International Scholarly Research Notices

International Scholarly Research Notices / 2012 / Article

Clinical Study | Open Access

Volume 2012 |Article ID 486425 |

Louis-Jacques van Bogaert, "Anogenital Lesions: Kaposi's Sarcoma and Its Mimicks", International Scholarly Research Notices, vol. 2012, Article ID 486425, 5 pages, 2012.

Anogenital Lesions: Kaposi's Sarcoma and Its Mimicks

Academic Editor: G. D'ettorre
Received31 Jul 2012
Accepted13 Sep 2012
Published31 Oct 2012


Kaposi's sarcoma (KS) is a low-grade vascular neoplasm associated with human herpes virus-8 (HHV-8) infection, and, in the epidemic form, with the human immunodeficiency virus (HIV). Although HHV-8 is present in all body fluids and is sexually transmitted, there are surprisingly few reports of anogenital KS. Clinically, especially in HIV/KS endemic areas, dark stained skin patches or nodules are prone to misdiagnosis, especially in dark-skinned individuals. Therefore, a biopsy is recommended. The histologic appearance spans a broad spectrum of KS and non-KS lesions; therefore, the final diagnosis should be confirmed by HHV-8 immunohistochemistry. We report a series of 36 anogenital biopsies from a group of 16 documented HIV-positive patients; in 20 the HIV serostatus was unknown. There were ten KS (five in HIV-positive patients), and 26 non-KS (11 in HIV-positive subjects) lesions. In the era of HIV/AIDS, anogenital lesions may be the first manifestation of KS in immunocompromised individuals and should be biopsied. The histological diagnosis should be confirmed by HHV-8 immunohistochemistry.

1. Introduction

The human herpes virus-8 (HHV-8), also called Kaposi’s sarcoma herpes virus (KSHV), is the causative agent of all types of Kaposi’s sarcoma (KS), namely the classic, endemic, iatrogenic immunosuppression, and the epidemic/human immunodeficiency virus (HIV) related forms. The modes of acquisition of the KSHV and its transmission vary with age, gender, geography, and sexual practices [1]. Although the virus is omnipresent its incidence is highest in KS endemic regions such as sub-Saharan Africa (sSA).

In Uganda, HHV-8 DNA was detected in 28 percent of oral swabs and 27 percent of blood samples of healthy asymptomatic subjects [2]. Hence, saliva is a potential source of transmission. KSHV is transmitted to children from maternal and nonmaternal sources in KS-endemic regions, and occurs via nonsexual routes [36]. It has been shown that, in sSA, infection occurs during childhood mainly via maternal saliva and breast milk [7, 8]. Anthropologic research in sSA has identified that premastication of foods of infants and children is traditional, and that saliva, semen, and vaginal fluids are used while engaging in nonsexual practices associated with childcare [911].

The sexual transmission of KSHV is more controversial. In the industrialized world, there is evidence of transmission between men having sex with men (MSM) via anal but not oroanal sex [7, 12, 13]. Heterosexual transmission is affirmed by some [1418]. Others deny it [5, 19]. Since KSHV is present in semen and in uterine cervical scrapings, sexual transmission appears to be very plausible [17, 20, 21]. However, despite the high incidence of KSHV infection and its presence in the male and female genital tract, surprisingly few cases of anogenital KS have been reported in the literature, associated or not with HIV coinfection, in males or females [2227].

The purpose of this study was to describe the clinical and histopathological spectrum of anogenital lesions either under- or overdiagnosed as KS in a HIV/AIDS endemic province of South Africa.

2. Materials and Methods

The study was carried out at the Histopathology Department of the National Health Laboratory Service of the Limpopo Province. The population is mainly rural and is in excess of 5 M. The department receives and reports all the histology specimens from the public hospitals in the province.

The cases were retrieved from a prospective survey of 429 biopsy and LAN-1 immunohistochemically stained cases from March 2010 through July 2012 (Figure 1). Patients’ data were recorded from the biopsy request form and the laboratory data base. The following information was compiled: age, gender, clinical information, clinical provisional diagnosis, and HIV serostatus.

Routine streptavidin-biotin-peroxidase immunostaining with diaminobenzidine was performed on formalin-fixed paraffin-embedded tissue using a murine monoclonal antibody directed against the C-terminus of the latent nuclear antigen-1 (LNA-1) molecule of HHV-8 (clone 13B10; Novocastra, Newcastle upon Tyne, UK).

Patients’ anonymity was preserved. Ethical approval was obtained from the institutional research ethics committee.

3. Results

Figure 1 illustrates the distribution of cases by HIV status, immunohistochemically diagnosed KS, and mimicks. We collected a total of 36 cases of anogenital lesions: 15 in males and 21 in females. Sixteen (44.4%) had a documented HIV infection; 20 were of unknown HIV serostatus.

Table 1 shows the clinicopathology of male anogenital lesions. There were 4 KS and 11 mimicks; four (26.6%) were HIV-positive. Pyogenic granulomas accounted for 7 (46.6%) of non-KS lesions. KS was clinically suspected in one case only.

AgeHIV StatusClinical PresentationHistopathology

54UnknownScrotal massNodular stage KS
38PositivePerineal ulcerPlaque stage KS
29UnknownPenile ulcerNodular stage KS
35UnknownPenile KSEarly patch stage KS
49UnknownScrotal ulcerPyogenic granuloma
34PositiveScrotal ulcerPyogenic granuloma
27UnknownScrotal pyogenic granulomaPyogenic granuloma
72UnknownScrotal ulcerPyogenic granuloma
30UnknownPenile ulcerPyogenic granuloma
59PositivePerianal ulcerPyogenic granuloma
63UnknownPerianal ulcerPyogenic granuloma
47UnknownPerianal nodule Hemangioma
24UnknownScrotal noduleHemangioma
32PositiveFournier’s gangreneFournier’s gangrene
41UnknownPenile noduleMalignant fibrous histiocytoma

Table 2 illustrates the clinicopathological presentation of female anogenital lesions. Twelve (46.2%) were known to be HIV-positive. The clinical diagnosis of KS was made in cases with known disseminated KS.

AgeHIV StatusClinical PresentationHistopathology

48PositiveVulvar massNodular stage KS
31PositiveVulvar mass (disseminated KS)Nodular stage KS
33UnknownCervical erosionNodular stage KS
34PositiveVulvar noduleEarly patch stage KS
24UnknownVulvar noduleNodular stage KS
24PositiveVaginal KSNodular stage KS
19PositiveVulvar KSPyogenic granuloma
48UnknownAnal ulcerPyogenic granuloma
40UnknownVaginal ulcerPyogenic granuloma
35PositiveVulvar nodulePyogenic granuloma
44PositiveVulvar nodulePyogenic granuloma
22NegativeVulvar nodulePyogenic granuloma
44PositiveAnal ulcerPyogenic granuloma
25PositiveVulvar noduleFibrous histiocytoma
25PositiveVulvar carcinomaFibrous histiocytoma
49UnknownVulvar noduleFibrous histiocytoma
58UnknownCervical massPedunculated leiomyoma
49UnknownVulvar violaceous lesionLichen planus
42PositiveVulvar dark skin patchMelanocytic melanoma
45PositiveVulvar noduleHemangioma
43UnknownCervical erosionCervical cancer

4. Discussion

African endemic KS has been identified for many decades in the past. Currently, the increasing prevalence of HIV infection complicates all efforts to clearly distinguish the endemic variant from the HIV-related one [28]. The clinical presentation and natural history of the endemic KS are now blending with those of the epidemic or AIDS-associated disease [29]. The distinction is clinically relevant because, although it is amenable to highly active antiretroviral treatment (HAART), AIDS-associated KS carries a poor prognosis [30]. Unfortunately, in South Africa, there is still widespread reluctance to be tested for HIV. This is attributable to the official opt-in policy (voluntary counseling and testing), and the fear of stigma and discrimination. This adds to the difficulty in distinguishing endemic from epidemic KS cases.

Early reports on African KS concentrated on the gender differences and histological features [31, 32]. One publication indicated that the most common presentation was cutaneous; it emphasised the rarity of anogenital location [33]. In a textbook of 1957, Bluefarb cited six patients with KS of the glans penis [34]. A series of 29 KS cases retrospectively collected from 1973 till 1985 in Uganda mentioned external genital involvement of 15 [35]. A Nigerian report mentioned that anogenital involvement was more common in HIV-positive cases [36]. A more recent publication of 66 biopsy-confirmed KS and HIV-seropositive patients found 10 (15.2%) genital sites (not otherwise specified); no genital KS was found in 11 cases of endemic KS [28]. Among twenty biopsy-proven Nigerian KS, the penis and rectum were involved in what appears to be cases of disseminated KS [37]. In an Ugandan series of 197 HIV-associated KS (only 62% biopsy-proven) it was reported that 6% were located on the genitals (no gender distribution or precise anatomic location); half of the series had lesions in two or more anatomic locations [38]. The difficulty with most of these reports is that the anogenital location seems to have been part of multicentric or disseminated KS, and that none was LNA-1 confirmed.

It is now well established that both the clinical and histological diagnosis of KS is fraught with over- and underdiagnosis because of the wide range of mimickers [39, 40]. Therefore, especially in HIV/AIDS and KS endemic areas, a clinical lesion suspect of KS should be biopsied, and the histopathological diagnosis must be supported by HHV-8 immunohistochemistry. Clinically, the most common mimicks are seborrheic keratosis, haemangioma, and pyogenic granulomas. Histopathologically, around thirty lesions are part of the differential diagnosis [39, 40]. Seborrheic keratosis mimicks early patch stage KS. Pyogenic granulomas and haemangioma mimick nodular stage KS. Fibrous histiocytoma and tendosynovitis mimick the plaque stage, to name only a few and most common ones.

Literature case reports all illustrate that vulvar KS appeared clinically as a mass, a papilloma, or an abscess; none was initially suspected to be a KS [2226]. In the present series, KS was clinically diagnosed only in one instance; one was overdiagnosed microscopically as KS before LAN-1 immunostaining.

In conclusion, anogenital KS is rare and easily misdiagnosed even in HIV/KS endemic regions. Therefore, a high clinical suspicion threshold should prompt a biopsy, and the diagnosis of KS should be confirmed by LNA-1 immunohistochemistry to avoid misdiagnosis and wrong management.

Conflict of Interests

The author declares no conflict of interests.


  1. B. Biryahwaho, S. C. Dollard, R. M. Pfeiffer et al., “Sex and geographic patterns of human herpesvirus 8 infection in a nationally representative population-based sample in Uganda,” Journal of Infectious Diseases, vol. 202, no. 9, pp. 1347–1353, 2010. View at: Publisher Site | Google Scholar
  2. C. Johnston, J. Orem, F. Okuku et al., “Impact of HIV infection and Kaposi Sarcoma on human herpesvirus-8 mucosal replication and dissemination in Uganda,” PLoS ONE, vol. 4, no. 1, Article ID e4222, 2009. View at: Publisher Site | Google Scholar
  3. S. M. Mbulaiteye, R. M. Pfeiffer, D. Whitby, G. R. Brubaker, J. Shao, and R. J. Biggar, “Human herpesvirus 8 infection within families in rural Tanzania,” Journal of Infectious Diseases, vol. 187, no. 11, pp. 1780–1785, 2003. View at: Publisher Site | Google Scholar
  4. S. Mbulaiteye, V. Marshall, R. K. Bagni et al., “Molecular evidence for mother-to-child transmission of Kaposi sarcoma-associated herpesvirus in Uganda and K1 gene evolution within the host,” Journal of Infectious Diseases, vol. 193, no. 9, pp. 1250–1257, 2006. View at: Publisher Site | Google Scholar
  5. A. A. Adjei, H. B. Armah, F. Gbagbo, I. Boamah, C. Adu-Gyamfi, and I. Asare, “Seroprevalence of HHV-8, CMV, and EBV among the general population in Ghana, West Africa,” BMC Infectious Diseases, vol. 8, article 111, 2008. View at: Publisher Site | Google Scholar
  6. L. M. Butler, W. A. Were, S. Balinandi et al., “Human herpesvirus 8 infection in children and adults in a population-based study in rural Uganda,” Journal of Infectious Diseases, vol. 203, no. 5, pp. 625–634, 2011. View at: Publisher Site | Google Scholar
  7. R. Bagni and D. Whitby, “Kaposi's sarcoma-associated herpesvirus transmission and primary infection,” Current Opinion in HIV and AIDS, vol. 4, no. 1, pp. 22–26, 2009. View at: Publisher Site | Google Scholar
  8. M. Dedicoat, R. Newton, K. R. Alkharsah et al., “Mother-to-child transmission of human herpesvirus-8 in South Africa,” Journal of Infectious Diseases, vol. 190, no. 6, pp. 1068–1075, 2004. View at: Publisher Site | Google Scholar
  9. J. M. Wojcicki, “Traditional behavioural practices, the exchange of saliva and HHV-8 transmission in sub-Saharan African populations,” British Journal of Cancer, vol. 89, no. 10, pp. 2016–2017, 2003. View at: Publisher Site | Google Scholar
  10. J. M. Wojcicki, R. Newton, M. I. Urban et al., “Risk factors for high anti-HHV-8 antibody titers (≥1:51,200) in black, HIV-1 negative South African cancer patients: a case control study,” BMC Infectious Diseases, vol. 3, article 21, 2003. View at: Publisher Site | Google Scholar
  11. J. M. Wojcicki, C. Kankasa, C. Mitchell, and C. Wood, “Traditional practices and exposure to bodily fluids in Lusaka, Zambia,” Tropical Medicine and International Health, vol. 12, no. 1, pp. 150–155, 2007. View at: Publisher Site | Google Scholar
  12. G. J. P. van Griensven, E. C. Boucher, and R. A. Coutinho, “Oro-anal sex and the occurrence of Kaposi's sarcoma,” Genitourinary Medicine, vol. 69, no. 1, pp. 77–78, 1993. View at: Google Scholar
  13. E. A. Engels, J. O. Atkinson, B. I. Graubard et al., “Risk factors for human herpesvirus 8 infection among adults in the United States and evidence for sexual transmission,” Journal of Infectious Diseases, vol. 196, no. 2, pp. 199–207, 2007. View at: Publisher Site | Google Scholar
  14. M. A. Eltom, S. M. Mbulaiteye, A. J. Dada, D. Whitby, and R. J. Biggar, “Transmission of human herpesvirus 8 by sexual activity among adults in Lagos, Nigeria,” AIDS, vol. 16, no. 18, pp. 2473–2478, 2002. View at: Publisher Site | Google Scholar
  15. L. Lavreys, B. Chohan, R. Ashley et al., “Human herpesvirus 8: seroprevalence and correlates in prostitutes in Mombasa, Kenya,” Journal of Infectious Diseases, vol. 187, no. 3, pp. 359–363, 2003. View at: Publisher Site | Google Scholar
  16. C. Henke-Gendo and T. F. Schultz, “Transmission and disease association of Kaposi's sarcoma-associated herpes virus: recent developments,” Current Opinion in Infectious Diseases, vol. 17, no. 1, pp. 53–57, 2004. View at: Publisher Site | Google Scholar
  17. O. Bagasra, D. Patel, L. Bobroski et al., “Localization of human herpesvirus type 8 in human sperms by in situ PCR,” Journal of Molecular Histology, vol. 36, no. 6-7, pp. 401–412, 2005. View at: Publisher Site | Google Scholar
  18. A. Dupuy, T. Schulz, S. Chevret et al., “Asymmetrical transmission of human herpesvirus 8 among spouses of patients with Kaposi sarcoma,” British Journal of Dermatology, vol. 160, no. 3, pp. 540–545, 2009. View at: Publisher Site | Google Scholar
  19. T. B. Campbell, M. Borok, B. Ndemera et al., “Lack of evidence for frequent heterosexual transmission of human herpesvirus 8 in zimbabwe,” Clinical Infectious Diseases, vol. 48, no. 11, pp. 1601–1608, 2009. View at: Publisher Site | Google Scholar
  20. P. Monini, L. de Lellis, M. Fabris, F. Rigolin, and E. Cassai, “Kaposi's sarcoma-associated herpesvirus DNA sequences in prostate tissue and human semen,” The New England Journal of Medicine, vol. 334, no. 18, pp. 1168–1172, 1996. View at: Publisher Site | Google Scholar
  21. P. K. S. Chan, W. H. Li, M. Y. M. Chan, and A. F. B. Cheng, “Detection of human herpesvirus 8 in cervical cells of Chinese women with abnormal Papanicolaou smears,” Clinical Infectious Diseases, vol. 29, no. 6, pp. 1584–1585, 1999. View at: Publisher Site | Google Scholar
  22. A. F. Audouin, P. Lopes, and Y. Lenne, “Kaposi's sarcoma of the uterine cervix and atypical condyloma in a female patient with a heart transplant (during the postpartal period),” Archives d'Anatomie et de Cytologie Pathologiques, vol. 36, no. 5-6, pp. 226–228, 1988. View at: Google Scholar
  23. S. B. Rajah, J. Moodley, D. J. Pudifin, J. Duursma, and K. Cooper, “Kaposi's sarcoma associated with acquired immunodeficiency syndrome presenting as a vulval papilloma. A case report,” South African Medical Journal, vol. 77, no. 11, pp. 585–586, 1990. View at: Google Scholar
  24. M. A. Macasaet, A. Duerr, W. Thelmo, S. D. Vernon, and E. R. Linger, “Kaposi sarcoma presenting as a vulvar mass,” Obstetrics and Gynecology, vol. 86, no. 4, pp. 695–697, 1995. View at: Publisher Site | Google Scholar
  25. R. M. Riggs and J. McCarthy, “Vulvar Kaposi's sarcoma in a woman with AIDS: a case report,” Journal of Reproductive Medicine for the Obstetrician and Gynecologist, vol. 50, no. 9, pp. 730–732, 2005. View at: Google Scholar
  26. B. W. Laartz, C. Cooper, A. Degryse, and J. T. Sinnott, “Wolf in sheep's clothing: advanced kaposi sarcoma mimicking vulvar abscess,” Southern Medical Journal, vol. 98, no. 4, pp. 475–477, 2005. View at: Publisher Site | Google Scholar
  27. K. H. Kim, J. I. Choi, K. H. Ryu et al., “Primary classic Kaposi's sarcoma of the penis in an HIV-negative patient,” Korean Journal of Urology, vol. 51, no. 11, pp. 803–806, 2010. View at: Publisher Site | Google Scholar
  28. G. Wamburu, E. J. Masenga, E. Z. Moshi, P. Schmid-Grendelmeier, W. Kempf, and C. E. Orfanos, “HIV—associated and non—HIV associated types of Kaposi's sarcoma in an African population in Tanzania. Status of immune suppression and HHV-8 seroprevalence,” European Journal of Dermatology, vol. 16, no. 6, pp. 677–682, 2006. View at: Publisher Site | Google Scholar
  29. O. W. Mwanda, P. Fu, R. Collea, C. Whalen, and S. C. Remick, “Kaposi's sarcoma in patients with and without human immunodeficiency virus infection, in a tertiary referral centre in Kenya,” Annals of Tropical Medicine and Parasitology, vol. 99, no. 1, pp. 81–91, 2005. View at: Publisher Site | Google Scholar
  30. K. M. Chu, G. Mahlangeni, S. Swannet, N. P. Ford, A. Boulle, and G. Van Cutsem, “AIDS-associated Kaposi's sarcoma is linked to advanced disease and high mortality in a primary care HIV programme in South Africa,” Journal of the International AIDS Society, vol. 13, no. 1, article 23, 2010. View at: Publisher Site | Google Scholar
  31. J. A. Gordon, “Kaposi's sarcoma: a review of 136 Rhodesian African cases,” Postgraduate Medical Journal, vol. 43, no. 502, pp. 513–519, 1967. View at: Google Scholar
  32. K. M. O'Connell, “Kaposi's sarcoma: histopathological study of 159 cases from Malawi,” Journal of Clinical Pathology, vol. 30, no. 8, pp. 687–695, 1977. View at: Google Scholar
  33. G. Slavin, H. M. Cameron, and H. Singh, “Kaposi's sarcoma in mainland Tanzania: a report of 117 cases,” British Journal of Cancer, vol. 23, no. 2, pp. 349–357, 1969. View at: Google Scholar
  34. S. M. Bluefarb, Kaposi's Sarcoma, Charles Thomas, Springfield, Ill, USA, 1957.
  35. E. Katongole-Mbidde, C. Banura, and M. Nakakeeto, “Diagnostic implications of genital Kaposi's sarcoma,” East African Medical Journal, vol. 66, no. 8, pp. 499–502, 1989. View at: Google Scholar
  36. A. Z. Mohammed, E. J. C. Nwana, and A. N. Manasseh, “Changing patterns of Kaposi's sarcoma in Nigerians,” Tropical Doctor, vol. 35, no. 3, pp. 168–169, 2005. View at: Publisher Site | Google Scholar
  37. M. B. Kagu, H. A. Nggada, H. I. Garandawa, B. H. Askira, and M. A. Durosinmi, “AIDS-associated Kaposi's sarcoma in Northeastern Nigeria,” Singapore Medical Journal, vol. 47, no. 12, pp. 1069–1074, 2006. View at: Google Scholar
  38. W. Phipps, F. Ssewankambo, H. Nguyen et al., “Gender differences in clinical presentation and outcomes of epidemic kaposi sarcoma in Uganda,” PLoS ONE, vol. 5, no. 11, Article ID e13936, 2010. View at: Publisher Site | Google Scholar
  39. S. R. Long, M. J. Whitfeld, C. Eades, J. E. Koehler, A. P. Korn, and C. J. Zaloudek, “Bacillary angiomatosis of the cervix and vulva in a patient with AIDS,” Obstetrics and Gynecology, vol. 88, no. 4, pp. 709–711, 1996. View at: Publisher Site | Google Scholar
  40. J. L. Urquhart, A. Uzieblo, and S. Kohler, “Detection of HHV-8 in pyogenic granuloma-like kaposi sarcoma,” American Journal of Dermatopathology, vol. 28, no. 4, pp. 317–321, 2006. View at: Publisher Site | Google Scholar

Copyright © 2012 Louis-Jacques van Bogaert. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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