Plummer-Vinson syndrome pathophysiology

Plummer-Vinson syndrome Microchapters
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Overview
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Pathophysiology
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Differentiating Plummer-Vinson syndrome from other Diseases
Epidemiology and Demographics
Risk Factors
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Natural History, Complications and Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
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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. However, the precise relationship of anemia Other possible factors include malnutrition, genetic predisposition or even autoimmune processes. The dysphagia in Plummer-Vinson syndrome results from postcricoid web or stricture. However, recent studies have shown that some patients do not exhibit these obstructive lesions and the dysphagia is likely due to 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)