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Increased
severity of Kaposi's sarcoma in HIV-1-infected Zimbabwean women
Tom
Egwang
April 12, 2007
http://www.aidsmap.com/en/news/A587BF63-65CF-4C34-862F-FB0545C6CC4A.asp
Zimbabwean women with
HIV/AIDS who present with AIDS-related Kaposi sarcoma (AIDS-KS)
are younger than male counterparts of similar AIDS-KS status and
have a more severe course of KS, according to the findings of a
cross-sectional study published in the March 1st edition of the
Journal of Acquired Immune Deficiency Syndromes.
KS was first described
in 1872 by Moritz Kaposi as a disease of elderly Mediterranean or
Jewish men. KS typically manifests itself as multiple purple-coloured
skin lesions. When HIV/AIDS emerged in the early 1980's, KS
was one of the first recognized clinical manifestations of HIV infection.
Recent findings of a herpetic-like viral DNA in Kaposi's sarcoma
tissue have suggested an infectious co-factor for AIDS-KS and human
herpesvirus 8 is found in Kaposi's sarcoma tumors of all types.
The epidemiology of AIDS-KS
appears to be complex with gender differences playing some unknown
role. In North America and Europe, the risk of AIDS-KS is greater
in men; this gender difference can be explained by the epidemiology
of HIV-1 and KS herpesvirus (KSHV). However, in Sub-Saharan Africa
where the seroprevalence of HIV-1 and KSHV are similar, men still
have a greater risk for AIDS-KS.
AIDS-KS is rare in women
outside sub-Saharan Africa and the current published data indicate
a more extensive disease and worse outcome in women. Given the paucity
of data on AIDS-KS in sub-Saharan women and the lack of explanation
for gender-related differences in the manifestations of AIDS-KS,
a team of Zimbabwean and US researchers investigated clinical, immunologic,
and virologic markers in Zimbabwean men and women with AIDS-KS.
The study took place
in Parirenyatwa Hospital KS Clinic in Harare. All men and women
diagnosed with AIDS-KS between 1998 and 2001 were eligible to participate.
In all 438 men and 166 women with AIDS-KS participated; all were
antiretroviral-naive. Participants were interviewed regarding weight
loss, fever, or night seats and underwent a complete physical examination.
Laboratory investigations
included liver function tests, a complete blood cell count, chest
radiography, and HIV serology; CD4 counts were available for most
patients. KS was confirmed by biopsy of a suspected lesion for all
patients. The clinical stage of KS was established by an established
staging classification. KSHV DNA in blood cells or plasma was determined
by real-time polymerase-chain reaction (PCR).
In general, female patients
were younger than male patients (median and range of 33 (19-73)
versus 38 (17-73); p < 0.001). This suggested that women were
either infected with HIV-1 at an earlier age than men or that the
immunosuppression due to HIV-1 infection and KS pathogenesis progresses
more rapidly in women. These possibilities were addressed by employing
a statistical model to adjust for age; no gender differences in
CD4 counts were found.
Systemic symptoms included
fever, diaphoresis, or weight loss. A multivariate model which adjusted
for age and CD4 counts revealed no significant gender-related differences
in all the measured parameters except that women were more likely
than men to have systemic symptoms (OR =1.8, 95 % CI 1.2-2.7; p
= 0.008).
A multivariate model
which adjusted for the effect of prior treatment also provided a
similar conclusion (OR =1.7, 95 % CI 1.1-2.7; p = 0.009). Univariate
analysis confirmed that the frequency of systemic symptoms were
significantly higher in females by comparison with males (52 % versus
38 %; p = 0.001). Overall, there were no statistically significant
gender-related differences in AIDS-KS stages, prior or current chemotherapy
or radiation, CD4 counts, plasma or cellular KSHV DNA load, nor
the frequency of KSHV DNA detectable by PCR.
The study by Amie Meditz
and Thomas Campbell of the University of Colorado is the first systematic
description of AIDS-KS in African women and the first comparison
of viral and immunologic markers between men and women, and the
first to demonstrate that there might be gender-related differences
in the biology and pathogenesis of AIDS-KS since women are at a
significantly higher risk of systemic symptoms than men.
The authors speculate
that other co-infections in women, which were not considered in
the study, might have contributed to the gender-related differences
in disease severity. For example, the increased proinflammatory
cytokines associated with such infections might have contributed
to the AIDS-KS pathogenesis. However, the authors did not specify
the gender-specific co-infections that might have been responsible.
The policy implication
of the study is that health care workers should pay more attention
to women with AIDS-KS since they bear the brunt of the morbidity.
The authors call for additional studies designed to unravel the
mechanisms which result in the differential susceptibility of women
to the ravages of AIDS-KS. The authors specifically cite parity,
menstrual status, and female sex hormones as gender-specific factors
which could be investigated further.
A landmark discovery
by Kaleeba and Berger recently identified the receptor by which
KSHV infects human cells and which might play a crucial role in
the development of KS. It would be informative to establish whether
there are gender-related differences in the expression of this receptor.
These and other studies
might provide the vital information which will inform on the development
of novel interventions for women with AIDS-KS.
References
Meditz AL et
al. Gender differences in AIDS-associated Kaposi sarcoma in Harare,
Zimbabwe. J Acquir Immune Defic Syndr 44: 306-308, 2007.
Kaleeba JAR
and Berger EA. Kaposi's sarcoma-associated herpesvirus fusion-entry
receptor: cystine transporter xCT. Science 311(5769):1921-4, 2006.
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