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Long-term alcohol consumption and gene mutations are the most important causes of chronic pancreatitis. In addition to mutations in acinar genes, such as digestive enzymes and their inhibitors, defects in genes that primarily or exclusively affect the duct cells have also been described in recent years. Genetic changes are found not only in patients with a positive family history (hereditary pancreatitis) but also in so-called idiopathic and, to a lesser extent, in alcoholic chronic pancreatitis. The coming years will likely show that there are very complex interactions between environmental influences and numerous genetic factors.Langjähriger Alkoholkonsum und Genmutationen sind die wichtigsten Ursachen einer chronischen Pankreatitis. Neben Mutationen in azinären Genen wie Verdauungsenzymen und deren Inhibitoren sind in den letzten Jahren auch genetische Defekte beschrieben worden, die vornehmlich oder ausschließlich die Gangzellen betreffen. Genveränderungen finden sich nicht nur bei Patienten mit positiver Familienanamnese (hereditäre Pankreatitis), sondern auch bei sogenannter idiopathischer und – in geringerem Maße – bei alkoholischer chronischer Pankreatitis. In den nächsten Jahren wird sich wahrscheinlich zeigen, dass sehr komplexe Interaktionen zwischen Umwelteinflüssen und zahlreichen genetischen Faktoren bestehen.

A scrotal mass as initial manifestation of necrotising pancreatitis is very rare. In addition, the diagnosis is very difficult because diseases that occur more frequently produce similar symptoms. Therefore, it is very important to think about rare entities in the differential diagnosis for testicular pain.

Chronic pancreatitis is characterized by recurrent abdominal pain due to chronic inflammation resulting in loss of exocrine and endocrine function. The main complications of chronic pancreatitis are pancreatic pseudocysts and pancreatic carcinoma. In most cases chronic pancreatitis is induced by excessive chronic alcoholism, but intake of small amounts of alcohol may be enough to induce chronic pancreatitis. Treatment of pain includes discontinuation of alcohol abuse, use of analgetics and endoscopic interventional and surgical treatment options.

Often, equivocal pancreatic cystic masses in a patient cannot be clearly identified. We report on a 74-year-old patient who consulted us with size-gaining multi-cystic lesions located at the pancreatic head and tail as well as with an increased CA 19-9 level. By using diagnostic methods as ultrasound, radiological images and innovative endoscopic techniques an intraductal papillary mucinous neoplasm (IPMN) was diagnosed. Evaluation of equivocal cystic lesions requires developing of further strategies as well as integration of new concepts: We present a diagnostic algorithm based on endoscopy that enables us to perform an adapted therapy by having a more accurate evaluation and the opportunity to gain samples where unclear lesions are given.

Portal vein thrombosis complicating acute pancreatitis is more often diagnosed today due to the improved imaging techniques (computed tomography, ultrasound, nmr). Nevertheless the outcome of recent portal vein thrombosis is ill-known. We report on the computed tomographic findings and clinical course of portal vein thrombosis in two patients suffering from acute pancreatitis. Both patients showed spontaneous recanalization of the thrombosis.

Chronic pancreatitis is characterized clinically by recurrent or persistent abdominal pain, as well as exocrine, and possibly also endocrine, pancreatic insufficiency. The diagnosis is established with the aid of imaging procedures and the investigation of pancreatic function. Treatment comprises pain amelioration, possibly also applying endoscopic and surgical measures, and the treatment of exocrine and endocrine insufficiency.

The oesophagus, stomach and pancreas are primary target organs for ethanol-related diseases. In the oesophagus and stomach, ethanol induces motility disorders and mucosal lesions that are dose-dependent and reversible under acute conditions. Chronic consumption of alcohol causes a significant increase in the risk for squamous carcinoma of the oesophagus. All of these effects are mainly caused by direct contact of alcohol or its metabolite acetaldehyde with the mucosa. Non-alcoholic components are responsible for many effects of alcoholic beverages, including the powerful stimulation of gastric acid secretion by beverages that are produced by fermentation. In the exocrine pancreas, alcohol induces secretory alterations that are mainly affected by the manner and duration of alcohol exposure, the additional administration of food, the type of beverage or the basal secretory state of the gland. Because the pancreas is not topically exposed to ethanol, these ethanol effects on pancreatic secretion are primarily caused by systemic cholinergic mechanisms of the vagus nerve. Chronic alcohol abuse may cause chronic alcoholic pancreatitis after recurrent subclinical inflammatory episodes. Genetic predispositions are believed to play an additional role in the pathomechanism of the disease. In contrast to the cardiovascular system, moderate consumption of alcoholic beverages does not have any beneficial health effects on the oesophagus, stomach or pancreas. Future research needs to define the exact molecular mechanisms and the role of different genetic predispositions for alcohol-induced diseases as well as the effects of the non-alcoholic components of alcoholic beverages.

Chronic pancreatitis is mostly caused by heavy alcohol consumption and is characterized by the onset of symptoms in the fourth and fifth decade. Beginning in patients older than 65 years of age is rare. Leading symptom is recurrent or persisting abdominal pain which is missed only in approximately 5% of the cases. Chronic pancreatitis is classified as idiopathic if there is no anamnesis of alcohol abuse or some rare specific causes. The Idiopathic Chronic Senile Pancreatitis (ICSP) is a subset of the non-alcoholic pancreatitis and is characterized by advanced age at the time of first manifestation. Although life expectancy especially in chronic alcoholic pancreatitis is reduced, there are many patients who reach older age. The natural history in all forms of chronic pancreatitis shows a decrease in pain and the manifestation of exocrine and endocrine insufficiency as late complications. Especially in the elderly loss of weight may occur with steatorrhea and pancreatic diabetes mellitus as the dominating clinical problem of chronic pancreatitis. If pain persists treatment is symptomatically with analgesics. The possibility of causal surgery or the indication for endoscopic treatment of painful chronic pancreatitis should be proven in every single case. Standard pancreatin treatment consisting of large amounts of enzymes will abolish maldigestion. Pancreatic diabetes requires often insulin, there is a tendency to hypoglycaemia. In contrast to chronic pancreatitis cancer of the pancreas is a typical and frequent disease of the elderly. The prognosis is bad and one year life expectancy is just about 11%. One of the reasons is, that the diagnosis is found lately because early symptoms are missing. Specific symptoms like pain, weight loss or jaundice occur lately. In suspicion of pancreatic cancer a lot of methods of morphological diagnostic are available such as CT, MRCP, ultrasound, ERCP and PET, in addition the specific tumor markers CA 19-9 and CEA. After diagnostic is completed, curative resection is possible in only a low percentage of all cases. Old age is no contraindication for surgery, prognosis and the risk of surgery don't differ to other age groups. In most cases palliative therapy is the only possible option because of an advanced tumor stage. Sufficient pain therapy, endoscopic stenting in case of obstructive jaundice or gastroenterostomy in case of duodenal are useful interventions.

Chronic pancreatitis: Only recently mutations in several genes were found in patients with chronic pancreatitis. In those with a familial chronic pancreatitis mutations of the cationic trypsinogen were identified and the variants N29I and R122H lead to an autosomal dominant disease. In this group of patients the mutation N34S of the trypsin inhibitor SPINK1 was detected. In so-called idiopathic pancreatitis both variants of the SPINK1 and of the CFTR (cystic fibrosis transmembrane conductance regular) were identified. Alterations in both genes were also found in patients with alcoholic chronic pancreatitis. The strongest risk factor for chronic pancreatitis were trypsinogen mutations N29I and R122H mutations. However, both SPINK1 and CFTR increased the risk for chronic pancreatitis to a higher level than alcohol consumption. A genetic investigation should be performed in familial disease and younger age, but also in patients without family history and higher age a mutation could be found. Pancreas cancer: In 10% of the patients with pancreas cancer other members of the family were affected from the disease. Some of them belong to well characterized familial syndroms like HNPCC or Peutz-Jeghers-syndrom. In a minority of the others a genetic factor may be found, too. In sporadic disease the development of the tumor is characterized by continued acquirement of genetic alterations described by the PanIN model (pancreatic intraepithelial neoplesia). This means that the evolution of the neoplasia progresses from normal tissue via epithelial hyperplasy (PanIN 1A), papillary hyperplasy without (PanIN 1B) and with dysplasy (PanIN 2) and carcinoma in situ (PanIN 3) to invasive pancreas cancer. The progression is associated with genetic alterations of the cells (mutations of ki-ras, p16, p53 etc.). This results in deterioration of control of the cell cycle and the apoptosis and explains the malignancy of the disease. These findings may be used in the future to develop newer therapeutic principles in order to improve the dismal prognosis of this disease.

A 44-year-old patient was transferred for further treatment of pyogenic liver abscess and a severe attack of a chronic pancreatitis for strong upper right quadrant abdominal pain and recurring fever.Laboratory results revealed a significant inflammatory constellation. Abdominal ultrasound was performed which showed a big pyogenic abscess in the right lobe of the liver. Escherichia coli and Enterococcus faecalis could be isolated from abscess aspirates. Endoscopic retrograde cholangiography (ERC) without access of the pancreatic duct showed stenosis of the Ductus hepatocholedochus which was treated with a biliary endoprothesis.Antibiotic treatment and percutaneous drainage led to complete remission of the abscess. A few days after discharge the patient returned with identical clinical symptoms. Abdominal ultrasound showed recurrence of the abscess. Because of excessively high pancreatic amylase in aspirated abscess material the patient underwent endoscopic retrograde cholangiopancreaticography (ERCP). There, a pancreatico-hepatic fistula was seen, probably the result of necrosis caused by a severe acute attack of the chronic pancreatitis. After insertion of a naso-fistular drainage, continous rinse and appropriate antibiotic therapy both abscess and fistula completely disappeared without recurrence.The rare case of a pancreatic fistula should be considered when a pyogenic liver abscess follows an episode of acute pancreatitis or attack of chronic pancreatitis. Determination of pancreatic amylase in aspired abscess material can be an important step towards correct diagnosis.

A 43-year-old, cachectic, alcohol-addicted patient was admitted to the hospital due to hemoptysis and fever of up to 40 degrees C for the last 4 days. Physical examination revealed pleural rubs in the right lower lung and a diffuse pain in the right upper quadrant of the abdomen. The right upper quadrant of the abdomen also showed scars from several surgical interventions on the small intestine, the liver and the biliary tract and deformed caudal ribs due to an accident 23 years earlier.Chest X-ray, ultrasound and computed tomography (CT) showed abscess cavities in lung and liver communicating through the diaphragm. Under antibiotic therapy the abscess was drained. Cultures showed Klebsiella pneumoniae and Streptococcus viridans. Continuous lavage of the abscess cavities and antibiotic therapy led to an improvement in parameters of inflammation and clinical status. Imaging after 10 days of treatment showed a contrast enrichment in the abscess cavities and a bronchobiliary fistula accounting for temporary biliptysis. The drainage was removed after 29 days, when similar imaging revealed no further sign of an abscess cavity and a previous CT follow-up had proven a distinct decrease of the abscesses.Bronchobiliary fistulas are very rare. In most cases they are caused by hepatic or subphrenic abscesses, resulting from different conditions. The development of an bronchobiliary fistula originating from a Klebsiella pneumoniae pneumonia, as indicated by this report, has not been described so far. In the patient presented here, treatment was achieved due to continuous drainage despite the large extent of the abscess.

Chronic alcohol abuse is of significant clinical and economic relevance. A major part of internal medical pathology is associated with chronic alcoholism. 50% of all accidents with subsequent traumatic injuries are related to alcohol intake. Patients who are chronic alcohol abusers have prolonged hospital stays and substantial increases in postoperative morbidity. A sophisticated diagnosis of alcoholism within standard clinical routine is often difficult, and in most cases the treatment of alcohol-related diseases and complications is protracted and requires increased energy expenditure by the treating physicians. In surgical patients, chronic alcohol abuse is associated with a 3- to 4-fold risk of infections, sepsis, cardiac and bleeding complications. Therefore, the patients themselves, along with the general practitioner and an in-hospital interdisciplinary team should cooperate in medical and operative treatment in order to attain better clinical outcome. Each patient history should include a detailed assessment of the quantity of daily alcohol intake. Alcoholic diagnostic regimens including questionnaires (i.e. CAGE, AUDIT) in combination with specific laboratory markers (CDT, GGT, MCV), if implemented, could prove valuable, especially in cases where major surgical procedures are considered. Strict abstinence by alcoholic patients with organ pathology in medical and elective surgical settings as well as the prophylactic treatment of pre-operative alcohol withdrawal appear to be useful strategies to reduce the risk of complications. Short-term interventions are associated with reduced alcohol intake and decreased incidence of re-trauma. Considering the clinical relevance of alcohol abuse, sufficient screening, interventions, and open approaches to address alcohol problems should be important components of the daily clinical routine in outpatient clinics, emergency rooms, in GPs' offices and in general hospitals.

Extensive fibrosis combined with the development of pseudocysts, calcifications and concomittant loss of acinar cells are the characteristic features in the pathogenesis of chronic pancreatitis. In some patients an inflammatory mass is generated which is most frequently located in the pancreatic head. The inflammatory pancreatic head tumor has been postulated to be the pace maker of the course of the disease. Over expression of growth factors (GF) has been discussed to be the molecular basis of focal development of fibrosis. Aim of this study was to correlate the expression of GF-m-RNA (acidic und basic fibroblast growth factor: a/b FGF; plateled derived growth factor: PDGF-A/B) in pancreatic specimens from patients with chronic pancreatitis taken from different parts of the pancreatic gland to the generation of an inflammatory mass in the pancreatic head. Using quantitative PCR, northern blotting and in-situ-hybridisation m-RNA expression of a/b FGF and PDGF-A/B was nearly identical in the pancreatic head, corpus and tail. Furthermore the expression of these GF did not correlate to the development of an inflammatory mass in the pancreatic head. From the results of this study a causal relation between expression of these GF and the development of an inflammatory mass in the pancreatic head could not be confirmed.

Selection of the optimal treatment strategy in severe acute pancreatitis (SAP) is a serious clinical challenge largely due to difficult differential diagnosis of patients with early SAP. The aim of this study is a retrospective evaluation of the first experiences in the treatment of patients with SAP and early SAP according to a new complex clinical protocol (CCP).A total of 210 patients complied with Atlanta recommendations for SAP and were included in the retrospective study. Patients were stratified into two groups according to the diagnostic and treatment strategy. Non-protocol (NP) group comprised 154 patients who had received their treatment based on previous clinical routine and subjective decision of physicians in charge. 56 patients who were managed according to the new CCP developed for SAP comprised the CCP group. CCP included:- Early assessment of the severity of acute pancreatitis (APACHE II score, presence of SIRS and/or organ dysfunction); - Immediate ICU monitoring including routine measurement of the intraabdominal pressure; - Conservative treatment including early enteral nutrition, colloids, antibacterial prophylaxis and early continuous venovenous hemofiltration (CVVHF) when indicated; - Surgical treatment when conservative treatment was not effective (progression of the organ dysfunction) or presence of infection was evident. Hospital, ICU stays and outcomes were analysed. Statistical comparison was done by Mann-Whitney U-test and Chi-square test.The age structure and severity of the disease were similar in both groups with mean of 51.3 (15.6) vs. 46.8 (15.2) years and 9.7 (5.1) vs. 9.8 (4.4) APACHE II points in groups NP and CCP, respectively. Male/female ratio was 2 : 1, and alcohol was the main etiologic factor in about 55 % of cases in both groups. Early SAP was diagnosed in 33 % to 46 % of patients according to the results of the SOFA scoring. The results of the conservative therapy considerably improved after implementation of the CCP treatment. Surgical intervention was done in 46-52 % of patients. MODS was the main cause of death in both groups. Remarkable decrease in early mortality (within the first week from admission) was a real advantage of CCP treatment comprising 1.8 % vs. 22.1 % in NP patients, p0.01. Mortality from early SAP was reduced by CCP treatment to 3.8 % compared to 33 % in NP group, p0.01. There was a considerable reduction in postoperative mortality with CCP treatment comprising 10.3 % vs. 32.7 % in patients who did not receive CCP treatment, p0.05. Overall mortality associated with CCP treatment ranged to 5 %, compared to 34 % mortality in the NP treatment group, p0.01. Due to the considerable number of early deaths among NP patients, there was statistically longer ICU and hospital stay in CP group with mean of 14.1 (14.1) vs. 9.6 (15.2) days and 37.9 (26.7) vs. 23.4 (21.8) days, compared to NP group, p0.01.Timely recognition and complex therapy of SAP including ICU monitoring, colloids, antibacterial prophylaxis, early enteral nutrition, and CVVHF is the most effective way how to manage this category of patients. Implementation of a specialised treatment protocol considerably improves outcome and reduces the number of deaths associated with surgery and early SAP.

GENETIC RISK FACTORS: Recently, several genetic risk factors for chronic pancreatic diseases were found. In patients with chronic pancreatitis several mutations of the cationic trypsinogen were identified. In the majority of these subjects an autosomal dominant disease was observed. Mutations in the pancreatic secretory trypsin inhibitor (SPINK 1) were found in 20% of subjects with idiopathic, in 5% of those with alcoholic chronic and in 50% of those with tropical pancreatitis. Further variants were identified in CFTR (Cystic Fibrosis Transmembrane Conductance Regulator), a chlorid transporter initially identified a disease-causing molecule in cystic fibrosis. In approximately 20-25% of the patients with chronic pancreatitis a mutation of one of these genes can be found.A genetic investigation is useful when there is evidence for a family history of chronic pancreatitis and, at absence of typical risk factors, in patients with onset of disease earlier than 35-40 years of age.In addition to alcohol abstinence the patients should be advised not to smoke. National and international registers as well as self-aid groups exist.

Pancreaticojejunal anastomosis. Indication, technique and results. Pancreaticojejunal anastomoses are performed for the treatment of chronic pancreatitis and after resection of pancreatic carcinomas. In chronic pancreatitis by drainage procedures (Partington-Rochelle and Puestow-Gillesby) one can expect good long term results, if the diameter of the pancreatic duct is at least 1 cm and the length of the anastomosis 6 cm. The duodenumpreserving head resection (Beger or Frey) is a combination of resection and drainage and is significant in the therapy of inflammatory head processes. In the surgical treatment of pancreatic carcinomas pancreaticojejunostomies are applied after head resection (Whipple-, pyloruspreserving modification). The end-to-side mucosa-mucosa anastomosis offers the best results concerning postoperativ complications and mortality rates.

A 69-year-old woman complained of recurrent cramp-like symptoms in the upper abdomen. She admitted excessive alcohol intake. Physical examination revealed swelling and inflammation of both ankles. All other findings were unremarkable.Sonography and computed tomography scan showed a cystic structure (5 cm) in the head of the pancreas. Biochemical testing revealed an anemia (Hb 7,5 mg/dl) and an elevated serum lipase (4494 U/l). Intestinal hemorrhage could not be confirmed by endoscopy. An involvement of parapancreatic structures with the pseudocyst could not be demonstrated by combination of endoscopic retrograde cholangiopancreatography (ERCP) and computed tomography (CT).The patient died unexpectedly. Autopsy showed a rupture of the pancreatic pseudocyst into the portal vein leading to portal vein thrombosis. The cause of death was an embolism of the pulmonary arteries. Postmortal reevaluation of CT and ERCP clarified diagnostic features.Erosion of peripancreatic vessels is one of the life threatening complications in chronic pancreatitis. The complication is uncommon but should be included into differential diagnosis of recurrent intestinal bleeding.

Incarceration of a pancreatic stone fragment in the distal pancreatic duct after ESWL-therapy.A partial or total absence of stones in pancreaticolithiasis therapy can be reached by using ESWL. We report on a patient who happened to get an incarceration of a fragment in the distal pancreatic duct after having been treated by ESWL without a previous sphincterotomy to the ductus Wirsungianus. This emphasizes the recommendation to carry out a papillotomy of the pancreatic main duct before applying ESWL to pancreatic stones.

It is difficult to provide valid data with regard to changes in incidence and prevalence of acute pancreatitis in Germany. The lack of information is due to strict legal regulations to protect personal data, a certain lack of interest in epidemiological research and the lack of exact statistics of diseases treated in hospitals. The incidence of acute pancreatitis in other industrialized Western countries is about 10 new cases per year and 100,000 inhabitants. The increase of alcohol consumption over the last 30 years is associated with an increase of ethanol-induced pancreatitis. One may speculate that due to improved diagnostic possibilities, such as CT scan, cases where acute pancreatitis is diagnosed at autopsy are rare. Due to the increase in alcohol consumption it can be assume that the incidence and prevalence of chronic pancreatitis have increased in Germany similar to well-documented data from Denmark. Since alcohol consumption is slightly decreasing in Germany it is likely that the present incidence of about 10 cases of chronic pancreatitis per 100,000 inhabitants will also decrease.

The standard treatment of acute pancreatitis is primarily supportive, including a well standardized conservative therapy and additionally specific interventions in complicated disease. The role of early endoscopic retrograde cholangiopancreatography in acute pancreatitis has been discussed for about 20 years. The etiology of pancreatitis plays an important role in making the decision for early interventional treatment. The results of clinical trials about early interventional treatment of acute biliary pancreatitis demonstrate that the outcome of patients without signs of biliary stone impaction or acute cholangitis is burdened by more severe complications than in patients treated conservatively. Urgent endoscopic retrograde cholangiopancreatography, endoscopic sphincterotomy and stone extraction within 72 hours of admission reduces the frequency of major complications only in patients with acute biliary pancreatitis with obstructive jaundice or biliary sepsis.

Differential diagnosis of cystic lesions in the abdomen may be very difficult. We present the clinical manifestation and the diagnostic steps of a rare case of an aneurysm of the gastroduodenal artery mimicking a cystic lesion. We also discuss the imaging methods we used to verify the diagnosis such as colour Doppler sonography and 3D-sonography.A 42-year old woman with chronic pancreatitis was admitted to our hospital after an extended diagnostic program (sonography, computed tomography and laparoscopy) with the diagnosis of a pancreatic pseudocyst with vascular erosion. Using conventional sonography we found a cystic lesion of 5 x 5 cm diameter with parietal deposits between pancreas and coeliac trunk. After colour Doppler sonography we found an arterial jet in the cystic tumor; initially the source of the jet seemed to be the hepatic artery. We referred the patient to our department of radiology with the diagnosis of hepatic artery aneurysm. The aneurysm was confirmed by the angiography and was embolised with coils in the same session. However, the source of the aneurysm was not the hepatic, but the gastroduodenal artery. By postangiographical 3D-sonography we could clearly reconstruct the relation of the aneurysm to the gastroduodenal artery.Colour Doppler sonography should be the first imaging tool for clarifying cystic lesions in the abdomen. 3D-sonography is a reliable and useful method to identify visceral vessels of the abdomen. Nowadays the "gold standard" angiography should preferably be used as a therapeutic procedure.

Thoracic manifestations of internal pancreatic fistulas caused by chronic pancreatitis are rare conditions. The three main types of these manifestations are mediastinal pseudocysts, pancreatico pleural fistulas and pancreaticobronchial fistulas. We report on one patient with the clinical presentation of all three thoracic internal pancreatic fistulas with a communication to a pseudoaneurysm of the splenic artery caused by chronic alcohol-related pancreatitis. Conservative therapy over four weeks was not successful. Resection of the pseudoaneurysm, debridement of the mediastinal pseudocyst and duodenum preserving resection of the pancreas treated all complications and prevents recurrence in this patient with chronic pancreatitis.

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.

Interventional (non-surgical) therapy is a relative new approach in the management of chronic pancreatitis. Indications for endoscopic therapy are pseudocysts and strictures or stones of the main pancreatic duct. Endoscopic sphincterotomy, extraction of pancreatic duct stones, extracorporal shock-wave lithotripsy (ESWL), pancreatic duct stenting and drainage of pseudocysts are all methods with a high success rate but with a low complication rate. Therefore in patients with chronic pancreatitis and with a failure of conservative management interventional techniques have to be considered. They may be an alternative to surgical procedures.

Despite numerous experimental and clinical investigations there is no consensus on the evolution of chronic pancreatitis (CP). In the 1970s and 1980s, Sarles persistently emphasised the de novo evolution of CP due to pancreatolithiasis. In recent years, however, clinical and morphological studies have provided strong evidence for the initial proposal of acute pancreatitis progressing to chronic pancreatitis. The so-called necrosis-fibrosis-sequence theory is supported by immunohistochemical work suggesting that inflammatory mediators primarily contribute to tissue destruction and that infiltration of pancreatic nerves by immune cells is a pathogenetic factor for the generation of pain in CP. While Sarles postulates that acinar hypersecretion and an imbalance of pancreatic stone promoting and inhibiting factors trigger the evaluation of CP, the necrosis-fibrosis-sequence theory also involves other pathomechanisms (e.g. changes in ductal permeability, ischemia, oxidative stress) which have been shown to cause (acute) pancreatic injury. Despite this unifying template, which also lessens the need to identify independent mechanisms for the pathogenesis of acute and chronic alcoholic pancreatitis, there are still open questions, e.g. on genetic factors that (like in hereditary CP) may explain the different susceptibility of the pancreas to injury and the individual immunological response.

Pancreatitic pseudocysts of the spleen are rare events. We report two cases of conservative management of splenic involvement in pancreatitis by ultrasound-guided aspiration. The first patient was admitted with clinical and biochemical signs of acute exacerbation of chronic pancreatitis. The ultrasound examination showed a subcapsular anechoic zone in the spleen as well as pancreatic pseudocysts. The laboratory examination of the fluid obtained by ultrasound-guided aspiration confirmed the presence of an intrasplenic pancreatitic pseudocyst which disappeared completely after a second percutaneous aspiration. The second patient was admitted with acute exacerbation of chronic pancreatitis and septic symptoms caused by an abscess near the left lobe of the liver. After successful surgical drainage of the abscess the patient developed an expanding anechoic subcapsular fluid zone in the spleen. Quantitative decompression by ultrasound guided fine needle-aspiration confirmed the pancreatitic origin of the lesion which vanished within a few days without further treatment. We conclude that fine-needle aspiration of splenic pseudocysts under ultrasound control permits a differential diagnostic distinction from splenic abscess or hematoma and accelerates healing. There is thus a nonsurgical option for treatment of pancreatitic intrasplenic pseudocysts, provided that the patient is under close clinical observation.

The etiology of acute pancreatitis is based on several causes, among which idiopathic nature (30%) is second to biliary stone disease (60-70%). It is still under debate whether alcohol as the main cause of chronic pancreatitic disease can cause acute pancreatitis. Based on Opie's "obstruction theory" of 1901 and experimental data, it is now widely accepted that the gallstone passage into or through the terminal biliopancreatic ductal system triggers acute (necrotizing) pancreatitis by causing pancreatic ductal obstruction. However, the sequential intracellular mechanisms in the pathogenesis of acute pancreatitis remain unclear. A co-localization hypothesis has been proposed to explain the premature intracellular activation of trypsinogen to trypsin: due to a yet unknown defect in the intracellular protein transport and sorting system within the acinar cell, lysosomal hydrolases (i.e. cathepsin B) and secretory proteins (i.e. trypsinogen) co-localize in a fragile postgolgi vacuole where activation can occur. In addition, alterations of exo- and endocytosis at the apical pole exist (i.e. secretion block). The pathophysiological events are characterized by local and systemic hypovolemia and (micro)circulatory failure aggravating necrosis, followed by ARDS, renal failure and several other severe complications (i.e. sepsis and DIC). The systemic overflow of proteolytic enzymes (i.e. PLA-2) and kinins plays a major role as mediating factor in severe cases, resulting in multiorgan failure.

Alcohol abuse and gallstones are the most important factors in the pathogenesis of acute pancreatitis. Other factors are less frequent, and in some patients one is unable to identify any risk factor. Even in the most frequent forms of alcoholic or biliary pancreatitis little is known about the cellular and molecular mechanisms which lead to severe pancreatitis. New experimental studies have shown that many biochemical and morphological events are similar in different experimental models of pancreatitis as well as in human disease. These changes include intracellular premature activation of trypsin, blockade of luminal enzyme secretion and appearance of intracellular vacuoles. Although activated trypsin triggers the activation of other proteases, it is not trypsin but other proteases (e.g. elastase, chymotrypsin and phospholipase) which damage the pancreatic acinar cell. These pathogenetic findings may lead to the development of inhibitors which more effectively inhibit the latter cell-toxic proteases and may thereby help to improve the therapy.

Based on own studies and on results of other centers the multiorgan failure (MOF) resp. the systemic inflammatory response syndrome (SIRS) in acute necrotizing pancreatitis seems to be no longer an compelling reason for surgery in the absence of proven infection of pancreatic necrosis. Growing experience of continuous veno-venous hemofiltration (CVVH) facilitates successful conservative treatment of-formerly often lethal-cases of serious necrotizing pancreatitis. If infection of necrosis is documented surgical intervention should be performed. Our present regime of therapy of necrotizing pancreatitis consists in conservative intensive medical treatment, immediately after admission; a pancreas penetrating antibiotic medication starting on admission; early use of continuous veno-venous hemofiltration if MOF or SIRS occurs, surgical intervention, if infection of necrosis is proved. Other indications for surgery are massive bleeding or bowel perforation due to tryptic lesions.

15 to 30% of the patients with chronic pancreatitis develop an inflammatory mass in the pancreatic head. The leading symptoms of these patients are severe upper abdominal pain and complications of the surrounding organs. From 1969 to 1995, 380 patients were treated with a duodenumpreserving pancreatic head resection. The cause of the disease was alcohol abuse in 81%. 93% of the patients suffered from severe pain with recurrent pain attacks. CT-scan revealed enlargement of the pancreatic head (4 cm in diameter) in 79% of the patients. 83% of the patients had an impaired exocrine pancreatic function; 48% of the patients had an impaired glucose tolerance or were diabetic. The hospital mortality was 0.8%; 5% of all patients had to be reoperated. The mean duration of the hospitalization was 13.9 days. 89% of the patients showed an unchanged endocrine function in the early postoperative course. The glucose metabolism was improved in 9%, 2% had a deteriorated function. The duodenum-preserving pancreatic head resection is a procedure with a low postoperative mortality and morbidity without deterioration of the endocrine pancreatic function.

Two patients were admitted to hospital for diagnosis of recurrent upper gastrointestinal bleeding. Both had chronic pancreatitis with alcohol abuse. Their general condition was satisfactory. Physical examination showed no diagnostic abnormalities other than mild epigastric pain on pressure in one patient.In case 1 angiography revealed pseudoaneurysm of the splenic artery as a complication of chronic pancreatitis to be the cause of the bleeding. In case 2 sonography demonstrated multiple pancreatic pseudocysts after recurrent pancreatitis. Duplex sonography revealed one of the cyst to be a partly thrombosed pseudoaneurysm of the splenic artery and the source of the bleeding.In both cases a fistula between splenic artery and pancreatic duct having been shown to be the source of the bleeding, transcatheter embolisation of the splenic artery with platinum coils was successfully undertaken. Both patients remained symptom-free 4 and 10 months later.Although haemosuccus pancreaticus is a rare cause of upper gastrointestinal bleeding, given certain features in the patient's history and the clinical findings, it should be included in the differential diagnosis.