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Lymphangiosarcoma of Dogs: a Review

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Lymphangiosarcoma of Dogs: a Review Review article — Oorsigartikel Lymphangiosarcoma of dogs: a review J H Williamsa amount of fibrous tissue in the hilus, sug- ABSTRACT gesting obstruction to lymph flow2. Many Lymphangiosarcoma in dogs, an extremely rare tumour with only 16 cases reported in the of the dogs reported with primary literature, is reviewed. Lymphangiosarcoma in humans, also very rare, and known in lymphoedema have had small or absent post-mastectomy, chronically-lymphoedematous patients as ‘Stewart-Treves’ syndrome, is lymph nodes, the initial defect having briefly outlined, as well as the various other causes of lymphoedema, both primary and been reported, as in humans, as fibrosis of secondary, which usually precede malignancy. Comparisons between human and canine 8 lymphoedema are made when such references were found. The genetic links to primary the lymph nodes and leading to second- lymphoedema and the manifestation thereof in humans are mentioned. Lymphangio- ary obstructive changes in lymph vessels sarcoma in the majority of human and canine patients is an aggressively malignant tumour due to chronic overdistension, loss of with few patients surviving despite various attempted treatments. The tumour most contractility and/or non-functional lym- commonly arises in the subcutaneous tissues and rapidly invades underlying tissues and phatic valves. The remaining human may spread widely internally via haematogenous and lymphatic routes, with frequent cases either had a reduced number of pleural and chest involvement. The tumour has been reported mostly in medium- to lymphatics on lymphography, described large-breed dogs, in slightly more males than females, and in an age-range of 8 weeks to 13 as ‘obliterated’ lymphatics, and were years, with more cases aged 5 years and older. Methods of diagnosis, with the variations possibly born with too few lymphatics encountered, including routine histopathology, immunohistochemistry, electron micros- (hypoplasia) if they manifested early copy, tissue culture characteristics and endothelial expression of glycocongugates, are clinically; or those manifesting later in life discussed. may have acquired obliterative disease of Key words: diagnosis, dogs, genetics, lymphoedema, human, lymphangiosarcoma, review, obscure cause – this latter group compris- treatment. ing the majority of lymphoedemas2. Williams J H Lymphangiosarcoma of dogs: a review. Journal of the South African Veterinary In humans, primary lymphoedema has Association (2005) 76(3): 127–131 (En.). Department of Paraclinical Sciences, Section of been classified into hereditary and non- Pathology, Faculty of Veterinary Science, University of Pretoria, Private Bag X04, Onderste- hereditary,with the oedema in hereditary poort, 0110 South Africa. cases present at birth or in early child- hood (Milroy’s Disease), with late onset between the 1st decade and puberty INTRODUCTION been secondary to inflammatory disease, (Meige’s disease), or, exceptionally, after One of the very rare complications of surgical procedures, or radiation6, but age 35 years3. Non-hereditary primary chronic lymphoedema in humans is the other rare associations are with traumatic, lymphoedema may also occur at birth or development of lymphangiosarcoma, idiopathic, congenital or filarial lymph- later in life3. Genetic mapping of the which is an aggressively malignant oedema13. autosomal dominant form of hereditary tumour3,22. In some cases of lymphangiosarcoma in primary lymphoedema (Milroy’s disease) This neoplasm arises from lymphatic humans following lymphoedema, the suggests a mutation that inactivates the lining endothelium, and was originally lymphoedema was considered primary6 vascular endothelial growth factor C reported in humans by Stewart and and was present for an average of 21 years receptor (VEGFR-3) tyrosine kinase sig- Treves in 1948 in chronically oedematous (range of 1.5 to 46 years) before malig- nalling mechanism felt to be specific to extremities occurring mostly after radical nancy. Primary lymphoedema may be lymphatic vessels22,33. This was recently mastectomy, which included lymph node defined as that caused by a primary ab- used immunohistochemically to show resection and/or radiation for breast normality or disease of the lymph- up lymphatic-origin vessels in normal carcinoma. Lymphangiosarcoma arising conducting elements of the lymph vessels skin and vascular tumours of lymphatic in these circumstances thereafter became or lymph nodes, leading to excessive origin16,30. Other congenital lymph- known as ‘Stewart-Treves’ syndrome6,3,22,29. accumulation of protein-rich lymph/ oedemas mostly cluster in families, with The postmastectomy oedema in one plasma ultrafiltrate in the interstitial an autosomal dominant pattern of trans- report6 preceded the multicentric, poly- tissues2,6. Three groups are recognised mission and involving various genes, lo- morphous, patchy, nodular to bullous, where the functional abnormality and cus heterogeneity and/or environmental ecchymotic soft tissue malignancy in the its cause is known, namely large-vessel determinants22,33. ‘Lymphoedema – subcutaneous tissue by an average of abnormalities such as congenital aplasia, distichiasis’ syndrome in humans is an approximately 9.5 years but ranged from hypoplasia or obstruction of the thoracic autosomal dominant disorder character- 1.5 to 26 years and neoplasia occurred in duct or cisterna chyli; congenital lymphatic ised by lymphoedema of the lower limbs, less than1%ofcases. The lymphoedema valvular incompetence and congenital together with a 2nd row of eyelashes in cases of lymphangiosarcoma not aplasia or hypoplasia of peripheral lym- growing from the meibomian glands, as associated with mastectomy has usually phatics, which includes lymph node ab- well as other developmental defects, 2,27 aDepartment of Paraclinical Sciences, Section of Pathol- sence, hypoplasia or fibrosis . Some including cardiac defects, cleft palate and ogy, Faculty of Veterinary Science, University of Pretoria, humans with unilateral whole leg lymph- extradural cysts. This suggests a gene Private Bag X04, Onderstepoort, 0110 South Africa. E-mail: [email protected] oedema have been found to have small defect with pleiotropic effects acting 33 Received: May 2005. Accepted: August 2005. shrunken lymph nodes with an increased during development . Apart from the 0038-2809 Jl S.Afr.vet.Ass. (2005) 76(3): 127–131 127 VEGFR-3 gene mutation, a 2nd gene, the pathogenesis of lymphangiosarcoma ments. Occasional patients are long-term FOXC2, which directs development of a in humans due to aggravation of lym- survivors, with tumour morphology variety of embryonic tissues, was identi- phatic occlusion, but some cases had no not appearing to influence prognosis4,6. fied33. It is also known that an inactivated radiation therapy, or the tumour arose in Therapeutic consensus has not been 2nd X chromosome or else the Y chromo- the contralateral non-irradiated limb6. reached in human medicine on account of some is necessary to prevent XO Turner Lymphangiosarcoma is known to extend the rarity of the tumour. In metastatic or syndrome in man33. It is hypothesized rapidly in the subcutaneous tissues distally, locally advanced tumours use of more that a gene or genes expressed from circumferentially and proximally, with recent cytotoxic drugs known to be effec- non-inactivated portions of the inactive X infiltration along the deep intramuscular tive on soft tissue tumours may be consid- or the Y chromosome are involved in the fascial septae, and with lymphatic and ered13. development of the lymphatic system, haematogenous metastases to the thoracic and a deficiency of the product of wall, pleura and lungs most frequently, DIAGNOSIS this gene is responsible for the Turner but few organs may be spared. Mean The characteristic normal histological syndrome phenotype, which includes human survival time was just over 1.5 lymphatic phenotype has been desig- peripheral lymphoedema33. Down syn- years with a range of 2 months to 5.5 nated as staining negative for PAL-E drome (trisomy 21) may occasionally years6 and overall prognosis is considered (vesicular component in blood vessel present with foetal cystic hygroma, poor3,13 to extremely poor29. endothelium), PECAM, CD34, basement lymphoedema and intestinal lymphan- Chronically lymphoedematous tissue is membrane components laminin and giectasis, in addition to anomalies of the prone to recurrent infection, microbial Type IV collagen and von Willebrand’s blood vessels and heart33. growth being encouraged by the surplus factor (vWf or factor VIII-related antigen), Primary lymphoedema may manifest at protein-rich interstitial fluid. Lymphatic and positive for VEGFR-3, alkaline any phase of life but most commonly dysfunction also impairs local immune phosphatase, 5’endonuclease, podoplanin, appears at puberty in humans. However, response and regional immunosurveil- junctional protein desmoplakin, LYVE-1 acquired lymphoedema is much more lance 7,22,31, sometimes being referred to as (a homologue of the hyaluronan receptor common28,33, occurring secondary to espe- ‘immunodysregulation’33. In chronic CD44)33, vimentin26 and proliferating cell cially parasitic (filarial) and other infec- lymphoedema, macrophages are dor- nuclear antigen (PCNA)26. However, tions, and less commonly to cancer mant, no longer functioning to lyse the these staining characteristics may vary invasion, cancer treatment (surgery large amount of protein in the interstitial with species, vessel calibre, stage of and irradiation)
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