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Pathology Quiz Case 2: Diagnosis

Pathology Quiz Case 2: Diagnosis Diagnosis: Angiolymphoid hyperplasia with eosinophilia (AHE) Angiolymphoid hyperplasia with eosinophilia, which was first described in the English-language literature by Wells and Whimster1in 1969, is a benign vascular lesion that forms nodules in the head and neck. The term epithelioid hemangioma(EH) has also been used to further classify these lesions as benign vascular neoplasms, thereby differentiating them from histiocytoid hemangioma,2which includes all vascular lesions characterized by histiocytoid endothelium, whether benign or malignant. Angiolymphoid hyperplasia with eosinophilia appears predominantly in the third to fifth decades of life, with a peak incidence occurring during the fourth decade and a male-female ratio of nearly 2:1.3,4It typically presents as single or multiple nodules involving the head and neck region, especially the ear, periauricular area, forehead, and scalp; a few lesions can also be found in the extremities.4The lesions involve the subcutaneous tissue (82%), followed by the dermis and the deep soft tissue.4Common symptoms are pruritus, pain, bleeding, and lesional growth.5The duration of the lesions varies between 5 weeks and 15 years, with the majority of cases being present for 6 months or less.4Regional lymphadenopathy, peripheral blood eosinophilia, and increased serum IgE levels are not commonly seen in AHE.6 Histologically, AHE consists of a generally well-circumscribed proliferation of dermal vessels and inflammatory cells.3,5,7The vascular component is composed of thick- and thin-walled vessels with lumina lined by plump “epithelioid” endothelial cells, which will often partially or completely obliterate the vascular lumina.5,7,8The plump epithelioid endothelial cells not only have much larger nuclei than ordinary capillary endothelial cells, they also have abnormally vesicular, acidophilic, and sometimes vacuolated cytoplasm as well. The vascular component is usually contained within a bed of reticular fibers, while elastic fibers are not typically found within the vessels.7 The inflammatory component varies in density from lesion to lesion and consists of a mixture of lymphocytes, mononuclear cells (which may be histiocytes), numerous eosinophils, and mast cells.7,8The inflammatory component is diffusely arranged surrounding the vascular component, sometimes making the vascular component difficult to recognize. Lymphoid follicles may be found within these lesions and, if present, are usually found within the deeper aspects of the lesion.8The stromal tissue that contains the vascular and cellular components consists mainly of elongated mesenchymal cells with a few collagen bundles scattered within the lesion.7 The pathogenesis of AHE/EH remains a subject of debate, with there being 2 main schools of thought. First, the vascular proliferation seen in AHE is a primary neoplastic process leading to a secondary inflammatory response.5,6Factors believed to be a possible stimulus for vascular proliferation are nonspecific traumatic events and an altered estrogen state such as pregnancy.5,6The second school of thought is that AHE/EH is, at least in part, a nonneoplastic, reactive process that is stimulated by preceding trauma.4The differential diagnosis of AHE includes many benign and malignant vascular lesions of the skin and various reactive states dominated by lymphocytes and eosinophils, such as granuloma pyogenicum, Kaposi sarcoma, angiomatous lymphoid hamartoma, eosinophilic granuloma, malignant lymphoma, angiosarcoma, and reaction to insect bites.5,6 The primary modality of treatment for AHE is complete surgical excision. Inadequate excision yields a recurrence rate of 33%.5A second modality of treatment that has proved beneficial is carbon dioxide laser vaporization. This modality is especially valuable in patients who are poor surgical candidates or when the lesion is relatively inaccessible.9The carbon dioxide laser has been shown to vaporize the lesion, with no residual disease or recurrence at 15 months.9Other interventions such as low-dose irradiation, intralesional steroid injections, and cryotherapy have been used with minimal success.6 Disclaimer:The views expressed herein are those of the author(s) and do not reflect the official policy or position of the Department of the Army, the Department of Defense, or the US government. Box Section Ref ID Submissions Residents and fellows in otolaryngology are invited to submit quiz cases for this section and to write letters to the Archivescommenting on cases presented. Quiz cases should follow the patterns established. See Instructions for Authors (http://archotol.ama-assn.org/misc/ifora.dtl). Material for CLINICALPROBLEMSOLVING: PATHOLOGYshould be submitted electronically via the online submission and review system at http://manuscripts.archoto.com. Reprints are not available from the authors. References 1. Wells GCWhimster IW Subcutaneous angiolymphoid hyperplasia with eosinophilia. Br J Dermatol 1969;81 (1) 1- 15PubMedGoogle ScholarCrossref 2. Rosai FGold JLandy R The histiocytoid hemangiomas: a unifying concept embracing several previously described entities of skin, soft tissue, large vessels, bone, and heart. Hum Pathol 1979;10 (6) 707- 730PubMedGoogle ScholarCrossref 3. Urabe ATsuneyoshi MEnjoji M Epithelioid hemangioma versus Kimura's disease. Am J Surg Pathol 1987;11 (10) 758- 766PubMedGoogle ScholarCrossref 4. Fetsch JFWeiss SW Observations concerning the pathogenesis of epithelioid hemangioma (angiolymphoid hyperplasia). Mod Pathol 1991;4 (4) 449- 455PubMedGoogle Scholar 5. Don DMIshiyama AJohnstone AKFu YAbemayor E Angiolymphoid hyperplasia with eosinophilia and vascular tumors of the head and neck. Am J Otolaryngol 1996;17 (4) 240- 245PubMedGoogle ScholarCrossref 6. Chong WThomas AGoh C Kimura's disease and angiolymphoid hyperplasia with eosinophilia: two disease entities in the same patient: case report and review of the literature. Int J Dermatol 2006;45 (2) 139- 145PubMedGoogle ScholarCrossref 7. Mehregan AHShapiro L Angiolymphoid hyperplasia with eosinophilia. Arch Dermatol 1971;103 (1) 50- 57PubMedGoogle ScholarCrossref 8. Henry PGBurnett JW Angiolymphoid hyperplasia with eosinophilia. Arch Dermatol 1978;114 (8) 1169- 1172PubMedGoogle Scholar 9. Hobbs ERBailin PLRatz JLYarbrough CL Treatment of angiolymphoid hyperplasia of the external ear with carbon dioxide laser. J Am Acad Dermatol 1988;19 (2, pt 1) 345- 349PubMedGoogle ScholarCrossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Otolaryngology - Head & Neck Surgery American Medical Association

Pathology Quiz Case 2: Diagnosis

Archives of Otolaryngology - Head & Neck Surgery , Volume 134 (2) – Feb 1, 2008

Pathology Quiz Case 2: Diagnosis

Abstract

Diagnosis: Angiolymphoid hyperplasia with eosinophilia (AHE) Angiolymphoid hyperplasia with eosinophilia, which was first described in the English-language literature by Wells and Whimster1in 1969, is a benign vascular lesion that forms nodules in the head and neck. The term epithelioid hemangioma(EH) has also been used to further classify these lesions as benign vascular neoplasms, thereby differentiating them from histiocytoid hemangioma,2which includes all vascular lesions characterized by...
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Publisher
American Medical Association
Copyright
Copyright © 2008 American Medical Association. All Rights Reserved.
ISSN
0886-4470
eISSN
1538-361X
DOI
10.1001/archoto.2007.29-b
Publisher site
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Abstract

Diagnosis: Angiolymphoid hyperplasia with eosinophilia (AHE) Angiolymphoid hyperplasia with eosinophilia, which was first described in the English-language literature by Wells and Whimster1in 1969, is a benign vascular lesion that forms nodules in the head and neck. The term epithelioid hemangioma(EH) has also been used to further classify these lesions as benign vascular neoplasms, thereby differentiating them from histiocytoid hemangioma,2which includes all vascular lesions characterized by histiocytoid endothelium, whether benign or malignant. Angiolymphoid hyperplasia with eosinophilia appears predominantly in the third to fifth decades of life, with a peak incidence occurring during the fourth decade and a male-female ratio of nearly 2:1.3,4It typically presents as single or multiple nodules involving the head and neck region, especially the ear, periauricular area, forehead, and scalp; a few lesions can also be found in the extremities.4The lesions involve the subcutaneous tissue (82%), followed by the dermis and the deep soft tissue.4Common symptoms are pruritus, pain, bleeding, and lesional growth.5The duration of the lesions varies between 5 weeks and 15 years, with the majority of cases being present for 6 months or less.4Regional lymphadenopathy, peripheral blood eosinophilia, and increased serum IgE levels are not commonly seen in AHE.6 Histologically, AHE consists of a generally well-circumscribed proliferation of dermal vessels and inflammatory cells.3,5,7The vascular component is composed of thick- and thin-walled vessels with lumina lined by plump “epithelioid” endothelial cells, which will often partially or completely obliterate the vascular lumina.5,7,8The plump epithelioid endothelial cells not only have much larger nuclei than ordinary capillary endothelial cells, they also have abnormally vesicular, acidophilic, and sometimes vacuolated cytoplasm as well. The vascular component is usually contained within a bed of reticular fibers, while elastic fibers are not typically found within the vessels.7 The inflammatory component varies in density from lesion to lesion and consists of a mixture of lymphocytes, mononuclear cells (which may be histiocytes), numerous eosinophils, and mast cells.7,8The inflammatory component is diffusely arranged surrounding the vascular component, sometimes making the vascular component difficult to recognize. Lymphoid follicles may be found within these lesions and, if present, are usually found within the deeper aspects of the lesion.8The stromal tissue that contains the vascular and cellular components consists mainly of elongated mesenchymal cells with a few collagen bundles scattered within the lesion.7 The pathogenesis of AHE/EH remains a subject of debate, with there being 2 main schools of thought. First, the vascular proliferation seen in AHE is a primary neoplastic process leading to a secondary inflammatory response.5,6Factors believed to be a possible stimulus for vascular proliferation are nonspecific traumatic events and an altered estrogen state such as pregnancy.5,6The second school of thought is that AHE/EH is, at least in part, a nonneoplastic, reactive process that is stimulated by preceding trauma.4The differential diagnosis of AHE includes many benign and malignant vascular lesions of the skin and various reactive states dominated by lymphocytes and eosinophils, such as granuloma pyogenicum, Kaposi sarcoma, angiomatous lymphoid hamartoma, eosinophilic granuloma, malignant lymphoma, angiosarcoma, and reaction to insect bites.5,6 The primary modality of treatment for AHE is complete surgical excision. Inadequate excision yields a recurrence rate of 33%.5A second modality of treatment that has proved beneficial is carbon dioxide laser vaporization. This modality is especially valuable in patients who are poor surgical candidates or when the lesion is relatively inaccessible.9The carbon dioxide laser has been shown to vaporize the lesion, with no residual disease or recurrence at 15 months.9Other interventions such as low-dose irradiation, intralesional steroid injections, and cryotherapy have been used with minimal success.6 Disclaimer:The views expressed herein are those of the author(s) and do not reflect the official policy or position of the Department of the Army, the Department of Defense, or the US government. Box Section Ref ID Submissions Residents and fellows in otolaryngology are invited to submit quiz cases for this section and to write letters to the Archivescommenting on cases presented. Quiz cases should follow the patterns established. See Instructions for Authors (http://archotol.ama-assn.org/misc/ifora.dtl). Material for CLINICALPROBLEMSOLVING: PATHOLOGYshould be submitted electronically via the online submission and review system at http://manuscripts.archoto.com. Reprints are not available from the authors. References 1. Wells GCWhimster IW Subcutaneous angiolymphoid hyperplasia with eosinophilia. Br J Dermatol 1969;81 (1) 1- 15PubMedGoogle ScholarCrossref 2. Rosai FGold JLandy R The histiocytoid hemangiomas: a unifying concept embracing several previously described entities of skin, soft tissue, large vessels, bone, and heart. Hum Pathol 1979;10 (6) 707- 730PubMedGoogle ScholarCrossref 3. Urabe ATsuneyoshi MEnjoji M Epithelioid hemangioma versus Kimura's disease. Am J Surg Pathol 1987;11 (10) 758- 766PubMedGoogle ScholarCrossref 4. Fetsch JFWeiss SW Observations concerning the pathogenesis of epithelioid hemangioma (angiolymphoid hyperplasia). Mod Pathol 1991;4 (4) 449- 455PubMedGoogle Scholar 5. Don DMIshiyama AJohnstone AKFu YAbemayor E Angiolymphoid hyperplasia with eosinophilia and vascular tumors of the head and neck. Am J Otolaryngol 1996;17 (4) 240- 245PubMedGoogle ScholarCrossref 6. Chong WThomas AGoh C Kimura's disease and angiolymphoid hyperplasia with eosinophilia: two disease entities in the same patient: case report and review of the literature. Int J Dermatol 2006;45 (2) 139- 145PubMedGoogle ScholarCrossref 7. Mehregan AHShapiro L Angiolymphoid hyperplasia with eosinophilia. Arch Dermatol 1971;103 (1) 50- 57PubMedGoogle ScholarCrossref 8. Henry PGBurnett JW Angiolymphoid hyperplasia with eosinophilia. Arch Dermatol 1978;114 (8) 1169- 1172PubMedGoogle Scholar 9. Hobbs ERBailin PLRatz JLYarbrough CL Treatment of angiolymphoid hyperplasia of the external ear with carbon dioxide laser. J Am Acad Dermatol 1988;19 (2, pt 1) 345- 349PubMedGoogle ScholarCrossref

Journal

Archives of Otolaryngology - Head & Neck SurgeryAmerican Medical Association

Published: Feb 1, 2008

Keywords: epithelioid hemangioma of skin,internship and residency,otolaryngology,medical residencies

References