Endoscopic diagnostics and therapy of pancreatobiliary diseases in persons after gastric resection according to Billroth I.

The stomach resection according to Billroth I (B I) is very rarely done. The aim of this retrospective study is to evaluate our experience with diagnostic and therapeutic endoscopic retrograde cholangiopancreatography (ERCP) in patients after stomach resection according to Billroth I. In patients with a condition after stomach resection according to B I, a study of the group of 20 years (November 1994 - December 2014) took place. Three patients were evaluated retrospectively after B I stomach resection with biliary obstruction. For the ERCP was used the Olympus therapeutic videotheroscop in all cases with the standard (as in normal anatomical situation). Cannulation success in diagnostic ERCP was achieved in 3 out of 3 patients - 100% success rate of ERC diagnosis. For all these 3 patients CDL was found in the ERCP. In addition, endoscopic treatment was performed immediately after ERCP diagnosis in all 3 patients with a CDL pathologic ERCP diagnosis, the initial endoscopic papillotomy (EPT) performed in the standard procedure (as in normal anatomy). Subsequently, endoscopic extraction of all CDL from hepatocholedocus to duodenum was performed. Overall the ERCP was completely successful in all 3 of the 3 (100% of 3) patients who initially started endoscopic therapy. There were no complications in our group of 3 patients. For ERCP in patients with BI stomach resection, we had 100% success rate of diagnostic and therapeutic ERCP in all of these patients (3 CDL patients).

[Relapsing autoimmune pancreatitis type 1: case report]. / Relabující autoimunitní pankreatitida 1. typu: kazuistika.

Autoimmune pancreatitis (AIP) is a rare form of chronic pancreatitis, classified into 2 subtypes - AIP type 1 and AIP type 2. We present a case of a 31-years-old female admitted to our institution with upper abdominal pain and obstructive jaundice. Endoscopic retrograde cholangiopancreatoscopy (ERCP) revealed stenosis of intrapancreatic distal bile duct. Diffuse parenchymal enlargement and typical features of AIP were shown by computed tomography (CT) and endoscopic ultrasonography (EUS). The patient´s serum IgG4 was elevated at 3.8 g/l (range 0.08-1.4 g/l). She was diagnosed with AIP type 1 and treated with prednisone (initial dose of 30 mg per day, then tapered by 5 mg/day every week). The maintenance dose of 5 mg per day was continued for 6 months. Despite clinical and radiological remission, serum levels of IgG4 remained elevated. The patient experienced disease relapse 25 months after first attack. Moreover, new finding of calcifications occured in pancreas. The relapse was managed with corticosteroids and maintenance immunosupression with azathioprin was started. Literature review on risk factor of relapse, long-term immunosupressive therapy indication and optimal follow-up of AIP type 1 patients are discussed.Key words: autoimmune pancreatitis type 1 - long-term follow-up - relapse - therapy.

[The role of metabolic syndrome in gastroenterology]. / Role metabolického syndromu v gastroenterologii.

GOAL: Metabolic syndrome and its components play an important part in the development of not only cardiovascular conditions, but also digestive and pancreaticobiliary system diseases. The aim of our study is to present a comprehensive overview of the diseases where metabolic syndrome is an inducing risk factor, or where it affects the course of the disease. RESULTS: Metabolic syndrome is a significant risk factor of induction of gastroesophageal reflux and its complication, which is Barretts esophagus. Metabolic syndrome was described as the disease closely linked to idiopathic intestinal inflammations, diseases of the biliary tree and pancreas. Acute pancreatitis, both its development in obese individuals and the burden of its course, are in close correlation with metabolic syndrome, similarly as the course of chronic, mainly alcoholic pancreatitis. Study of non-alcoholic steatopancreatitis presents a challenge, most importantly with regard to the function of pancreatic B cells in obese individuals. Non-alcoholic hepatic steatosis and its forms may as much as lead to the stage of cirrhosis of the liver and they pose a risk of hepatocellular carcinoma. Metabolic syndrome was also described in a population study as a risk factor for carcinoma of the colon. SUMMARY: Metabolic syndrome and its components present an important risk factor in relation to inducing some benign as well as malignant gastrointestinal and pancreaticobiliary diseases. A systemic approach to influencing the metabolic syndrome and its components is therefore one of the important approaches to influencing the development and course of not only cardiovascular conditions.

[Autoimmune pancreatitis - diagnostic consensus]. / Autoimunitní pankreatitida - diagnostický konsenzus.

The autoimmune type of pancreatitis represents the specific disease of pancreas, with significant contribution of autoimmune processes in its etiopathogenesis. Currently, there are two proved subtypes of this particular pancreatopathy, which are defined clinically, histomorphologically and serologically. They have many histomorphological signs in common, but differ in the presence of so-called granulocytic epithelial lesions (GEL), which are absent in subtype 1. The subtype 1 is characterized by the presence of gammaglobulines, esp. immunoglobuline G4 and IgG4 positive extrapancreatic lesions. The subtype 2 is typically associated with the inflammatory bowel diseases, esp. ulcerative colitis. But the common characteristic of both subtypes is the fact response to applied steroid treatment. Due to diverse diagnostic criteria in the past, in 2011 the consensus for the diagnosis of autoimmune pancreatitis was announced. It is based on clinical symptoms, biochemical results, the results got by using of imaging methods, histomorphology and positive response to steroid treatment. The matter to be solved is the question of early differential diagnosis between focal autoimmune pancreatitis and adenocarcinoma of pancreatic head. From imaging methods are MRI/CT, MRCP (in Asia ERCP), EUS with targeted biopsy of the gland (under EUS control), are recommended as the methods of choice.

Pancreatic pain.

Pain is a common symptom of many diseases. Recently, the pain has been classified and analyzed exactly. Its particular components/types are described to the maximum of their depths and details. That is why each particular pain present in a specific disease (pancreatopathies included) has to be treated according to the presence of the specific type of pain. In diseases of pancreas, there are nociceptive, neuropathic, and inflammatory components of pain participating, frequently. Especially long-lasting, not well-controlled pain sets off the process of neuromodulation. The recent pioneering applications/administrations of various neuromodulatory therapeutic approaches represent the promising discoveries for the treatment of long-term, severe, drug-resistant pain syndromes, including chronic pancreatitis. In this article, we summarized the characteristics of pain, the therapeutic strategy, and algorithms of analgesic treatment (in general and applied for pancreatopathies), including new therapeutic trends and approaches.

Autoimmune pancreatitis.

INTRODUCTION: Autoimmune pancreatitis (AIP) is the specific type of chronic pancreatitis due to autoimmune background and mechanism. CHARACTERISTICS: The main clinical symptoms of AIP are obstructive jaundice and abdominal discomfort. The typical histological findings are lymphocytes and IgG4 plasma cells infiltration, fibrosis and venulitis within pancreatic gland. Plasma level of IgG4 is usually extremely high. DIAGNOSIS: High level IgG4 positive plasma cells in serum, lymphoplasmatic infiltration found on histological staining of pancreatic tissue, "sausage-like" pancreas in ultrasound and CT scans, and response to steroid therapy are crucial for making of diagnosis. Classification of AIP: AIP can be classified into two subtypes. Type 1 was recognized as the pancreatic manifestation of multiorgan disorder, called IgG4 related disease. Type 2 is a pancreas-specific disorder not associated with IgG4, with similar histological signs as type 1, but also with the positivity of GEL (granulocythic epithelial lesion). THERAPY: Due to its high effectivity in AIP treatment, steroid therapy is the first-line option. The alternative therapy is using immunosuppressants (azathioprine). Recently, there are also first experience in biological therapy already published. CONCLUSION: Before the start of AIP therapy - the differential diagnosis between pancreatic cancer and AIP is essential.

Could rising BUN predict the future development of infected pancreatic necrosis?

BACKGROUND: Infected (peri)pancreatic necrosis (IPN) in acute pancreatitis (AP) is associated with organ failure (OF) and high mortality. There are no established early markers of primary IPN. This study aimed to assess the association of simple parameters with primary IPN in AP. METHODS: We retrospectively studied 281 patients with AP admitted to Mayo Clinic hospitals and identified those with microbiologically confirmed infections in (peri)pancreatic necrosis and collections. We defined primary IPN as infection of (peri)pancreatic necrotic tissue that developed before interventions. We recorded admission hematocrit, BMI, BUN, serum creatinine, SIRS score and development of persistent organ failure within 48 h of admission; and performed serial SIRS and BUN calculations for at least 48 h. We used univariate and multivariable analysis to assess associations and expressed results as odds ratio (OR)[95% CI]. RESULTS: 27 (9.6%) patients developed IPN, of which 21 (77.7%) had primary IPN. 38.1% had Gram positive, 9.5% Gram negative and 52.3% mixed bacterial infections. Five (23.8%) of the patients with IPN had fungal infection. On univariate analysis, SIRS ≥ 2 at admission, rise in BUN by 5 mg/dL within 48 h of admission, persistence of SIRS for 48 h and development of persistent OF within 48 h of disease had significant association with development of primary IPN with OR (95% CI) of 4.12 (1.53-11.15), 10.25 (3.95-26.61), 1.19 (1.69-10.39) and 7.62 (2.58-21.25) [2-tailed p = 0.004, <0.0001, 0.002 and <0.0001] respectively. On multivariable analysis, only rise in BUN by 5 mg/dL within 48 h of admission was associated with primary IPN (p = 0.007). CONCLUSIONS: Rising BUN within 48 h of admission can be used to predict development of primary IPN in AP.

Incidence of pancreatic carcinoma in patients with chronic pancreatitis.

BACKGROUND/AIMS: Pancreatic carcinoma belongs to the area of conditions with late diagnosis and there is no effective screening method. One possible approach to diagnosing so called early adenocarcinoma, therefore, lies in the identification and systematic examination of individuals in risk for this condition. METHODOLOGY: Between 1992 and 2005 we systematically observed 223 individuals diagnosed with chronic pancreatitis. In this 14-year period we performed classical biochemical tests, endoscopic ultrasound, CT scans and ERCP, we asked about the number of cigarettes smoked per year and classified individuals consuming regularly more than 80 g of alcohol per day for 5 years for men and 50 g of alcohol per day for 5 years for women as having the alcoholic form of chronic pancreatitis. The remaining patients were classified according to TIGARO classification. RESULTS: Alcohol-related etiology was detected in 73.1% of patients, 21.5% had the chronic obstructive form and only 5.4% were classified as idiopathic pancreatitis. Pancreatic carcinoma was detected in 13 patients with chronic pancreatitis (5.8%), three patients were diagnosed with gastric carcinoma and one with esophageal carcinoma. Pancreatic malignancy developed mainly in patients with the alcoholic form of pancreatitis (4.5%). In the 14 year period 11 subjects died, out of which eight cases were related to pancreatic carcinoma. CONCLUSION: Pancreatic and extra-pancreatic cancer localized in the gastrointestinal tract are among the serious complications of chronic nonhereditary pancreatitis. Systematic observation of patients with chronic pancreatitis must be performed with the aim of early diagnosis of pancreatic, but not only pancreatic malignancies.

Inhibitory effects of interferon-gamma on activation of rat pancreatic stellate cells are mediated by STAT1 and involve down-regulation of CTGF expression.

Pancreatic stellate cells (PSCs) are the main source of extracellular matrix proteins in pancreatic fibrosis, a pathological feature of chronic pancreatitis and pancreatic cancer. Interferon-gamma (IFN-gamma) is an antifibrotic cytokine, but how precisely it exerts its effects on PSCs is largely unknown. Here, we have focussed on the role of STAT1 as well as target genes of IFN-gamma signalling. Our data indicate that IFN-gamma regulates the expression of two autocrine mediators of PSC activation, connective tissue growth factor and endothelin-1, in a transforming growth factor-beta1-antagonistic manner. STAT1 overexpression under the control of a tetracycline-dependent promoter revealed a close correlation between STAT1 expression and activation, the biological effects of IFN-gamma (growth inhibition, induction of apoptosis), and target gene expression. Our data further support the hypothesis that IFN-gamma interferes with stellate cell activation in the pancreas and suggest activated STAT1 as an inductor of a quiescent PSC phenotype.