FDA-approved Treatments
Experimental Treatments
Top New Articles
 Google Custom Search
Persistent AIDS-related Kaposi Sarcoma in the HAART Era Reveals Need for New Therapies

Kaposi sarcoma (KS) continues to be one of the most common malignancies among people with HIV, despite dramatic declines in its incidence since the advent of highly active antiretroviral therapy (HAART).

Prior to the HAART era, treatment for AIDS-related KS had been mainly palliative, involving the use of chemotherapy that resulted in minimal or short-term response.

Use of HAART by patients with AIDS-related KS has been associated with improved survival and prolonged time to treatment failure. Cases of complete KS resolution with antiretroviral therapy alone have been documented, but few studies have examined the response to HAART in a clinical setting.

Patients with advanced KS rarely respond to HAART alone, but antiretroviral therapy in combination with chemotherapy improves response rates to 50%-82%. Neither the relative roles of HAART and chemotherapy, nor the predictors of response to both HAART and chemotherapy in persons with KS have been extensively studied. In addition, evaluations of treatment with both HAART and chemotherapy in primary care settings, where adherence may be an issue, do not exist.

The objective of the current retrospective study, published in the May 11, 2008 issue of AIDS, was to evaluate the role of HAART and chemotherapy on tumor response and to identify factors associated with response among patients with AIDS-related KS in routine primary care at 2 HIV clinics (University of Washington and the Fred Hutchinson Cancer Research Center, Seattle, WA).

A total of 114 patients from these clinics with a diagnosis of AIDS-related KS were identified via a clinical database. Records were reviewed to confirm the KS diagnosis and abstract clinical and chemotherapy information. Demographics, laboratory values and HAART use were abstracted electronically. Cox's proportional hazards models identified predictors of KS improvement and resolution.

Results
Among 64 patients with confirmed KS, 36 months following diagnosis, the rate of improvement was 77% and the rate of complete resolution was 51%.

In univariate analyses, recent chemotherapy was associated with KS improvement.

Lower recent HIV viral load and HAART were associated with both improvement and resolution.

No measured baseline characteristics (tumor stage, year of diagnosis, CD4 cell count, HIV viral load, prior HAART) or recent CD4 count predicted KS improvement or resolution.

In multivariate analyses, recent chemotherapy and HAART were predictors of KS improvement.

Only recent HAART was associated with resolution.

KS response was not associated with type of HAART (non-nucleoside reverse transcriptase inhibitor, protease inhibitor, or ritonavir-boosted protease inhibitor-based regimens).

Conclusion

Kaposi's sarcoma, seen here on the thigh, was once a rare malignancy of the blood vessels, but is now associated with AIDS.

Based on these results, the study authors concluded, "Highly active antiretroviral therapy and chemotherapy are important in clinical Kaposi sarcoma response."

In addition, they noted that despite the widespread availability of HAART, KS continues to be a clinical problem.

Finally, with only half the patients in the cohort achieving complete resolution of KS, the authors concluded that, "New therapeutic approaches are needed."

Department of Epidemiology, Department of Laboratory Medicine, Department of Medicine, University of Washington; Program in Biostatistics and Vaccine and Infectious Disease Institute, Fred Hutchinson Cancer Research Center, Seattle, WA.

5/09/08

Reference
HQ Nguyen, AS Magaret, MM Kitahata, and others. Persistent Kaposi sarcoma in the era of highly active antiretroviral therapy: characterizing the predictors of clinical response. AIDS 22(8): 937-945. May 11, 2008.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Protease Inhibitors (PIs)
Note: Most PIs are now used
in combination with low-dose
ritonavir (Norvir)
Agenerase
Agenerase (amprenavir)
Aptivus
Aptivus (tipranavir)
Crixivan
Crixivan (indinavir)
Invirase
Invirase (saquinavir )
Kaletra
Kaletra (lopinavir/ritonavir)
Lexiva
Lexiva (fosamprenavir)
Norvir
Norvir (ritonavir)
Prezista
Prezista (darunavir)
Reyataz
Reyataz (atazanavir)
Viracept
Viracept (nelfinavir)
Nucleoside / Nucleotide
Reverse Transcriptase
Inhibitors (NRTIs)
Combivir
Combivir (zidovudine + lamivudine)
Epivir
Epivir (lamivudine; 3TC)
Emtriva
Emtriva (emtricitabine; FTC)
Epzicom
Epzicom (abacavir + lamivudine)
Retrovir
Retrovir (zidovudine; AZT)
Trizivir
Trizivir (abacavir + zidovudine +lamivudine)
Truvada
Truvada  (tenofovir + emtricitabine)
Videx
Videx (didanosine; ddI)
Viread
Viread (tenofovir)
Zerit
Zerit (stavudine; d4T)
Ziagen
Ziagen (abacavir)
non Nucleoside 
Reverse Transcriptase
 Inhibitors
(nNRTIs)
Rescriptor
Intelence (etravirine)
Rescriptor
Rescriptor (delavirdine)
Sustiva
Sustiva (efavirenz)
Viramune
Viramune (nevirapine)
Entry / Fusion Inhibitors
Fuzeon (enfuvirtide)
Selzentry/Celsentri ( maraviroc)
Fixed-dose Combinations
Atripla
Atripla (efavirenz + emtricitabine + tenofovir)
Combivir
Combivir (zidovudine + lamivudine)
Trizivir
Trizivir (abacavir + zidovudine + lamivudine)
Truvada
Truvada (tenofovir + emtricitabine)
Integrase Inhibitors
Isentress (raltegravir)