Palmar plantar erythrodysesthesia pathophysiology: Difference between revisions
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* In cases caused by capecitabine, higher expression of the capecitabine-activating enzyme thymidine phosphorylase in the skin of the palms<sup>10</sup> | * In cases caused by capecitabine, higher expression of the capecitabine-activating enzyme thymidine phosphorylase in the skin of the palms<sup>10</sup> | ||
==Microscopic Pathology== | ==Microscopic Pathology== | ||
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | ||
* The pathologic features of PPE are non-specific. | |||
* However, since PPE involves a cytotoxic reaction primarily affecting keratinocytes the histopathologic findings are similar to histologic manifestation of direct toxic reactions: | |||
** Dominantly an interface dermatitis with a cell-poor infiltrate | |||
** A variable degree of epidermal (keratinocytes) necrosis<ref name="pmid8468414">{{cite journal| author=Fitzpatrick JE| title=The cutaneous histopathology of chemotherapeutic reactions. | journal=J Cutan Pathol | year= 1993 | volume= 20 | issue= 1 | pages= 1-14 | pmid=8468414 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8468414 }} </ref> | |||
* Generally, in mild cytotoxic reactions (PPE WHO grades 1 and 2) necrosis is restricted to basal keratinocytes. | |||
* In severe cytotoxic reactions (WHO grades 3 and 4) destruction of the entire basal layer occurs, and a blister along with complete epidermal necrosis may also be seen97. | |||
* Other histologic manifestations in epidermis include: | |||
** Vacuolar degeneration of the basal cell layer of epidermis | |||
** Mild spongiosis | |||
** Hyperkeratosis | |||
** Lymphohistiocytic infiltrates | |||
** Apoptosis of keratinocytes | |||
** Partial separation of the epidermis from the dermis. | |||
*Dermal changes include: | |||
** Superficial perivascular infiltration of dermis composed of lymphocytes and eosinophils | |||
** Papillary dermal edema | |||
** Neutrophilic eccrine hidradenitis | |||
** Eccrine squamous syringometaplasia, in severe PPE (WHO grades 3 and 4) | |||
* Histologic evidence of small-fiber neuropathy, as shown by reduced epidermal nerve fiber density, has been suggested to be responsible for occurrence of neuropathic pain, dysesthesias, paresthesias, and temperature intolerance in PPE. <ref name="pmid19078798">{{cite journal| author=Stubblefield MD, Custodio CM, Kaufmann P, Dickler MN| title=Small-Fiber Neuropathy Associated with Capecitabine (Xeloda)-induced Hand-foot Syndrome: A Case Report. | journal=J Clin Neuromuscul Dis | year= 2006 | volume= 7 | issue= 3 | pages= 128-32 | pmid=19078798 | doi=10.1097/01.cnd.0000211401.19995.a2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19078798 }} </ref> | |||
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Palmar plantar erythrodysesthesia Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mandana Chitsazan, M.D.
Overview
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)[1]
- Concentration and excretion of cytotoxic drug in eccrine sweat glands causing damage or alteration in these structures [2] [3]
- A type I (immunoglobulin E [IgE]-mediated) allergic reaction [4], 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 [2] [5] [6]
- High density of eccrine sweat glands [7]
- Absence of folliculosebaceous units (hair follicles and sebaceous glands)[7]
- Thick stratum corneum [7]
- Wide dermal papillae [7]
- High proliferation 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
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- The pathologic features of PPE are non-specific.
- However, since PPE involves a cytotoxic reaction primarily affecting keratinocytes the histopathologic findings are similar to histologic manifestation of direct toxic reactions:
- Dominantly an interface dermatitis with a cell-poor infiltrate
- A variable degree of epidermal (keratinocytes) necrosis[8]
- Generally, in mild cytotoxic reactions (PPE WHO grades 1 and 2) necrosis is restricted to basal keratinocytes.
- In severe cytotoxic reactions (WHO grades 3 and 4) destruction of the entire basal layer occurs, and a blister along with complete epidermal necrosis may also be seen97.
- Other histologic manifestations in epidermis include:
- Vacuolar degeneration of the basal cell layer of epidermis
- Mild spongiosis
- Hyperkeratosis
- Lymphohistiocytic infiltrates
- Apoptosis of keratinocytes
- Partial separation of the epidermis from the dermis.
- Dermal changes include:
- Superficial perivascular infiltration of dermis composed of lymphocytes and eosinophils
- Papillary dermal edema
- Neutrophilic eccrine hidradenitis
- Eccrine squamous syringometaplasia, in severe PPE (WHO grades 3 and 4)
- Histologic evidence of small-fiber neuropathy, as shown by reduced epidermal nerve fiber density, has been suggested to be responsible for occurrence of neuropathic pain, dysesthesias, paresthesias, and temperature intolerance in PPE. [9]
References
- ↑ J. E. Fitzpatrick. "The cutaneous histopathology of chemotherapeutic reactions". Journal of cutaneous pathology. PMID 8468414.
- ↑ 2.0 2.1 Baack BR, Burgdorf WH (1991). "Chemotherapy-induced acral erythema". J Am Acad Dermatol. 24 (3): 457–61. PMID 2061446.
- ↑ Hiromi Tsuboi, Kohzoh Yonemoto & Kensei Katsuoka. "A case of bleomycin-induced acral erythema (AE) with eccrine squamous syringometaplasia (ESS) and summary of reports of AE with ESS in the literature". The Journal of dermatology. PMID 16361756.
- ↑ Perry, Michael (2012). Chemotherapy source book. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 9781451101454.
- ↑ W. S. Susser, D. L. Whitaker-Worth & J. M. Grant-Kels. "Mucocutaneous reactions to chemotherapy". Journal of the American Academy of Dermatology. PMID 10071309.
- ↑ Yvonne Lassere & Paulo Hoff. "Management of hand-foot syndrome in patients treated with capecitabine (Xeloda)". European journal of oncology nursing : the official journal of European Oncology Nursing Society. doi:10.1016/j.ejon.2004.06.007. PMID 15341880.
- ↑ 7.0 7.1 7.2 7.3 Cox GJ, Robertson DB (1986). "Toxic erythema of palms and soles associated with high-dose mercaptopurine chemotherapy". Arch Dermatol. 122 (12): 1413–4. PMID 2947543.
- ↑ Fitzpatrick JE (1993). "The cutaneous histopathology of chemotherapeutic reactions". J Cutan Pathol. 20 (1): 1–14. PMID 8468414.
- ↑ Stubblefield MD, Custodio CM, Kaufmann P, Dickler MN (2006). "Small-Fiber Neuropathy Associated with Capecitabine (Xeloda)-induced Hand-foot Syndrome: A Case Report". J Clin Neuromuscul Dis. 7 (3): 128–32. doi:10.1097/01.cnd.0000211401.19995.a2. PMID 19078798.