Pathology of AIDS related malignant tumours

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Pathology of AIDS - Related Malignant Tumours

Patients with HIV infection are at increased risk for developing Kaposi's sarcoma, non-Hodgkin's lymphoma, and several other cancers.

Accumulating data suggest that HIV-infected patients also are at increased risk for developing Hodgkin's lymphoma, cervical carcinoma in situ (CIS), other anogenital neoplasms (invasive cancer and CIS), leiomyosarcoma, and conjunctival squamous cell carcinoma.

AIDS is caused by the human immunodeficiency viruses HIV-I (present globally) and HIV-II (mainly restricted to West Africa and contacts with that zone).

It is generally assumed that HIV-1 infection play a passive role in cancer development by impairing the host immune surveillance and increasing the risk of oncogenic virus infection.

Recent insights, however, indicate that HIV-1 infection more actively promotes cancer growth.

HIV is not per se oncogenic, but a wide range of tumours is now described with increased incidence among HIV-infected people and/or with a more aggressive clinical course, compared with HIV-uninfected people.

In most cases, cellular immunosuppression, caused by HIV-related destruction of CD4+ T-cells, is the major factor in inducing tumours.

Co-factors, usually oncogenic viruses, are now being demonstrated.

The range of tumours in HIV/AIDS patients overlap with but is not identical to that seen in patients immunosuppressed for other reasons (Example: organ transplantation).

Related posts: Kaposi’s Sarcoma (KS):

One of the earliest opportunistic diseases that defined AIDS (even before the etiological link of AIDS with infection by HIV was recognized) was Kaposi’s Sarcoma in skin and viscera.

Whether Kaposi’s Sarcoma is a genuine neoplasm or a reactive hyperplasia of endothelium is still disputed.

The incidence of Kaposi’s Sarcoma among HIV-infected people varies with risk-factors for HIV transmission and geography.

It is high in homosexual men and African adults and children, low in haemophiliacs and more frequent in east than West Africa.

In 1994, a new herpes virus-HHV-8- was described in association with KS tissues.

Epidemiological blood and tissue studies support its etiological role in development of Kaposi’s Sarcoma.

Lymphoma:

High-grade B-cell lymphoma, particularly in the central nervous system, is a major cause of morbidity and mortality in HIV/AIDS.

Tumours are usually extra-nodal and destructive.

They are commonly associated with Epstein-Barr Virus infection.

Incidence is inversely related to CD4+ T-cell count, which may explain why it is less common in patients in Africa and India.

T-cell lymphomas, Hodgkin’s disease and myeloma have a slightly increased incidence compared with HIV-uninfected people.

Anogenital Carcinoma:

At present, there is no strong evidence linking increased incidence of invasive cervical cancer to the HIV epidemic; however, some studies have demonstrated an association between HIV and the increased prevalence of human papilloma virus (HPV) and cervical intraepithelial neoplasia (CIN).

Most studies do not reveal an increased incidence of invasive carcinoma of cervix, some show a more aggressive clinico-pathological course of carcinoma.

HPV-16 and 18 are associated infection.

HIV-infected homosexual men have a 1000-fold increased risk of developing anal carcinoma compared with HIV-uninfected, associated with HPV infection. However, in clinical practice much anal intraepithelial neoplasia (AIN) is encountered but little invasive carcinoma.

Conjunctival carcinoma:

The incidence of conjunctival squamous cell carcinoma is closely related to exposure to ultraviolet light.

In equatorial, though not elsewhere, there is an epidemic of this malignancy among HIV-infected adults.

A proven co-factor in a proportion of cases is HPV-16.

Other Tumours:

Small series and case reports of cancers in HIV-infected patients strongly suggest an increased incidence and more aggressive behaviour of other epithelial tumours.

These include skin squamous cell carcinoma and basal cell carcinoma and melanoma.

They are generally present in the later stages of HIV disease.

The relative risks for the most common epithelial cancers in the general population (lung, breast, colon/rectum, stomach, liver, and prostate) are not increased substantially in people with AIDS, however.

There is inconclusive evidence, however, with regard to HIV infection being associated with invasive cervical cancer, testicular seminoma, or hepatocellular carcinoma.

Most cancers seen in the AIDS setting are related to oncogenic virus infections, such as Epstein-Barr virus (EBV), Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) and human papillomavirus (HPV).

Clinical evidence suggests that the oncogenicity of HPV is altered by the presence of HIV-1 infection irrespective of host immune status.

The introduction of highly active antiretroviral therapy (HAART) has dramatically decreased the incidence of KS whereas the impact of HAART is variable in EBV-related lymphoma and HPV - related cervical cancer, suggesting that additional factors are involved in the pathogenesis of these cancers.

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