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Related Concept Videos

Acute Pancreatitis II: Clinical Manifestations and Management01:30

Acute Pancreatitis II: Clinical Manifestations and Management

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Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...
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Acute Pancreatitis I: Introduction01:27

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Pancreatitis is inflammation of the pancreas, an organ located behind the stomach. It can be either acute or chronic.
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
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A Mouse Model for Chronic Pancreatitis via Bile Duct TNBS Infusion
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Diabetic Bone Marrow Cell Injection Accelerated Acute Pancreatitis Progression.

Xiao-Min Luo1, Cen Yan1, Yue-Jie Zhang1

  • 1Department of Science and Technology, Beijing Youan Hospital, Capital Medical University, Beijing 100069, China.

Journal of Immunology Research
|September 6, 2021
PubMed
Summary
This summary is machine-generated.

Diabetic bone marrow cells worsen acute pancreatitis severity. In a mouse model, these cells increased inflammation and acinar cell damage, highlighting diabetes as a risk factor for severe pancreatitis.

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Area of Science:

  • Gastroenterology and Hepatology
  • Endocrinology and Metabolism
  • Immunology

Background:

  • Acute pancreatitis (AP) is a significant cause of hospitalization, with a subset progressing to severe forms.
  • Diabetes mellitus is an established independent risk factor for AP incidence and severity.
  • The precise mechanisms by which diabetes influences AP progression remain incompletely understood.

Purpose of the Study:

  • To investigate the role of diabetic bone marrow cells (BMC) in the progression of acute pancreatitis.
  • To elucidate the impact of diabetic BMC on inflammation and acinar cell injury during AP.

Main Methods:

  • Acute pancreatitis was induced in wild-type mice using caerulein injections.
  • Bone marrow cells were isolated from both wild-type and diabetic (db/db) mice.
  • These BMC were transplanted into recipient mice, followed by AP induction and subsequent analysis of serum markers, histology, and cytokine production.

Main Results:

  • Mice receiving diabetic BMC exhibited significantly elevated serum lipase activity and overall pancreatitis severity scores compared to controls and wild-type BMC recipients.
  • Histological examination revealed increased acinar cell necrosis and vacuolization in mice treated with diabetic BMC.
  • Diabetic BMC produced higher levels of pro-inflammatory cytokines, including IL-6, GM-CSF, and IL-10, and attracted more myeloperoxidase-positive cells.

Conclusions:

  • Bone marrow cells from diabetic mice exacerbate acute pancreatitis.
  • Diabetic BMC enhance the inflammatory response and acinar cell damage, contributing to AP progression.
  • These findings underscore the detrimental role of diabetes-associated BMC in AP pathogenesis.