PATHOLOGY OF VASCULAR SKIN LESIONS - PART 5 pptx

122 Sangüeza and Requena / Pathology of Vascular Skin Lesions 13. Albrecht S, Kahn HJ. Immunohistochemistry of intravascular papillary endothelial hyperplasia. J Cutan Pathol 1990;17:16–21. 14. Rosai J, Akerman LR. Intravascular atypical vascular proliferation. Arch Dermatol 1974;109:704–17. 15. Cooper PH. Vascular tumors. In: Farmer R, Hood AF, eds. Pathology of the Skin. Norwalk, CT, Appleton & Lange, 1990:804–46. 16. Pins MR, Rosenthal DI, Springfield DS, Rosemberg AE. Florid extravascular papillary endothelial hyperplasia (Masson’s pseudoangiosarcoma) presenting as a soft-tissue sarcoma. Arch Pathol Lab Med 1993;117:259–63. 17. Chen KT. Extravascular papillary endothelial hyperplasia. J Surg Oncol 1987;36:52–4. 18. Borrelli L, Ciniglio M, Faffulli N, Del Torto M. Intravascular papillary endothelial hyperplasia in the hand of a fencer. Pathologica 1992;84:551–6. 19. Inaloz HS, Patel G, Knight AG. Recurrent intravascular papillary endothelial hyperplasia developing from a pyogenic granuloma. J Eur Acad Dermatol Venereol 2000;15:156–8. 20. Hashimoto H, Daimaru Y, Enjoji M. Intravascular papillary endothelial hyperplasia. A clinicopatho- logic study of 91 cases. Am J Dermatopathol 1983;5:539–46. 21. Heyden G, Dahl I, Angervall L. Intravascular papillary endothelial hyperplasia in the oral mucosa. Oral Surg Oral Med Oral Pathol 1978;45:83–7. 22. Buchner A, Merrell PW, Carpenter WM, Leider AS. Oral intravascular papillary endothelial hyperpla- sia. J Oral Pathol Med 1990;19:419–22. 23. Stern Y, Braslavsky D, Shpitzer T, Feinmesser R. Papillary endothelial hyperplasia in the tongue: a benign lesion that may be mistaken for angiosarcoma. J Otolaryngol 1994;23:81–3. 24. Tosios K, Koutlas IG, Papanicolaou SI. Intravascular papillary endothelial hyperplasia of the oral soft tissues: report of 18 cases and review of the literature. J Oral Maxillofac Surg 1994;52:1263–8. 25. De Courten A, Fuffer R, Samson J, Lombardi T. Intravascular papillary endothelial hyperplasia of the mouth: report of six cases and literature review. Oral Dis 1999;5:175–8. 26. Wehbe MA, Otto NR. Intravascular papillary endothelial hyperplasia in the hand. J Hand Surg [Am] 1986;11:275–9. 27. Schwartz IS, Parris A. Cutaneous intravascular papillary endothelial hyperplasia: a benign lesion that may simulate angiosarcoma. Cutis 1982;29:66–9. 28. Dekio S, Tsujino Y, Jidoi J. Intravascular papillary endothelial hyperplasia on the penis: report of a case. J Dermatol 1993;20:10:657–9. 29. Cisco RW, McCormac RM. Intravascular papillary endothelial hyperplasia of the foot. J Foot Ankle Surg 1994;33:610–6. 30. Kato H. Two cases of intravascular papillary endothelial hyperplasia developing on the sole. J Dermatol 1996;23:655–7. 31. Stewart M, Smoller BR. Multiple lesions of intravascular papillary endothelial hyperplasia (Masson’s lesions). Arch Pathol Lab Med 1994;118:315–6. 32. Romani J, Puig L, Costa I, de Moragas JM. Masson’s intravascular papillary endothelial hyperplasia mimicking Stewart-Treves syndrome: report of a case. Cutis 1997;59:148–50. 33. Renshaw AA, Rosai J. Benign atypical vascular lesions of the lip. A study of 12 cases. Am J Surg Pathol 1993;17:557–65. 34. Levere SM, Barsky SH, Meals RA. Intravascular papillary endothelial hyperplasia: a neoplastic “actor” representing an exaggerated attempt at recanalization mediated by basic fibroblast growth factor. J Hand Surg [Am] 1994;19:559–64. 35. Katzman B, Caliguri DA, Klein DM, Nicastri AD, Chen P. Recurrent intravascular papillary endothelial hyperplasia. J Hand Surg [Br] 1997;22:113–5. 36. Yamamoto T, Marui T, Mizuno K. Recurrent intravascular papillary endothelial hyperplasia of the toes. Dermatology 2000;200:72–4. 07/Sangüeza/99-132/F 01/14/2003, 12:12 PM122 Chapter 7 / Cutaneous Vascular Hyperplasias 123 6. PSEUDO-KAPOSI’S SARCOMA Pseudo-Kaposi’s sarcoma is an unfortunate term applied to two completely different processes, acroangiodermatitis of Mali and the Stewart-Bluefarb syndrome. Acroangio- dermatitis of Mali (1) refers to skin lesions on the lower extremities of patients with chronic venous insufficiency, and Stewart-Bluefarb syndrome (2) is an arteriovenous malformation that clinically resembles Kaposi’s sarcoma. Clinical Features Clinically, the Stewart-Bluefarb syndrome usually presents early in life and involves the lower extremities of young adults unilaterally (Fig. 13). Purple papules and macules appear, which in some instances are painful and become ulcerated. The affected limb may have an increased temperature, with varicose veins, and a palpable thrill can be felt as an expression of the underlying arteriovenous shunt. Similar changes have been described at the site of cutaneous shunts for hemodyalisis (3–5) (Figs. 14 and 15) in paralyzed extremities (6,7) and in patients with Klippel-Trenaunay syndrome (8,9). Acroangio- dermatitis of Mali is simply exaggerated stasis dermatitis. The lesions are usually bilat- eral and develop in elderly patients with chronic venous insufficiency (Fig. 16). They have a predilection for the dorsal aspect of the feet and ankles. The lesions begin as violaceous macules and patches that develop slowly into soft, nontender, red to purple papules and nodules. Patients also present with scaly and indurated purple plaques, and Fig. 13. Stewart-Bluefarb syndrome in the lower extremity of young male patient. An underlying arteriovenous shunt was present. 07/Sangüeza/99-132/F 01/14/2003, 12:12 PM123 124 Sangüeza and Requena / Pathology of Vascular Skin Lesions changes of stasis dermatitis are evident on the adjacent skin. Lesions identical to those of acroangiodermatitis of Mali may be seen in the distal part of an amputation stump (10,11) (Fig. 17) induced by a suction-socket prosthesis (12). H ISTOPATHOLOGIC FEATURES Both types of pseudo-Kaposi’s sarcoma resemble Kaposi’s sarcoma clinically, but histopathologically they are completely different. In the Mali’s variant, the histopatho- logic findings are those of stasis dermatitis, namely, there is an increased number of thick- walled vessels lined by plump endothelial cells, extravasation of erythrocytes, and deposits of hemosiderin (Fig. 18). These changes are confined to the upper half of the dermis. In Stewart-Bluefarb syndrome, the entire dermis may be affected and, in large specimens, an arteriovenous shunt may be identified. Histopathologically, the differen- tial diagnosis with early stages of Kaposi’s sarcoma is usually straightforward, keeping in mind that the patch and plaque stages of Kaposi’s sarcoma are characterized by a proliferation of irregular jagged blood vessels, which are present around preexisting venules and adnexa and are lined by thin endothelial cells. As a rule, the papillary dermis is spared in the early stages of Kaposi’s sarcoma. Recently, the expression of CD34 antigen has been proposed as a feature to histopathologically distinguish lesions of pseudo-Kaposi’s sarcoma from authentic Kaposi’s sarcoma. CD34 positivity is detected in both endothelial cells and perivascular spindle cells of Kaposi’s sarcoma, whereas no such expression is seen in pseudo-Kaposi’s sarcoma (13). Furthermore; HHV-8 is not demonstrated in lesions of pseudo-Kaposi’s sarcoma (14). Fig. 14. Acroangiodermatitis involving the forearm and the hand, distally to the site of a cutaneous arteriovenous shunt for hemodialysis. Fig. 15. Acroangiodermatitis involving the inner aspect of the forearm distally to the site of a cutaneous arteriovenous shunt for hemodialysis. The lesion showed the appearance of a purpu- ric plaque. 07/Sangüeza/99-132/F 01/14/2003, 12:12 PM124 Chapter 7 / Cutaneous Vascular Hyperplasias 125 Fig. 16. Acroangiodermatitis of Mali involving the inner aspect of the ankle of an elderly male. Fig. 17. Acroangiodermatitis of Mali involving the distal part of an amputation stump. 07/Sangüeza/99-132/F 01/14/2003, 12:12 PM125 126 Sangüeza and Requena / Pathology of Vascular Skin Lesions TREATMENT Treatment of acroangiodermatitis of Mali is unsatisfactory and often unnecessary. If it is required, treatment of venous insufficiency of the lower extremities may be followed by slow improvement of the cutaneous lesions. Patients with Stewart-Bluefarb syndrome should consult with a vascular surgeon in order to embolize or excise the arteriovenous shunt under angiographic control (15). References 1. Mali JWH, Kuiper JT, Hamers AA. Acro-angiodermatitis of the foot. Arch Dermatol 1965;92:515–8. 2. Bluefarb SM, Adams LA. Arteriovenous malformation with angiodermatitis. Stasis dermatitis simulat- ing Kaposi’s disease. Arch Dermatol 1967;96:176–81. 3. Goldblum OM, Kraus E, Bronner AK. Pseudo-Kaposi’s sarcoma of the hand associated with an acquired, iatrogenic arteriovenous fistula. Arch Dermatol 1985;121:1038–40. 4. Landthaler M, Stolz W, Eckert F, Schmoeckel C, Braun-Falco O. Pseudo-Kaposi’s sarcoma occurring after placement of arteriovenous shunt. A case report with DNA content analysis. J Am Acad Dermatol 1989;21:499–505. Fig. 18. Histopathologic features of acroangiodermatitis. (A) Scanning magnification show lobu- lar proliferations of capillaries at the superficial dermis. (B) Higher magnification demonstrates that the lobules are composed of plump endothelial cells with extravasation of erythrocytes and deposits of hemosiderin. 07/Sangüeza/99-132/F 01/14/2003, 12:12 PM126 Chapter 7 / Cutaneous Vascular Hyperplasias 127 5. Kim TH, Kim KH, Kang JS, Kim JH, Hwang IY. Pseudo-Kaposi’s sarcoma associated with acquired arteriovenous fistula. J Dermatol 1997;24:28–33. 6. Meynadier J, Malbos S, Guilhon JJ, et al. Pseudo-angiosarcomatose de Kaposi sur membre paralytique. Dermatologica 1980;16:190–7. 7. Landthaler M, Langehenke H, Holzmann H, Braun Falco O. Akroangiodermatitis Mali (“Pseudo- Kaposi”) and gelähmten Beinen. Hautarzt 1988;39:304–7. 8. Lund Kofoed M, Klemp P, Thestrup-Pedersen K. The Klippel-Trenaunay syndrome with acro- angiodermatitis (pseudo-Kaposi’s sarcoma). Acta Derm Venereol 1985;65:75–7. 9. Lyle WG, Given KS. Acroangiodermatitis (pseudo-Kaposi’s sarcoma) associated with Klippel- Trenaunay syndrome. Ann Plast Surg 1996;37:654–6. 10. Kolde G, Wörheide J, Baumgartner R, Bröcker EB. Kaposi-like acroangiodermatitis in an above-knee amputation stump. Br J Dermatol 1989;120:575–80. 11. Gucluer H, Gurbuz O, Kotiloglu E. Kaposi-like acroangiodermatitis in an amputee. Br J Dermatol 1999;141:380–1. 12. Badell A, Marcoval J, Graells J, Moreno A, Peyri J. Kaposi-like acroangiodermatitis induced by a suction-socket prosthesis. Br J Dermatol 1994;131:915–7. 13. Kanitakis J, Narvaez D, Claudy A. Expression of the CD34 antigen distinguishes Kaposi’s sarcoma from pseudo-Kaposi’s sarcoma (acroangiodermatitis). Br J Dermatol 1996;134:44–6. 14. Krengel S, Goerdt S, Kruger K, Schnitzler P, Geiss M, Tebbe B, Blume-Peytavi U, Orfanos CE. Kaposiforme, HHV-8-negative Akroangiodermatitis bei chronisch-venoser insuffizienz. Hautarzt 1999;50:208–13. 15. Utermann S, Kahle B, Petzoldt D. Erfolgreiche Langzeittherapie bei Stewart-Bluefarb-Syndrom. Hautarzt 2000;51:336–9. 07/Sangüeza/99-132/F 01/14/2003, 12:12 PM127 128 Sangüeza and Requena / Pathology of Vascular Skin Lesions 7. REACTIVE ANGIOENDOTHELIOMATOSIS Angioendotheliomatosis is a broad term that encompasses two different processes, one malignant and the other benign. Malignant angioendotheliomatosis is an intravascu- lar form of malignant lymphoma, whereas the reactive or benign form of angio- endotheliomatosis is a self-limited intravascular proliferation of endothelial cells that occurs in the skin as a response to a different stimuli (1). C LINICAL FEATURES Reactive angioendotheliomatosis is usually limited to the skin, and, in contrast to what was initially thought, is not necessarily associated with an underlying infection. Cases of reactive angioendotheliomatosis have been described in patients with subacute bacterial endocarditis, Chagas’ disease, allergic response to cow’s milk protein, pulmonary tuber- culosis, cryoproteinemia, chronic lymphatic leukemia, hepatopathy and hypertensive portal gastropathy, antiphospholipid syndrome, rheumatoid arthritis, dermal amyloid angiopathy, and severe peripheral vascular atherosclerotic disease, but also in patients with no underlying disease (2–16). Clinically, the lesions appear as red-brown or violaceous nodules or plaques over the face (Fig. 19), arms, and legs (2). In addition, petecchiae, ecchymoses, and small areas Fig. 19. Reactive angioendotheliomatosis in a patient with cryoglobulinemia. Purpuric plaques on the cheeks of an elderly woman. 07/Sangüeza/99-132/F 01/14/2003, 12:12 PM128 Chapter 7 / Cutaneous Vascular Hyperplasias 129 of necrosis are frequently observed (3,5). The pathogenesis remains unclear, but a circu- lating angiogenic factor has been proposed by some investigators (4,6). Wick and Rocamora (1) suggested that reactive angioendotheliomatosis is an unusual residual of leukocytoclastic vasculitis. In cases associated with cryoglobulinemia or cold aggluti- nins, the luminal deposits of cryoproteins may be the stimulus to induce the proliferation of endothelial cells (7,17). A similar pathogenesis has been proposed for glomeruloid hemangioma in POEMS syndrome (18). Reactive intravascular angiomatosis of the skin with local deposits of intravascular immunoglobulin resulting in a vascular proliferation with a glomeruloid pattern has also been described in patients with monoclonal gammopathy and chronic lymphocytic B-leukemia (19). In the cases of peripheral atherosclerotic disease, vascular insufficiency from the occluded arteries appears to be the inciting factor for the endothelial proliferation, because when the blood flow is restored by a graft bypass, the lesions resolve (8,20). We have seen examples of both intravascular and diffuse dermal reactive angioendo- theliomatosis that appeared in acral areas of the forearm and hand secondary to iatrogenic arteriovenous fistulas for hemodialysis that resolved when the arteriovenous fistula was removed. We postulated that a local increase of vascular endothelial growth factor, as is the case in hypoxia, was the cause of the endothelial proliferation (21). Kunstfeld et al. (22) have recently described an example of diffuse dermal reactive angioendotheliomatosis with lesions involving the trunk in a patient undergoing chronic hemodialysis. H ISTOPATHOLOGIC FEATURES Histopathologically, the intravascular form of reactive angioendotheliomatosis exhib- its dilated blood vessels that contain a proliferation of endothelial cells often occluding the lumina of the vessels; occasionally there are associated fibrin thrombi (Fig. 20). Focally, recanalized “glomeruloid” blood vessels are seen, especially in the cases asso- ciated with cryoglobulinemia (7,17). Endothelial cells do not show atypia, and mitotic figures are not identified. Involved vessels are surrounded by a scanty inflammatory infiltrate of lymphocytes, neutrophils, and extravasated erythrocytes. In the cases of reactive angioendotheliomatosis associated with severe peripheral vascular atheroscle- rotic disease, the histopathologic picture is different. In these cases the proliferation is not localized to preexisting vessels, or if it is, proliferation is minimal; what is more promi- nent is the presence of diffuse, interstitial proliferations of endothelial cells that percolate between the collagen bundles of the reticular dermis (8,20–23). Immunohistochemical studies have demonstrated that the proliferating cells in reactive angioendotheliomatosis are endothelial cells, because they expressed factor VIII-related antigen, Ulex europaeus I lectin, CD34, CD31, and vimentin, but they failed to express leukocyte antigens such as leukocyte common antigen, LN2, MT1, UCHL1, and L26, as well as epithelial membrane antigen and cytokeratins (1,7,8,18,22). In some cases, pro- liferation of pericytic myoepithelial cells, identified by their staining with antibodies to muscle-associated proteins, are present within and around affected blood vessels (1,9,22). In rare instances of intravascular reactive angioendotheliomatosis, the proliferating intravascular cells did not mark with endothelial cell markers but with markers of histio- cytic differentiation; for this type of lesion the term of intravascular histiocytosis has been proposed (24,25). PCRs carried out in paraffin-embedded sections of reactive angioendo- theliomatosis for HHV-8 DNA have been negative (22). 07/Sangüeza/99-132/F 01/14/2003, 12:12 PM129 130 Sangüeza and Requena / Pathology of Vascular Skin Lesions TREATMENT Cutaneous lesions of reactive angioendotheliomatosis require no treatment; most of them regress spontaneously when the cause is eliminated. In two recently described cases of diffuse dermal reactive angioendotheliomatosis, the lesions responded respectively to treatment with oral methylprednisolone (22) and isotretinoin (23). Fig. 20. Histopathologic features of reactive angioendotheliomatosis. (A) Low power shows numerous vascular structures scattered at different levels of the dermis. (B) Higher magnification demonstrates plump endothelial cells and fibrin thrombi occluding the lumina of the vessels. (C) Immunohistochemical studies reveal that most of the endothelial cells express immunoreactivity for CD31. 07/Sangüeza/99-132/F 01/14/2003, 12:12 PM130 Chapter 7 / Cutaneous Vascular Hyperplasias 131 References 1. Wick MR, Rocamora A. Reactive and malignant “angioendotheliomatosis”: a discriminant clinico- pathologic study. J Cutan Pathol 1988;15:260–71. 2. Pleger L, Tappeiner I. Zuz kenntnis der systemisierteu Endotheliomatose der cutanen Blutgefasse (Reticuloendotheliose?). Hautarzt 1959;10:359–63. 3. Ruiter M, Mandema E. New cutaneous syndrome in subacute bacterial endocarditis. Arch Inten Med 1964;113:283–90. 4. Pasyk K, Depowski M. Proliferating systemized angioendotheliomatosis of a 5-month- old infant. Arch Dermatol 1978;114:1512–5. 5. Gottron HA, Nickolowski W. Extrarenale Löhlein Herdnephritis der Haut bei Endocarditis. Arch Klin Exp Dermatol 1958;207:156–76. 6. Person JR. Systemic angioendotheliomatosis. A possible disorder of a circulating angiogenic factor. Br J Dermatol 1977;96:329–31. 7. LeBoit PE, Solomon AR, Santa Cruz DJ, Wick MR. Angiomatosis with luminal cryoprotein deposition. J Am Acad Dermatol 1992;27:969–73. 8. Krell JM, Sanchez RL, Solomon AR. Diffuse dermal angiomatosis: a variant of reactive cutaneous angioendotheliomatosis. J Cutan Pathol 1994;21:363–70. 9. Lazova R, Slater C, Scott G. Reactive angioendotheliomatosis. Case report and review of the literature. Am J Dermatopathol 1996;18:63–9. 10. Martin S, Pitcher D, Tschen J, Wolf JE Jr. Reactive angioendotheliomatosis. J Am Acad Dermatol 1980;2:117–23. 11. Schmidt K, Hartig C, Stadler R. Reaktive Angioendotheliomatose bei chronisch lymphatischer Leukamie. Hautartz 1996;47:550–5. 12. Quinn TR, Alora MB, Momtaz KT, Taylor CR. Reactive angioendotheliomatosis with underlying hepatopathy and hypertensive portal gastropathy. Int J Dermatol 1998;37:382–5. 13. Creamer D, Black MM, Calonje E. Reactive angioendotheliomatosis with the antiphospholipid syn- drome. J Am Acad Dermatol 2000;42:903–6. 14. Tomasini C, Soro E, Pippione M. Angioendotheliomatosis in a woman with rheumatoid arthritis. Am J Dermatopathol 2000;22:334–8. 15. Ortonne N, Vignon-Pennamen MD, Majdalani G, Pinquier L, Janin A. Reactive angioendotheliomatosis secondary to dermal amyloid angiopathy. Am J Dermatopathol 2001;23:315–9. 16. Brazzelli V, Baldini F, Vasallo C, et al. Reactive angioendotheliomatosis in an infant. Am J Dermatopathol 1999;21:42–5. 17. Porras-Luque JI, Fernandez-Herrera J, Dauden E, Fraga J, Fernández-Villalta MJ, García-Díez A. Cutaneous necrosis by cold agglutinins associated with glomeruloid reactive angioendotheliomatosis. Br J Dermatol 1998;139:1068–72. 18. Chan JKC, Fletcher CDM, Hicklin GA, et al. Glomeruloid hemangioma: a distinctive cutaneous lesion of multicentric Castleman’s disease associated with POEMS syndrome. Am J Surg Pathol 1990;14:1036–46. 19. Salama SS, Jenkin P. Angiomatosis of skin with local intravascular immunoglobulin deposits, associ- ated with monoclonal gammopathy. A potential cutaneous marker for B-chronic lymphocytic leukemia. A report of unusual case with immunohistochemical and immunofluorescence correlation and review of the literature. J Cutan Pathol 1999;26:206–12. 20. Kimyai-Asadi A, Nousari HC, Ketabchi N, Henneberry JM, Costarangos C. Diffuse dermal angioma- tosis: a variant of reactive angioendotheliomatosis associated with atherosclerosis. J Am Acad Dermatol 1999;40:257–9. 21. Requena L, Fariña MC, Renedo G, Alvarez A, Sanchez Yus E, Sangueza OP. Intravascular and diffuse dermal reactive angioendotheliomatosis secondary to iatrogenic arteriovenous fistulas. J Cutan Pathol 1999;26:159–64. 22. Kunstfeld R, Petzelbauer P. A unique case of benign disseminated angioproliferation combining fea- tures of Kaposi’s sarcoma and diffuse dermal angioendotheliomatosis. J Am Acad Dermatol 2001;45:601–5. 23. McLaughlin ER, Morris R, Weiss SW, Arbiser JL. Diffuse dermal angiomatosis of the breast: response to isotretinoin. J Am Acad Dermatol 2001;45:462–5. 24. O’Grady JT, Shahidullah H, Doherty VR, Al-Nafussi A. Intravascular histiocytosis. Histopathology 1994;24:265-8. 25. Rieger E, Soyer HP, LeBoit PE, Metze D, Slovak R, Kerl H. Reactive angioendotheliomatosis or intravascular histiocytosis? An immunohistochemical and ultrastructural study in two cases of intravas- cular histiocytic cell proliferation. Br J Dermatol 1999;140:497–504. 07/Sangüeza/99-132/F 01/14/2003, 12:12 PM131 [...]... (bFGF) and vascular endothelial growth factor /vascular permeability factor (VEGF/ VPF) (69), as well as high levels of the intercellular adhesion molecule (ICAM )-3 (70), type IV collagenase (71), urokinase (71), and E-selectin (71) Interferon-β (IFN-β) is 08/Sangüeza/13 3-2 16/F 143 01/14/2003, 2 :57 PM 144 Sangüeza and Requena / Pathology of Vascular Skin Lesions Fig 12 Histopathologic features of congenital... hemangiomas scattered on the anterior chest of an adult man 08/Sangüeza/13 3-2 16/F 151 01/14/2003, 2 :58 PM 152 Sangüeza and Requena / Pathology of Vascular Skin Lesions Fig 15 Numerous small cherry hemangiomas scattered all over the skin This woman also had a prolactinoma Fig 16 Histopathologic features of cherry hemangioma (A) Low-power view shows a wellcircumscribed vascular proliferation (B) Higher magnification... Am Acad Dermatol 2000;43:37–41 21 Gupta G, Bilsland D A prospective study of the impact of laser treatment on vascular lesions Br J Dermatol 2000;143: 356 –9 08/Sangüeza/13 3-2 16/F 153 01/14/2003, 2 :58 PM 154 Sangüeza and Requena / Pathology of Vascular Skin Lesions 4 ARTERIOVENOUS HEMANGIOMA This lesion was first described in 1 956 by Biberstein and Jessner (1), who termed it cirsoid aneurysm, because... early years of life, a stable period, and then characteristically, spontaneous regression Virtually, 100% of infantile hemangiomas undergo some degree of 08/Sangüeza/13 3-2 16/F 137 01/14/2003, 2 :57 PM 138 Sangüeza and Requena / Pathology of Vascular Skin Lesions Fig 4 Ulcerated infantile hemangioma on the dorsum of the neck spontaneous regression (Fig 5) It has been estimated that approx 30% of infantile... Waidelich W, Braun-Falco O A three-year experience with the argon laser in dermatotherapy J Dermatol Surg Oncol 1984;10: 456 –61 19 Grekin RC, Flynn TC, Cooper D, Geisse J Efficacy of a 2-mm spot size lens for the treatment of superficial vascular lesions with a flashlamp-pumped dye laser Int J Dermatol 1997;36:8 65 9 20 Aghassi D, Anderson RR, Gonzalez S Time-sequence histologic imaging of laser-treated cherry... Giant hemangioma of the thigh (Kasabach-Merritt syndrome): resection with temporary clamping of the common iliac artery Br J Plast Surg 19 85; 38:426–32 08/Sangüeza/13 3-2 16/F 147 01/14/2003, 2 :58 PM 148 Sangüeza and Requena / Pathology of Vascular Skin Lesions 29 Evans J, Batchelor ADR, Stark G, et al Hemangioma with coagulopathy sustained response to prednisone Arch Dis Child 19 75; 50:809–12 30 Edgerton... therapy in the management of infantile hemangioma with Kasabach Merritt syndrome Pediatr Radiol 1987;17 :50 3–4 84 Enjolras O, Borsik M, Herbreteau D, Merland JJ, Hadjean E, Huy PT Indications chirurgicales dans les angiomes de face Ann Otolaryngol Chir Cervicofac 1993;110:192–7 08/Sangüeza/13 3-2 16/F 149 01/14/2003, 2 :58 PM 150 Sangüeza and Requena / Pathology of Vascular Skin Lesions 85 Chowdri NA, Darzi... coagulopathy (Kasabach-Merritt phenomenon) is associated with kaposiform hemangioendothelioma and not with common infantile hemangioma Plast Reconstr Surg 1997;100:1377–86 41 Alvarez-Mendoza A, Lourdes TS, Ridaura-Sanz C, Ruiz-Maldonado R Histopathology of vascular lesions found in Kasabach-Merritt syndrome: review based on 13 cases Pediatr Dev Pathol 2000;3 :55 6–60 42 Kishnani P, Iafolla AK, McConkie-Rosell A,... Diagnostic imaging in the evaluation of vascular birthmarks Dermatol Clin 1998;16: 455 –8 7 Dubois J, Garel L, Grignon A, et al Imaging of hemangiomas and vascular malformations in children Acad Radiol 1998 ;5: 390–400 8 Jacobs AH, Walton RG The incidence of birthmarks in the neonate Pediatrics 1976 ;58 :218–22 9 Hidano A, Purwoko R, Jitsukawa K Statistical survey of skin changes in Japanese neonates Pediatr... the treatment of benign cutaneous vascular ectasia Dermatologica 1987;174:11–7 22 Long CC, Lanigan SW Treatment of angioma serpiginosum using a pulsed tunable dye laser Br J Dermatol 1997;136:631–2 08/Sangüeza/13 3-2 16/F 1 35 01/14/2003, 2 :57 PM 136 Sangüeza and Requena / Pathology of Vascular Skin Lesions 2 INFANTILE HEMANGIOMAS Infantile hemangiomas are the most common vascular proliferation in infancy . Pathology of Vascular Skin Lesions changes of stasis dermatitis are evident on the adjacent skin. Lesions identical to those of acroangiodermatitis of Mali may be seen in the distal part of an amputation. Stewart-Treves syndrome: report of a case. Cutis 1997 ;59 :148 50 . 33. Renshaw AA, Rosai J. Benign atypical vascular lesions of the lip. A study of 12 cases. Am J Surg Pathol 1993;17 :55 7– 65. 34. Levere SM, Barsky. Langzeittherapie bei Stewart-Bluefarb-Syndrom. Hautarzt 2000 ;51 :336–9. 07/Sangüeza/9 9-1 32/F 01/14/2003, 12:12 PM127 128 Sangüeza and Requena / Pathology of Vascular Skin Lesions 7. REACTIVE ANGIOENDOTHELIOMATOSIS Angioendotheliomatosis