Explore chapters and articles related to this topic
Sexually Transmitted Diseases
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Aarthy K. Uthayakumar, Christopher B. Bunker
HIV and neoplasms: HIV patients are found to have a 2-fold increased risk for skin cancer.3 Kaposi sarcoma, caused by Human herpesvirus 8 (HHV-8), can be disseminated in the context of HIV or AIDS, with gastrointestinal and pulmonary involvement. Cutaneous lesions can involve the oral mucosa and genitals (Figure 27.10). Localized treatments include cryotherapy, radio-therapy, topical retinoids, or surgical removal, for example, with curettage and electrodesiccation. Systemic chemotherapy is required for advanced stage Kaposi sarcoma. With the introduction of ARV, the incidence of Kaposi sarcoma has declined; however, non-AIDS-defining cancers, of which skin cancer is the most common, are increasing. Actinic keratoses are extremely common, and both basal cell cancer (BCC) and squamous cell cancer (SCC) may present at younger ages and with an atypical appearance. Melanoma may be more common and more dangerous in HIV.
Antiviral Drugs as Tools for Nanomedicine
Published in Devarajan Thangadurai, Saher Islam, Charles Oluwaseun Adetunji, Viral and Antiviral Nanomaterials, 2022
The human herpesvirus-8 (HHV-8), also called Kaposi sarcoma herpesvirus (KSHV), belongs to the family of DNA viruses, herpeseviridae. It causes Kaposi sarcoma (a vascular malignancy) and B cell lymphoproliferative diseases, such as primary effusion lymphoma (PEL) and multicentric Castleman disease (MCD) (Weiss et al. 1998).
Kaposi's Sarcoma
Published in Debjani Sahni, Adam Lerner, Bilal Fawaz, Advanced Skin Cancer, 2022
Kaposi’s sarcoma (KS) is a rare angioproliferative neoplasm that presents in a variety of clinical settings.1–3 A common feature to all variants is the association with human herpesvirus-8 (HHV-8), which is thought to play an essential role in its pathogenesis.1 The four principal clinical variants include classic KS, African-endemic KS, KS due to iatrogenic immunosuppression, and acquired immunodeficiency syndrome (AIDS)-associated epidemic KS.2,3 More recently, a fifth variant, termed non-epidemic KS, has been increasingly reported in young, otherwise healthy men who have sex with men (MSM). Non-epidemic KS patients lack the other risk factors typically associated with KS and appear to have a favorable prognosis overall.4
Eyelid margin Kaposi sarcoma leading to AIDS diagnosis
Published in Baylor University Medical Center Proceedings, 2021
Olivia A. Moharer, Ivan M. Vrcek
A 51-year-old man presented to the clinic for evaluation of a pigmented lesion involving the left lower eyelid. The lesion was enlarging and causing local irritation despite treatment with antibiotic eyedrops and warm compresses. It was a raised, flesh-colored lesion along the left lower lid margin (Figure 1). A shave biopsy of the lesion revealed dermal accumulation of dilated, jagged vascular channels surrounded by atypical spindle cells (Figure 2a) that stained positive for human herpesvirus 8 (Figure 2b). The lesion was classified as KS, an angioproliferative malignancy considered to be an AIDS-defining illness. Initial lab work for the patient following diagnosis revealed a CD4 count of 47 cells/mm3 and an HIV viral load of 189,856 copies/mL. The patient was subsequently diagnosed with AIDS and started on a highly active antiretroviral therapy regimen consisting of darunavir, cobicistat, emtricitabine, and tenofovir alafenamide fumarate, with prophylactic azithromycin and trimethoprim-sulfamethoxazole. At the 9-month follow-up, the patient’s viral load had decreased to 40 copies/mL, and the CD4 count was 181 cells/mm3. Following definitive excisional surgery, there was no evidence of KS recurrence.
A lymphoproliferative pericardial mass
Published in Baylor University Medical Center Proceedings, 2020
Barbara Mantilla, Kenneth Nugent, Ximena Solis, Pablo Paz, Haneen Mallah, John Makram, Safaa Labib, Andres Yepes-Hurtado
Castleman disease (CD) is a benign lymphoid disorder that affects <200,000 people in the United States.1 It can be classified clinically into unicentric and multicentric and can be divided by histologic subtypes, including hyaline-vascular and plasma cell variants.1,2 Most CD cases are unicentric, with 75% of these belonging to the hyaline-vascular variant.1 The unicentric type is well circumscribed, involving one or more lymph nodes in the same anatomic site and predominantly above the diaphragm. Thus, it is often asymptomatic and amenable to surgical resection. Unicentric CD usually becomes symptomatic when the mass compresses adjacent organs. On the other hand, the multicentric variant is a systemic lymphoproliferative disorder encompassing groups of lymph nodes in different locations. It has a higher risk of malignancy and is frequently associated with a state of immunosuppression, secondary to HIV or human herpesvirus–8 infection.1 We discuss a rare case of hyaline-vascular unicentric CD presenting as an incidental pericardial mass.
Diffuse dermal angiomatosis of the breast
Published in Baylor University Medical Center Proceedings, 2020
Nicholas Nguyen, Annika S. Silfvast-Kaiser, Jillian Frieder, Marcus Zaayman, Alan Menter
DDA is a unique variant of RAE commonly reported on the lower extremities and, more recently, in women with large, pendulous breasts.1,2 DDAB tends to affect individuals aged 40 to 60 years who have multiple risk factors for atherosclerosis (i.e., hypertension, hyperlipidemia, diabetes mellitus, chronic smoking history, previous heart disease, and stroke).10,13 The differential diagnosis includes acroangiodermatitis, Kaposi sarcoma, and low-grade angiosarcoma. Histologically, a proliferation of endothelial cells and microscopic capillaries in the dermis is seen, in contrast to the intraluminal proliferation of endothelial cells seen in classic RAE.2,14 CD31, CD34, and ERG stains are positive, underscoring benign dermal endothelial cell proliferation. Human herpesvirus 8 testing is negative.3,9,14–16 Although the pathogenesis of DDA remains unclear, it is postulated that angiogenesis is due to up-regulation of vascular endothelial growth factor, secondary to chronic ischemia and hypoxia.4