Palmar plantar erythrodysesthesia pathophysiology

Palmar plantar erythrodysesthesia Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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

The exact pathogenesis of palmar plantar dysesthesia is not completely understood. Suggested explanations include:

• Direct toxic effect of the chemotherapeutic drug against epidermal cells (keratinocytes)

• Concentration and excretion of cytotoxic drug in eccrine sweat glands causing damage or alteration in these structures ^4,5

• A type I (immunoglobulin E [IgE]-mediated) allergic reaction⁶, suggested based on the occasional co-occurrence of facial erythema/edema, papular rash, and fever.

Unique characteristics of the palms and the soles which justify their involvement as the preferred sites of involvement include^4,7,8: 

·       High density of eccrine sweat glands⁹

·       Absence of folliculosebaceous units (hair follicles and sebaceous glands)⁹

·       Thick stratum corneum⁹

·       Wide dermal papillae⁹

·       High proliferative rate of epidermal basal cells

·       The temperature and pressure gradient

·       Gravitation forces

·       Vascular anatomy peculiar to these areas

·       In cases caused by capecitabine, higher expression of the capecitabine-activating enzyme thymidine phosphorylase in the skin of the palms¹⁰

Pathogenesis

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

OR

• It is understood 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.

OR

Genes involved in the pathogenesis of [disease name] include:

• [Gene1]
• [Gene2]
• [Gene3]

OR

The development of [disease name] is the result of multiple genetic mutations such as:

• [Mutation 1]
• [Mutation 2]
• [Mutation 3]

Associated Conditions

Conditions associated with [disease name] include:

• [Condition 1]
• [Condition 2]
• [Condition 3]

Gross Pathology

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

Microscopic Pathology

On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].