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Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
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Acute Pancreatitis I: Introduction01:27

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Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models
09:54

Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models

Published on: December 3, 2019

GVHD pathophysiology: is acute different from chronic?

Tomomi Toubai1, Yaping Sun, Pavan Reddy

  • 1Department of Internal Medicine, Division of Hematology/Oncology, University of Michigan Comprehensive Cancer Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109-0942, USA.

Best Practice & Research. Clinical Haematology
|May 28, 2008
PubMed
Summary
This summary is machine-generated.

Graft-versus-host disease (GVHD) is a major complication following allogeneic hematopoietic cell transplantation (HCT). This chapter contrasts the distinct pathophysiologies of acute and chronic GVHD, highlighting key differences in their onset and mechanisms.

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Last Updated: Jul 5, 2026

Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models
09:54

Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models

Published on: December 3, 2019

Area of Science:

  • Immunology
  • Transplantation Medicine
  • Hematology

Background:

  • Graft-versus-host disease (GVHD) is a significant complication after allogeneic hematopoietic cell transplantation (HCT).
  • GVHD presents in two main forms: acute and chronic.
  • Acute GVHD typically occurs within 100 days post-HSCT, driven by donor T cells reacting to host antigens.

Purpose of the Study:

  • To discuss and contrast the pathophysiologies of acute and chronic GVHD.
  • To elucidate the differing mechanisms underlying acute and chronic GVHD.
  • To provide a foundational understanding of GVHD subtypes in HCT.

Main Methods:

  • Comparative analysis of pathophysiological mechanisms.
  • Review of established literature on GVHD.
  • Discussion of T cell involvement in GVHD.

Main Results:

  • Acute GVHD is characterized by donor T cell response to mismatched histocompatibility antigens, manifesting early post-transplant.
  • Chronic GVHD, occurring later, shares features with autoimmune diseases and involves less understood mechanisms and antigens.
  • Both acute and chronic GVHD are T cell-mediated but differ in timing, antigen targets, and underlying cellular processes.

Conclusions:

  • Understanding the distinct pathophysiologies of acute and chronic GVHD is crucial for managing HCT complications.
  • Further research is needed to fully elucidate the mechanisms of chronic GVHD.
  • Differentiating between acute and chronic GVHD is essential for appropriate clinical management and treatment strategies.