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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.

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.

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., (Copyright © 2013 IAP and EPC. Published by Elsevier B.V. All rights reserved.)

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.