Plummer-Vinson syndrome pathophysiology

Plummer-Vinson syndrome Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:

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Overview

The exact pathogenesis of [disease name] is not fully understood.

OR

It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].

OR

[Pathogen name] is usually transmitted via the [transmission route] route to the human host.

OR

Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.

OR

[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].

OR

The progression to [disease name] usually involves the [molecular pathway].

OR

The pathophysiology of [disease/malignancy] depends on the histological subtype.

Pathophysiology

Pathogenesis

• Plummer-Vinson syndrome is a rare condition characterized by iron-deficiency anemia, glossitis and dysphagia.
• The exact pathogenesis of Plummer-Vinson syndrome is not fully understood. It is postulated that Plummer-Vinson syndrome results from iron deficiency. Other possible factors include malnutrition, genetic predisposition or even autoimmune processes.
  • Iron plays a major role in the expression of citric acid cycle enzymes such as citrate synthase, isocitric dehydrogenase, and succinate dehydrogenase.
  • Iron replete cells with normal citric acid cycle have an increased formation of reducing equivalents (NADH) thus leading to increased ATP formation via oxidative phosphorylation.
  • In patients with iron deficiency, all these metabolic pathways (oxidative phosphorylation) are reduced. This promotes anaerobic metabolism with increased consumption of glucose and increased production of lactic acid.
  • In patients with iron deficiency the iron-dependent oxidative enzymes are unable to function at optimum level and may lead to myasthenic changes in muscles. These myasthenic changes are often seen in muscles involved in swallowing and may lead to atrophy of the esophageal mucosa, and formation of esophageal webs.

• The dysphagia in Plummer-Vinson syndrome results from postcricoid web or stricture. However, recent studies have shown that patients who do not exhibit obstructive lesions may have dysphagia resulting from muscular in-coordination.

OR

• It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
• [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
• Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
• [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
• The progression to [disease name] usually involves the [molecular pathway].
• The pathophysiology of [disease/malignancy] depends on the histological subtype.

Genetics

• [Disease name] is transmitted in [mode of genetic transmission] pattern.
• Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
• The development of [disease name] is the result of multiple genetic mutations.

Gross Pathology

• On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

On microscopic histopathological analysis, Plummer-Vinson syndrome presents with the following findings:

• Epithelial atrophy
• Chronic submucosal inflammation
• Epithelial atypia or dysplasia (in advanced cases)