Kaposi's Sarcoma Lesions Research Articles

Analysis of tumor infiltrating immune cells in Kaposi sarcoma lesions discovers shifts in macrophage populations.

Limited information exists about the types of immune cells present in Kaposi sarcoma (KS) lesions, especially in KS in the gastrointestinal tract. Using previously reported RNA-sequencing results from Kaposi sarcoma lesions in skin and gastrointestinal tract with normal matched tissues from the same patients at the same time, we investigated changes in lymphocytes in these tissues. We employed a computational method that determines changes in cell type distributions using KS lesion transcriptome data compared to a reference set of RNA expression patterns of purified immune cells. Since secreted cytokines and chemokines from KSHV-infected cells may influence the microenvironment of Kaposi sarcoma lesions, we performed cytokine profiling of conditioned media from KSHV-infected primary human dermal lymphatic endothelial cells. We also measured how this conditioned media altered the differentiation of macrophages in cell culture assays. These results suggested that factors in conditioned media from KSHV-infected endothelial cells promoted differentiation of a promonocytic cell line to proinflammatory macrophages.

Survival Following Diagnosis of HIV-Associated Kaposi Sarcoma Among Adults in East Africa in the "Treat-All" Era.

Despite widespread access to antiretroviral therapy (ART) in the "Treat All" era, HIV-associated Kaposi sarcoma (KS) remains among the most common malignancies in sub-Saharan Africa. Survival after KS diagnosis has historically been poor in Africa, but knowledge whether survival has changed at the population level in the contemporary era has been limited by lack of community-representative surveillance and monitoring systems. We identified all adult persons living with HIV (PLWH) with a new diagnosis of KS made between 2016 and 2019 during outpatient or inpatient care at prototypical primary care-providing medical facilities in Kenya and Uganda using rapid case ascertainment. Participants were subsequently followed for vital status, including community tracking for those who became lost to follow-up. Among 411 participants with newly diagnosed KS, 71% were men, median age was 34 (IQR: 30 to 41) years, and 91% had ACTG T1 tumor extent. Over a median follow-up of 7.8 (IQR: 2.4 to 17.9) months, cumulative incidence of death (95% CI) at months 6, 12 and 18 were 34% (30% to 39%), 41% (36% to 46%) and 45% (40% to 51%), respectively. Having the highest number of anatomic sites (11 to 16) harboring KS lesions (hazard ratio 2.2 (95% CI: 1.3-3.8) compared to 1 to 3 sites) and presence of oral KS lesions (hazard ratio 2.2 (95% CI: 1.4-3.3)) were independently associated with higher mortality. Lower hemoglobin and CD4 count as well as higher plasma HIV RNA were also associated with higher mortality. Among PLWH with newly diagnosed KS in East Africa in the "Treat All" era, survival was poor and related to mucocutaneous extent of KS. The findings emphasize the need for better control of KS in Africa, including novel approaches for earlier detection, better linkage to oncologic care, and more potent therapy.

Evaluation of interleukin-23 expression in classic kaposi’s sarcoma and AIDS-Associated

Kaposi’s sarcoma (KS) is a low-grade vascular tumor that presents most frequently with skin lesions. Multiple factors are related to KS pathogenesis. The interleukin-23 (IL-23) is an immunomodulatory cytokine with pro-carcinogenic role. The aim of this study was to evaluate the detection of IL-23 in cutaneous lesions of patients with KS classic and KS-AIDS. This was a cross-sectional study conducted at the public Hospital in Natal, Rio Grande do Norte, Brazil. This study included 13 biopsies of patients which presented KS with histopathological confirmation. For detection of IL-23, the immunohistochemical analysis was made with monoclonal antibody anti-IL-23. The immunostaining for IL-23 in biopsies was positive in 61.5% (8/13) of cases. Of seven lesions classified as patch-stage, three were positive for IL-23 (42.8%); two of three samples classified as plaque-stage were positive for IL-23 (66.7%); all the nodular-stage lesions were positive for IL-23. The positivity found in KS-AIDS lesions was 66.7% (6/9) and KS classic 50% (2/4). Our data supports the concept that IL-23 might be a pro-carcinogenic mediator, detected in KS lesions, probably favoring the progression of the tumor. KEY WORDS: Sarcoma; Kaposi; interleukin-23; tumor microenvironment.

KSHV/HHV-8 Associated Multicentric Castleman Disease in 80 HIV Negative Patients

Introduction : KSHV/HHV-8 associated multicentric Castleman disease (HHV-8 MCD) is a rare lymphoproliferative disorder associating lymphadenopathy, splenomegaly, fever and inflammatory symptoms with high serum CRP, hypergammaglobulinemia and high plasma HHV-8 DNA viral load. HHV-8 MCD mainly affects HIV infected patients but can also be observed in HIV negative patients born in countries with high HHV-8 prevalence or in men who have sex with men. In a large cohort of HIV negative patients, we sought to describe patient and disease characteristics and to compare them with those observed in a large cohort of HIV-infected patients with HHV8 MCD. Methods : We analysed a cohort of 80 HIV negative patients with HHV8+ MCD and compared them to 228 HIV-infected patients with HHV8+ MCD. These patients have been prospectively enrolled in the national registry for Castleman disease held by the Reference Center for Castleman Disease in Paris, over a 30-year period. Results : Most of these patients (67,5 %) originated from Sub saharan or Northern Africa. The baseline characteristics were similar in HIV- and HIV+ patients although HIV negative patients were older at MCD diagnosis (median, 67 vs 43 years) with 20% of the patients above 75 years, and the male predominance was slightly lower in the HIV negative population (74% vs 82%). They also presented less frequently with previous Kaposi sarcoma lesions (34% vs 52%). Biological markers including cytopenia, serum CRP and gamma globulins levels as well as blood HHV8 DNA viral load were very similar in both groups, although MCD attacks in HIV negative patients were rather less agressive than in HIV-infected patients. Of notice, the median CD4 + T cell count was normal in the HIV negative group (600 x10 6/L) The incidence of lymphoma during follow-up remains high but very similar in both groups : 3,12 /100 pt.y. in HIV negative patients and 3,10 /100 pt.y. in HIV-infected patients The median overall survival (OS) was 8,8 years (95%CI, 5,5-15) in HIV- patients and 20,6 years (95%CI, 6,3-24,1) in HIV-infected patients (p=0.19). Although the follow-up was shorter in HIV negative patients (24 vs 56 months), the 5-year probability of survival (79,2%; 95%CI 61,7-89,4) was very similar to that observed in HIV-infected patients (81,2% ; CI95% 74,6-86,2). Death was related to HHV8 complications or treatment in 6 /15 (40%) HIV negative patients and in 31 /57 (54%) HIV-infected patients. The slightly higher proportion of deaths not related to HHV8 in the HIV negative population might be explained by the older age of these patients. Conclusions : Using a large cohort of HIV negative patients, we could show that HHV8 MCD in this population is very similar to that observed in HIV-infected patients. Despite the fact that these patients were older at diagnosis, the overall survival was similar to that observed in HIV-infected patients, at least at 5-year from diagnosis.

Lymphedema and Kaposi sarcoma: A narrative review

Kaposi sarcoma (KS), due to HHV-8 infection is classified in 4 subtypes: epidemic, endemic, HIV-related and iatrogenic essentially after organ transplant. Lymphedema is a complication of KS. We reviewed the interactions between HHV-8 infection and lymphedema according an analysis of the literature. HHV-8 can infect different types of cells, among them a privileged tropism for lymphatic endothelial cells. It induces multi-centric endothelial proliferation leading to the occlusion of lymphatic vascular lumen. Lymphatic obstruction progressively lead to the blockage of lymphatic drainage, lymph stasis and lymphedema. Lymphedema mostly involved the lower limb affected by KS. It can then develop simultaneously or after the appearance of KS lesions but also be the first sign of KS, a long time before KS skin lesion onset. Lymphedema diagnosis is clinical and lymphoscintigraphy can confirm it if necessary. Lymphedema may be associated with active lesions of KS or non-evolutive, with only cicatricial lesions. KS should be treated according to the KS subtype, aggressive form, with local or systemic treatments associating with causal treatment, such as HIV infection or reducing immuno-suppressive drugs in transplant patients. In most of the cases, KS treatment may slightly reduce (or not) lymphedema volume which remains a chronic disease. Lymphedema management should be associated in order to reduce the volume and then stabilizing it. Low-stretch bandage, elastic garments and skin care are the cornerstone of treatment. Lymphedema is a frequent complication of KS, and may reveal KS or occurs throughout its course. Association of KS and lymphedema must be known because lymphedema is a chronic disease affecting the quality of life. Beyond the treatment of KS, its management must be specific including a long follow-up to optimize the patient's observance required to maintain the best lymphedema control.

A retrospective study of Kaposi's sarcoma in Hotan region of Xinjiang, China.

Kaposi sarcoma (KS) is the most common cancer in patients with human immunodeficiency virus/acquired immunodeficiency syndrome (AIDS). In 1994, Chang and Moore discovered Kaposi sarcoma associated herpesvirus for the first time in KS lesions in AIDS patients. KS is a low-grade mesenchymal neoplasm of blood and lymphatic vessels that primarily affects the skin, although the disease may become disseminated to the lymphatic system, lungs, airways, or abdominal viscera. In this research, clinical characteristics and treatment of patients of Kaposi sarcoma were retrospectively analyzed in Hotan District, Xinjiang China. We look into the clinical traits, prognosis, and therapy of Kaposi sarcoma. From May 2017 to August 2022, 32 patients were treated in the People's Hospital of Hotan District, Xinjiang Uygur Autonomous Region, China. Twenty-two of these were classic Kaposi sarcomas (cKS), and 10 of these were Kaposi sarcomas linked to AIDS (AIDS-KS). The majority of KS patients were Uyghur. In terms of age at onset, AIDS-KS patients were younger than cKS patients. cKS and AIDS-KS are most frequently manifested in the feet and lower limbs. Ten patients with AIDS-KS have treated with combination antiretroviral therapy (combination antiretroviral therapy) combination chemotherapy, 5 of 10 patients had a complete response, 2 patients achieved partial response, the overall effective rate was 70%, and CD4 + T cells were greater than before. For cKS and AIDS-KS, the median overall survival was 56 and 50.8 months, respectively (P > .05). As a result, antiviral combination chemotherapy can also improve the prognosis of AIDS-KS patients.

Clinical Course of Kaposi Sarcoma in Persons Living with HIV And Aids (PLWHA) Treated with Combined Antiretroviral Therapy (cART) in Cameroon

Kaposi sarcoma (KS) is a low-grade vascular tumor believed to be caused by a virus known as Kaposi sarcoma herpesvirus/ human herpesvirus 8 (KSHV/HHV8) and is usually but not always associated with HIV infection. Although it can affect any organ or anatomical location, kaposi sarcoma lesions are most frequently found in mucosal surfaces and the skin.

A prospective cohort study identifies two types of HIV+ Kaposi Sarcoma lesions: proliferative and inflammatory.

Kaposi sarcoma (KS) is the most common cancer in people living with HIV (PLWH) in many countries where KS-associated herpesvirus is endemic. Treatment has changed little in 20 years, but the disease presentation has. This prospective cohort study enrolled 122 human immunodeficiency virus (HIV) positive KS patients between 2017 and 2019 in Malawi. Participants were treated with bleomycin, vincristine and combination antiretroviral therapy, the local standard of care. One-year overall survival was 61%, and progression-free survival was 58%. The 48-week complete response rate was 35%. RNAseq (n = 78) differentiated two types of KS lesions, those with marked endothelial characteristics and those enriched in inflammatory transcripts. This suggests that different KS lesions are in different disease states consistent with the known heterogeneous clinical response to treatment. In contrast to earlier cohorts, the plasma HIV viral load of KS patients in our study was highly variable. A total of 25% of participants had no detectable HIV; all had detectable KSHV viral load. Our study affirms that many KS cases today develop in PLWH with well-controlled HIV infection and that different KS lesions have differing molecular compositions. Further studies are needed to develop predictive biomarkers for this disease.

Elevated iNOS and 3′-nitrotyrosine in Kaposi's Sarcoma tumors and mouse model

Kaposi's Sarcoma (KS) is a heterogenous, multifocal vascular malignancy caused by the human herpesvirus 8 (HHV8), also known as Kaposi's Sarcoma-Associated Herpesvirus (KSHV). Here, we show that KS lesions express iNOS/NOS2 broadly throughout KS lesions, with enrichment in LANA positive spindle cells. The iNOS byproduct 3-nitrotyrosine is also enriched in LANA positive tumor cells and colocalizes with a fraction of LANA-nuclear bodies. We show that iNOS is highly expressed in the L1T3/mSLK tumor model of KS. iNOS expression correlated with KSHV lytic cycle gene expression, which was elevated in late-stage tumors (>4 weeks) but to a lesser degree in early stage (1 week) xenografts. Further, we show that L1T3/mSLK tumor growth is sensitive to an inhibitor of nitric oxide, L-NMMA. L-NMMA treatment reduced KSHV gene expression and perturbed cellular gene pathways relating to oxidative phosphorylation and mitochondrial dysfunction. These finding suggest that iNOS is expressed in KSHV infected endothelial-transformed tumor cells in KS, that iNOS expression depends on tumor microenvironment stress conditions, and that iNOS enzymatic activity contributes to KS tumor growth.

Koebner Phenomenon in Kaposi's Sarcoma: A Large Single-Center Case Series and Review of Current Knowledge.

occasional case reports have described the appearance of Kaposi's sarcoma (KS) on previously unaffected skin after incidental or accidental injury, but the association is probably under-reported. to present a large case series of patients suffering from Koebner phenomenon (KP) in KS and describe their main epidemiological, clinical, and therapeutic features. we have retrospectively analyzed our clinical and photographic records of 524 patients who had been diagnosed with KS between 2009 and 2021. 31 of 524 (6%) KS patients developed KP. Among these 31 patients, 24 (77%) had KS lesions after surgery, 4 (13%) after electrochemotherapy, laser therapy and cryotherapy, and 3 (10%) on areas affected by bullous diseases. trauma, including surgery or other medical procedures, can trigger KS, underlying the importance of treatment options which cause the least injury to the skin.

Iatrogenic Kaposi’s sarcoma in the anovulvar area

Kaposi’s sarcoma (KS) is an indolent angioproliferative tumor that depends on viral replication (HHV-8) and inflammatory cytokines produced by infected immune and endothelial cells [1]. It is a multifocal disease, with its evolutionary spectrum varying from a locoregional “indolent” form to a disseminated and fulminant form. KS lesions are rarely limited to unusual mucocutaneous areas. To our knowledge, there have been no reports of iatrogenic KS confined to the female external genitalia. Herein, we report the first case of iatrogenic KS restricted to the vulva and anus in an HIV-negative patient.

Clinical, Dermoscopic, Ultrasonographic, and Histopathologic Correlations in Kaposi's Sarcoma Lesions and Their Differential Diagnoses: A Single-Center Prospective Study.

(1) Background: Kaposi's sarcoma (KS) is an angioproliferative neoplasm typically appearing as angiomatous patches, plaques, and/or nodules on the skin. Dermoscopy and ultrasonography have been suggested as an aid in the diagnosis of KS, but there is little evidence in the literature, especially regarding its possible differential diagnoses. Our aim is to describe and compare the clinical, dermoscopic, and ultrasonographic features of KS and KS-like lesions. (2) Methods: we conducted a prospective study on 25 consecutive patients who were first referred to our tertiary care center from January to May 2021 for a possible KS. (3) Results: 41 cutaneous lesions were examined by means of dermoscopy, Doppler ultrasonography, and pathology, 32 of which were KS-related, while the remaining 9 were lesions with clinical resemblance to KS. On dermoscopy, a purplish-red pigmentation, scaly surface, and the collarette sign were the most common features among KS lesions (81.3%, 46.9%, and 28.1%, respectively). On US, all 9 KS plaques and 21 KS nodules presented a hypoechoic image. Dermoscopic and Doppler ultrasonographic findings of KS-like lesions, such as cherry angioma, venous lake, glomus tumor, pyogenic granuloma, and angiosarcoma were also analyzed. (4) Conclusions: dermoscopy and Doppler ultrasonography can be useful to better assess the features of KS lesions and in diagnosing equivocal KS-like lesions.

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The Body in History, Culture, and the Arts

Higher Rate of Relapse of KSHV/HHV-8 Associated Multicentric Castleman Disease after Rituximab Therapy in HIV- Patients Than in HIV+ Patients

KSHV/HHV-8 associated multicentric Castleman disease (HHV-8 MCD) is a rare lymphoproliferative disorder associating lymphadenopathy, splenomegaly, fever and inflammatory symptoms with high serum CRP, hypergammaglobulinemia and high plasma HHV-8 DNA viral load. HHV-8 MCD mainly affects HIV infected patients but can also be observed in HIV negative patients born in countries with high HHV-8 prevalence. We retrospectively analysed a cohort of 99 patients (73 HIV+ and 26 HIV-) with HHV-8 MCD treated with rituximab (off-label). The baseline characteristics were similar in HIV- and HIV+ patients although HIV- patients were older at MCD diagnosis (median, 65 vs 42 years) and presented less frequently with previous Kaposi sarcoma lesions (15% vs 40%). Out of these 99 patients, 95 patients (25 HIV- and 70 HIV+) achieved CR after a rituximab based therapy. After a median follow-up of 51 months (743 visits), 36 patients were considered as in treatment failure because of MCD relapse, KS progression, lymphoma or death. The 5-year progression-free survival (PFS) was 54,4 % [IC95% 40,8-66,0]. Relapse or progression of HHV-8 disease occured in 12 /25 (48%) HIV- patients and in 24 /75 (32%) HIV+ patients. The 5-year PFS was lower in HIV- patients than in HIV+ patients : 25,7 % [IC95% 5,2-53,6] and 61,6% [IC95% 46,2-73,7], respectively (p= 0.02 ). We have retrospectively analysed the kinetics of blood HHV-8 DNA, CD19+ B-cells and serum CRP after a first rituximab induced CR. The median times for a rise of plasma HHV-8 DNA above 3 logs/mL (n=57), CD19+ B-cells above 1/mm3 (n=59) and serum CRP above 20 mg/L (n=42) were 5,8 months [IQR 2,8-19,8], 8 months [IQR 4,7-13,4] and 13,1 months [IQR 3,4-27,8], respectively. The median time for treatment failure after such events were 4,5 months [IQR 0-16,4] for HHV8-DNA, 13,9 months [IQR 2,7-22,5] for CD19+ B-cells and 2 months [IQR 0-6,9] for CRP. These data show that in most patients, B cells became detectable again and that plasma HHV-8 DNA rose above 3 logs/mL during the first year post-rituximab and that these events could be followed by a rise in serum CRP preceding treatment failure. We suggest that these covariates should be monitored every 4-6 months although the decision of reintroducing specific therapy should still rely on the occurrence of clinical symptoms. The lower rate of relapse observed in the HIV+ population despite a longer follow-up period, may be due to a younger age and to the possible immune reconstitution upon antiretroviral therapy in this population. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

Oral–visceral iatrogenic Kaposi sarcoma following treatment for acute lymphoblastic leukemia: a case report and review of the literature

BackgroundThere have hardly been any reported cases of children presenting with Kaposi sarcoma as a second malignancy following treatment for acute lymphoblastic leukemia outside a transplant setting.Case presentationWe report a case of a 5-year-old boy of Bantu origin, which, to our knowledge, could be only the second reported case of oral–visceral Kaposi sarcoma after acute lymphoblastic leukemia treatment. The patient presented with a 1-month history of progressive, non-painful, soft tissue oral mass, 1 month after completing treatment for high-risk acute lymphoblastic leukemia. He was successfully treated for Kaposi sarcoma on a two-drug regimen (bleomycin and vincristine) with good clinical response.ConclusionVisceral Kaposi sarcoma as a second malignancy may occur after pediatric acute lymphoblastic leukemia treatment, but its rarity makes it unlikely to raise suspicion among clinicians, thus precluding early diagnosis and treatment. We recommend routine evaluation for Kaposi sarcoma lesions in children undergoing long-term surveillance following treatment for childhood acute leukemia.

S2431 A Rare Case of Esophageal Kaposi Sarcoma Causing Dysphagia

Introduction: Kaposi sarcoma (KS) is an angioproliferative disorder(low grade vascular tumor) caused by human herpesvirus-8 in immunocompromised patients. The disease is multifocal, ranging from indolent skin manifestations to extensive visceral involvement. We are describing a rare case of esophageal KS causing dysphagia. Case Description/Methods: A 57-year-old bisexual male with a medical history of hypertension, syphilis and recent diagnosis of HIV (untreated) admitted for hypotension, tachycardia, nausea, vomiting,hemoptysis and dysphagia to soilds. He was noted to have oropharyngeal lesions and biopsy of the lesions were obtained. An EGD performed for evaluation of dysphagia (denied odynophagia) showed circumferential erythema, purplish plaques and friability of the esophagus. Biopsies were obtained from esophagus. Pathology from tongue, gingiva, proximal and distal esophagus returned positive for Kaposi sarcoma with positive staining for HHV-8 and CD31. CD4 count was 31/uL and HSV8 PCR showed 1,000,000 copies. Patient was treated with Bictegravir, emtricitabine and tenofovir alafenamide. Hematology was consulted for potential pulmonary KS and patient was started on liposomal doxorubicin. He developed Ventricular fibrillation and cardiac arrest. He was revived and intubated. Patient improved initially but developed neutropenic fever. Infectious disease treated him with empirical antibiotics and antivirals. Patient further developed Castleman’s disease, respiratory failure, acute kidney failure requiring CRRT, and altered mental status. Despite aggressive measures patient did not survive (Figure). Discussion: AIDS-related KS varies in clinical progression and occurs in 20% of patients with AIDS. The CD4 count will typically be less than 150 cells per cubic millimeter with a high viral load ranging from greater than 10,000 copies per millimeter. Gastrointestinal manifestation is the most common extra-cutaneous site of KS in AIDS-related cases though rarely does it occur without cutaneous involvement. The majority of the patients are asymptomatic, roughly 75%. Symptomatic patients present with nonspecific findings such as abdominal discomfort, cramps, nausea, vomiting, diarrhea, and upper or lower GI bleed. KS lesions causing dysphagia are extremely rare. The mainstay of therapy is combined antiretroviral therapy (ART). Local intralesional chemotherapy can be utilized to manage limited lesions. Systemic therapy with liposomal anthracyclines is recommended for patients with advanced or rapidly progressive disease.Figure 1.: Kaposi Sarcoma Lesions.

A major role for Nrf2 transcription factors in cell transformation by KSHV encoded oncogenes.

Kaposi’s sarcoma (KS) is the most common tumor in AIDS patients. The highly vascularized patient’s skin lesions are composed of cells derived from the endothelial tissue transformed by the KSHV virus. Heme oxygenase-1 (HO-1) is an enzyme upregulated by the Kaposi´s sarcoma-associated herpesvirus (KSHV) and highly expressed in human Kaposi Sarcoma (KS) lesions. The oncogenic G protein-coupled receptor (KSHV-GPCR or vGPCR) is expressed by the viral genome in infected cells. It is involved in KS development, HO-1 expression, and vascular endothelial growth factor (VEGF) expression. vGPCR induces HO-1 expression and HO-1 dependent transformation through the Ga13 subunit of heterotrimeric G proteins and the small GTPase RhoA. We have found several lines of evidence supporting a role for Nrf2 transcription factors and family members in the vGPCR-Ga13-RhoA signaling pathway that converges on the HO-1 gene promoter. Our current information assigns a major role to ERK1/2MAPK pathways as intermediates in signaling from vGPCR to Nrf2, influencing Nrf2 translocation to the cell nucleus, Nrf2 transactivation activity, and consequently HO-1 expression. Experiments in nude mice show that the tumorigenic effect of vGPCR is dependent on Nrf2. In the context of a complete KSHV genome, we show that the lack of vGPCR increased cytoplasmic localization of Nrf2 correlated with a downregulation of HO-1 expression. Moreover, we also found an increase in phospho-Nrf2 nuclear localization in mouse KS-like KSHV (positive) tumors compared to KSHV (negative) mouse KS-like tumors. Our data highlights the fundamental role of Nrf2 linking vGPCR signaling to the HO-1 promoter, acting upon not only HO-1 gene expression regulation but also in the tumorigenesis induced by vGPCR. Overall, these data pinpoint this transcription factor or its associated proteins as putative pharmacological or therapeutic targets in KS.

Scrotal Kaposi’s sarcoma in an immunocompetent patient: A case report and review of the literature

Kaposi’s sarcoma (KS) is a malignancy that generally affects the skin. It may be systemic with internal organ involvement, originating from the vascular endothelium. It is an acquired immunodeficiency syndrome (AIDS)-defining illness. Human herpes virus-8 (HHV-8) infection is involved in its pathogenesis. KS lesions have a general distribution, often involving the skin of the feet and legs and, to a lesser extent, the hands, arms, and trunk. Isolated scrotal involvement in an immunocompetent patient is a highly rare presentation. Herein, we present an immunocompetent Saudi patient with scrotal KS. A review of the related literature is also presented.

Histologic Variants of Kaposi Sarcoma in the Gastrointestinal Tract: A Contemporary Multi-institutional Clinicopathologic Analysis of 46 Cases.

Kaposi sarcoma (KS) can pose diagnostic challenges in biopsy specimens. Multiple histologic variants of cutaneous KS have been described; however, the histomorphologic spectrum of gastrointestinal (GI) KS has not been systematically studied. This large series comprehensively evaluated 46 cases of KS involving the GI tract and identified 7 histomorphologic variants, some that have not been previously described. Five of them are inconspicuous but have unique morphologic patterns, including lymphangioma/lymphangiectatic-like (n=17), mucosal hemorrhage/telangiectatic-like (n=17), mucosal inflammation-like (n=15), granulation tissue-like (n=13), and mucosal prolapse-like (n=4) variants. These variants can be easily misdiagnosed or misinterpreted on routine examination if KS is not considered, and if the immunohistochemical stain for human herpesvirus-8 is not performed. The other 2 morphologic variants present as spindle cell proliferations and are the GI stromal tumor-like (n=8) and inflammatory myofibroblastic tumor-like (n=2). These variants raise a broad differential diagnosis of spindle cell tumors of the GI tract and could pose diagnostic challenges. In summary, GI KS lesions exhibit variable, often unconventional histomorphologic patterns. KS should be included in the differential diagnosis even if features of conventional KS are not seen, particularly in limited biopsies in immunocompromised patients, such as those with human immunodeficiency virus infection. Although the clinical significance of these morphologic variants is yet to be determined, they are nonetheless important from a diagnostic standpoint. Misdiagnosis and delay in appropriate management can be avoided by recognizing the morphologic diversity of GI KS and appropriately utilizing the human herpesvirus-8 immunohistochemical stain.

Cutaneous and subcutaneous Kaposi's sarcoma lesions treated with electrochemotherapy.

Kaposi's sarcoma (KS) is a locally aggressive mesenchymal tumor that involves the lymphovascular system, with a tendency to become multifocal. Electrochemotherapy (ECT) is considered a valuable treatment option in selected patients with cutaneous and subcutaneous KS lesions. We report a retrospective study that included 14 classic and endemic KS patients that underwent ECT sessions for the treatment of KS cutaneous and subcutaneous lesions at our institution. According to Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 criteria, our patients had an overall response rate (ORR) of 100% to the ECT treatment. A complete response (CR) was obtained in 92.8% of patients after one or more ECT sessions. Only one patient had a progressive disease (PD). The treatment was well tolerated with a low complication rate, mainly transitory local pain or skin ulceration. ECT represents a locoregional therapy for containment and symptomatic control of classic and endemic KS cutaneous and subcutaneous lesions. Further studies including different subtypes of KS patients should also be performed.