Kaposi’s Sarcoma Restricted to an Immunocompromised District

opportunistic oncogenesis, especially in reference to vascular tumors. From this lymphological perspective, it has even been assumed that KS and Stewart-Treves angiosarcoma may not be completely different entities, but merely variant expressions of a similar underlying abnormality consisting of impairments in lymph drainage and immune control [6] . This is supported by the existence of borderline cases [12] . Clinical observations and experimental investigations have confirmed the parallel course of the lymphatic and immune functions in body regions affected with KS [3–9] or Stewart-Treves angiosarcoma [13, 14] . In this light, the two conditions may only differ in etiology, with human herpes virus 8 (HHV-8) always being causative of KS, while unknown viruses might be responsible for other angiosarcomas (though occasionally the same HHV-8 has been suspected) [12, 15] . The transformation of a common wart into a squamous cell carcinoma in a patient with chronic lymphedema [16] clearly indicates how a viral infection (human papilloma virus infection in this example) can evolve into an ‘opportunistic’ tumor (squamous cell carcinoma in this example) in the presence of persistent lymph stasis. In summary, the case reported by Kostaki et al. [1] features a typical example of an immunocompromised district due to repeated surgical procedures that impaired both lymph circulation and immune control in the traumatized area. Bearing in mind that an immunocompromised district may harbor opportunistic and immunity-related disorders – such as infections, tumors and immune reactions [2] – the onset of KS lesions is not at all surprising here, since KS has an infectious etiology (HHV-8), a tumor morphology (angiogenic neoplasm), and an immune pathogenesis (immunosuppression often confined to acral body regions [3– 10] ).