Takanori Inagaki

Interleukin-6 is a useful marker for early prediction of the severity of acute pancreatitis.

Twelve patients with acute pancreatitis admitted to our department between January 1993 and December 1994 were studied prospectively and classified into two groups (severe group, five patients; mild group, seven patients), according to the criteria for grading severity of acute pancreatitis proposed by the Research Committee for Intractable Diseases of the Pancreas, Japanese Ministry of Health and Welfare (1990). To evaluate markers for early estimation of the severity of acute pancreatitis, we measured serum changes in various parameters. In the severe group interleukin-6 (IL-6) levels were increased significantly 5, 24, 72, and 120 h after the onset (p < 0.01), compared with the mild group. C-reactive protein (CRP), thrombin antithrombin III, and α2-plasmin inhibitor plasmin complex levels were significantly increased only at the 72-h time point. Peak values of interleukin-8 (IL-8) and soluble human E selectin were observed at 5 and 72 h, respectively, after the onset. There was a significant correlation between IL-6 at 5 h and both pancreatic secretory trypsin inhibitor (r = 0.85) and CRP (r = 0.94) at 72 h. We therefore conclude that IL-6 is a useful marker for assessment of the severity of acute pancreatitis in its early stages.

Pancreaticopleural fistula imaged with magnetic resonance pancreatography

Accessible online at: www.karger.com/journals/pan Pancreaticopleural fistula is a rare complication of inflammatory pancreatic disease. Although its demonstration is often difficult, endoscopic retrograde pancreatography (ERP) and CT have been employed for diagnostic purposes [1–4]. Recently, magnetic resonance pancreatography (MRP) has proven effective in a number of studies, with results generally equivalent to conventional ERP [5]. Here we present the contributions of MRP to the diagnosis and treatment plan of a patient with a pancreaticopleural fistula. A 58-year-old male was admitted to our hospital because of abdominal pain and anorexia. He had a history of moderate alcohol intake since the age of 20 years and a remote history of pancreatitis. Physical examination on admission revealed diminished breath sounds in the right chest and moderate tenderness in the upper quadrant of the abdomen. Chest films revealed a massive right pleural effusion. Laboratory data on admission were as follows: serum amylase was

Decreased pancreatic exocrine function in the mutant Eisai hyperbilirubinemic rat (EHBR)

The Eisai hyperbilirubinemic rat (EHBR) is a Sprague-Dawley rat (SDR) mutant with conjugated hyperbilirubinemia as an autosomal recessive trait. EHBRs manifest jaundice from birth, which is permanent except for a transient decrease at 6-8 weeks of age. To investigate whether the hyperbilirubinemia affects pancreatic exocrine function and acinar cell growth, EHBRs at 6 (without jaundice) and 12 weeks (with jaundice) of age were compared, along with SDRs as controls. Pancreatic wet weights did not significantly differ, but amylase content of acini was lower in EHBRs than SDRs. No correlation was found between pancreatic wet weight and serum bilirubin levels in EHBRs. In vitro amylase release in response to 1-100 pM cholecystokinin octapeptide (CCK-8), 1 microM 12-O-tetradecanoylphorbol 13-acetate, and 2.5 microM calcium ionophore A23187, and in vivo pancreatic secretion stimulated by CCK-8 (0.08 microg/kg body weight/h) were significantly lower in the EHBR cases than in the SDRs. At the electron microscopic level, many acinar cell nuclei were pyknotic, most elements of their Golgi complexes were atrophied, some mitochondria demonstrated fusion, and the rough-surfaced endoplasmic reticulum (RER) was dilated in EHBRs. These findings are indicative of a hypofunctional state. However, no differences between EHBRs at 6 and 12 weeks of age were evident, suggesting that the hyperbilirubinemia does not exert any pronounced influence on acinar cell growth or pancreatic exocrine function.

Impaired pancreatic exocrine function in rats with carbon tetrachloride-induced liver cirrhosis.

SummaryBackgroundSubstantial numbers of studies have revealed the close correlation between chronic pancreatitis and cirrhosis in human. However, the situation with regard to pancreatic enzyme secretion is less clear.AimThe aim of the study was to investigate pancreatic exocrine function in rat with carbon tetrachloride-induced liver cirrhosis in rats.MethodsPancreatic exocrine function and morphology in Sprague-Dawley rats with carbon tetrachloride-induced liver cirrhosis were investigated. Pancreatic exocrine functions stimulated by cholecystokinin-8 and other secretagogs were assessed in isolated pancratic acini, and in vivo and morphological changes were studied by routine were assessed in isolated pancreatic acini, and in vivo and morphological changes were studied by routine histological examination and electron microscopy.ResultsThe basal and cholecystokinin-8-stimulated amylase releases from acini and acinar amylase content were significantly lower in the cirrhotic rats than the control. None of the secretagogs induced the some amount of amylase release in cirrhotic as in control rats. Volume of the pancreatic juice and outputs of amylase and protein were significantly decreased under basal and cholecystokinin-8-stimulated conditions in vivo. Electron microscopy revealed most of the rough-surfaced endoplasmic reticulum accompanying less numbers of ribosomes to be dilated and some mitochondria to be swollen in cirrhotic rats.ConclusionPancreatic exocrine functions are decreased in cirrhotic rats owing to alterations at the electron microscopic levels, reflecting an impaired acinar intracellular messenger system.