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Related Concept Videos

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Inflammation01:38

Inflammation

Overview
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...

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Ultrasonography of the Adult Male Urinary Tract for Urinary Functional Testing
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Published on: August 14, 2019

Correlation between benign prostatic hyperplasia and inflammation.

Yakup Bostanci1, Amir Kazzazi, Shabnam Momtahen

  • 1Department of Urology, New York University School of Medicine, New York, NY, USA.

Current Opinion in Urology
|November 20, 2012
PubMed
Summary
This summary is machine-generated.

Prostatic inflammation may contribute to benign prostatic hyperplasia (BPH) development and lower urinary tract symptoms (LUTS). Evidence suggests BPH is an immune inflammatory disease, potentially offering new treatment strategies.

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Area of Science:

  • Urology
  • Immunology
  • Pathology

Background:

  • Benign prostatic hyperplasia (BPH) is a common condition in aging men.
  • The exact mechanisms driving BPH pathogenesis and progression remain incompletely understood.

Purpose of the Study:

  • To review and evaluate existing evidence on the role of prostatic inflammation in BPH development and progression.
  • To explore the link between inflammation and lower urinary tract symptoms (LUTS) associated with BPH.

Main Methods:

  • Systematic review of current scientific literature.
  • Analysis of studies examining prostate tissue, inflammatory markers, and clinical outcomes in BPH patients.

Main Results:

  • Inflammatory infiltrates are common in BPH prostate tissues and correlate with prostate size.
  • Inflammation may drive cytokine production, angiogenesis, and stromal hyperproliferation in the prostate.
  • A pro-inflammatory microenvironment, oxidative stress, and hypoxia are implicated in BPH progression.

Conclusions:

  • Emerging evidence strongly suggests BPH is an immune inflammatory disease.
  • T-cell activity and autoimmune responses may promote epithelial and stromal cell proliferation in BPH.
  • Understanding inflammation's role can improve BPH risk stratification and guide novel therapeutic approaches.