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PubMed1976

[Neuropsychiatric disorders of the diseases of exocrine pancreas (author's transl)].

Neuropsychiatric and psychosomatic disorders occurring the exocrine pancreatic diseases are not rare, nevertheless didn't it seem to be very interesting in research and there exists no summarizing work of this disorders. Therefore we tried to give a comprehensive representation of those neuropsychiatric problems which are connected with the function of this organ. At first we give a description of psychopathology and pathogenesis of the functional pancreatic psychosis. The problematic of the reciprocal relationship of nervous system and pancreatitis, alcoholism and pancreatitis are demonstrated as well as the psychic disorders occurring the pancreas insufficiency, cystes of pancreas and congenital pancreatic diseases. Psychosomatic and mental disorders of pancreas carcinoma and mucoviscidosis are shown in detail. The question of the interrelation between pancreatic function and amyotrophic lateral sclerosis or parathyreotic diseases are discussed just as themes of neuropsychiatric pharmacotherapie and pancreatic function and mental disorders in pancreatic treatment.

Acute Disease↗

PubMed1975

[The valve of selective retrograde cholangiography in the radiological diagnosis of diseases of the biliary passages(author's transl)].

The value of selective endoscopic retrograde cholangiography in the radiological diagnosis of diseases of the biliary passages and neighbouring organs is discussed on the basis of 400 retrograde pancreatocholangiograms. The results of this endoscopic examination were compared with the findings of all the other preoperative examinations carried out. The diagnostic usefulness and limitations of various methods are discussed in relation to stenosis of the papilla, pancreatitis, carcinoma of the pancreas, tumours of the extrahepatic bile ducts and postoperative bile duct abnormalities. The diagnostic accuracy of 97% emphasises the value of co-operation between radiologists and endoscopists.

Adult↗

PubMed1980

[Examination of pancreatic function in children with special reference to the PABA-test (author's transl)].

To establish the diagnosis of acute pancreatitis the estimation of amylase in serum and urine, lipase and radio-immunoreactive trypsin in the serum are useful. Lipase estimations are more helpful than measuring amylase values. Trypsin-RIA-tests are increasingly important adults. But in chronic pancreatitis and inborn secretory insufficiencies of the pancreas these methods are less helpful. PABA-test, pancreolauryl-test (PLT), and the estimation of chymotrypsin in faeces are screening procedures, although their results correlate well amongst each other. As compared to the chymotrypsin estimation in faeces PABA test and PLT allow for some semiquantitative estimation of the secretory function and dynamics of the gland. The influence of malabsorption, liver and kidney diseases on these parameters is not yet quite clarified. Besides screening they are undoubtedly of value for judging the course and therapy of cystic fibrosis, Shwachman-syndrome, iatrogenic lesions by cytostatics (immunosuppressives and corticosteroids). Quantitative estimations of fat in faces and the pancreozymin test are no longer of significance.

4-Aminobenzoic Acid↗

PubMed1999

Chronic pancreatitis.

In the past year, numerous important papers were published on chronic pancreatitis, its causes, and its diagnosis; the cause of fibrosis; and pain in pancreatic cancer. More than 750 mutations have been described in the cystic fibrosis transmembrane regulator (CFTR) gene. Some mutations cause relatively mild reductions in CFTR function and may lead to disease in one organ without clinical involvement of other organs. Two groups of investigators recently reported that "idiopathic" chronic pancreatitis may be the sole manifestation of some CFTR mutations. Some recent reports may enhance our understanding of pancreatic fibrogenesis and may lead to therapies for painful chronic pancreatitis. Pancreatic stellate cells are vitamin A-containing cells that resemble hepatic stellate cells and were recently isolated from rat and human pancreas. They respond to inflammatory cytokines by producing collagen. Two studies show that endoscopic ultrasonography (EUS) correlates well with endoscopic retrograde cholangiopancreatography in moderate to severe chronic pancreatitis. However, in patients who have a few nondiagnostic abnormalities on EUS, these results have poor correlation with the results of endoscopic retrograde cholangiopancreatography and the secretin test. The clinical significance of these abnormalities is unclear, and the diagnosis of chronic pancreatitis should not be based on EUS findings alone. Painful chronic pancreatitis is a complex and difficult management problem. A recent study of alcoholic chronic pancreatitis suggests that the best predictors of pain relief are an intermittent pattern of pain and the presence of surgically correctable complications (eg, pseudocysts or biliary obstruction). An American Gastroenterological Association technical review of painful chronic pancreatitis emphasized the lack of controlled studies supporting any form of therapy. Further evidence that longstanding chronic pancreatitis is a premalignant condition has been provided by recent epidemiologic, pathologic, and molecular biology studies.

Journal Article↗

PubMed1997

An update on diseases of the pancreas in children.

The aim of this review is to describe recent developments in the field of pancreatic disorders in children. First, recent developments in the genetic research of hereditary pancreatitis are discussed. Subsequently, several issues of acute pancreatitis are presented. These include a description of the potential hazardous morbidity and mortality of this disorder in children. In addition, various novel etiologies that have been described lately in the medical literature are illustrated. Next, this paper discusses two examples of pancreatic disorders associated with systemic manifestations, i.e., ganglioneuromatosis and diabetes mellitus. Finally, a few rare genetic syndromes with pancreatic involvement are touched upon, an association that is not very well recognized. Cystic fibrosis is not covered.

Acute Disease↗

PubMed2002

Chloride transport in microperfused interlobular ducts isolated from guinea-pig pancreas.

Isolated interlobular ducts from the guinea-pig pancreas secrete a HCO3--rich fluid in response to secretin. To determine the role of Cl- transporters in this process, intracellular Cl- concentration ([Cl-]i) was measured in ducts loaded with the Cl--sensitive fluoroprobe, 6-methoxy-N-ethylquinolinium chloride (MEQ). [Cl-]i decreased when the luminal Cl- concentration was reduced. This effect was stimulated by forskolin, was not dependent on HCO3- and was not inhibited by application of the anion channel/transporter inhibitor H2DIDS to the luminal membrane. It is therefore attributed to a cAMP-stimulated Cl- conductance, probably the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel. [Cl-]i also decreased when the basolateral Cl- concentration was reduced. This effect was not stimulated by forskolin, was largely dependent on HCO3- and was inhibited by basolateral H2DIDS. It is therefore mediated mainly by Cl-/HCO3- exchange. With high Cl- and low HCO3- concentrations in the lumen, steady-state [Cl-]i was 25-35 mM in unstimulated cells. Stimulation with forskolin caused [Cl-]i to increase by approximately 4 mM due to activation of the luminal anion exchanger. With low Cl- and high HCO3- concentrations in the lumen to simulate physiological conditions, steady-state [Cl-]i was 10-15 mM in unstimulated cells. Upon stimulation with forskolin, [Cl-]i fell to approximately 7 mM due to increased Cl- efflux via the luminal conductance. We conclude that, during stimulation under physiological conditions, [Cl-]i decreases to very low levels in guinea-pig pancreatic duct cells, largely as a result of the limited capacity of the basolateral transporters for Cl- uptake. The resulting lack of competition from intracellular Cl- may therefore favour HCO3- secretion via anion conductances in the luminal membrane, possibly CFTR.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed2001

Immortalized bovine pancreatic duct cells become tumorigenic after transfection with mutant k-ras.

Mutation of the K-ras gene is thought to be an early and important event in pancreatic carcinogenesis. In order to study the role of this molecular alteration in the transition from the normal to the neoplastic pancreatic cell, bovine pancreatic duct cells were first immortalized by SV40 large T antigen (Ag) complementary (c)DNA transfection and then transfected with a mutated K-ras gene. As did primary duct cells, the immortalized duct cells (more than 100 passages) expressed cytokeratins, carbonic anhydrase type-II, cystic fibrosis transmembrane conductance regulator (CFTR), and multidrug resistance (mdr). They grew as a single layer after transplantation under plastic domes and formed three-dimensional structures resembling ducts when grown on Matrigel. Cell growth was stimulated by insulin, epidermal growth factor (EGF), transforming growth factor (TGF)-alpha, but cells did not respond to gastrin and CCK-8. They did not form colonies in soft agar nor did they form tumors in nude mice. Immortalized cells transfected with mutated K-ras acquired the ability to form tumors after orthotopic injection into the nude mouse pancreas. It is concluded that SV 40 immortalized bovine pancreatic

Animals↗

PubMed1983

Postprandial release of gastric inhibitory polypeptide (GIP) and pancreatic polypeptide in dogs with pancreatic acinar atrophy. Correction of blunted GIP response by addition of pancreatic enzymes to a meal.

In order to evaluate the enteropancreatic hormone axis in dogs with pancreatic acinar atrophy, we measured the release of gastric inhibitory polypeptide and pancreatic polypeptide in response to a standard meal and a meal containing pancreatic enzymes in affected dogs and controls. Postprandial release of pancreatic polypeptide was normal in dogs with pancreatic atrophy and was not affected by addition of pancreatic enzymes to the food. Gastric inhibitory polypeptide was not released after a standard meal in affected dogs, but this blunted response was corrected by the addition of pancreatic enzymes to the food. Feeding the enzyme alone did not stimulate a gastric inhibitory polypeptide response. These results, in part, support similar observations previously reported in children with exocrine pancreatic insufficiency associated with cystic fibrosis. We conclude that dogs with idiopathic pancreatic acinar atrophy can be used as an animal model for future study of enteropancreatic hormonal abnormalities that occur in human beings with exocrine pancreatic insufficiency.

Animals↗

PubMed2000

Embryonic epithelial membrane transporters.

Embryonic epithelial membrane transporters are organized into transporter families that are functional in several epithelial organs, namely, in kidney, lung, pancreas, intestine, and salivary gland. Family members (subtypes) are developmentally expressed in plasma membranes in temporospatial patterns that are 1) similar for one subtype within different organs, like aquaporin-1 (AQP1) in lung and kidney; 2) different between subtypes within the same organ, like the amiloride-sensitive epithelial sodium channel (ENaC) in lung; and 3) apparently matched among members of different transporter families, as alpha-ENaC with AQP1 and -4 in lung and with AQP2 in kidney. Finally, comparison of temporal expression patterns in early embryonic development of transporters from different families [e.g., cystic fibrosis transmembrane conductance regulator (CFTR), ENaC, and outer medullary potassium channel] suggests regulatory activating or inactivating interactions in defined morphogenic periods. This review focuses on embryonic patterns, at the mRNA and immunoprotein level, of the following transporter entities expressed in epithelial cell plasma membranes: ENaC; the chloride transporters CFTR, ClC-2, bumetanide-sensitive Na-K-Cl cotransporter, Cl/OH, and Cl/HCO(3); the sodium glucose transporter-glucose transporter; the sodium/hydrogen exchanger; the sodium-phosphate cotransporter; the ATPases; and AQP. The purpose of this article is to relate temporal and spatial expression patterns in embryonic and in early postnatal epithelia to developmental changes in organ structure and function.

Animals↗

PubMed2001

The pck rat: a new model that resembles human autosomal dominant polycystic kidney and liver disease.

BACKGROUND: The pck rat is a recently identified model of polycystic kidney disease (PKD) and liver disease (PLD) that developed spontaneously in the rat strain Crj:CD/SD. Its pattern of inheritance is autosomal recessive. METHODS: To characterize this new model, we studied pck rats derived from F9 breeding pairs from Charles River Japan and control Sprague-Dawley rats. Blood and tissues (kidneys, liver, and pancreas), obtained from these rats at 1, 7, 21, 70, and 182 days of age, were used for biochemical determinations, light and electron microscopy, and immunohistochemistry. RESULTS: The pck rats develop progressive cystic enlargement of the kidneys after the first week of age, and liver cysts are evident by day 1. The renal cysts developed as a focal process from thick ascending loops of Henle, distal tubules, and collecting ducts in the corticomedullary region and outer medulla. Flat and polypoid epithelial hyperplasia were common in dilated tubules and cysts. Apoptosis was common and affected normal, as well as dilated tubules, but less frequently cysts lined by flat epithelium. The basement membranes of the cyst walls exhibited a variety of alterations, including thinning, lamellation, and thickening. Focal interstitial fibrosis and inflammation were evident by 70 days of age. Segmental glomerulosclerosis and segmental thickening of the basement membrane with associated effacement of the podocyte foot processes were noted in some rats at 70 days of age. The PKD was more severe in male than in female pck rats, as reflected by the higher kidney weights, while there was no gender difference in the severity of the PLD. Mild bile duct dilation was present as early as one day of age. With age, it became more severe, and the livers became markedly enlarged. Even then, however, there was only a mild increase in portal fibrosis, without formation of fibrous septae. Slight elevations of plasma blood urea nitrogen levels were detected at 70 and 182 days of age. CONCLUSIONS: The pck rat is a new inherited model of PKD and PLD with a natural history and renal and hepatic histologic abnormalities that resemble human autosomal dominant PKD. This model may be useful for studying the pathogenesis and evaluating the potential therapies for PKD and PLD. The identification of the pck gene may provide further insight into the pathogenesis of autosomal dominant PKD.

Animals↗

PubMed1990

Solid, infiltrating variety of papillary cystic neoplasm of the pancreas.

Four tumors with histologic, histochemical, and ultrastructural characteristics of papillary cystic neoplasm of the pancreas but lacking the capsule commonly observed in papillary cystic neoplasm and infiltrating interiorly into the pancreatic parenchyma were seen in two men and two women who were 39 to 51 years old. These tumors contrasted with typical encapsulated papillary cystic neoplasms that show extrapancreatic growth and that are detected as a palpable abdominal mass in young women. These four tumors, although unpalpable, were all detected by nodular images of calcification in abdominal plain radiography. The tumors had a mean diameter of 3.1 cm (range, 1.7 to 4.5 cm), were confined within the pancreatic parenchyma, and showed central fibrosis accompanied by dystrophic changes such as calcification and ossification. A small necrotic cyst contiguous to the fibrous focus also was observed in the tumor in three patients. Tumor cells similar to those of a papillary cystic neoplasm had infiltrated among the pancreatic parenchyma in solid and pseudopapillary patterns, and pleomorphic atypism was observed in some parts of the tumor in three patients. These tumors were tentatively designated solid, infiltrating variety of papillary cystic neoplasms to differentiate them from ordinary encapsulated papillary cystic neoplasms. Although no signs of recurrence have been noticed after surgical treatment in these patients, the infiltrating growth pattern and the presence of pleomorphic atypism suggest higher malignancy than the ordinary papillary cystic neoplasm. The contrasting growth pattern and possible malignancy may warrant establishment of these tumors as a papillary cystic neoplasm subclass.

Adult↗

PubMed2002

Heterotopic pancreatitis: gastric outlet obstruction due to an intramural pseudocyst and hamartoma.

Heterotopic pancreas, usually a silent gastrointestinal malformation, may become clinically evident when complicated by chronic inflammation. We report a case of pancreatitis and extensive pseudocyst formation in the gastric antrum, which caused gastric outlet obstruction. The diagnosis was obscured by a history of emesis during pregnancy and a previously resected gastric polyp. The nature of the obstructive lesion was not diagnosed preoperatively in spite of endosonographic evaluation. Intraoperatively, a cystic tumor of the stomach wall was found, the lesion was excised, and a pyloroplasty was performed to close the excision site. Histology revealed heterotopic pancreatic tissue with chronic inflammation, fibrosis and pseudocyst formation and adjacent to this lesion a myoglandular hamartoma. The patient is symptom-free two years after surgery and no recurrence was found. The nature of heterotopic pancreatic tissue, its diagnosis and management are discussed.

Adult↗

PubMedDate not supplied

Pancreatic disease in children and young adults: evaluation with CT.

In children with pancreatic disease, computed tomography (CT) has a primary role in the evaluation of pancreatitis, trauma, and malignancy. At CT, pancreatic abnormalities may manifest as pancreatic enlargement (tumor, acute pancreatitis), pancreatic atrophy (cystic fibrosis, chronic pancreatitis), cystic lesions (pseudocysts, congenital simple cysts, autosomal dominant polycystic kidney disease, von Hippel-Lindau disease, cystic fibrosis, cystic neoplasms), or fatty replacement (cystic fibrosis, Shwachman-Diamond syndrome, history of steroid therapy, Cushing syndrome, Johanson-Blizzard syndrome, obesity). CT is the best modality for evaluation of pancreatitis, allowing detection of pancreatic abnormalities as well as abnormal extrapancreatic fluid collections. In children who have undergone blunt abdominal trauma, CT has been shown to be the best initial imaging study, being more sensitive than ultrasound for detection of pancreatic injury. In neoplastic conditions, CT demonstrates the extent of disease, enables characterization of the tissue components of the tumor, and allows accurate posttreatment follow-up. Although the various diseases of the pancreas may have overlapping appearances at CT, the correct diagnosis can often be made on the basis of the CT findings in combination with the clinical history, laboratory data, and the patient's age.

Adolescent↗

PubMed2000

Intraductal papillary tumors of the pancreas. Histopathologic correlation of MR cholangiopancreatography findings.

PURPOSE: To evaluate MR cholangiopancreatography (MRCP) findings of intraductal papillary tumors of the pancreas and correlate them with histopathology. MATERIAL AND METHODS: Seventeen patients with intraductal papillary tumor of the pancreas underwent MRCP before surgery. MRCP findings were correlated to histopathology with regard to the presence of septa and excrescent nodules in the cystic lesion, communication between the cystic lesion and the main pancreatic duct (MPD), degree of dilatation of MPD, and dilatation of the common bile duct (CBD). RESULTS: MRCP demonstrated septa in 17 cases (100%), excrescent nodules in 8 cases (47.1%), communication between the intraductal papillary tumor and the MPD in 14 cases (82.3%), dilatation of MPD over 50% in 6 cases (35.3%), and dilatation of CBD in 3 cases (17.6%). These findings showed excellent correlation with histopathology. The septum on MRCP corresponded with a layer of connective tissue with pancreatic duct epithelium. Excrescent nodules in the carcinomas consisted not only of malignant cells, but also of dysplasia and adenoma. Excrescent nodules in adenomas were consistent not only with minimal papillary growth of adenoma, but also with proliferation of fibrosis, and hematoma and organized fibrin with minimal fibrosis. Pancreatic tissue was affected by chronic pancreatitis in all cases. Cases with dilatation of CBD on MRCP were due to microscopic invasion by the carcinoma. CONCLUSION: MRCP appearances of intraductal papillary tumors are well correlated with the findings at histopathology.

Adenocarcinoma, Papillary↗

PubMed1988

Bilateral renal dysplasia, pancreatic fibrosis, intrahepatic biliary dysgenesis, and situs inversus totalis in a boy.

This is a case report of a Japanese newborn infant showing bilateral renal dysplasia, severe pancreatic fibrosis simulating cystic fibrosis, intrahepatic biliary dysgenesis, and situs inversus totalis. The chromosomal analysis was normal. A review of the literature showed that there was another case exactly the same. These two rare cases had no difinite evidence of blood relationship, but occurred in the same town in a remote area.

Bile Ducts, Intrahepatic↗

PubMed1981

Optimization and validation of assays to estimate pancreatic esterase activity using well-characterized micellar solutions of cholesteryl oleate and tocopheryl acetate.

Studies have been carried out to determine the maximal solubilization of cholesteryl oleate and tocopheryl acetate within mixed bile salt-fatty acid micelles and to establish reproducible assays for pancreatic esterase activity using these micellar substrates. At pH 8.5, using 30 mM sodium taurocholate and 10 mM oleic acid, reproducible micellar solutions of the esters could be prepared giving micellar concentrations of 0.4 mM and 0.1 mM for tocopheryl acetate and cholesteryl oleate, respectively. Conditions were then optimized to estimate pancreatic esterase activity using these micellar-solubilized substrates. Maximal activity was obtained at pH 8.5 with 2-4 mM oleic acid and 15-30 mM sodium taurocholate, and gave coefficients of variation for the assays of 7.4% and 20.2% using tocopheryl acetate and cholesteryl oleate, respectively, as substrates. Micellar-solubilized cholesteryl oleate and tocopheryl acetate, together with a non-micellar system using p-nitrophenyl acetate, were used to estimate esterase activity in human duodenal aspirates and rat pancreatic homogenates. Esterase activity in children with cystic fibrosis was greatly reduced and paralleled tryptic and pancreatic lipase activity, which suggested that the esterase activity was pancreatic in origin. The results of this study, therefore, provide a basis for future investigations concerned with the hydrolysis and absorption of dietary esters.

Animals↗

PubMed2005

Genetic polymorphisms in alcoholic pancreatitis.

BACKGROUND: Chronic, excessive alcohol consumption is clearly associated with acute and chronic pancreatitis. However, both clinical and laboratory studies demonstrate that alcohol consumption alone does not directly cause alcoholic chronic pancreatitis. Growing evidence suggests that environmental and possibly genetic cofactors must also be present to overcome the redundant mechanisms protecting the pancreas from pancreatitis and facilitating complete recovery. METHODS: The SAPE hypothesis model was used to organize potential triggering factors, susceptibility factors and disease-modifying factors based on insights from animal studies. A systematic review of genetic studies on alcoholic pancreatitis was conducted and the results were analyzed in the context of animal studies. RESULTS: To date, no major genetic cofactors for susceptibility or progression have been identified in approximately 90% of cases of human alcoholic chronic pancreatitis. Mutations have been identified in the pancreatic secretory trypsin inhibitor gene (SPINK1) in about 8% of cases, and an excess in cystic fibrosis transmembrane conductance inhibitor (CFTR) gene variants have been reported, but the details of the complex genetics with CFTR have not been clarified. None of the polymorphisms in alcohol-metabolizing genes or detoxifying genes appear to explain pancreatic susceptibility. CONCLUSIONS: New, adequately powered genetic studies are needed. Several major genetic epidemiology studies are underway in both Europe and the United States to help determine why only a subset of alcoholics develop alcoholic chronic pancreatitis.

Acute Disease↗

PubMed1999

Epithelial P2X purinergic receptor channel expression and function.

P2X purinergic receptor (P2XR) channels bind ATP and mediate Ca(2+) influx--2 signals that stimulate secretory Cl(-) transport across epithelia. We tested the hypotheses that P2XR channels are expressed by epithelia and that P2XRs transduce extracellular ATP signals into stimulation of Cl(-) transport across epithelia. Electrophysiological data and mRNA analysis of human and mouse pulmonary epithelia and other epithelial cells indicate that multiple P2XRs are broadly expressed in these tissues and that they are active on both apical and basolateral surfaces. Because P2X-selective agonists bind multiple P2XR subtypes, and because P2X agonists stimulate Cl(-) transport across nasal mucosa of cystic fibrosis (CF) patients as well as across non-CF nasal mucosa, P2XRs may provide novel targets for extracellular nucleotide therapy of CF.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗