- Phase II evaluation of low-dose oral etoposide for the treatment of relapsed or progressive AIDS-related Kaposi's sarcoma: an AIDS Clinical
- Development of Kaposi's sarcoma at the site of a biopsy.
- Development of Kaposi's sarcoma in a surgical wound.
- Vascular endothelial growth factor levels in serum do not increase following HIV type 1 and HHV8 seroconversion and lack correlation with
- Kaposi's sarcoma: clinico-pathological analysis of human immunodeficiency virus (HIV) and non-HIV associated cases.
Table of Contents
1
UI - 12149296
AU - Evans SR; Krown SE; Testa MA; Cooley TP; Von Roenn JH
TI -
Phase II evaluation of low-dose oral etoposide for the treatment of
relapsed or progressive AIDS-related Kaposi's sarcoma: an AIDS Clinical
Trials Group clinical study.
SO - J Clin Oncol 2002 Aug 1;20(15):3236-41
AD - Center for Biostatistics in AIDS Research, Department of Biostatistics,
Harvard School of Public Health, Boston, MA, USA.
PURPOSE: Liposomal anthracyclines and paclitaxel are considered the best
available cytotoxic therapies for Kaposi's sarcoma (KS), but relapse is
common. To identify new interventions for relapsed or progressive KS, a
phase II study of low-dose etoposide to assess its toxicity and efficacy
was conducted. PATIENTS AND METHODS: Thirty-six patients with high-risk
KS were treated with oral etoposide 50 mg/d for 7 consecutive days of
every 2-week cycle. All patients' disease had relapsed or progressed
after prior combination chemotherapy or anthracycline therapy. For
patients without a complete or partial response after two cycles of
therapy and no toxicity greater than grade 2, the dose of etoposide was
escalated to 100 mg/d orally on days 1 to 7 of each 14-day cycle.
Treatment-related and disease-specific quality of life was evaluated
using patient reports on the General Health Self-Assessment Form and a
KS-specific measure. RESULTS: One patient achieved a complete response,
12 patients had a partial response (overall response rate, 36.1%), and
stable disease was observed in 12 patients (33.3%). Tumor responses were
seen in all disease sites. Fourteen patients had their dose escalated,
of whom five responded. The median time to response was 17.7 weeks; the
median duration of response was 25 weeks. The most frequent hematologic
abnormality was neutropenia, which was grade 4 in seven patients and
grade 3 in six. Opportunistic infections occurred in eight patients
during the treatment period. Both response to treatment and toxicity
influenced patient-reported quality of life. CONCLUSION: We conclude
that low-dose oral etoposide at a dose of 50 mg/d is safe and effective
for the treatment of refractory or progressed AIDS-related KS and has an
overall positive effect on the quality of life of responding patients.
2
UI - 12213952
AU - Yarchoan R; Davis DA
TI -
Development of Kaposi's sarcoma at the site of a biopsy.
SO - N Engl J Med 2002 Sep 5;347(10):763-4; discussion 763-4
3
UI - 11961149
AU - Webster-Cyriaque J
TI -
Development of Kaposi's sarcoma in a surgical wound.
SO - N Engl J Med 2002 Apr 18;346(16):1207-10
AD - School of Dentistry, University of North Carolina at Chapel Hill, Chapel
Hill 27599-7455, USA. jennifer@med.unc.edu
4
UI - 12167275
AU - Renwick N; Weverling GJ; Brouwer J; Bakker M; Schulz TF; Goudsmit J
TI -
Vascular endothelial growth factor levels in serum do not increase
following HIV type 1 and HHV8 seroconversion and lack correlation with
AIDS-related Kaposi's sarcoma.
SO - AIDS Res Hum Retroviruses 2002 Jul 1;18(10):695-8
AD - Department of Human Retrovirology, Academic Medical Center, University
of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands.
The utility of vascular endothelial growth factor (VEGF) concentrations
in serum as a predictive marker for AIDS-KS was studied. Sera were
obtained from 40 homosexual men who seroconverted for HIV-1 and HHV8
prior to or during their participation in the Amsterdam Cohort Studies
(1984-2000). We designed an ELISA to detect VEGF and measured VEGF prior
to either infection, at HIV-1 and HHV8 seroconversion, after both
infections, at AIDS-KS diagnosis (n = 11), and in the most recently
available serum sample. The geometric mean serum VEGF concentration was
81.5 pg/ml in those with AIDS-KS and 80.4 pg/ml in those with AIDS but
without KS. Median serum VEGF concentrations did not differ between the
time points described above. Higher VEGF concentrations in serum were
observed at higher CD4(+) cell counts. Serum concentrations of VEGF were
not influenced by HIV-1 or HHV8 infection or by the conditions leading
to AIDS-KS. Sequential measurement of VEGF in serum is not expected to
contribute to the prediction or therapeutic monitoring of AIDS-KS.
5
UI - 11994760
AU - Hong A; Lee CS
TI -
Kaposi's sarcoma: clinico-pathological analysis of human
immunodeficiency virus (HIV) and non-HIV associated cases.
SO - Pathol Oncol Res 2002;8(1):31-5
AD - Royal Prince Alfred Hospital, Department of Radiation Oncology
Mis-senden Road, Camperdown, New South Wales, 2050, Australia.
Kaposi s sarcoma (KS) is a angioformative lesion that classically occurs
in elderly Eastern European and Mediterranean males but is also common
in immunosuppressed individuals particularly human immunodeficiency
virus (HIV)-infected patients. This study investigates the clinical and
histopathological features of 47 patients with Kaposi s sarcoma from a
teaching hospital in Sydney, Australia, in which 44 cases had adequate
clinical follow-up information over a 10-year period. Most of the
lesions were of late stage (37/47 cases; 79%), consisting of 11 cases of
plaque stage KS and 26 cases of nodular stage KS with only 10 cases of
early or patch stage KS. The majority of the HIV-positive cases (23/33;
70%) and all of the HIV-negative (14/14; 100%) cases had late stage
lesions (p=0.020; X 2 -test). The histopathological features that were
more common in the KS lesions of HIV-negative patients were lesional
cell mitosis (p=0.0002), single cell necrosis (p=0.001), apoptosis
(p=0.0001) and single cell anaplasia (p=0.0001). The KS lesions in
HIV-positive patients tended to have dissecting blood vessels (14/33
cases; 42%) unlike those seen in HIV-negative patients (0/14 cases; 0%)
(p=0.004). Most HIV-positive cases (30/33; 90%) were males (p=0.0068);
and all these patients (33/33 cases; 100%) were <60 years old, in
contrast to HIV-negative patients (1/11 cases; 9%) (p=0.0001). HIV
status does not affect the occurrence of multiplicity of KS lesions.
However, extracutaneous or visceral KS lesions were more likely to occur
in HIV-positive patients (p=0.027). The number of cases of
histologically proven KS cases has decreased markedly over the recent 5
year period of 1995-1999 (n=14), which was less than half of the number
of the preceding 5 year period, 1990-1994 (n=33). In summary, there are
distinct differences in the clinical and histopathological features of
Kaposi s sarcoma lesions in HIV-positive and HIV-negative patients.
Despite the recent discovery of the HHV8 virus as the initiating and
promoting factor of most of the KS lesions, these differences indicated
that there might be different mechanisms that occur in HIV-positive and
HIV-negative patients in the development of this lesion.
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