoholic pancreatitis (68.5 +/- 22.8 milliseconds; P < 0.001) or alcohol dependence (65.3 +/- 23.6 milliseconds; P < 0.001) were significantly greater than in the control group (42.8 +/- 13.2 milliseconds). Both QT dispersion and QTc dispersion were longer in patients with alcoholic pancreatitis than those with alcohol dependence (P = 0.011 and P = 0.039, respectively). Simple linear regression analysis of the relationship between the RR and QT intervals revealed that the regression lines for patients with alcoholic pancreatitis and alcohol dependence were almost parallel. However, the slope of the regression line for the control group was significantly greater (P < 0.05) than for the other 2 lines. CONCLUSION: The findings demonstrate increased QT and QTc dispersions in patients with either alcoholic pancreatitis or alcohol dependence. The QT dispersion and QTc dispersion were longer in patients with alcoholic pancreatitis than those with alcohol dependence.

Arrhythmias, Cardiac↗
PubMed2004

[Role of apoptosis in severe acute pancreatitis].

The role of apoptosis in a severe acute pancreatitis is recently given the most attention, but it is hardly known in a clinical study. We show three assumptions between apoptosis and the pathophysiological mechanisms of severe acute pancreatitis in this paragraph. First, the apoptosis of pancreatic acinar cell might prevent from a worsening in acute pancreatitis due to diminish leakage of pancreatic enzyme and extension of inflammation. Secondly, impairment cellular immunity due to peripheral lymphocyte apoptosis might be linked to the development of subsequent infectious complications in acute pancreatitis. Third, apoptosis in various major organs might be involved in the mechanism of multiple organs failure in acute pancreatitis. These findings might lead the new development in the therapeutic strategy of acute pancreatitis.

Acute Disease↗
PubMed2002

The effect of steroid pulse therapy on the development of acute pancreatitis induced by closed duodenal loop in rats.

BACKGROUND: The aim of the present study was to evaluate the effect of a high dose of methylprednisolone (MP) on the development of acute pancreatitis (AP) in rats induced by closed duodenal loop (CDL). METHODS: Pancreas web weight, volume of ascites, hematocrit, serum amylase activity, concentrations of interleukin (IL)-1beta and IL-6, organ blood flow in both the pancreas and the kidney, and histological findings of the pancreas were studied 6 h after the induction of AP. RESULTS: The intravenous administration of MP (30 mg/kg body weight) significantly reduced the increase in pancreas web weight, volume of ascites, hematocrit, serum amylase activity, concentrations of IL-1beta and IL-6, histological edema, and necrosis observed in CDL pancreatitis. The administration of MP also apparently improved both the pancreatic and the renal blood flow. CONCLUSIONS: The present results suggest that these cytokines influence at least the progression of AP, and that the mechanism by which MP pulse therapy inhibits the development of AP partly involves the inhibition by MP of the release of the cytokines.

Acute Disease↗