childhood aids increases cancer risk later in life

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Childhood AIDS Increases Cancer Risk Later in Life

March 7, 2011 (Boston, Massachusetts) ² An analysis of more than 5800 people diagnosed with AIDS in

childhood prior to the 1996 initiation of highly active antiretroviral therapy (HAART) has revealed that such

people have an increased risk for Kaposi's sarcoma and non-Hodgkin's lymphoma.

Although the risk for these cancers has declined in the HAART era, their risk in this population remains

higher than in the general population, and the risk for leiomyosarcoma is unchecked by HAART. Follow-

up of the cohort has been as long as 10 years.

The study results, presented here at the 18th Conference on Retroviruses and Opportunistic Infections by

Edgar Simard, PhD, from the National Cancer Institute in Bethesda, Maryland, point out the importance of

close monitoring of this segment of the AIDS population during adolescence and adulthood.

"This is the largest study to date to evaluate the long-term effect of childhood AIDS. People who are

diagnosed with AIDS during their childhood or early adolescence and who survive remain at risk for

Kaposi's sarcoma and non-Hodgkin's lymphoma, although the risk of these cancers has declined in the

HAART era. As well, those diagnosed with AIDS during childhood remain at greater risk for

leiomyosarcoma," Dr. Simard told Medscape Medical News.

The study was prompted by the findings that HAART does not completely restore the immune damage

caused by HIV infection. The consequence might be more maladies ² including cancer ² in children,

adolescents, and young adults than in older individuals with AIDS.

"This is the most comprehensive and perhaps the first study to investigate children who contracted HIV

and their cancer incidence," Dirk P. Dittmer, PhD, from the University of North Carolina School of

Medicine in Chapel Hill, told Medscape Medical News.

AIDS registry records from 15 regions in the United States were matched with cancer registries to identify

cancers diagnosed up to 10 years after the diagnosis of AIDS in 5846 subjects, ranging in age from birthto 14 years at the time of diagnosis. The cancer risks relative to the general population in the pre-HAART

era (1980 to 1995) and HAART era (1996 to 2008) were assessed with standardized incidence ratios

(SIR). The changes in cancer incidence in those diagnosed with AIDS were determined in the 2 time

periods.

Of the 5846 people, 72.5% were diagnosed with AIDS in the pre-HAART era and 27.5% were diagnosed

in the HAART era. The majority were male (51.7%), non-Hispanic blacks (61.7%), and 4 years or younger

at AIDS onset (67.5%).

The 10-year risk for any cancer was higher in those diagnosed with AIDS than in the general population

in the pre-HAART era (SIR, 41; 95% confidence interval [CI], 32 to 51) and, although reduced, was also

higher in the HAART era (SIR, 19; 95% CI, 13 to 26).

More specifically, the widespread implementation of HAART was associated with a lower incidence of all

cancers (relative risk [RR], 0.38; 95% CI, 0.23 to 0.64; n = 106), Kaposi's sarcoma (RR, 0.13; 95% CI,

0.02 to 0.75; n = 20), and non-Hodgkin's lymphoma (RR, 0.39; 95% CI, 0.21 to 0.74; n = 64).

However, the rate of Kaposi's sarcoma remained higher in comparison to the general population, even in

the HAART era (pre-HAART SIR, 1706; 95% CI, 994 to 2832; HAART SIR, 1254; 95% CI, 259 to 3666).



The rate of non-Hodgkin's lymphoma declined significantly following the advent of HAART, compared with

the general population (pre-HAART SIR, 341; 95% CI, 245 to 463; HAART SIR, 130; 95% CI, 82 to

194; P < .001).

The only non-AIDS-defining cancer that displayed an elevated risk was leiomyosarcoma (pre-HAART

SIR, 870; 95% CI, 237 to 2229; HAART SIR, 554; 95% CI, 180 to 1292; P = .41; n = 9).

"Treatment may not differ for those who have survived childhood AIDS. But we need to recognize that, for

this population, the risk of cancer is greater. We need data from longer-term observations to investigate

the influence of lifestyle factors and to expand the research to include other factors, such as economic

status," Dr. SimardtoldMedscape Medical News.

"This work highlights the changing dynamics of the HIV epidemic. As people with HIV live longer thanks

to HAART, we urgently need to understand how to treat their comorbidities. Foremost among them is

cancer. The risk of cancer following a childhood AIDS diagnosis is elevated, compared with the general

population," Dr. Dittmer noted.

"This raises several questions: Should we increase screening for AIDS-defining cancers or predisposingcancer virus infections in HIV positive adolescents? What is the biological mechanism that leads to an

increased risk of leiomyosarcoma in HIV positive children?" Dr. Dittmer asked.

REFERENCE: www.Medscape.com;18th Conference on Retroviruses and Opportunistic Infections

(CROI): Abstract 82LB. Presented March 1, 2011

Kaposi's sarcoma (KS) is a tumor caused by Human herpesvirus 8 (HHV8), also known as Kaposi's

sarcoma-associated herpesvirus (KSHV). It was originally described by Moritz Kaposi(KA-po-she), a

Hungarian dermatologist practicing at the University of Vienna in 1872.[1]

It became more widely known as

one of the AIDS defining illnesses in the 1980s. The viral cause for this cancer was discovered in 1994.

Although KS is now well-established to be caused by a virus infection, there is widespread lack of

awareness of this even among persons at risk for KSHV/HHV-8 infection[2]

.

Restated, Kaposi¶s sarcoma (KS) is a systemic disease which can present with cutaneous lesions with or

without internal involvement. Four subtypes have been described: Classic KS, affecting middle aged men

of Mediterranean and Jewish descent, African endemic KS, KS in iatrogenically immunosuppressed

patients, and AIDS-related KS. The erythematous to violaceous cutaneous lesions seen in KS have

several morphologies: macular, patch, plaque, nodular, and exophytic. The cutaneous lesions can be

solitary, localized or disseminated. KS can involve the oral cavity, lymph nodes, and viscera. The

pathogenesis of KS is still being elucidated, though infection with HHV-8 appears to be associated with

KS development. Classic KS tends to be indolent, presenting with erythematous or violaceous patches on

the lower extremities. African endemic KS and AIDS-related KS tend to be more aggressive. The AIDS-

related KS lesions often rapidly progress to plaques and nodules affecting the upper trunk, face, and oral

mucosa. The diagnosis can be made with a tissue biopsy and, if clinically indicated, internal imaging

should be done.



The non-Hodgkin lymphomas (NHLs) are a diverse group of blood cancers that include any kind

of lymphoma except Hodgkin's lymphomas. Types of NHL vary significantly in their severity, from indolent

to very aggressive.

Lymphomas are types of cancer derived from lymphocytes, a type of white blood cell. Lymphomas are

treated by combinations of chemotherapy, monoclonal antibodies,immunotherapy, radiation,

and hematopoietic stem cell transplantation.

Non-Hodgkin lymphomas were classified according to the 1982 Working Formulation which recognizes

16 types. The Working Formulation is now considered obsolete, and the classification is commonly used

primarily for statistical comparisons with previous decades. The Working Formulation has been

superseded twice.

The latest lymphoma classification, the 2008 WHO classification, largely abandoned the "Hodgkin" vs.

"Non-Hodgkin" grouping. Instead, it lists over 70 different forms of lymphomas in four broad groups.



Non-Hodgkin lymphomas (NHLs)



Kaposi's sarcoma (KS)

childhood aids increases cancer risk later in life

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