Chronic pancreatitis, acute pancreatitis

MRCP has been recognized as a safe and noninvasive diagnostic method. In the present study we evaluated the usefulness of MRCP in diagnosis of chronic and acute pancreatitis. Two-dimensional fast asymmetric spin-echo (FASE) MRCP was performed in 40 patients with chronic pancreatitis and 13 with acute pancreatitis. In 29 patients (72.5%) with chronic pancreatitis and 9 (66.7%) with acute pancreatitis, main pancreatic duct (MPD) was visualized entirely. MRCP could demonstrate the characteristic findings of chronic pancreatitis such as dilatation and irregularity of MPD in most cases. In acute pancreatitis, MRCP indicated that MPD was normal in diameter, but irregular in configuration compared with that of the control group. MRCP may facilitate the diagnosis of chronic and acute pancreatitis.     

Chronic pancreatitis: diagnosis

Chronic pancreatitis is a chronic, inflammatory process leading to destruction of the exocrine tissue, filorosis, and in some patients a loss of endocrine function. Because chronic pancreatitis results in a permanent destruction of pancreatic tissue, exocrine and/or endocrine pancreatic insufficiency may follow. However, owing to the tremendous reserve of pancreatic function, insufficiency may be subclinical at least in the beginning of the disease. The diagnosis of chronic pancreatitis is not difficult; it is based on a typical medical history, specific imaging procedures, and pancreatic function testing. The main differential diagnosis is to separate chronic pancreatitis form pancreatic carcinoma. In the present summary, the different imaging procedures and pancreatic function tests are discussed.     

Chronic recurrent pancreatitis in pregnancy

This report describes a case of chronic recurrent pancreatitis due to gallstones arising in the first trimester of pregnancy. Total parental nutrition produced a normalization of pancreatic enzymes and a rapid regression of symptoms. Following another relapse of acute pancreatitis, a laparoscopic cholecystectomy was performed. The pregnancy continued normally and the patient had a spontaneous delivery at the 37th week.     

Chronic pancreatitis: terminology and classification

Rubidazone, the new semi-synthetic benzol hydrazone hydrochloride derivative of dauorubicin, has proved on a molecular weight basis to be less toxic than adriamycin and similar to daunorubicin in cardiac toxicity studies in the hamster as well as in other in vivo and in vitro test systems. It has proven effectiveness against several animal tumours and human acute leukaemias. We have compared the inhibitory effect of rubidazone to that of adriamycin on P388 leukaemia and normal bone marrow colony-forming units (CFU) using the spleen colony assay system in male DBA2 mice. The efficacy ratios (i.e., the ratio of the slopes of the normal bone marrow CFU to leukaemic CFU dose-survival curves) in the spleen colony assay system for rubidazone and adriamycin were 7-8 and 7-5 respectively. This near identity of efficacy ratios fro rubidazone and adriamycin correlated with the results of median survival time studies in the leukaemic mice. Their dose-median survival time curves were almost parallel, having nearly identical slopes. Rubidazone's equal therapeutic index as compared to adriamycin in the spleen colony assay system together with its known decreased toxicity to cardiac muscle cells makes it an extremely promising new anthracycline derivative to study in comparison to adriamycin in human malignancies.     

Chronic pancreatitis: a cause of cholestasis

The bile ducts were visualised using endoscopic retrograde cholangiopancreatography (ERCP), percutaneous or intravenous cholangiography in 38 patients with non-gallstone chronic pancreatitis. Stenosis of the intrapancreatic portion of the distal common bile duct was demonstrated in 11 patients. Ten of the 11 developed transient cholestasis during exacerbations of their chronic pancreatitis. In six cholestasis eventually persisted requiring surgical relief. Secondary biliary cirrhosis was present in one patient. No evidence of pancreatic carcinoma was found in the patients explored surgically. Ten of the patients are alive more than one year after diagnosis. Chronic pancreatitis was of alcoholic aetiology in 10 of the patients with biliary stenosis. Cholestasis and biliary stricture are common but poorly recognised complications of non-gallstone chronic pancreatitis, especially when pancreatitis is severe and due to alcohol.     

Chronic pancreatitis: nutrition and pain therapy

Therapy of chronic pancreatitis rests on five arms: Avoidance of alcohol, treatment of pain, replacement therapy for exocrine and endocrine insufficiency and adequate nutrition. Alcohol withdrawal improves pain and the patient's compliance. It also seems to retard the chronic inflammatory process. Therapy of pain depends on the pathomechanism of pain. There is a lack of prospective, controlled studies comparing various treatment regimens. Thus, treatment options are partly dependent on the experience of the physician taking care of the patient and include i.e. for pseudocysts: surgical vs percutaneous or endoscopic drainage; for stenosis of the main pancreatic duct close to the papilla: surgical vs endoscopic drainage (stents); for distal bile duct stenosis: endoscopic stents vs biliodigestive anastomosis vs pancreatic head resection; for pancreatic stones: extracorporal shock wave lithotripsy followed by endoscopic stone extraction vs surgery (pancreaticojejunostomy), finally for inflammatory tumor of the pancreatic head combined with pain with or without compression of the distal bile duct or duodenum: duodenum-preserving pancreatic head resection vs Whipple resection. Patients with pain resistant to medical treatment may be candidates for a transcutaneous blockade of the plexus coeliacus or for epidural nerve blockade before one choses a surgical procedure. Application of pancreatic enzymes does not seem to have a major beneficial effect on pancreatic pain. Modification of nutrition has become less restrictive. Thanks to improved substitution with acid resistant porcine pancreatic extracts with high lipase activity, fat restriction is no longer of paramount importance. However, supply with sufficient calories is still difficult due to pain, inadequate compliance and hypermetabolism.     

Chronic pancreatitis and neoplasia: correlation or coincidence

Renal biopsy specimens from patients with membranous nephropathy (MN) were studied using immunohistochemical labelling to clarify the aetiological significance of Helicobacter pylori antigen in this disease. Sixteen specimens were examined, from 7 male and 9 female MN patients. Renal specimens from patients with diabetic nephropathy and IgA nephropathy, and from autopsied patients without renal diseases were obtained as controls. Immunohistochemical labelling was performed using one polyclonal antibody and three monoclonal antibodies against H. pylori. Specimens from 11 of the MN patients revealed granular deposits along the glomerular capillary walls, which reacted positively with polyclonal antibody after trypsin pretreatment. None of the control specimens revealed positive labelling. The MN specimens showed no positive reaction with the primary antibody, which had been treated for immunoabsorption testing using sonicated H. pylori. We also determined H. pylori status in these MN patients histologically and/or serologically. Of the 11 patients whose glomeruli were positive for anti-H. pylori antibody, 7 were suitable for analysis, and all were regarded as positive for H. pylori infection. These results suggest that the presence of a specific antigen in the glomeruli of patients with MN and H. pylori infection may be involved in the pathogenesis of MN.     

Chronic pancreatitis: a complication of sarcoidosis?

Gastrointestinal localizations of sarcoidosis are rare. A total of 14 cases of pancreatic involvement in sarcoidosis has been reported previously. We report here a case of late onset idiopathic chronic pancreatitis diagnosed at the same time as sarcoidosis with liver, colonic, renal, mediastinal and neurologic involvement in a 56-year-old man. This case further suggests a possible relationship between idiopathic chronic pancreatitis and multisystem diseases.     

Chronic pancreatitis prevalence in liver cirrhosis. Morphological and functional study

In the present study we have examined the ability of the beta-amyloid peptide (A beta(25-35)) to modulate the respiratory burst activity of human monocytes in vitro. Incubation of the cells for 24 h with A beta(25-35) as well as with A beta(1-42) resulted in an enhanced production of reactive oxygen radicals (ROI) in response to phorbol 12-myristate 13-acetate (PMA). Such effect was additively increased by coincubation with interferon-gamma (IFN gamma), and was paralleled by modulation of gene and protein expression of some components of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system. Since the effects of A beta(25-35) were also reproduced in primary rat microglia, our findings indicate that A beta(25-35) can potentiate the ability of mononuclear phagocytes to produce ROI, and add further insights into its biological effects.     

Phenformin-associated pancreatitis

Although phenformin has been previously reported to be associated with acute pancreatitis, little emphasis of this association has been made in the literature. We report the case of a 70-year-old diabetic man who developed acute hemorrhagic pancreatitis and severe lactic acidosis while taking phenformin. The patient was not taking any other medications, nor did he have any of the known metabolic conditions associated with pancreatitis. We review the four previously published cases of patients who developed acute pancreatitis while taking phenformin. Three of those patients also developed lactic acidosis, a well-known complication of phenformin therapy. Although phenformin has been reported to increase the serum amylase activity and to alter the content of the pancreatic secretions in response to various stimuli, the manner in which the drug might cause acute pancreatitis remains completely unknown.     

Lupus pancreatitis

We report the case of a sixteen year old female patient, admitted to a general hospital due to fever, poliarthritis, malar rash and vasculitis. Diagnostic studies confirmed the existence of Systemic Lupus Erythematosus. Shortly after admission, the patient was transferred to an intensive care unit due to severe acute pancreatitis. In spite of its infrequency, the diagnosis of acute pancreatitis must always be considered whenever a patient with SLE presents abdominal pain. The authors emphasise the importance of an early diagnosis of this rare complication, with high mortality rates, and present a brief review of the international literature.     

Hereditary pancreatitis

Hereditary pancreatitis is an idiopathic form of chronic pancreatitis which affects multiple members of a family in an autosomal dominant mode of inheritance. Most of the case reports are in caucasians of European descent. In this report, we present our data on four affected members spanning three generations in a family from India. Current data on hereditary pancreatitis are summarized, to revive an interest in this rare form of chronic pancreatitis.     

Chronic pancreatitis is associated with increased concentrations of epidermal growth factor receptor, transforming growth factor alpha, and phospholipase C gamma

The epidermal growth factor (EGF) receptor is a transmembrane protein that binds EGF and transforming growth factor alpha (TGF alpha), and that stimulates phospholipase C gamma 1 (PLC gamma 1) activity. In this study the role of the EGF receptor in chronic pancreatitis was studied. By immunohistochemistry, the EGF receptor, TGF alpha, and PLC gamma 1 were found to be expressed at high concentrations in pancreatic ductal and acinar cells from chronic pancreatitis patients. Northern blot analysis showed that, by comparison with normal controls, 19 of 27 chronic pancreatitis tissues exhibited a 5.7-fold increase in EGF receptor mRNA concentrations, and 20 of 27 chronic pancreatitis tissues exhibited a sixfold increase in TGF alpha mRNA concentrations. In situ hybridisation confirmed that overexpression occurred in ductal and acinar cells, and showed that both mRNA moieties colocalised with their respective proteins. These findings suggest that TGF alpha may act through autocrine and paracrine mechanisms to excessively activate the overexpressed EGF receptor in the two major cell types of the exocrine pancreas, thereby contributing to the pathobiology of this disorder.