TS, MM, NES, GF and VBSK equally contributed

to the writing the other part of the review. All authors read and approved the final manuscript.”
“Background Kaposi’s Sarcoma (KS) is a tumour affecting mainly the skin, with multifocal expression and possible lymph nodal and visceral involvement [1]. Classically, it consists of four clinical variants: Classic KS (CKS) – or Mediterranean KS-, iatrogenic KS, African KS, and AIDS-KS. All four variants are associated with Human Herpesvirus-8 (HHV-8), and they show a similar histological pattern. HHV-8 infection of endothelial cells or circulating endothelial and/or haematopoietic progenitors leads to changes in their morphology, glucose metabolism, growth rate, lifespan and gene expression, resulting in the precipitation of KS [2]. In Italy, the most commonly

observed clinical variants are CKS, typically found in persons over 60 years of age, and the epidemic selleck form, AIDS-KS, which affects younger persons with HIV infection. In HIV-positive persons, KS constitutes an AIDS-defining condition [3]. Another subvariant of KS (termed “”gay Kaposi”") has also been described in HIV-negative homosexuals [4] and is possibly related to the sexual transmission of HHV-8 Navitoclax molecular weight infection [5]. The clinical onset of KS is characterised by violaceous macules and papules, which over the course of months or years tend to merge into plaques and nodules (in some cases ulcerated), which are associated with a characteristic oedema, particularly evident in the lower limbs. However, definitive diagnosis is based on histopathological evidence of spindle cell and the presence of HHV-8 latency associated nuclear antigen (LANA), in spindle cells and

vascular or lymphatic endothelial cells [6]. The clinical progression of CKS is generally slow and not very aggressive, although cases with rapidly growing lesions, with signs of local invasiveness, can be observed, as well as forms that fail to respond to physical or systemic treatment. By contrast, the natural history of AIDS-KS, which can affect mucous membranes, lymph nodes, the gastrointestinal tract, and the lungs, is more aggressive, particularly in untreated HIV-infected individuals [7]. Diverse classification methods have been proposed, based on the clinical AMP deaminase aspects and localization of lesions, which can also be assessed by roentgen-ray study, gastroscopy, and total body TC [8–10]. To define KS accurately, additional aspects can be considered, including immunological and virological parameters of HHV-8 and HIV infection, which could also be used to evaluate prognostic aspects and therapeutic indications [11–13]. Other non-invasive diagnostic techniques, in particular, telethermography and confocal microscopy, could be complementary to traditional staging instruments [14, 15].