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Pilonidal disease is a common acquired condition believed to arise from penetration of short hairs into the subcutaneous tissue that induces a cyst or sinus formation. Malignant degeneration is rare and is typically seen only after decades of antecedent disease presence. Condylomata acuminatum in association with pilonidal disease have been described in two prior case reports, however, the coexistence of condyloma with pilonidal disease complicated by malignant degeneration has not been previously reported. Condylomata have known potential for malignant degeneration and are correlated with human papilloma virus infection, with certain serotypes of higher oncogenic potential. Coinfection with human immunodeficiency virus and human papilloma virus is associated with higher rates of anal neoplasia, We report two cases of human immunodeficiency virus-infected patients with the constellation of pilonidal disease, condylomata acuminatum, and subsequent malignant degeneration into squamous-cell carcinoma. In contrast to other case reports in the literature, these two patients had considerably shorter antecedent periods of pilonidal disease before malignant degeneration was detected. Both cases also had intractable courses. We conclude that the existence of condylomata acuminatum and pilonidal disease in an immunocompromised patient may represent a more ominous condition than solitary pilonidal disease. Therefore, careful inspection of the pilonidal area in human immunodefiency virus-infected patients presenting with condylomata is important and earlier intervention should be considered. Moreover, further evaluation of the prevalence of squamous-cell carcinoma arising from pilonidal disease complicated by condylomata, particularly in the immunosuppressed, is warranted. [ABSTRACT FROM AUTHOR]

Purpose of Review: AIDS-related Kaposi's sarcoma results from co-infection with HIV and Kaposi's sarcoma herpesvirus/human herpesvirus-8, which leads to the development of an angiogenic-inflammatory state that is critical in the pathogenesis of the condition. Recent discoveries regarding Kaposi's sarcoma herpesvirus/human herpesvirus-8 infection and its activation of signal transduction have led to a greater understanding into Kaposi's sarcoma pathogenesis and have identified potential targets for therapy., Recent Findings: Kaposi's sarcoma is driven by Kaposi's sarcoma herpesvirus/human herpesvirus-8-specific pathways, which include viral G protein-coupled receptor, viral IL-6, and viral chemokine homologues. In addition, cellular growth/angiogenic pathways such as vascular endothelial growth factor, insulin growth factor, platelet-derived growth factor, angiopoietin and matrix metalloproteinases are 'pirated' by Kaposi's sarcoma herpesvirus/human herpesvirus-8. Recent findings show Kaposi's sarcoma herpesvirus/human herpesvirus-8 specific signaling pathways and pirated pathways to be important therapeutic targets., Summary: Numerous advances have been made recently that expand the understanding of Kaposi's sarcoma pathogenesis. These findings and recent clinical trials of targeted therapy for treatment are a prelude to a shift in the paradigm of how AIDS-related Kaposi's sarcoma is managed.

Purpose of Review: The incidence and spectrum of non-AIDS-defining cancers has continued to grow. As HIV-infected individuals live longer due to highly active antiretroviral therapy, their risk of dying from one of these cancers is increased. The recent literature pertaining to non-AIDS-defining cancers is reviewed., Recent Findings: Recent epidemiological studies have identified higher rates of carcinoma of the anus, lung, breast, skin, conjunctiva, liver and prostate; hematopoietic malignancies such as Hodgkin's lymphoma, plasma-cell neoplasia and leukemia; and other neoplasms like melanoma and leiomyosarcoma in HIV-positive patients. The role of HIV-induced immunosuppression in the development of these non-AIDS-defining cancers appears less important than lifestyle habits like smoking and sun exposure, as well as coinfection with human papilloma, hepatitis B, hepatitis C and Epstein-Barr viruses., Summary: It is unclear whether the growing number of reports on non-AIDS-defining cancers reflects a true increased incidence or merely the product of increased surveillance, detection and reporting. Highly active antiretroviral therapy not only promotes longevity in the HIV-positive population, but may increase their risk of developing cancer like Hodgkin's lymphoma. Assertive prevention strategies are needed to adequately deal with non-AIDS-defining cancers in an aging and growing HIV-positive population.

Kaposi sarcoma (KS) is a multicentric vascular neoplasm characterized histologically by the progressive proliferation of spindle-shaped tumor cells in all epidemiologic (AIDS-related, classic, endemic, and iatrogenic) forms. Human herpesvirus 8 (HHV8) is associated with all epidemiologic forms of KS and has been shown in vitro to induce the tyrosine receptor kinase c-kit in HHV8-infected cells. To date, c-kit immunoreactivity has not been systematically studied in KS lesions. Therefore, the aim of this study was to evaluate c-kit expression by immunohistochemistry in different proliferative stages and epidemiologic forms of KS. Archival cases of formalin-fixed, paraffin-embedded KS lesions, including 9 classic, 11 AIDS-related, and 15 African (endemic) forms at various histologic stages (5 patch, 8 plaque, 22 nodular), biopsied from different sites, were stained using immunohistochemistry with antibodies to HHV8 (LNA-1) and c-kit (CD117). C-kit immunoreactivity of lesional cells was demonstrated in 15 (43%) cases overall. A total of five (56%) classic, five (45%) AIDS-related, and five (33%) endemic KS cases were positive for c-kit. There was no difference in the intensity of c-kit staining between the different epidemiologic groups and histologic stages of KS. HHV8 (LNA-1) immunoreactivity was present in all (100%) classic, 10 (91%) AIDS-related, and 9 (60%) endemic cases. LNA-1 staining was demonstrated in 13 (93%) of the c-kit-positive and 15 (75%) of the c-kit-negative KS lesions. These findings indicate that c-kit expression in lesional cells can be detected by immunohistochemistry in different epidemiologic forms and histologic stages of KS. Furthermore, the expression of c-kit does not correspond with the presence of HHV8 (LNA-1) immunoreactivity in KS lesions.

Objectives: Myelodysplasia is a frequent consequence of HIV infection, but acute myeloid leukemia (AML) is rare. Clinical presentations and outcomes of patients with HIV and subsequent AML are reviewed., Methods: Five HIV-infected individuals who were subsequently diagnosed with AML were evaluated and treated. A further 42 cases of AML among patients with antecedent HIV infection were identified using MEDLINE, AIDSLINE, and CancerLit searches., Results: HIV infection was present for a median of 48 months (71-180) before AML was diagnosed and the median reported CD4 cell count was 210 x 106 cells/l. In five instances, a delay in diagnosis occurred when cytopenias were initially attributed to HIV or zidovudine-based therapy. In 45 patients, diagnosis was according to the French-American-British (FAB) leukemia classification schema and in two the FAB type was not specified. M2 (n = 15) and M4 (n = 14) subtypes represented 64% (29/45) of reported cases. Patients with a CD4 cell count < 200 x 106 cells/l (n = 11) had a median survival time of 7 weeks, while patients with a CD4 cell count >or= 200 x 106 cells/l (n = 7) had a median survival of 7 months (P = 0.005). Although long-lasting chemotherapy-induced responses were rare, the majority of treated patients did achieve complete hematologic remissions. Treatment-related morbidity did not appear to be excessive., Conclusion: In the absence of randomized and prospective clinical studies to guide decision making, this analysis indicates that induction chemotherapy may be a reasonable option for selected HIV-infected patients with AML and adequate immune function.

Objective: To assess the efficacy, safety and tolerance of oral 9-cis-retinoic acid in HIV-infected patients with Kaposi's sarcoma., Methods: Sixty-six patients with AIDS-related Kaposi's sarcoma were enrolled at 14 centers; 60 received the study medication and were analyzed and, of these, 45 (75%) had received prior therapy for Kaposi's sarcoma. Once daily oral 9-cis-retinoic acid (alitretinoin, Panretin) was administered at doses up to 140 mg/m2. Most patients (72%) received a maximum dose of 100 mg/m2. Response was assessed using AIDS Clinical Trials Group (ACTG) criteria., Results: The median age was 38 years and the median absolute CD4 cell count was 194 x 10(6) cells/l (range 6-784 x 10(6)). Despite the use of three- and four-drug antiviral regimens (83%), the median HIV RNA at baseline was 8701 copies/ml [range < 500 (lower limit of detection) to 4.24 x 10(6)]. The tumor response rate was 37% (95% confidence interval 25-49). Tumor response was associated with improved quality-of-life measures. There was a significant increase in interleukin 6 (IL-6) levels from baseline to week 4. Responders had significantly lower baseline soluble IL-6 receptor levels (P = 0.029) than non-responders. The median time to response was 9 weeks (mean, 13 weeks; range, 4-36). HIV RNA levels did not change significantly during therapy nor did they correlate with tumor responses. Study drug was discontinued by 28 patients for adverse events, which included headache (13) and skin toxicity (10)., Conclusion: Oral 9-cis-retinoic acid is an active antitumor drug for AIDS-related Kaposi's sarcoma. Treatment is associated with skin and constitutional toxicity and further studies are needed to improve its long-term tolerance.