Chronic pancreatitis caused by an autoimmune abnormality

Yoshida, Kenji; Toki, Fumitake; Takeuchi, Tadashi; Watanabe, Shinichiro; Shiratori, Keiko; Hayashi, Naoaki

doi:10.1007/bf02285209

Cited by 1,284 publications

(258 citation statements)

References 22 publications

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“…We previously demonstrated induction of acinar cell apoptosis, with infiltration of CD8 and CD4 T cells and tacrolimus, an immunosuppressant, attenuates this apoptosis and chronic inflammation in this model (Hashimoto et al, 2000;Yamada et al, 2001). Clinical investigations have demonstrated that infiltration of CD4 and CD8 T cells and high expression of major histocompatibility complex class I and class II antigens by pancreatic epithelial cells is observed in human chronic pancreatitis, suggesting that cell-mediated autoimmune mechanisms are at work (Anderson et al, 1988;Bedossa et al, 1990;Jalleh et al, 1993;Yoshida et al, 1995). Furthermore, autoimmune chronic pancreatitis has been recognized as a new entity in humans defined in terms of lymphocyte infiltration, autoantibody production, and effectiveness of steroid administration (Okazaki et al, 2000).…”

Section: Discussionmentioning

confidence: 73%

Candesartan, an Angiotensin II Receptor Antagonist, Suppresses Pancreatic Inflammation and Fibrosis in Rats

Yamada¹,

Kuno²,

Masuda³

et al. 2003

J Pharmacol Exp Ther

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Angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists attenuate fibrosis in the kidney, heart, and liver by suppressing transforming growth factor-␤1 mRNA and decreasing production of extracellular matrix proteins. We recently demonstrated that lisinopril, an angiotensin-converting enzyme inhibitor, alleviates pancreatic inflammation and fibrosis in male Wistar Bonn/Kobori rats. The involvement of angiotensin II receptor and its receptor interaction in the pathogenesis of spontaneous chronic pancreatitis was assessed in this model. Candesartan, an angiotensin II receptor antagonist, was administered in drinking water (10.5, 42, or 125 mg/l) to 10-week-old male WBN/Kob rats for 10 weeks and inflammatory parameters, fibrosis, and gene expression of renin-angiotensin system components and transforming growth factor-␤1 were assessed in the pancreas. Immunostaining for ␣-smooth muscle actin was also performed. Candesartan significantly suppressed decrease in pancreatic weight and increases in pancreatic myeloperoxidase activity, hydroxyproline content, ratio of fibrous tissue, histologic scores, and ratio of ␣-smooth muscle actin-positive cells (activated pancreatic stellate cells) at 20 weeks. The high dose enhanced the expression of angiotensinogen and angiotensin II receptor type 2 mRNA and suppressed the overexpression of transforming growth factor-␤1 mRNA. The conclusion is that candesartan alleviates chronic pancreatitis and fibrosis by suppressing the overexpression of transforming growth factor-␤1, resulting in prevention of activation of pancreatic stellate cells in male WBN/Kob rats. We propose that angiotensin II receptor type 1 antagonists may be useful for the treatment of chronic pancreatitis involving angiotensin II interaction with its receptor.The renin-angiotensin system (RAS) plays an important role in regulation of the systemic blood pressure, body fluid, and electrolyte balance. Angiotensin II (AT-II), an octapeptide produced by proteolytic cleavage of its precursor angiotensin I by the angiotensin-converting enzyme (ACE), is a physiologically active product of the RAS (Matsusaka and Ichikawa, 1997). It stimulates the proliferation of mesangial cells, cardiac fibroblasts, and hepatic stellate cells (HSCs) and their increased synthesis of extracellular matrix proteins through induction of transforming growth factor (TGF)-␤1 expression both in vivo and in vitro (Matsusaka and Ichikawa, 1997;Bataller et al., 2000).Two subtypes of AT-II receptors, namely, type 1 (AT1 receptor) and type 2 (AT2 receptor) have been identified (Matsusaka and Ichikawa, 1997;Matsubara, 1998). AT1 receptor, which mediates most of the biological results of AT-II action, including vasoconstriction, cell proliferation, and production of extracellular matrix proteins, is found in the kidney, liver, adrenal cortex, and blood vessels. It is well documented that AT-II induces cell hypertrophy and ion transport in the kidney, heart, and liver, primarily through AT1 receptor (Matsusaka and Ichikawa, 1...

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Section: Discussionmentioning

confidence: 73%

Candesartan, an Angiotensin II Receptor Antagonist, Suppresses Pancreatic Inflammation and Fibrosis in Rats

Yamada¹,

Kuno²,

Masuda³

et al. 2003

J Pharmacol Exp Ther

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“…In 1992, Toki et al (9) reported the presence of diffuse irregular narrowing of the main pancreatic duct (MPD) on endoscopic retrograde pancreatography (ERP) in a patient with an unusual type of chronic pancreatitis. In 1995, Yoshida et al (10) proposed referring to the disease in these individuals as "autoimmune pancreatitis" (AIP). The findings in these patients include high serum gamma globulin or immunoglobulin G (IgG) levels, positivity for the presence of antinuclear antibodies (ANA), diffuse enlargement of the pancreas, and response to steroid therapy.…”

Section: Introductionmentioning

confidence: 99%

Atypical Manifestations of Pancreatitis with Autoimmune Phenomenon in an Adolescent Female

et al. 2005

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We report a case of an adolescent girl with atypical manifestations of pancreatitis with autoimmune phenomenon presenting with epigastralgia and back pain. While no abnormalities were detected on computed tomography and magnetic resonance imaging, apart from the absence of peripancreatic spread, laboratory and serological findings, such as hypergammaglobulinemia, a high titer of immunoglobulin G, a high titer of immunoglobulin G4, slight positivity for antinuclear antibodies, and positivity for autoantibodies to lactoferrin, were suggestive of autoimmune pancreatitis (AIP). Magnetic resonance cholangiopancreatography imaging (MRCP) visualized only the main pancreatic duct (MPD) in the pancreas head region. Proteoclastic enzyme inhibitor treatment was ineffective but the patient responded well to oral prednisolone. The patient and her family did not consent to endoscopic retrograde pancreatography or biopsy/histopathological examination. The case could not be diagnosed as AIP due to lack of typical diagnostic criteria, and thus the final diagnosis was considered pancreatitis with autoimmune phenomenon. We considered that the MRCP finding of partly visible MPD was due to diffuse irregular narrowing of the MPD. This case suggests that while MRCP imaging of the MPD may be helpful in the diagnosis of pancreatitis with autoimmune phenomenon, a negative result does not preclude such diagnosis. (Internal Medicine 44: 886-891, 2005)

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“…This notion received no further attention in Japan until the mid 90's when Yoshida et al published a case of a patient with chronic pancreatitis and impaired exocrine function with associated autoimmunity [2]. The term AIP was first used here.…”

Section: Introductionmentioning

confidence: 99%

Clinically Mimicking Pancreatic and Dilation in Main Pancreatic Duct in Autoimmune Pancreatitis (AIP): A Case Report and Literature Review

Li¹,

Xiong²

2017

OALib

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Autoimmune pancreatitis (AIP) is a unique form of pancreatitis which has autoimmune features. AIP has clinical presentations that greatly mimic pancreatic cancer (PC). It is critical for clinicians to distinguish AIP from PC because their treatments and prognoses are entirely different. We report a 62-year-old man with obstructive jaundice and dilation in the main pancreatic duct (MPD). The diagnosis of AIP was based on diagnostic criteria by the elevated IgG-4 serum levels and the typical imaging such as diffuse pancreatic swelling and dilation in the common biliary duct (CBD). The difference of the imaging finding in our case is the expanding of the MPD, which is usually described to be stenosis in many literatures. Finally, the patient was confirmed with type I AIP according to the diagnosis criteria. After the steroid treatment lasting 3 months, the patient was gradually recovered. We present the case and take a review of literature in order to improve the early identification of AIP.

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Chronic pancreatitis caused by an autoimmune abnormality

Cited by 1,284 publications

References 22 publications

Candesartan, an Angiotensin II Receptor Antagonist, Suppresses Pancreatic Inflammation and Fibrosis in Rats

Candesartan, an Angiotensin II Receptor Antagonist, Suppresses Pancreatic Inflammation and Fibrosis in Rats

Atypical Manifestations of Pancreatitis with Autoimmune Phenomenon in an Adolescent Female

Clinically Mimicking Pancreatic and Dilation in Main Pancreatic Duct in Autoimmune Pancreatitis (AIP): A Case Report and Literature Review

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