DOCSLIB.ORG

Malignant Vascular Tumors&Mdash

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Malignant Vascular Tumors&Mdash Modern Pathology (2014) 27, S30–S38 S30 & 2014 USCAP, Inc All rights reserved 0893-3952/14 $32.00 Malignant vascular tumors—an update Cristina Antonescu Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA Although benign hemangiomas are among the most common diagnoses amid connective tissue tumors, sarcomas showing endothelial differentiation (ie, angiosarcoma and epithelioid hemangioendothelioma) represent under 1% of all sarcoma diagnoses, and thus it is likely that fewer than 500 people in the United States are affected each year. Differential diagnosis of malignant vascular tumors can be often quite challenging, either at the low end of the spectrum, distinguishing an epithelioid hemangioendothelioma from an epithelioid hemangioma, or at the high-grade end of the spectrum, between an angiosarcoma and a malignant epithelioid hemangioendothelioma. Within this differential diagnosis both clinico-radiological features (ie, size and multifocality) and immunohistochemical markers (ie, expression of endothelial markers) are often similar and cannot distinguish between benign and malignant vascular lesions. Molecular ancillary tests have long been needed for a more objective diagnosis and classification of malignant vascular tumors, particularly within the epithelioid phenotype. As significant advances have been recently made in understanding the genetic signatures of vascular tumors, this review will take the opportunity to provide a detailed update on these findings. Specifically, this article will focus on the following aspects: (1) pathological and molecular features of epithelioid hemangioendothelioma, including the more common WWTR1–CAMTA1 fusion, as well as the recently described YAP1–TFE3 fusion, identified in a morphological variant of epithelioid hemangioendothe- lioma; (2) discuss the heterogeneity of angiosarcoma clinical, morphological and genetic spectrum, with particular emphasis of MYC and FLT4 gene amplification in radiation-induced angiosarcoma; and (3) provide a practical guide in the differential diagnosis of epithelioid vascular tumors using molecular testing. Modern Pathology (2014) 27, S30–S38; doi:10.1038/modpathol.2013.176 Keywords: angiosarcoma; epithelioid hemangioendothelioma; WWTR1–CAMTA1; YAP1–TFE3 Epithelioid hemangioendothelioma classic and malignant EHE, based on mitotic activity and size, in an effort to reflect different biological Incidence, Demographics. and Terminology subsets.5,6 Epithelioid hemangioendothelioma (EHE) is a rare soft tissue tumor, substantially less common than Pathological Features angiosarcoma, but given the more indolent nature of EHEs have a propensity for angiocentric growth, the tumor it encompasses a larger prevalent popula- expanding the vessel wall, obliterating the lumen tion.1 It occurs in a younger population, with a peak and spreading centrifugally into surrounding tissue incidence in the 4th to 5th decade.2 Women appear where they induce a sclerotic response (Figures to be affected more commonly than men. In a survey 1a-c). Microscopically, EHE are arranged in single of EHE patients from an EHE support group, overall files, cords and small nests (Figures 1d,e), typically survival was 73% at 5 years.3 lacking well-formed vascular channels, with only EHE of soft tissue was first described by Weiss and immature, intracytoplasmic lumina being observed Enzinger.4 As its clinical behavior is intermediate (Figures 1f). Other distinctive features include an between a benign hemangioma and a high-grade infiltrative growth pattern, encasing surrounding angiosarcoma, the term ‘hemangioendothelioma’ structures and lack of a lobular growth pattern was suggested. Subsequently, EHE of soft tissue typically seen with benign hemangiomas. EHE cells was stratified into two risk groups of malignancy, are separated by a characteristic extracellular sul- fated acid-rich matrix, varying from a light blue Correspondence: Dr C Antonescu, MD, Department of Pathology, (myxoid, myxo-chondroid, Figures 1f,g) to a deep Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New pink (hyaline, Figure 1h) extracellular stroma. The York, NY 10065, USA. Email: [email protected] cells have a pale to more densely eosinophilic Received 18 July 2013; revised 3 September 2013; accepted 4 cytoplasm containing vacuoles, which deform the September 2013 cytoplasm, so-called ‘blister cells’. Some vacuoles www.modernpathology.org Malignant vascular tumors C Antonescu S31 Figure 1 Conventional epithelioid hemangioendothelioma, pathological findings: (a) gross appearance of an epithelioid hemangioen- dothelioma (EHE) of the superior vena cava, tumor being entirely confined to the vein wall; (b) van Gieson elastic stain highlighting the elastic structure of a vessel wall showing complete obliteration with tumor; (c) angiocentric growth involving a small vessel wall in a soft tissue EHE; microscopic appearance showing cords (d) or solid sheets (e) of epithelioid cells with moderate amount of pale eosinophilic cytoplasm; (f) the presence of intracytoplasmic lumens (blisters cells) is a common feature, as is the myxochodnroid quality of the extracellular stroma; occasionally the matrix may more myxoid (g) or hyalinized (h) in appearance. (i) Malignant EHE with hyperchromasia, nuclear pleomorphism and increased mitotic activity. contain fragmented erythrocytes. In most cases, the transcriptional factor activation and signaling in the cells show a low nuclear grade, however, a small hippo pathway that is normally highly expressed in subset of cases show moderate to marked nuclear endothelial cells.10 WWTR1 fuses to CAMTA1,on pleomorphism, with overt hyperchromasia and 1p36, which belongs to a family of calmodulin- increased mitotic activity (Figure 1i). This latter binding transcription activators, normally found only appearance may be quite challenging to separate in brain. The 1p36 region is frequently lost in from angiosarcoma in a small biopsy sample. neuroblastoma and gliomas, implicating CAMTA1 as a tumor suppressor gene.11,12 Most cases with classic morphology (ie, lacking mature vascular Genetics channel formation) examined so far contain this translocation,8,9 which is not directly targetable with A t(1;3)(p36.3;q25) translocation was initially present day therapeutics, but may reveal downstream reported in two cases of EHE, suggesting that this targets in future studies. may represent a recurrent abnormality in this In 50% of cases, EHE have a multifocal clinical subgroup of tumors.7 Ten years later, two back-to- presentation.3 It has long been debated if this back studies, using different methodologies, occurrence is truly multifocal or represents an were able to clone the genes involved in the unusual pattern of loco-regional metastasis. This is t(1;3)(p36.3;q25) translocation.8,9 WWTR1 (also particularly relevant in visceral EHE, where the called TAZ), on 3q25, is a gene involved in 14-3-3 multifocal disease is limited to one organ (ie, liver, Modern Pathology (2014) 27, S30–S38 Malignant vascular tumors S32 C Antonescu lung), without dissemination to other distant sites. activity and tumor size have been used to stratify As a result of this clinical behavior, patients with tumors into low and high-risk groups: patients with multifocal liver EHE are candidates for liver trans- tumors 43 cm in diameter and having more than plantation. Thus, by analysis of WWTR1–CAMTA1 three mitoses/50 HPFs have a 5-year disease-specific breakpoints in multiple nodules from two patients survival of 59% in contrast to 100% survival in with multifocal hepatic EHE, we were able to prove patients whose tumors lacked these features.5 In recently that this phenomenon is monoclonal, their study, however, the presence of nuclear representing metastatic implants of the same pleomorphism and necrosis were not indicative of neoplastic clone rather than a ‘field-effect’ or adverse outcome. Furthermore, these criteria do not synchronous occurrence of multiple neoplastic apply for multifocal presentation and visceral clones.13 locations. Thus, larger studies are needed to better In a recent study, we identified the presence of define prognostic criteria in molecularly defined YAP1–TFE3 gene fusion in a specific subset of EHE, EHE patients. lacking the WWTR1–CAMTA1 fusion and displaying a somewhat distinct morphology and strong TFE3 expression by immunohistochemistry.14 YAP1 trans- Angiosarcoma criptional co-activator is a major downstream effector of the Hippo pathway and shares signifi- Incidence and Demographics cant functional and sequence homology with Angiosarcoma may arise in any part of the body, but WWTR1. As the S127 14-3-3 binding site, WW is more common in soft tissue than in bone. The domain and its C-terminal transactivation domain peak age of incidence appears to be the 7th decade, are not retained in the fusion, it is most likely that and men are affected more than women. The head YAP1 provides a strong promoter to the oncogenic and neck area is probably the most common site of 14 TFE3 function of the fusion protein. The anatomic diagnosis, and the most common site of radiation- distribution of these lesions is mainly within soft induced angiosarcoma development is the breast. tissue, ranging from head and neck, trunk and After rhabdomyosarcoma, angiosarcoma is probably extremities, with only one case occurring in the the second most common sarcoma to arise from bone (vertebral body). Additional cases were seen in germ cell tumors.16 the lung, with multifocal presentation.The
Load more

Recommended publications
  • Recurrent Targetoid Hemosiderotic Hemangioma in a 26-Year-Old Man
    CASE REPORT Recurrent Targetoid Hemosiderotic Hemangioma in a 26-Year-Old Man LT Sarah Broski Gendernalik, DO, MC (FS), USN LT James D. Gendernalik, DO, MC (FS), USN A 26-year-old previously healthy man presented with a 6-mm violaceous papule that had a surrounding 1.5-cm annular, nonblanching, erythematous halo on the right-sided flank. The man reported the lesion had been recurring for 4 to 5 years, flaring every 4 to 5 months and then slowly disap - pearing until the cycle recurred. Targetoid hemosiderotic hemangioma was clinically diagnosed. The lesion was removed by means of elliptical excision and the condition resolved. The authors discuss the clinical appearance, his - tology, and etiology of targetoid hemosiderotic heman - giomas. J Am Osteopath Assoc . 2011;111(2);117-118 argetoid hemosiderotic hemangiomas (THHs) are a com - Tmonly misdiagnosed presentation encountered in the primary care setting. In the present case report, we aim to pro - Figure. A 6-mm violaceous papule with a surrounding 1.5-cm annular, nonblanching, erythematous halo in a 26-year-old man. vide general practitioners with an understanding of the clin - ical appearance, pathology, and prognosis of THH. Report of Case A 26-year-old previously healthy man presented to our primary around it and itched and burned each time it developed. The care clinic with a 6-mm violaceous papule with a surrounding lesion faded completely to normal-appearing skin between 1.5-cm annular, nonblanching, erythematous halo on the right- episodes, without evidence of a papule or postinflammatory sided flank ( Figure ). The patient stated that the lesion had hyperpigmentation.
    [Show full text]
  • Hemangiosarcoma Philip J
    Ettinger & Feldman – Textbook of Veterinary Internal Medicine Client Information Sheet Hemangiosarcoma Philip J. Bergman What is hemangiosarcoma? Hemangiosarcoma (HSA; angiosarcoma or malignant hemangioendothelioma) is an extremely aggressive tumor of blood vessel origin. Because blood vessels are present throughout the body, virtually any site in the body can have HSA. HSA occurs most frequently in dogs (approximately 2% of all tumors) and the most common site is the spleen. However, additional common sites include the heart, liver, muscle, lung skin, bones, kidney, brain, abdomen, and oral cavity. In three large canine splenic disease studies encompassing approximately 2000 dogs, a “rule of two thirds” was found suggesting that approximately two thirds of dogs with a splenic mass have a cancer (therefore one third are not malignant) and two thirds of the malignant tumors of the spleen are HSA. HSA is a disease generally of older dogs and cats with an average onset of 9 to 10 years; however, there are reports of extremely young dogs and cats with this disease (5 to 6 months to a few years of age). German shepherd dogs are most commonly diagnosed with HSA; however, other large breed dogs such as golden retrievers and Labrador retrievers may also be overrepresented. In cats, the most common breed is the domestic shorthair. The cause of HSA in dogs and cats is presently unknown. Exposures to toxins such as chemicals, insecticides, and radiation have been reported in humans to be associated with HSA. Ultraviolet light exposure from the sun may be a potential cause of HSA in dogs, as HSAs of the skin are commonly seen in dogs with light hair and poor pigmentation (e.g., Salukis, Whippets, and white Bulldogs).
    [Show full text]
  • Tumors and Tumor-Like Lesions of Blood Vessels 16 F.Ramon
    16_DeSchepper_Tumors_and 15.09.2005 13:27 Uhr Seite 263 Chapter Tumors and Tumor-like Lesions of Blood Vessels 16 F.Ramon Contents 42]. There are two major classification schemes for vas- cular tumors. That of Enzinger et al. [12] relies on 16.1 Introduction . 263 pathological criteria and includes clinical and radiolog- 16.2 Definition and Classification . 264 ical features when appropriate. On the other hand, the 16.2.1 Benign Vascular Tumors . 264 classification of Mulliken and Glowacki [42] is based on 16.2.1.1 Classification of Mulliken . 264 endothelial growth characteristics and distinguishes 16.2.1.2 Classification of Enzinger . 264 16.2.1.3 WHO Classification . 265 hemangiomas from vascular malformations. The latter 16.2.2 Vascular Tumors of Borderline classification shows good correlation with the clinical or Intermediate Malignancy . 265 picture and imaging findings. 16.2.3 Malignant Vascular Tumors . 265 Hemangiomas are characterized by a phase of prolif- 16.2.4 Glomus Tumor . 266 eration and a stationary period, followed by involution. 16.2.5 Hemangiopericytoma . 266 Vascular malformations are no real tumors and can be 16.3 Incidence and Clinical Behavior . 266 divided into low- or high-flow lesions [65]. 16.3.1 Benign Vascular Tumors . 266 Cutaneous and subcutaneous lesions are usually 16.3.2 Angiomatous Syndromes . 267 easily diagnosed and present no significant diagnostic 16.3.3 Hemangioendothelioma . 267 problems. On the other hand, hemangiomas or vascular 16.3.4 Angiosarcomas . 268 16.3.5 Glomus Tumor . 268 malformations that arise in deep soft tissue must be dif- 16.3.6 Hemangiopericytoma .
    [Show full text]
  • Lymphangioma Circumscriptum of the Vulva- a Case Series Dermatology Section
    DOI: 10.7860/JCDR/2021/47435.14553 Case Series Lymphangioma Circumscriptum of the Vulva- A Case Series Dermatology Section RASHMI S MAHAJAN1, YOGESH S MARFATIA2, ATMAKALYANI R SHAH3, KISHAN R NINAMA4 ABSTRACT Vulval dermatoses pose a diagnostic and therapeutic challenge for the dermatologists. Lymphangioma Circumscriptum (LC) is a form of lymphangioma affecting the skin and subcutaneous tissues that is characterised by benign dilation of lymphatic channels. This uncommon condition is known to occur over the chest, mouth, axilla, tongue, and rarely in the vulva. In this series, authors present three cases of LC of vulva in women between the age group of 45 to 60 years with late-onset fluid-filled lesions over the vulva. The first case had history of hysterectomy prior to onset of lesions, the second case had a spontaneous onset of lesions while the third was a suspected case of pelvic tuberculosis with secondary lymphangioma. Keywords: Lymphangiectasia, Vulvar, Vulval epithelium INTRODUCTION Disorders of vulval epithelium are a confusing spectrum of disorders. They are broadly classified as-1) Inflammatory, 2) Ulcerative and Bullous, 3) Infections, 4) Benign tumours and 5) Malignancies. It is essential to know the exact aetiology to plan successful therapy. LC is a benign lymphatic malformation characterised by dilation of lymphatic vessels in the skin and subcutaneous tissue with lesions erupting locally as isolated or grouped translucid, thin-walled vesicles filled with a clear liquid [1]. These pathological lymphatic malformations have no communication with the normal lymphatics [2]. The precise cause of LC is not established. It could be congenital or acquired as a result of damage to the lymphatic vessels secondary to various aetiologies.
    [Show full text]
  • Glomus Tumor in the Floor of the Mouth: a Case Report and Review of the Literature Haixiao Zou1,2, Li Song1, Mengqi Jia2,3, Li Wang4 and Yanfang Sun2,3*
    Zou et al. World Journal of Surgical Oncology (2018) 16:201 https://doi.org/10.1186/s12957-018-1503-6 CASEREPORT Open Access Glomus tumor in the floor of the mouth: a case report and review of the literature Haixiao Zou1,2, Li Song1, Mengqi Jia2,3, Li Wang4 and Yanfang Sun2,3* Abstract Background: Glomus tumors are rare benign neoplasms that usually occur in the upper and lower extremities. Oral cavity involvement is exceptionally rare, with only a few cases reported to date. Case presentation: A 24-year-old woman with complaints of swelling in the left floor of her mouth for 6 months was referred to our institution. Her swallowing function was slightly affected; however, she did not have pain or tongue paralysis. Enhanced computed tomography revealed a 2.8 × 1.8 × 2.1 cm-sized well-defined, solid, heterogeneous nodule above the mylohyoid muscle. The mandible appeared to be uninvolved. The patient underwent surgery via an intraoral approach; histopathological examination revealed a glomus tumor. The patient has had no evidence of recurrence over 4 years of follow-up. Conclusions: Glomus tumors should be considered when patients present with painless nodules in the floor of the mouth. Keywords: Glomus tumor, Floor of mouth, Oral surgery Background Case presentation Theglomusbodyisaspecialarteriovenousanasto- A 24-year-old woman with a 6-month history of swelling mosisandfunctionsinthermalregulation.Glomustu- in the left floor of her mouth was referred to our institu- mors are rare, benign, mesenchymal tumors that tion. Although she experienced slight difficulty in swal- originate from modified smooth muscle cells of the lowing, she did not experience pain or tongue paralysis.
    [Show full text]
  • Benign Hemangiomas
    TUMORS OF BLOOD VESSELS CHARLES F. GESCHICKTER, M.D. (From tke Surgical Palkological Laboratory, Department of Surgery, Johns Hopkins Hospital and University) AND LOUISA E. KEASBEY, M.D. (Lancaster Gcaeral Hospital, Lancuster, Pennsylvania) Tumors of the blood vessels are perhaps as common as any form of neoplasm occurring in the human body. The greatest number of these lesions are benign angiomas of the body surfaces, small elevated red areas which remain without symptoms throughout life and are not subjected to treatment. Larger tumors of this type which undergb active growth after birth or which are situated about the face or oral cavity, where they constitute cosmetic defects, are more often the object of surgical removal. The majority of the vascular tumors clinically or pathologically studied fall into this latter group. Benign angiomas of similar pathologic nature occur in all of the internal viscera but are most common in the liver, where they are disclosed usually at autopsy. Angiomas of the bone, muscle, and the central nervous system are of less common occurrence, but, because of the symptoms produced, a higher percentage are available for study. Malignant lesions of the blood vessels are far more rare than was formerly supposed. An occasional angioma may metastasize following trauma or after repeated recurrences, but less than 1per cent of benign angiomas subjected to treatment fall into this group. I Primarily ma- lignant tumors of the vascular system-angiosarcomas-are equally rare. The pathological criteria for these growths have never been ade- quately established, and there is no general agreement as to this par- ticular form of tumor.
    [Show full text]
  • Infantile Hemangioendothelioma of the Parotid Gland
    Elmer ress Case Report Int J Clin Pediatr. 2015;4(4):184-185 Infantile Hemangioendothelioma of the Parotid Gland Veeranna A. Kotrashettia, Vijay Baburao Sonawanea, b, Kapil Bainadea, Reshu Agarwala Abstract parotid region, 4 × 3 cm in size, smooth in surface, no pulsa- tions with no signs of inflammation (Fig. 1). Tumors of salivary glands are uncommon in children (less than 5%). Complete blood count was normal. USG revealed en- Hemangioma is the commonest tumor of salivary gland tumors (more larged parotid gland measuring 3.1 × 2.2 × 2.5 cm with in- than 50%). We report a rare case of infantile hemangioma (IH) of creased vascularity. parotid gland. MRI showed well-defined, lobulated homogenously en- hancing leison diffusely involving the superficial and deep Keywords: Hemangioma; Hemangioendothelioma; Parotid gland layers of parotid gland (Fig. 2). Findings are suggestive of in- fantile hemangioendothelioma. Introduction Discussion Infantile hemangiomas (IHs) are the most common tumor of IH of parotid gland is the most common tumor. Weiss and oth- infancy and have a well-described natural history of rapid growth during early infancy followed by gradual involution [1, 2]. Congenital capillary hemangioma is classified as true hemangioma of infancy [3]. It is usually not noticed in new- born period but becomes prominent in first months of life. Most common age of presentation is about 4 months. Parotid hemangioma demonstrates rapid growth in first months of life but usually regresses after 18 months [4]. MRI is the best im- aging technique to demonstrate parotid hemangioma. MRI shows hyperintense parotid gland hemangioma con- taining vascular flow voids.
    [Show full text]
  • Angiosarcomas and Other Sarcomas of Endothelial Origin
    Angiosarcomas and Other Sarcomas of Endothelial Origin a,b a Angela Cioffi, MD , Sonia Reichert, MD , c a,b,d, Cristina R. Antonescu, MD , Robert G. Maki, MD, PhD, FACP * KEYWORDS Angiosarcoma Epithelioid hemangioendothelioma Vascular sarcoma Kaposi sarcoma VEGF KDR FLT4 Translocation Organ transplant KEY POINTS Vascular sarcomas are rare and collectively affect fewer than 600 people a year in the United States (incidence approximately 2/million). Because angiosarcomas, hemangioendotheliomas, and other vascular tumors have unique embryonal derivation, it is not surprising that they have a unique sensitivity pattern to chemotherapy agents. Surgery, when possible, remains the primary treatment for angiosarcomas. Adjuvant radiation for primary disease seems prudent for at least some angiosarcoma, given the high local-regional recurrence rate of these tumors. Angiosarcomas also have a high rate of metastasis, but it is not clear that adjuvant chemotherapy improves survival. Epithelioid hemangioendothelioma is a unique form of sarcoma often presenting as multi- focal disease. Most patients can do well with observation alone, although a fraction of pa- tients have more aggressive disease and have difficulties in both local control and metastatic disease. Continued Disclosures: R.G. Maki receives clinical research support from Morphotek/Eisai, Ziopharm, and Imclone/Lilly. He has also consulted for Eisai, Morphotek/Eisai, Imclone/Lilly, Taiho, Glaxo- SmithKline, Merck, Champions Biotechnology, and Pfizer. He has received speaker’s fees from Novartis. He is an unpaid consultant for the Sarcoma Foundation of America, SARC: Sarcoma Alliance for Research through Collaboration, n-of-one, and 23 & me. C.R. Antonescu, A. Cioffi, and S. Reichert report no conflicts.
    [Show full text]
  • View Open Access Histological Variants of Cutaneous Kaposi Sarcoma Wayne Grayson1 and Liron Pantanowitz*2
    Diagnostic Pathology BioMed Central Review Open Access Histological variants of cutaneous Kaposi sarcoma Wayne Grayson1 and Liron Pantanowitz*2 Address: 1Histopathology Department, Ampath National Laboratory Support Services, Johannesburg, South Africa and 2Department of Pathology, Baystate Medical Center, Tufts University School of Medicine, Springfield, Massachusetts, USA Email: Wayne Grayson - [email protected]; Liron Pantanowitz* - [email protected] * Corresponding author Published: 25 July 2008 Received: 23 July 2008 Accepted: 25 July 2008 Diagnostic Pathology 2008, 3:31 doi:10.1186/1746-1596-3-31 This article is available from: http://www.diagnosticpathology.org/content/3/1/31 © 2008 Grayson and Pantanowitz; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract This review provides a comprehensive overview of the broad clinicopathologic spectrum of cutaneous Kaposi sarcoma (KS) lesions. Variants discussed include: usual KS lesions associated with disease progression (i.e. patch, plaque and nodular stage); morphologic subtypes alluded to in the older literature such as anaplastic and telangiectatic KS, as well as several lymphedematous variants; and numerous recently described variants including hyperkeratotic, keloidal, micronodular, pyogenic granuloma-like, ecchymotic, and intravascular KS. Involuting lesions as a result of treatment related regression are also presented. Introduction progression, (2) KS variants alluded to in the older litera- Kaposi sarcoma (KS) is a vascular lesion of low-grade ture, (3) more recently described KS variants, and (4) KS malignant potential that presents most frequently with lesions as a consequence of therapy.
    [Show full text]
  • Two Cases of Lymphangioma Circumscriptum Successfully Treated
    Letters to the Editor REFERENCES 8. Kato N. Vertically growing ectopic nail. J Cutan Pathol 1992;19:445‑7. 9. Nath AK, Udayashankar C. Congenital onychogryphosis: Leaning Tower nail. Dermatol Online J 2011;17:9. 1. Barad P, Fernandes J, Ghodge R, Shukla P. Vertically growing Nail. 10. Zaias N. The Nail in Health and Disease. 2nd ed. Norwalk, CT: Appleton Indian Dermatol Online J 2015;6;288‑9. and Lange; 1990. p. 164. 2. Fleckman P. Structure and function of the nail unit. In: 3rd, editors. Nails: 11. Ohata C, Shirabe H, Takagi K. Onychogryphosis with granulation tissue Therapy, Diagnosis and Surgery :Saunders; 2005. p. 13‑26. of proximal nail fold. Skin Res 1996;38:626‑9. 3. Kligman AM. Why do nails grow out instead of up? Arch Dermatol 1961;84:313‑5. 4. Kikuchi I, Ogata K, Idemori M. Vertically growing ectopic nail: Nature’s Access this article online experiment on nail growth direction. J Am Acad Dermatol 1984;10:114‑6. Quick Response Code: 5. Baran R. Nail growth direction revisited. Why do nails grow out instead of up? J Am Acad Dermatol 1981;4:78‑84. 6. Grover C, Bansal S, Nanda S, Reddy BS, Kumar V. En bloc excision of Website: www.idoj.in proximal nail fold for treatment of chronic paronychia. Dermatol Surg 2006;32:393‑9. 7. Hashimoto K. Ultrastructure of the human toenail. I. Proximal nail matrix. J Invest Dermatol 1971;56:235‑46. Letter to the Editor twice per year. Nothing in particular was noted in her family Two cases of lymphangioma history or her laboratory tests.
    [Show full text]
  • Vascular Malformations, Skeletal Deformities Including Macrodactyly, Embryonic Veins
    1.) Give a general classification and nomenclature to think about when evaluating these patients 2.) Share some helpful tips to narrow the differential in a minute or less of interaction 3.) Discuss some helpful imaging recommendations focusing on ultrasound Vascular Anomalies Tumors: Malformations: Hemangiomas: Low flow: Infantile Hemangioma (IH) Capillary malformation (CM) Rapidly involuting congenital hemangioma (RICH) Non-involuting congenital hemangioma (NICH) Venous malformation (VM) Kaposiform Hemangioendothelioma Lymphatic malformation (LM) (KHE) High flow: Arteriovenous malformation (AVM) Tufted Angioma (TA) Combined including syndromic VA. Other rare tumors www.issva.org • 2014 ISSVA classification is now 20 pages long • The key is that the imaging characteristics have not changed • Rapidly growing field • Traditionally, options were always the same – Surgery – Do nothing • With the increase in awareness and research as well as the development of the specialty of vascular anomalies: New Treatment Options Available – Treatment directly linked to diagnosis • Today, we have: – Interventional catheter based therapies – Laser surgery – Ablation technologies: Cryo, RFA, Microwave, etc. – Direct image-guided medications to administer – Infusion medicines – Oral medicines – Surgery- although much less common – Do Nothing- a VERY important alternative • Survey sample of 100 Referred patients – 47% wrong Dx – 35% wrong Tx • 14% wrong Tx with correct Dx • VAC – 14% indeterminate or wrong Dx – only 4% leave with no Tx plan • Important because
    [Show full text]
  • Mesenchymal) Tissues E
    Bull. Org. mond. San 11974,) 50, 101-110 Bull. Wid Hith Org.j VIII. Tumours of the soft (mesenchymal) tissues E. WEISS 1 This is a classification oftumours offibrous tissue, fat, muscle, blood and lymph vessels, and mast cells, irrespective of the region of the body in which they arise. Tumours offibrous tissue are divided into fibroma, fibrosarcoma (including " canine haemangiopericytoma "), other sarcomas, equine sarcoid, and various tumour-like lesions. The histological appearance of the tamours is described and illustrated with photographs. For the purpose of this classification " soft tis- autonomic nervous system, the paraganglionic struc- sues" are defined as including all nonepithelial tures, and the mesothelial and synovial tissues. extraskeletal tissues of the body with the exception of This classification was developed together with the haematopoietic and lymphoid tissues, the glia, that of the skin (Part VII, page 79), and in describing the neuroectodermal tissues of the peripheral and some of the tumours reference is made to the skin. HISTOLOGICAL CLASSIFICATION AND NOMENCLATURE OF TUMOURS OF THE SOFT (MESENCHYMAL) TISSUES I. TUMOURS OF FIBROUS TISSUE C. RHABDOMYOMA A. FIBROMA D. RHABDOMYOSARCOMA 1. Fibroma durum IV. TUMOURS OF BLOOD AND 2. Fibroma molle LYMPH VESSELS 3. Myxoma (myxofibroma) A. CAVERNOUS HAEMANGIOMA B. FIBROSARCOMA B. MALIGNANT HAEMANGIOENDOTHELIOMA (ANGIO- 1. Fibrosarcoma SARCOMA) 2. " Canine haemangiopericytoma" C. GLOMUS TUMOUR C. OTHER SARCOMAS D. LYMPHANGIOMA D. EQUINE SARCOID E. LYMPHANGIOSARCOMA (MALIGNANT LYMPH- E. TUMOUR-LIKE LESIONS ANGIOMA) 1. Cutaneous fibrous polyp F. TUMOUR-LIKE LESIONS 2. Keloid and hyperplastic scar V. MESENCHYMAL TUMOURS OF 3. Calcinosis circumscripta PERIPHERAL NERVES II. TUMOURS OF FAT TISSUE VI.
    [Show full text]