Yoshio Sogame

Evidence-based clinical practice guidelines for chronic pancreatitis 2015.

Chronic pancreatitis is considered to be an irreversible progressive chronic inflammatory disease. The etiology and pathology of chronic pancreatitis are complex; therefore, it is important to correctly understand the stage and pathology and provide appropriate treatment accordingly. The newly revised Clinical Practice Guidelines of Chronic Pancreatitis 2015 consist of four chapters, i.e., diagnosis, staging, treatment, and prognosis, and includes a total of 65 clinical questions. These guidelines have aimed at providing certain directions and clinically practical contents for the management of chronic pancreatitis, preferentially adopting clinically useful articles. These revised guidelines also refer to early chronic pancreatitis based on the Criteria for the Diagnosis of Chronic Pancreatitis 2009. They include such items as health insurance coverage of high-titer lipase preparations and extracorporeal shock wave lithotripsy, new antidiabetic drugs, and the definition of and treatment approach to pancreatic pseudocyst. The accuracy of these guidelines has been improved by examining and adopting new evidence obtained after the publication of the first edition.

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.

Ultrasonographic Splanchnic Arterial Flow Measurement in Severe Acute Pancreatitis

Introduction Duplex ultrasonographic technology is now capable of detecting flow signals in the various splanchnic vessels and calculating the concomitant flow velocities using fast-Fourier transformation. Aim To use Doppler sonography to investigate how splanchnic hemodynamics vary during the early stage of severe acute pancreatitis. Methodology Six patients with severe acute pancreatitis (age, 59.0 ± 6.57 years; four men, two women) and seven with mild to moderate acute pancreatitis (age, 60.1 ± 7.41 years; five men, two women) were examined with Doppler sonography immediately after disease onset. The maximum velocity, minimum velocity, mean velocity, pulsatility index, and resistive index were determined from the Doppler spectra from the proper hepatic artery, celiac artery, and superior mesenteric artery. We also examined 15 healthy subjects (age, 59.3 ± 4.60 years; 10 men, five women) as controls. Results The maximum velocity of the proper hepatic artery in patients with severe acute pancreatitis was significantly higher than that in patients with mild to moderate acute pancreatitis (p = 0.011) and in control subjects (p = 0.0047). Similarly, significant increases in both the minimum velocity and the mean velocity of the proper hepatic artery were observed in patients with severe acute pancreatitis. Neither pulsatility index nor resistive index of the proper hepatic artery showed a significant difference among the three groups. There were no significant differences among the three groups with respect to the flow velocity of the superior mesenteric artery. In contrast, the pulsatility index of the superior mesenteric artery in patients with severe acute pancreatitis was significantly lower than that in patients with mild to moderate acute pancreatitis (p = 0.0058) or in control subjects (p = 0.0024). For patients with acute pancreatitis, a significant inverse correlation was obtained between the maximum velocity of the proper hepatic artery and the pulsatility index of the superior mesenteric artery (r = −0.658, p = 0.0145). Conclusion The increase in the hepatic arterial flow velocity and the decrease in the superior mesenteric arterial pulsatility index may represent early events of the severe type of acute pancreatitis.

Relation between morphologic changes in the main pancreatic duct and exocrine pancreatic function after a secretin test.

Introduction Because pancreatic exocrine function testing methods are problematic, both imaging and functional tests are important in the diagnosis of chronic pancreatitis. Aim To evaluate the usefulness of ultrasonographic monitoring of the main pancreatic duct after a secretin test. Methodology A total of 70 subjects (30 control subjects, 26 patients with probable chronic pancreatitis, and 14 patients with definite chronic pancreatitis) were selected. The main pancreatic duct diameters were measured serially after an injection of secretin (100 IU/body). The relation between the magnitude of the duct dilation and exocrine pancreatic function on the secretin test was evaluated. Results The main pancreatic duct dilated immediately after a bolus injection of secretin, showed a peak after 2–5 minutes, and recovered gradually. The response curve of the definite group had a flatter pattern than that of the other groups. For the maximal to basal duct diameter ratio, statistically significant differences were found between the control and definite groups and between the control and probable groups. In addition, the ratio correlated significantly with the maximal bicarbonate concentration and secretory volume on the secretin test. Conclusions The results of the current study indicate that exocrine pancreatic function and the morphologic changes of the main pancreatic duct are significantly related. Dynamic ultrasonographic findings may reflect pancreatic function; consequently, this test may be a useful tool in the diagnosis of chronic pancreatitis.

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.

Molecular Cloning and Characterization of Chymopasin, a Novel Serine Protease from Rat Pancreas

Introduction Pancreas secretes many enzymes for food digestion into the pancreatic juice. We cloned a novel serine protease, chymopasin, from rat pancreas. Aims To know the localization of this enzyme in the pancreas and to analyze the enzymatic characteristics. Methodology We cloned chymopasin cDNA using 3′ and 5′ RACEs. Northern blot and in situ hybridization were used to study the expression of this enzyme. Recombinant chymopasin protein produced by E. coli was analyzed by Western blot using specific antibody, and its enzymatic characteristics were examined using commercially available synthetic substrates, fibrin and gelatin. Results The open reading frame of rat chymopasin consisted of 792 bp encoding 264 amino acid residues. The deduced amino acid sequence contained the essential catalytic triad characteristic of the serine protease family. There was no putative N-glycosylation site. The amino acid sequence of rat chymopasin showed 54.5% identity to rat chymotrypsin B. Northern blot analysis showed that the transcript was strongly expressed in the pancreas. In situ hybridization with digoxigenin-labeled cRNA probe showed that the positive signals were observed in the acinar cells, but not in the islet or duct cells. Chymopasin protein was detected in the pancreas homogenate and bile-pancreatic juice. Further, cerulein stimulated the secretion of rat chymopasin into bile-pancreatic juice. Conclusion These results suggested that rat chymopasin might be a digestive enzyme secreted from the acinar cells. From the enzyme assay using synthetic substrates, the purified recombinant chymopasin expressed in Escherichia coli showed chymotrypsin-like activity. In addition, rat recombinant chymopasin showed fibrinolytic and gelatinolytic activities. These results suggested a role in the pathogenesis of pancreatic damage.