scholarly journals Etiological significance of the hepatitis C virus among other infectious factors of chronic pancreatitis

2019 ◽  
Vol 42 (1) ◽  
pp. 41-45
Author(s):  
O.R. Shayhen ◽  
L.S. Babinets

The article presents a review of modern literature data on the role of various etiological factors in the development of chronic recurrent pancreatitis. Much attention is paid to infectious agents (viruses of epidemic parotiditis, hepatitis B and C, enteroviruses, adenoviruses, mycoplasmas, salmonellae) in the formation of the inflammatory process in the pancreatic tissue. The features of the pathogenesis of chronic pancreatitis associated with viral infection B and C are considered; it has been shown that the lesion of the pancreas is caused by the replication of viruses directly in the cells of this organ, immunopathological changes in the liver, and concomitant immunological disorders. The probability of developing diabetes mellitus, as one of the clinical manifestations of viral replication in pancreatic endocrine cells, is underlined. The clinical manifestations of exocrine and endocrine insufficiency of the pancreas during infection with various viruses, including Coxsackie B and enteroviruses, are described in detail; the features of the course of diabetes caused by infection of these pathogens are listed. The peculiarities of chronic pancreatitis in HIV-infected and AIDS patients, in patients with parasitic pathology (opisthorchiasis, clonorchosis, ascariasis, giardiasis) are considered; the role of helicobacteria in the development of a chronic inflammatory process in pancreatic tissue is characterized. It has been suggested that a given organ may be simultaneously affected by several infectious factors; the importance of identifying pathogens of infectious diseases for the timely formulation of the correct diagnosis and the selection of adequate therapy is emphasized.

2021 ◽  
Author(s):  
Meritxell Rovira ◽  
Goutham Atla ◽  
Miguel Angel Maestro ◽  
Vane Grau ◽  
Javier García-Hurtado ◽  
...  

SUMMARYUnderstanding genomic regulatory mechanisms of pancreas differentiation is relevant to the pathophysiology of diabetes mellitus, and to the development of replacement therapies. Numerous transcription factors promote β cell differentiation, although less is known about negative regulators. Earlier epigenomic studies suggested that the transcriptional repressor REST could be a suppressor of endocrine gene programs in the embryonic pancreas. However, pancreaticRestknock-out mice failed to show increased numbers of endocrine cells, suggesting that REST is not a major regulator of endocrine differentiation. Using a different conditional allele that enables profound REST inactivation, we now observe a marked increase in the formation of pancreatic endocrine cells. REST inhibition also promoted endocrinogenesis in zebrafish and mouse early postnatal ducts, and induced β-cell specific genes in human adult duct-derived organoids. Finally, we define REST genomic programs that suppress pancreatic endocrine differentiation. These results establish a crucial role of REST as a negative regulator of pancreatic endocrine differentiation.


2017 ◽  
Vol 8 (5) ◽  
pp. 96-102
Author(s):  
Mikhail P. Korolev ◽  
Leonid E. Fedotov ◽  
Ruben G. Avanesyan ◽  
Elena A. Mikhailova ◽  
Georgiy M. Lepekhin ◽  
...  

Chronic pancreatitis with pancreatic hypertension is extremely rare in childhood. Chronic pancreatitis in this age is usually always associated with a сongenital defect of the pancreatic duct system. The article describes the case of long-term clinical observation and minimally invasive treatment of chronic calculous pancreatitis, first diagnosed in a girl at the age of 16 years. Despite the fact that clinical manifestations were observed from the age of 3 years, the correct diagnosis could be made only at the age of 16, by joint application of ultrasound, Magnetic Resonance Imaging (MRI) and Magnetic Resonance Cholangiopancreatography (MRCP). The cause of chronic pancreatitis were concrements and strictures of the main and additional pancreatic ducts that caused pancreatic hypertension. Attempt of endoscopic retrograde lithoextraction from the pancreatic ducts was impossible because of the presence of severe stricture. Therefore, it was decided to apply a combined approach using percutaneous access under ultrasound navigation. The patient underwent series of minimally invasive combined procedures including the lithoextraction, balloon dilatation and transcutaneous drainage of the pancreatic ducts with the endoscopic and percutaneous access with ultrasound and radiologic control. For the prevention of restenosis, the antegrade stenting of the main pancreatic duct with self-expanding coated nitinol stent was used with further removal of the stent. Due to the treatment, there was no pancreatitis within 5 years after stent removal.


2009 ◽  
Vol 126 ◽  
pp. S307
Author(s):  
Mathieu Gouzi ◽  
Kerstin Johansson ◽  
Nancy Thompson ◽  
Josselin Soyer ◽  
Gérard Gradwohl ◽  
...  

Author(s):  
B. O. Kulevich ◽  
A. Yu. Razumovsky ◽  
V. V. Kholostova ◽  
Z. B. Mitupov ◽  
A. I. Khavkin ◽  
...  

Chronic pancreatitis is one of the most pressing problems of pediatric gastroenterology and surgery of hepatopancreatobiliary organs. Diagnosis and treatment of this category of patients requires a comprehensive examination using modern highly sensitive research methods and the collegial participation of a surgeon, gastroenterologist and endocrinologist. Due to the fact that the algorithm for managing these patients is not regulated, patients often receive enzyme replacement therapy for a long time, with indications for surgical treatment. In addition, the non-specificity of complaints and clinical manifestations of chronic pancreatitis, the asymptomatic course and the initial detection of exo- and endocrine insufficiency lead to a later choice of the optimal treatment method and increase the risk of complications. The key to effective care for children with chronic pancreatitis is the staging and continuity in research and treatment. At the Center for the Treatment of Developmental Anomalies and Diseases of the Hepatopancreatobiliary System in Children on the basis of the Filatov Hospital, highly effective interventions are carried out for chronic pancreatitis in children, the purpose of which is to ensure an adequate outflow of pancreatic juice using longitudinal pancreaticojejunostomy, which, in addition to draining the pancreas, allows to achieve clinical remission and stop the progression pathological process, including diabetes mellitus. The article reflects the experience of diagnosis and treatment of chronic pancreatitis in children.


2017 ◽  
Vol 37 (3) ◽  
pp. 30-35
Author(s):  
T. N. Hristich

Aim of this paper is to consider the role of hormones of the adipose tissue in mechanisms of obesity, metabolic syndrome, type 2 diabetes mellitus upon chronic pancreatitis. Materials and methods. The literature review indicates the value of visceral fat in the development of insulin resistance, dyslipidemia, including atherogenic one, taking into account the possible infiltration of pancreatic tissue by adipocytes. Participation of some adipocytokines of adipose tissue in the development of obesity upon chronic pancreatitis is highlighted. It is shown that in some cases the hormones of visceral adipose tissue, penetrating through the portal vein to the liver and then to the pancreas, aggravated the course of systemic chronic inflammation of the inherent chronic pancreatitis, promote steatosis and development of fatty pancreatic disease. Conclusion. Literary sources indicate the leading role of visceral adipose tissue and its hormones in the formation of obesity in chronic pancreatitis. Due to the infiltration of the pancreatic tissue by adipocytes, lipoidosis and steatosis develop. With the progression of the process type 2 diabetes mellitus, fatty liver or pancreatic disease, or cancer of these orhans. Consequently, there is a need for serious differentiated preventive and curative measures aimed at promoting a healthy lifestyle to improve the quality of life of patients suffering from chronic pancreatitis.


2018 ◽  
Vol 39 (1) ◽  
pp. 4-9
Author(s):  
T. N. Hristich

Aim is to consider the role of hormones in the adipose tissue of obesity mechanisms of metabolic syndrome, type 2 diabetes mellitus in chronic pancreatitis. Materials and methods. Literature review indicates the value of visceral fat in the development of insulin resistance, dyslipidemia, including atherogenic one, taking into account the possible infiltration of pancreatic tissue by adipocytes. Participation of some adipocytokines of adipose tissue in the development of obesity in chronic pancreatitis is highlighted. It is shown that in some cases the hormones of visceral adipose tissue, penetrating through the portal vein to the liver and then to the pancreas, aggravated the course of systemic chronic inflammation typical for the inherent chronic pancreatitis, formed steatosis and promoted development of fatty disease of the pancreas. Conclusion. Literary sources show the leading role of visceral adipose tissue and its hormones in the formation of obesity in chronic pancreatitis. Lipoidosis or steatosis develop due to the infiltration of the liver and pancreatic tissue by adipocytes. Upon the progression of the type 2 diabetes, fatty liver or pancreatic disease, or cancer of these organs may develop. Consequently, there is a strong need for a serious differentiated preventive and curative measures aimed at promoting a healthy lifestyle to improve the quality of life of patients suffering from chronic pancreatitis.


2020 ◽  
Vol 11 (10) ◽  
Author(s):  
L. Xia ◽  
Z. Xu ◽  
X. Zhou ◽  
F. Bergmann ◽  
N. Grabe ◽  
...  

Abstract Chronic pancreatitis (CP) is associated with elevated plasma levels of bacterial lipopolysaccharide (LPS) and we have demonstrated reduced acinar cell autophagy in human CP tissue. Therefore, we investigated the role of autophagy in experimental endotoxin-induced pancreatic injury and aimed to identify LPS in human CP tissue. Pancreatic Atg7-deficient mice were injected with a single sub-lethal dose of LPS. Expression of autophagy, apoptosis, necroptosis, and inflammatory markers was determined 3 and 24 h later utilizing immunoblotting and immunofluorescence. The presence of LPS in pancreatic tissue from mice and from patients and healthy controls was determined using immunohistochemistry, immunoblots, and chromogenic assay. Mice lacking pancreatic autophagy exhibited local signs of inflammation and were particularly sensitive to the toxic effect of LPS injection as compared to control mice. In response to LPS, Atg7Δpan mice exhibited enhanced vacuolization of pancreatic acinar cells, increase in TLR4 expression coupled to enhanced expression of NF-κΒ, JNK, and pro-inflammatory cytokines by acinar cells and enhanced infiltration by myeloid cells (but not Atg7F/F controls). Cell death was enhanced in Atg7Δpan pancreata, but only necroptosis and trypsin activation was further amplified following LPS injection along with elevated pancreatic LPS. The presence of LPS was identified in the pancreata from all 14 CP patients examined but was absent in the pancreata from all 10 normal controls. Altogether, these results support a potential role for metabolic endotoxemia in the pathogenesis of CP. Moreover, the evidence also supports the notion that autophagy plays a major cytoprotective and anti-inflammatory role in the pancreas, and blunting metabolic endotoxemia-induced CP.


2018 ◽  
Vol 314 (2) ◽  
pp. G211-G222 ◽  
Author(s):  
Murli Manohar ◽  
Alok K. Verma ◽  
Sathisha Upparahalli Venkateshaiah ◽  
Anil Mishra

Eosinophilic pancreatitis (EP) is reported in humans; however, the etiology and role of eosinophils in EP pathogenesis are poorly understood and not well explored. Therefore, it is interesting to examine the role of eosinophils in the initiation and progression of pancreatitis pathogenesis. Accordingly, we performed anti-major basic protein immunostaining, chloroacetate esterase, and Masson’s trichrome analyses to detect eosinophils, mast cells, and collagen in the tissue sections of mouse and human pancreas. Induced eosinophils accumulation and degranulation were observed in the tissue sections of human pancreatitis, compared with no eosinophils in the normal pancreatic tissue sections. Similarly, we observed induced tissue eosinophilia along with mast cells and acinar cells atrophy in cerulein-induced mouse model of chronic pancreatitis. Additionally, qPCR and ELISA analyses detected induced transcript and protein levels of proinflammatory and profibrotic cytokines, chemokines like IL 5, IL-18, eotaxin-1, eotaxin-2, TGF-β1, collagen-1, collagen-3, fibronectin, and α-SMA in experimental pancreatitis. Mechanistically, we show that eosinophil-deficient GATA1 and endogenous IL-5-deficient mice were protected from the induction of proinflammatory and profibrotic cytokines, chemokines, tissue eosinophilia, and mast cells in a cerulein-induced murine model of pancreatitis. These human and experimental data indicate that eosinophil accumulation and degranulation may have a critical role in promoting pancreatitis pathogenesis including fibrosis. Taken together, eosinophil tissue accumulation needs appropriate attention to understand and restrict the progression of pancreatitis pathogenesis in humans.NEW & NOTEWORTHY The present study for the first time shows that eosinophils accumulate in the pancreas and promote disease pathogenesis, including fibrosis in earlier reported cerulein-induced experimental models of pancreatitis. Importantly, we show that GATA-1 and IL-5 deficiency protects mice form the induction of eosinophil active chemokines, and profibrotic cytokines, including accumulation of tissue collagen in an experimental model of pancreatitis. Additionally, we state that cerulein-induced chronic pancreatitis is independent of blood eosinophilia.


2019 ◽  
Vol 42 (1) ◽  
pp. 36-40
Author(s):  
D. O. Hontsariuk ◽  
T. M. Hristich

The review contains modern statistical data on the prevalence and incidence of chronic pancreatitis, the role of nutrition in the development of the chronic inflammatory process in the pancreas, the influence of nutritional culture on the formation of the disease. The pathophysiological changes occurring in the pancreas upon alcohol abuse are revealed. The components of food and beverages that can disrupt the metabolism of nutrients, activate specific enzymes, initiate lipid peroxidation processes and provoke an inflammatory process in the gland tissue are listed. The objective signs of chronic pancreatitis and the dominant clinical syndromes are described in detail. A brief historical excursion into the peculiarities of dietary nutrition in patients with chronic pancreatitis is presented, modern ideas on the rational nutrition of patients with chronic pancreatitis are described. Emphasis is made on the dietary habits of patients in remission; the importance of adaptation to adequate ration during the period of attenuation of exacerbation of chronic pancreatitis is underlined. The recommendations for the prevention of diabetes mellitus are set, nutritional measures that can improve the processes of absorption and digestion are listed. The feasibility of an individual approach to the development of an optimal diet, taking into account the peculiarities of the course of chronic pancreatitis, the patient’s condition, which helps prevent the progression of exo- and endocrine pancreatic insufficiency, is considered. The importance of diet in the rehabilitation of patients with chronic pancreatitis is discussed.


Sign in / Sign up

Export Citation Format

Share Document