Dilatation of Pre-existing Vessels
Dilatation of pre-existing vessels include spider angioma (nevus araneus), capillary aneurysm-venous lake, telangiectasies, angiokeratomas and lymphangiectasias. The diagnosis of spider angioma is mostly clinical and is characterized by a central, slightly elevated, red punctum from which blood vessels radiate.

Capillary aneurysm and venous lake are different stages of the same disease. Clinically these are characterized by the sudden development of a growing dark papule seen on elderly patients. Histologically, capillary aneurysm presents as a thin-walled venule beneath the epidermis, lined by a single layer of endothelial cells and filled with a thrombus. When the thrombus dissolves the lesions acquire the appearance of a venous lake.

Telangiectasia denotes a condition that is characterized by the permanent dilatation of vessels. They can be either primary or secondary. Primary telangiectases can be seen in the following diseases: unilateral nevoid telangiectasia, generalized essential telangiectasia, hereditary hemorrhagic telangiectasia, hereditary benign telangiectasia, ataxia-telangiectasia, and cutaneous collagenous vasculopathy. Secondary telangiectases are seen in numerous, disparate conditions such as collagen vascular diseases, cutaneous mastocytosis and chronic graft versus host disease; but they also appear as a consequence of trauma, sun damage or radiodermatitis. Histopathologically, telangiectases are characterized by the presence of dilated blood vessels, mostly capillaries in the superficial dermis. Angiokeratoma is a group of several unrelated conditions, whose common denominator is the presence of dilated blood vessels in association with epidermal hyperplasia. Four clinical variants of angiokeratomas have been recognized: solitary, Fordyce's angiokeratoma, Mibelli's angiokeratoma and angiokeratoma corporis diffusum. The latter has been associated with different diseases of which Fabry's disease is the most common. Histopathologically, all variants of angiokeratomas are identical under a conventional microscope. Common features of all angiokeratomas include the presence of dilated thin-walled blood vessels, lined by a layer of endothelial cells, in the papillary dermis and a variable degree of hyperkeratosis.

Lymphangiectases are the result of permanent dilatation of lymphatic capillaries and develop in areas of the skin affected by obstruction or destruction of lymphatic drainage. Clinically, lymphangiectases are localized on genital or plantar skin and may mimic warts. Histopathologically, lymphangiectasias are characterized by the presence of dilated lymphatic vessels positioned within papillary dermis.

Hyperplasias
Hyperplasia is defined as an abnormal increase in the absolute number of normal cells, in an appropriately arranged tissue. Inherent in this terminology is the premise that hyperplasia ceases when its initiating stimulus has been removed; thereafter the tissue may or may not completely revert to its normal state. This group includes pyogenic granuloma, bacillary angiomatosis, verruga peruana, intravascular papillary endothelial hyperplasia, pseudo-Kaposi's sarcoma and reactive angioendotheliomatosis. The first three lesions, at least in their initial phase, have in common the presence of an exhuberant proliferation of vessels of different sizes and shapes, lined by prominent endothelium embedded in an edematous stroma. But there are differences, BA is produced by organisms of the genus Bartonella (formerly Rochalimaea). [13] Two species of Bartonella cause bacillary angiomatosis: B. quintana and, B. henselae. This disease is seen mostly in immunosupressed individuals. Verruga Peruana is the cutaneous manifestation of Bartonellosis and is caused by Bartonella bacilliformis.

Intravascular papillary endothelial hyperplasia (IPEH) is not a specific entity, but a histopathologic pattern that can be found in multiple vascular proliferations. Histopathologically, the proliferation of endothelial cells is present within one or more vascular lumina that have been occluded by a thrombus. In fully developed lesions, numerous papillary fronds lined by a single layer of plump endothelial cells, extend from the wall of the vessel into the lumina.

Pseudo-Kaposi's sarcoma is an unfortunate term that is applied to two completely different processes. These are acro-angiodermatitis of Mali and Stewart-Bluefard syndrome. Acro-angiodermatitis of Mali, refers to skin lesions on the lower extremities of patients with chronic venous insufficiency; and Stewart-Bluefarb syndrome, is an arteriovenous malformation that clinically resembles Kaposi's sarcoma. In the Mali's variant, the histopathologic 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 while in the Stewart-Bluefarb syndrome the entire dermis may be affected and, in large specimens, an arterio-venous shunt may be identified.

Reactive angioendotheliomatosis is usually limited to the skin, and in contrast to what was initially thought, is not necessarily associated with an underlying infection. Histopathologically, the intravascular form of reactive angioendotheliomatosis shows dilated blood vessels that contain a proliferation of endothelial cells which often occlude the lumina of the vessels; occasionally there are associated fibrin thrombi.

Benign Neoplasms

a) With endothelial differentiation
Angioma serpiginosum is a neoplasm characterized by a proliferation of endothelial cells and formation of new capillaries not simply a dilatation of pre-existing capillaries as in telangiectases. Histopathologically, angioma serpiginosum consists of clusters of dilated capillaries housed in the dermal papillae and lined by thick walls.

Infantile hemangioma is the most common benign vascular proliferation and traditionally, has been considered a neoplasm. That may be true for a minority of these proliferations, however, the majority of infantile hemangiomas are better considered as hyperplasias. This particular group of lesions, after an initial proliferative phase, undergo complete regression, through a process of fibrosis, even in the absence of therapy. True neoplastic infantile hemangiomas included noninvoluting congenital hemangiomas and congenital non-progressive hemangiomas. These two lesions do not regress as do the other infantile hemangiomas. The histopathologic composition of infantile hemangiomas varies with the age of the lesion. Early hemangiomas are highly cellular and are characterized by plump endothelial cells aligned to vascular spaces with small inconspicuous lumina. As the lesions mature, blood flow increases, endothelium flattens, and the lumina of the vessels enlarge and become more obvious. During this interval the vessels convey a "cavernous" appearance that can be misinterpreted as a venous malformation. Regression is portrayed as progressive interstitial fibrosis and adipose metaplasia, a process without known stimulus.

Noninvoluting congenital hemangiomas are characterized by lobular collections of small, thin-walled vessels with large, often stellate, central lumina, separated by variable amounts of fibrous tissue richly supplied with normal and abnormal veins and arteries. Congenital non-progressive hemangiomas are highly cellular with multiple well-defined lobules of proliferating capillaries that anastomose with each other to form ribbons within the dermis or subcutaneous tissue.

Senile or cherry angiomas are among the most frequently acquired cutaneous vascular lesions. They appear early in adulthood, most commonly on the trunk and with time, may increase in number and size. Microscopically, the cherry angioma consists of dilated capillary blood vessels localized in the superficial dermis.

Arteriovenous hemangioma is a neoplasm that occurs in mid-adult life and presents as a blue to red papule measuring 0.5 to 1.0 cm, mainly affecting facial skin. Histopathologically, acral arteriovenous hemangioma consists of a well-circumscribed proliferation of thick-walled muscle-containing blood vessels, lined by a single layer of endothelial cells involving the upper and mid reticular dermis.

Microvenular hemangioma is an acquired, slow growing asymptomatic lesion with angiomatous appearance. It is usually solitary and varies in size from 0.5 to 2 cm. It most commonly affects the upper limbs, particularly the forearms. Histopathologically, microvenular hemangioma appears as a poorly circumscribed proliferation of irregularly branched, round to oval, thin-walled blood vessels lined by a single layer of endothelial cells.

Tufted angioma most commonly affects children and young adults, but both congenital and very late onset cases have been described. The lesions have a predilection for the perineal area, thighs, neck, upper chest, back, and shoulders. Tufted angioma grows slowly and insidiously, and may eventually come to cover a large area of the trunk or neck. In most cases the growth is halted after some years and there is a slight tendency towards spontaneous regression. Histologically, TA presents with multiple individual vascular lobules within the dermis and subcutaneous fat. These aggregations are more prominent in the middle and lower part of the dermis. Each lobule is composed of aggregates of endothelial cells that form a concentric whorl around a preexisting vascular plexus. Some lobules bulge into the walls of dilated thin-walled vascular structures, giving these vessels a slit-like or semilunar appearance.

The term glomeruloid hemangiomas describe a distinctive vascular proliferation that occurs in patients affected with the POEMS syndrome. POEMS is an acronym for the syndrome which includes: polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy (M protein), and skin lesions. Microscopically, glomeruloid hemangioma consists of multiple ectatic vascular structures containing aggregates of capillary loops resembling renal glomeruli. The capillaries are lined with either flat or plump endothelial cells with vacuoles and surrounded by pericytes. The vacuoles in the cytoplasm of the endothelial cells contain eosinophilic PAS positive globules that represent deposits of immunoglobulins absorbed through circulation.

Acquired elastotic hemangioma develops during adulthood on chronic sun-damaged skin, on the extensor surface of the forearms or the lateral aspects of the neck. It mainly affects middle aged and elderly women. Acquired elastotic hemangioma presents as a slightly elevated, irregularly shaped, solitary lesion with violaceous coloration. Histopathologically, acquired elastotic hemangioma consists of a proliferation of capillary blood vessels involving the superficial dermis and in a band-like arrangement parallel to the epidermis. A narrow band of non-involved papillary dermis separates the newly formed capillaries from the normal or flattened epidermis.

Kaposiform hemangioendothelioma is a rare but distinctive vascular neoplasm that most commonly affects children. Though the retroperitoneum is the most frequent location, [1, 2, 3, 4, 5] it may also be found in the skin. When the neoplasm is positioned in deep soft tissue, mediastinum or retroperitoneum, it may be associated with the consumption coagulopathy that characterizes Kasabach-Meritt syndrome. Kaposiform hemangioendothelioma combines features of cellular infantile hemangioma and Kaposi's sarcoma. Characteristically, the neoplasm is composed of several ill-circumscribed nodules separated by connective tissue. Each nodule is formed by an admixture of small round capillaries and solid glomeruloid nests containing round to oval endothelial cells with epithelioid features.

Sinusoidal hemangioma lesions most frequently affect adult women and present as solitary, acquired subcutaneous nodule, however, examples of sinusoidal hemangioma in children have been also described in children. Widely dilated, thin-walled vascular channels that interconnect with each other characterize sinusoidal hemangioma. In some areas the neoplasm shows a pseudopapillary pattern. These thin-walled vessels branch and anastomose with each other to a much greater extent than conventional hemangiomas do.

Spindle cell hemangiomas most often occur in the distal regions of the extremities of children and young adults. However, examples of this lesion have been reported in other locations. Several cases of spindle cell hemangioma have been described in patients with Maffucci syndrome. Histopathologically, spindle cell hemangioma show well circumscribed but not encapsulated nodules that combine the features of hemangioma and Kaposi's sarcoma. They are rich in dilated thin walls and blood vessels sometimes occupied by organized thrombi and phleboliths. Interspersed between the blood vessels, is a stroma of spindle cells in fascicles closely resembling Kaposi's sarcoma.

The lesions of benign lymphangioendothelioma are reddish or bruise-like, slowly enlarging plaques that lack site predilection. Benign lymphangioendotheliomas appear histologically as delicate, thin-walled, endothelium-lined spaces entrapped between collagen bundles. The appearance may be confined to the papillary dermis but may extend into the reticular dermis and subcutaneous fat. In superficial areas, the vascular channels are arranged horizontally, often becoming smaller and more twisted at deeper levels.

The cutaneous lesions include: papules, small vesicles and erythematous plaques. Benign lymphangiomatous papules and plaques are the most common. Under low magnification, these lesions appear as relatively well-circumscribed capillary proliferations centered in the dermis, without extension into the subcutaneous fat. Most lesions show irregularly dilated lymphatic spaces, that branch and anastomose within the superficial dermis. Multiple papillary projections, covered by a single layer of endothelium, project into the lumina of the dilated lymphatic.

Lesions of hobnail hemangioma are characterized by a brown to violaceous central papule, surrounded by a thin, pale area and a peripheral ecchymotic ring. The ecchymotic halo ultimately disappears in contrast to the central papule that persists. Histopathologically, hobnail hemangioma shows a distinctive biphasic appearance. The center of the lesion is composed of dilated, irregular, thin-walled ectatic vascular spaces positioned in the superficial dermis. These vascular spaces sometimes exhibit intraluminal papillary projections and fibrin thrombi at different stages of organization. Prominent, plump, endothelial cells with a hobnail appearance line the papillary projections. The deep areas are distinct from the peripheral areas of the lesion because they show irregular, angulated thin-walled slit-shaped vascular channels that dissect the collagen bundles of the dermis.

Glomus tumors are uncommon neoplasms that arise from modified smooth muscle cells normally present in specialized arteriovenous shunts in acral sites, mainly the fingertips. Two types of glomus tumors have been described, solitary, and multiple. The solitary glomus tumor is more common. It creates a small, purple nodule preferentially in acral areas of the extremities, especially the nail beds of the fingers and toes. Frequently, the lesion create severe paroxysmal pain, usually precipitated by exposure to cold or minor pressure. Multiple glomus tumors are much less common than their solitary counterpart. They are termed glomangiomas descriptively in accordance with their angiomatous appearance. In contrast to the solitary glomus lesion, glomangiomas present during childhood as small bluish nodules situated deep in the dermis and widely scattered in the skin. Histopathologically, solitary glomus tumors are customarily solid, as a well-circumscribed nodule surrounded by compressed fibrous tissue. The neoplasm is cytologically formed of clusters of round or polygonal monomorphous glomus cells with large round, plump nuclei and scant eosinophilic cytoplasm. Glomangiomas are less well-circumscribed lesions than solitary glomus tumors. Some are made up of several nodules within the dermis and may have an appearance that calls to mind a hemangioma. These are composed of irregular dilated endothelial lined vascular channels that contain red blood cells and as a distinctive feature have small intramural aggregations of glomus cells. Glomus cells may form cords or small clusters in adjacent stroma, but numerically they are sparse relative to their numbers in a solitary glomus tumor.

Malignant Neoplasms

Kaposi's sarcoma
The clinical features and the biological behavior of Kaposi's sarcoma are different and depend on the epidemiological type. There are four types: the classical type of Kaposi's sarcoma which affects mainly elderly patients; the African-endemic variant; Kaposi's sarcoma associated with immunosuppressive drugs (iatrogenic) and AIDS-associated Kaposi's sarcoma. The earliest lesions of Kaposi's sarcoma known as the patch stage are characterized by inconspicuous changes and may produce the erroneous impression of an inflammatory condition. At scanning magnification these lesions show sparse, superficial and deep perivascular mononuclear cell infiltrates in conjunction with an increased number of irregular, jagged, vascular spaces lined by thin endothelial cells. The vessels are mainly found in the upper part of the dermis. The neoplastic vessels of Kaposi's sarcoma show a tendency to be present around pre-existing normal adnexae and blood vessels producing the so-called "promontory sign". In other areas, the blood vessels infiltrate collagen bundles of the dermis giving the appearance that they are "dissecting" the stroma. The inflammatory cells present are predominantly lymphocytes and plasma cells. The presence of plasma cells around newly formed irregular blood vessels is a helpful clue in the histopathologic diagnosis of the patch stage of Kaposi's sarcoma. Plaque lesions of Kaposi's sarcoma tend to involve the entire dermis and even the upper part of the subcutaneous fat. At this stage, there is an increased number of spindle cells arranged in short fascicles between collagen bundles centered around proliferating vascular channels. The spindle cells line irregularly shaped, slit-like vascular spaces that contain isolated erythrocytes. They display minimal or no atypia, with few or no mitotic figures. When the number of spindle cells increases, lesions of Kaposi's sarcoma become nodular. Then, the spindle cells are arranged in interwoven fascicles with erythrocytes scattered in the interstices. Nuclear atypia, pleomorphism and mitotic figures may be seen, but are usually not very prominent. In rare instances, however, especially in the African variant, a significant number of mitotic figures and atypical cells may be seen in lesions of Kaposi's sarcoma. A rather characteristic, but probably not specific, histopathologic finding is the presence of the so-called hyaline globules. Although these are most common in the plaque and nodular lesions of Kaposi's sarcoma, they can be present at any stage of the disease. These globules are located both intra- and extracellularlyand are PAS-positive, diastase-resistant and consist of eosinophilic spherules measuring between 1 to 10μm, and are. Most likely these hyaline globules represent degenerated erythrocytes that are phagocytized and confined to the phagolysosomes of the neoplastic cells.

Low grade angiosarcomas
This group of lesions includes: epithelioid hemangioendothelioma, retiform hemangioendothelioma and Dabska's tumor. These three neoplasms share many similarities both clinically and histologically, so they are best considered as part of a spectrum. Clinically, they usually appears as solitary, slightly painful tumors, which in some cases may ulcerate. They occur at any age and affects both sexes in approximately equal proportion. Histopathologically, the lesions of epithelioid hemangioendothelioma present as circumscribed dermal or subcutaneous nodules. The neoplasm is composed of cords, strands and nests of plump, epithelioid cells embedded in a fibromyxoid or sclerotic stroma. Many of the neoplastic cells contain vacuoles in their cytoplasm as a sign of primitive vascular differentiation. Slight cellular pleomorphism and occasional mitotic figures may be seen. Dabska's tumor is composed of interconnecting vascular channels lined by atypical endothelial cells. The vascular spaces vary in size and shape ranging from narrow channels to large vascular structures. The most characteristic histopathologic feature consists of papillary plugs of atypical endothelium, with a central sclerotic core of connective tissue, projecting into the lumina and producing a glomeruloid appearance. The endothelial cells are round to polyhedral with an atypical, hyperchromatic and eccentrically placed nuclei, located in the luminal border of the cell, producing a surface bulge, accounting for the term "hobnail" or "matchstick." Retiform hemangioendothelioma consists of elongated, arborizing blood vessels involving the dermis, arranged in an architectural pattern reminiscent to that of the normal rete testis. Monomorphic hobnail endothelial cells line the vessels composing the neoplasm. Cytologic atypia is minimal in the hobnail cells of retiform hemangioendothelioma and few or no mitotic figures are seen. In some areas, the retiform pattern is obscured by the presence of a dense inflammatory infiltrate of mature lymphocytes.

Angiosarcoma
Angiosarcomas are highly aggressive neoplasms that can present in three different settings, to wit: angiosarcoma of the face and scalp, angiosarcoma associated with lymphedema and radiation-induced angiosarcoma. Angiosarcoma of the face and scalp predominantly affects elderly patients and is usually located on the scalp and upper forehead. Clinically; the lesions appear as ill-defined bruise-like areas that simulate a hematoma. More advanced lesions present as indurate plaques with raised, nodular, and occasionally ulcerated components accompanied by smaller satellite lesions in the same vicinity. More than 90% of all angiosarcomas associated with chronic lymphedema occur following mastectomy for breast carcinoma,but it has been described in areas of lymphedema secondary to other mechanisms The arm, most often the upper inner aspect, is the most frequent site for early involvement. Less commonly, the tumor appears more distally, on the elbow or on the forearm. Clinically, these lesions appear as bruise-like areas or violaceous nodules superimposed on the brown non-pitting edema of the affected limb. After the appearance of the lesions, there is a rapid increase in their number and size and they may undergo ulceration. Advanced cases spread distally to the hands and proximally to the chest wall. Post irradiation cutaneous angiosarcoma is a rare condition that has been described following the use of radiotherapy for the treatment of diverse conditions, both benign and malignant. Regardless of the clinical variant, angiosarcomas are histopathologically similar. Well-differentiated angiosarcomas appear as irregular, dilated vascular channels lined by flattened endothelial cells with an innocuous appearance, which may lead one to confuse them with a hemangioma, lymphangioma or an inflammatory process. However, careful observation of these lesions reveals the presence of irregular vascular channels dissecting the dermis. These channels tend to communicate with each other, forming an anastomosing network. Furthermore, some of the endothelial cells appear large, hyperchromatic, and pleomorphic, protruding within vascular lumina, forming small papillations. Poorly differentiated angiosarcomas, demonstrate solid proliferations of polygonal or spindle-shaped pleomorphic endothelial cells, with prominent mitotic activity and poorly-formed vascular spaces, which sometimes makes it difficult to distinguish them from carcinoma, melanoma or a high-grade fibrosarcoma. Of considerable value for the diagnosis of these cases is the presence of cytoplasmic vacuoles within the neoplastic cells. Patchy lymphoid infiltrates are also a common finding. The number of erythrocytes that are present within the vascular spaces varies from a few to none in the poorly differentiated areas. Pre-existing adnexal, neural and vascular structures of the dermis are frequently involved and destroyed by the tumor.

Malignant glomus tumor (glomangiosarcoma)
The lesions of glomangiosarcoma are larger and deeper than conventional glomus tumors, and they are predominantly located on the extremities where they appear as subcutaneous masses. The tumors equally affect both men and women. Metastatic disease has been documented in only ten cases of histopathologically malignant glomus tumor, and in eight of these patients, death was a consequence of the widespread metastases from the glomangiosarcoma. Locally aggressive behavior appears to be more common in these neoplasms. There are three proposed categories for malignant glomus tumors:

1. locally infiltrative glomus tumor; these are neoplasms that lack atypical features but show locally aggressive behavior (LIGT)
   
   
2. glomangiosarcomas that result from the transformation of a glomus tumor (GABG); these are the most common type of MGT, and remaining areas of typical GT can be identified
   
   
3. de novo glomangiosarcoma (GADN), the most unusual form of MGT

BENIGN PROLIFERATIONS DILATATION OF PREEXISTING VESSELS Blood vessels: Spider angioma (nevus araneus) Capillary aneurism-venous lake Telangiectases: Unilateral nevoid telangiectasia Generalized essential telangiectasia Hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber disease) Hereditary benign telangiectasia Ataxia-telangiectasia (Louis-Bar syndrome) Cutaneous collagenous vasculopathy Angiokeratomas: Solitary angiokeratoma Angiokeratoma of Fordyce Angiokeratoma of Mibelli Angiokeratoma corporis diffusum Lymphatic vessels: Lymphangiectases HYPERPLASIAS Pyogenic granuloma Bacillary angiomatosis Verruga peruana Intravascular papillary endothelial hyperplasia (Masson's pseudoangiosarcoma) Pseudo-Kaposi's sarcoma: Acroangiodermatitis of Mali Stewart-Bluefarb syndrome "Benign" angioendotheliomatosis (reactive angioendotheliomatosis) BENIGN NEOPLASMS Endothelial differentiation: Capillaries and venules: Angioma serpiginosum Infantile hemangioma Cherry angioma (senile angioma) Acral arteriovenous hemangioma Angiolymphoid hyperplasia with eosinophilia Microvenular hemangioma Tufted angioma (angioblastoma) Glomeruloid hemangioma Acquired elastotic hemangioma Kaposiform hemangioendothelioma Veins and arteries: Sinusoidal hemangioma Giant-cell angioblastoma Spindle-cell hemangioma (formerly, spindle cell hemangioendothelioma) Lymphatic vessels: Benign lymphangioendothelioma Benign vascular proliferations in irradiated skin Hobnail hemangioma (Targetoid hemosiderotic hemangioma) Glomus cell differentiation: Solitary glomus tumor Multiple glomus tumors (glomangiomas) Intravenous glomus tumor MALIGNANT PROLIFERATIONS Kaposi's sarcoma Low-grade cutaneous angiosarcomas: Epithelioid hemangioendothelioma Endovascular papillary angioendothelioma (Dabska's tumor) Retiform hemangioendothelioma Composite hemangioendothelioma High-grade cutaneous angiosarcomas: Classic angiosarcoma of the face and scalp of elderly patients Cutaneous angiosarcoma associated with lymphedema Radiation-induced cutaneous angiosarcoma Epithelioid angiosarcoma Malignant glomus tumor (glomangiosarcoma)

References

1. Sangueza OP, Requena L. Pathology of vascular skin lesions: Clinicopathologic correlations. Humana Press, Totowa, New Jersey 2003.
   
   
2. Witte CL, Hicks T, Renert W, Witte MH, Butler C. Vascular spider: a cutaneous manifestation of hyperdynamic blood flow in hepatic cirrhosis. South Med J 1975;68:246-8.
   
   
3. Weathers DR, Fine RH. Thrombosed varyx of oral cavity. Arch Dermatol 1971; 104:427-30.
   
   
4. Person JR, Ossi MJ, Mundra R, et al. Unilateral nevoid telangiectasia. Arch Dermatol 1979;115:1034.
   
   
5. Kumar MV, Thappa DM, Shanmugam S, Ratnakar C. Angiokeratoma circumscriptum of the oral cavity. Acta Derm Venereol 1988;78:472.
   
   
6. Mu XC, Tran TA, Dupree M, Carlson JA. Acquired vulvar lymphangioma mimicking genital warts. A case report and review of the literature. J Cutan Pathol 1999;26:150-4. Peterson WC Jr, Fusaro RM, Goltz RW. Atypical pyogenic granuloma: a case of benign hemangioendotheliomatosis. Arch Dermatol 1964;90:197-201.
   
   
7. Stoler MH, Bonfiglio TA, Steigbigel RT, et al. An atypical subcutaneous infection associated with acquired immune deficiency syndrome. Am J Clin Pathol 1983;80:714-8.
   
   
8. Cockerell CJ, Webster GF, Whitlow MA, et al. Epithelioid angiomatosis: a distinct vascular disorder in patients with the acquired immunodeficiency syndrome or AIDS-related complex. Lancet 1987;2:654-6.
   
   
9. LeBoit PE, Berger TG, Egbert BM, et al. Epithelioid hemangioma - like vascular proliferation in AIDS. Manifestation of cat-scratch disease bacillus or infection? Lancet 1988;1:960-3.
   
   
10. Arias-Stella J, Liberman PH, Erlandson RA, Arias-Stella J Jr. Histology, immunohistochemistry, and ultrastructure of the verruga in Carrion's disease. Am J Surg Pathol 1986;10:595-610.
    
    
11. LeBoit PE, Solomon AR, Santa Cruz DJ, Wick MR. Angiomatosis with luminal cryoprotein deposition. J Am Acad Dermatol 1992;27:969-73.
    
    
12. Mulliken JB. Diagnosis and natural history of hemangiomas. In: Mulliken JB, Young AE eds. Vascular Birthmarks. Hemangiomas and Malformations. Philadelphia, W.B. Saunders Company, 1988;41-61.
    
    
13. Enjolras O, Mulliken JB, Boon LM, Wassef M, Kozakewich HPW, Burrows PE. Noninvoluting congenital hemangioma: A rare cutaneous vascular anomaly. Plast Reconstr Surg 2001;107:1647-54.
    
    
14. North PE, Waner M, James CA, Mizeracki A, Frieden IJ, Mihm MC Jr. Congenital nonprogressive hemangioma. A distinct clinicopathologic entity unlike infantile hemangioma. Arch Dermatol 2001;137:1607-20.
    
    
15. Santa Cruz DJ, Aronberg J. Targetoid hemosiderotic hemangioma. J Am Acad Dermatol 1988;19:550-8.
    
    
16. Guillou L, Calonje E, Speight P, Rosai J, Fletcher CD. Hobnail hemangioma: a pseudomalignant vascular lesion with a reappraisal of targetoid hemosiderotic hemangioma. Am J Surg Pathol 1999;23:97-105.
    
    
17. Hunt SJ, Santa Cruz DJ, Barr RJ. Microvenular hemangioma. J Cutan Pathol 1991;18:235-40.
    
    
18. Nakagawa K. Case report of angioblastoma of the skin. Nippon Hifuka Gakkai Zasshi 1949;59:92-4.
    
    
19. Wilson Jones E, Orkin M. Tufted angioma (angioblastoma). A benign progressive angioma not to be confused with Kaposi's sarcoma or low-grade angiosarcoma. J Am Acad Dermatol 1989;20:214-25.
    
    
20. Chan JKC, Fletcher CDM, Hicklin GA, Rosai J. Glomeruloid hemangioma. A distinctive cutaneous lesion of multicentric Castleman's disease associated with POEMS syndrome. Am J Surg Pathol 1990;14:1036-46.
    
    
21. Tsang WYW, Chan JKC. Kaposi-like infantile haemangioendothelioma: a distinctive vascular neoplasm of the retroperitoneum. Am J Surg Pathol 1991;15:982-9.
    
    
22. Weiss SW, Enzinger FM. Spindle cell hemangioendothelioma: a low grade angiosarcoma resembling cavernous hemangioma and Kaposi's sarcoma. Am J Surg Pathol 1986;10:521-30.
    
    
23. Ambrojo P, Fernández-Cogolludo E, Aguilar A, et al. Cutaneous lymphangiectases after therapy for carcinoma of the cervix: a case with unusual clinical and histological features. Clin Exp Dermatol 1990;15:57-9.
    
    
24. Díaz-Cascajo C, Borghi S, Weyers W, Retzlaff H, Requena L, Metze D. Benign lymphangiomatous papules of the skin following radiotherapy. A report of five new cases and review of the literature. Histopathology1999;35:319-27.
    
    
25. DiGiovanna JJ, Safai B. Kaposi's sarcoma: retrospective study of 90 cases with particular emphasis on the occurrence, ethnic background, and prevalence of other diseases. Am J Med 1981;71:779-83.
    
    
26. Chang Y, Cesarman E, Pessin MS, Lee F, Knowles DM, Moore PS. Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma. Science 1994;266:1865-9.
    
    
27. Weiss SW, Enzinger FM. Epithelioid hemangioendothelioma. A vascular tumor often mistaken for a carcinoma. Cancer 1982;50:970-81.
    
    
28. Weiss SW, Ishak KG, Dial DH, Sweet DE, Enzinger FM. Epithelioid hemangioendothelioma and related lesions. Semin Diagn Pathol 1986;3:259-87.
    
    
29. Dabska M. Malignant endovascular papillary angioendothelioma of the skin in childhood. Clinicopathologic study of 6 cases. Cancer 1969;24:503-10.
    
    
30. de Dulanto F, Armijo Moreno M. Malignant endovascular papillary hemangioendothelioma of the skin. Acta Derm Venereol 1973;53:403-8.
    
    
31. Calonje E, Fletcher CDM, Wilson Jones E, Rosai J. Retiform hemangioendothelioma. A distinctive form of low-grade angiosarcoma delineated in a series of 15 cases. Am J Surg Pathol 1994;18:115-25.
    
    
32. Wilson Jones E. Malignant angioendothelioma of the skin. Br J Dermatol 1964;76:21-39.
    
    
33. Holden CA, Spittle MF, Wilson Jones E. Angiosarcoma of the face and scalp, prognosis and treatment. Cancer 1987;59:1046-57.
    
    
34. Woodward AH, Ivins JC, Soule EH. Lymphangiosarcoma arising in chronic lymphedematous extremities. Cancer 1972;30:562-72.
    
    
35. Enzinger FM, Weiss SW. Malignant vascular tumors. In: Soft Tissue Tumors. Third Edition. St. Louis, MO, Mosby, 2002:641-77.