The Experts below are selected from a list of 96 Experts worldwide ranked by ideXlab platform
Herbert P Goodheart - One of the best experts on this subject based on the ideXlab platform.
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Targetoid Hemosiderotic Hemangioma a dynamic vascular tumor report of 3 cases with episodic and cyclic changes and comparison with solitary angiokeratomas
Journal of The American Academy of Dermatology, 1999Co-Authors: Andrew J Carlson, Soume Daulat, Herbert P GoodheartAbstract:Abstract Background: Both Targetoid Hemosiderotic Hemangiomas (THH) and solitary angiokeratomas (SAK) are acquired vascular malformations formed by superficial vascular ectasias possibly caused by trauma. Objective: We compare the clinicopathologic findings of THHs with those of SAKs and report the clinicopathologic findings of 3 singular cases of THH affected by cyclic or episodic morphologic changes. Methods: We performed a clinicopathologic study on 33 cases of THH and compared this group with 20 cases of SAK. On selected cases, histochemical and immunohistochemical analyses were evaluated. Results: Overlap of all the clinical and pathologic features studied were identified for THH and SAK. Clinically, they both commonly exhibited a brown or black papule located over the lower extremities that mimicked a melanocytic lesion. Histologically, they both had ectatic papillary dermal vessels with overlying epidermal hyperplasia, and adjacent hemosiderin deposits, extravasated red blood cells, lymphocytic infiltrate, and lymphangiectases. Compared with SAKs, THHs were significantly larger (5.3 vs 3.2 mm), more often excised (elliptical excision) than shave or punch biopsied, and had deeper dermal vessel alterations, more frequent dissecting vascular spaces, and more extensive hemosiderin deposits (all P P = .001). Conclusion: THHs and SAKs differ in degree, not in type, of clinicopathologic characteristics. This finding suggests that THHs are larger variants of SAKs whose size is the cause of more extensive, prolonged, or recurrent vessel damage. The histologic findings of extravasated red blood cells, hemosiderin, telangiectases, lymphangiectases, and fibrosis implicate trauma in the cause of these acquired vascular malformations. (J Am Acad Dermatol 1999;41:215-24.)
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Targetoid Hemosiderotic Hemangioma a dynamic vascular tumor report of 3 cases with episodic and cyclic changes and comparison with solitary angiokeratomas
Annual Meeting of the American Society of Dermatopathology, 1999Co-Authors: J A Carlson, Soume Daulat, Herbert P GoodheartAbstract:Background: Both Targetoid Hemosiderotic Hemangiomas (THH) and solitary angiokeratomas (SAK) are acquired vascular malformations formed by superficial vascular ectasias possibly caused by trauma. Objective: We compare the clinicopathologic findings of THHs with those of SAKs and report the clinicopathologic findings of 3 singular cases of THH affected by cyclic or episodic morphologic changes. Methods: We performed a clinicopathologic study on 33 cases of THH and compared this group with 20 cases of SAK. On selected cases, histochemical and immunohistochemical analyses were evaluated. Results: Overlap of all the clinical and pathologic features studied were identified for THH and SAK. Clinically, they both commonly exhibited a brown or black papule located over the lower extremities that mimicked a melanocytic lesion. Histologically, they both had ectatic papillary dermal vessels with overlying epidermal hyperplasia, and adjacent hemosiderin deposits, extravasated red blood cells, lymphocytic infiltrate, and lymphangiectases. Compared with SAKs, THHs were significantly larger (5.3 vs 3.2 mm), more often excised (elliptical excision) than shave or punch biopsied, and had deeper dermal vessel alterations, more frequent dissecting vascular spaces, and more extensive hemosiderin deposits (all P <.01). THHs presenting with episodic changes were significantly larger than those without (11 vs 4.4 mm, P =.001). Conclusion: THHs and SAKs differ in degree, not in type, of clinicopathologic characteristics. This finding suggests that THHs are larger variants of SAKS whose size is the cause of more extensive, prolonged, or recurrent vessel damage. The histologic findings of extravasated red blood cells, hemosiderin, telangiectases, lymphangiectases, and fibrosis implicate trauma in the cause of these acquired vascular malformations.
Victor Kokta - One of the best experts on this subject based on the ideXlab platform.
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Targetoid Hemosiderotic Hemangiomas hobnail Hemangiomas are vascular lymphatic malformations a study of 12 pediatric cases
Journal of The American Academy of Dermatology, 2012Co-Authors: Rola Al Dhaybi, Christina Lam, Afshin Hatami, Julie Powell, Catherine Mccuaig, Victor KoktaAbstract:Background Targetoid Hemosiderotic Hemangioma (THH), also called hobnail Hemangioma, is a benign vascular lesion and thought to be of lymphatic origin. Objective We sought to perform a clinicopathologic analysis of cases diagnosed as THH in a tertiary care children's hospital. Methods Clinical and histopathologic data were obtained from a chart review of 12 confirmed pediatric cases of THH. To determine the presence or absence of lymphatic vessels in lesional biopsy specimens, we evaluated the expression of the lymphatic endothelial cell marker podoplanin using the D2-40 antibody. Wilms tumor-1 gene immunostaining and Ki-67 proliferation index were also performed to evaluate the proliferative nature of these lesions. Results Three children had a lesion since birth and 4 had a history of trauma before appearance of the THH. D2-40 immunostaining was positive in every case. Wilms tumor-1 gene immunostaining was negative in 9 cases, focally positive in two cases, and not performed in one case. The Ki-67 proliferation index was very low in all cases studied. Limitations The small number of cases and restriction to a pediatric population were limitations. Conclusion Our findings suggest that THH should be classified as a lymphatic vascular malformation.
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differentiation of vascular tumors from vascular malformations by expression of wilms tumor 1 gene evaluation of 126 cases
Journal of The American Academy of Dermatology, 2010Co-Authors: Rola Al Dhaybi, Julie Powell, Catherine Mccuaig, Victor KoktaAbstract:Background Vascular tumors and malformations can be challenging to diagnose. Although they may initially appear very similar, they have distinct clinical courses and management. Wilms tumor 1 (WT1) gene expression has been reported in many different tumors including hematologic malignancies and some solid tumors. Objective We sought to evaluate the expression of WT1 in 126 vascular lesions (64 vascular tumors, one Masson tumor, and 61 vascular malformations). Methods Based on the International Society for the Study of Vascular Anomalies classification of vascular anomalies, we studied the expression of WT1 in vascular tumors composed of infantile Hemangioma, congenital Hemangiomas (non-involuting, rapidly involuting, and not otherwise specified), pyogenic granuloma, tufted angioma, cherry angioma, Kaposi sarcoma, and angiosarcoma. We also studied WT1 expression in vascular malformations composed of angiokeratoma/verrucous Hemangioma, combined vascular malformations, venous malformations, glomuvenous malformations, lymphatic malformations/lymphangioma, telangiectasia, and Targetoid Hemosiderotic Hemangioma. Results All vascular tumors and proliferations had positive WT1 cytoplasmic endothelial immunostaining whereas only 3 vascular malformations were WT1 positive. Moreover the positivity of WT1 in these vascular malformations was focal and involved only re-endothelialized neovessels within thrombi. Limitations The low number of malignant vascular tumors is a limitation. Conclusions Immunohistochemical detection of WT1 could be a useful tool to routine evaluation of vascular anomalies allowing the distinction of vascular tumors and proliferations from vascular malformations. Staining for WT1 may guide the clinician in difficult cases, as positive results would suggest a proliferative vascular lesion whereas negative results might point to a vascular malformation.
Andrew J Carlson - One of the best experts on this subject based on the ideXlab platform.
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Targetoid Hemosiderotic Hemangioma a dynamic vascular tumor report of 3 cases with episodic and cyclic changes and comparison with solitary angiokeratomas
Journal of The American Academy of Dermatology, 1999Co-Authors: Andrew J Carlson, Soume Daulat, Herbert P GoodheartAbstract:Abstract Background: Both Targetoid Hemosiderotic Hemangiomas (THH) and solitary angiokeratomas (SAK) are acquired vascular malformations formed by superficial vascular ectasias possibly caused by trauma. Objective: We compare the clinicopathologic findings of THHs with those of SAKs and report the clinicopathologic findings of 3 singular cases of THH affected by cyclic or episodic morphologic changes. Methods: We performed a clinicopathologic study on 33 cases of THH and compared this group with 20 cases of SAK. On selected cases, histochemical and immunohistochemical analyses were evaluated. Results: Overlap of all the clinical and pathologic features studied were identified for THH and SAK. Clinically, they both commonly exhibited a brown or black papule located over the lower extremities that mimicked a melanocytic lesion. Histologically, they both had ectatic papillary dermal vessels with overlying epidermal hyperplasia, and adjacent hemosiderin deposits, extravasated red blood cells, lymphocytic infiltrate, and lymphangiectases. Compared with SAKs, THHs were significantly larger (5.3 vs 3.2 mm), more often excised (elliptical excision) than shave or punch biopsied, and had deeper dermal vessel alterations, more frequent dissecting vascular spaces, and more extensive hemosiderin deposits (all P P = .001). Conclusion: THHs and SAKs differ in degree, not in type, of clinicopathologic characteristics. This finding suggests that THHs are larger variants of SAKs whose size is the cause of more extensive, prolonged, or recurrent vessel damage. The histologic findings of extravasated red blood cells, hemosiderin, telangiectases, lymphangiectases, and fibrosis implicate trauma in the cause of these acquired vascular malformations. (J Am Acad Dermatol 1999;41:215-24.)
Rola Al Dhaybi - One of the best experts on this subject based on the ideXlab platform.
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Targetoid Hemosiderotic Hemangiomas hobnail Hemangiomas are vascular lymphatic malformations a study of 12 pediatric cases
Journal of The American Academy of Dermatology, 2012Co-Authors: Rola Al Dhaybi, Christina Lam, Afshin Hatami, Julie Powell, Catherine Mccuaig, Victor KoktaAbstract:Background Targetoid Hemosiderotic Hemangioma (THH), also called hobnail Hemangioma, is a benign vascular lesion and thought to be of lymphatic origin. Objective We sought to perform a clinicopathologic analysis of cases diagnosed as THH in a tertiary care children's hospital. Methods Clinical and histopathologic data were obtained from a chart review of 12 confirmed pediatric cases of THH. To determine the presence or absence of lymphatic vessels in lesional biopsy specimens, we evaluated the expression of the lymphatic endothelial cell marker podoplanin using the D2-40 antibody. Wilms tumor-1 gene immunostaining and Ki-67 proliferation index were also performed to evaluate the proliferative nature of these lesions. Results Three children had a lesion since birth and 4 had a history of trauma before appearance of the THH. D2-40 immunostaining was positive in every case. Wilms tumor-1 gene immunostaining was negative in 9 cases, focally positive in two cases, and not performed in one case. The Ki-67 proliferation index was very low in all cases studied. Limitations The small number of cases and restriction to a pediatric population were limitations. Conclusion Our findings suggest that THH should be classified as a lymphatic vascular malformation.
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differentiation of vascular tumors from vascular malformations by expression of wilms tumor 1 gene evaluation of 126 cases
Journal of The American Academy of Dermatology, 2010Co-Authors: Rola Al Dhaybi, Julie Powell, Catherine Mccuaig, Victor KoktaAbstract:Background Vascular tumors and malformations can be challenging to diagnose. Although they may initially appear very similar, they have distinct clinical courses and management. Wilms tumor 1 (WT1) gene expression has been reported in many different tumors including hematologic malignancies and some solid tumors. Objective We sought to evaluate the expression of WT1 in 126 vascular lesions (64 vascular tumors, one Masson tumor, and 61 vascular malformations). Methods Based on the International Society for the Study of Vascular Anomalies classification of vascular anomalies, we studied the expression of WT1 in vascular tumors composed of infantile Hemangioma, congenital Hemangiomas (non-involuting, rapidly involuting, and not otherwise specified), pyogenic granuloma, tufted angioma, cherry angioma, Kaposi sarcoma, and angiosarcoma. We also studied WT1 expression in vascular malformations composed of angiokeratoma/verrucous Hemangioma, combined vascular malformations, venous malformations, glomuvenous malformations, lymphatic malformations/lymphangioma, telangiectasia, and Targetoid Hemosiderotic Hemangioma. Results All vascular tumors and proliferations had positive WT1 cytoplasmic endothelial immunostaining whereas only 3 vascular malformations were WT1 positive. Moreover the positivity of WT1 in these vascular malformations was focal and involved only re-endothelialized neovessels within thrombi. Limitations The low number of malignant vascular tumors is a limitation. Conclusions Immunohistochemical detection of WT1 could be a useful tool to routine evaluation of vascular anomalies allowing the distinction of vascular tumors and proliferations from vascular malformations. Staining for WT1 may guide the clinician in difficult cases, as positive results would suggest a proliferative vascular lesion whereas negative results might point to a vascular malformation.
Soume Daulat - One of the best experts on this subject based on the ideXlab platform.
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Targetoid Hemosiderotic Hemangioma a dynamic vascular tumor report of 3 cases with episodic and cyclic changes and comparison with solitary angiokeratomas
Journal of The American Academy of Dermatology, 1999Co-Authors: Andrew J Carlson, Soume Daulat, Herbert P GoodheartAbstract:Abstract Background: Both Targetoid Hemosiderotic Hemangiomas (THH) and solitary angiokeratomas (SAK) are acquired vascular malformations formed by superficial vascular ectasias possibly caused by trauma. Objective: We compare the clinicopathologic findings of THHs with those of SAKs and report the clinicopathologic findings of 3 singular cases of THH affected by cyclic or episodic morphologic changes. Methods: We performed a clinicopathologic study on 33 cases of THH and compared this group with 20 cases of SAK. On selected cases, histochemical and immunohistochemical analyses were evaluated. Results: Overlap of all the clinical and pathologic features studied were identified for THH and SAK. Clinically, they both commonly exhibited a brown or black papule located over the lower extremities that mimicked a melanocytic lesion. Histologically, they both had ectatic papillary dermal vessels with overlying epidermal hyperplasia, and adjacent hemosiderin deposits, extravasated red blood cells, lymphocytic infiltrate, and lymphangiectases. Compared with SAKs, THHs were significantly larger (5.3 vs 3.2 mm), more often excised (elliptical excision) than shave or punch biopsied, and had deeper dermal vessel alterations, more frequent dissecting vascular spaces, and more extensive hemosiderin deposits (all P P = .001). Conclusion: THHs and SAKs differ in degree, not in type, of clinicopathologic characteristics. This finding suggests that THHs are larger variants of SAKs whose size is the cause of more extensive, prolonged, or recurrent vessel damage. The histologic findings of extravasated red blood cells, hemosiderin, telangiectases, lymphangiectases, and fibrosis implicate trauma in the cause of these acquired vascular malformations. (J Am Acad Dermatol 1999;41:215-24.)
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Targetoid Hemosiderotic Hemangioma a dynamic vascular tumor report of 3 cases with episodic and cyclic changes and comparison with solitary angiokeratomas
Annual Meeting of the American Society of Dermatopathology, 1999Co-Authors: J A Carlson, Soume Daulat, Herbert P GoodheartAbstract:Background: Both Targetoid Hemosiderotic Hemangiomas (THH) and solitary angiokeratomas (SAK) are acquired vascular malformations formed by superficial vascular ectasias possibly caused by trauma. Objective: We compare the clinicopathologic findings of THHs with those of SAKs and report the clinicopathologic findings of 3 singular cases of THH affected by cyclic or episodic morphologic changes. Methods: We performed a clinicopathologic study on 33 cases of THH and compared this group with 20 cases of SAK. On selected cases, histochemical and immunohistochemical analyses were evaluated. Results: Overlap of all the clinical and pathologic features studied were identified for THH and SAK. Clinically, they both commonly exhibited a brown or black papule located over the lower extremities that mimicked a melanocytic lesion. Histologically, they both had ectatic papillary dermal vessels with overlying epidermal hyperplasia, and adjacent hemosiderin deposits, extravasated red blood cells, lymphocytic infiltrate, and lymphangiectases. Compared with SAKs, THHs were significantly larger (5.3 vs 3.2 mm), more often excised (elliptical excision) than shave or punch biopsied, and had deeper dermal vessel alterations, more frequent dissecting vascular spaces, and more extensive hemosiderin deposits (all P <.01). THHs presenting with episodic changes were significantly larger than those without (11 vs 4.4 mm, P =.001). Conclusion: THHs and SAKs differ in degree, not in type, of clinicopathologic characteristics. This finding suggests that THHs are larger variants of SAKS whose size is the cause of more extensive, prolonged, or recurrent vessel damage. The histologic findings of extravasated red blood cells, hemosiderin, telangiectases, lymphangiectases, and fibrosis implicate trauma in the cause of these acquired vascular malformations.
