Disseminated bone lesions in AIDS‐associated Kaposi sarcoma, a bad prognosis? About four cases

• Published in: Journal of the International AIDS Society Vol. 15; pp. 1 - 3
• Main Authors: Wassilew, N, Ciaffi, L, Vu, D, Calmy, A, Toutous Trellu, L
• Format: Journal Article
• Language: English
• Published: Geneva International AIDS Society 01-11-2012; John Wiley & Sons, Inc
• Subjects: Acquired immune deficiency syndrome; AIDS; AIDS (Disease); Antiretroviral agents; Biopsy; Bone density; Bone mineral density; Chemotherapy; Complications and side effects; Diagnosis; HIV; Human immunodeficiency virus; Immune system; Kaposi's sarcoma; Kaposis sarcoma; Lesions; Medical imaging; Medical prognosis; Patients; Prognosis; Risk factors; Sarcoma; Sexually transmitted diseases; STD; Switzerland
• ISSN: 1758-2652; 1758-2652
• DOI: 10.7448/IAS.15.6.18437

Kaposi sarcoma (KS) can present with a wide range of clinical features ranging from minimal cutaneous disease to a rapidly progressing neoplasm. Bone lesions are most often discovered accidently in the context of radiological investigations done for the screening of KS‐visceral involvement [1]. Little is known on clinical outcome and response to antiretroviral therapy (ART) and/or chemotherapy of these lytic osseous lesions. We report four cases with bone involvement in the context of systemic KS and aim at describing the long‐term clinical outcome in two of these patients. Cases of AIDS‐associated KS with disseminated bone lesions were collected in the HIV Unit, University Hospital Geneva, Switzerland. Patients were compared on clinical, biological and radiological features and therapeutic responses. Between 2002 and 2012, four HIV1‐infected patients with T1 stage of KS presented disseminated osseous lesions (Table 1). Mean age was 43 years (range 39 ‐ 47 years), mean time of follow up until our analysis was 48.5 months (SD 53.8), and mean CD4 count at KS diagnosis was 190.5 c/mL (SD 202.8). All patients showed hypodense bone lesions predominating the axial skeleton (figure 1), but no radiological imaging was performed to search for peripheral bone lesions.
No patient reported pain or experienced pathological fractures. In one patient a dual‐energy X‐ray absorptiometry (DXA) showed a bone mineral density within normal range after 10 years of KS diagnosis with disseminated bone lesions. No radiological change was observed in that patient despite stable KS disease after 13 cycles of liposomal doxorubicin and ART (figure 1). We describe a well‐documented long‐term follow up of disseminated osseous AIDS‐associated KS disease. In our four cases, lytic bone lesions were asymptomatic and were not associated with bone fragility. We even could confirm the KS nature of the lesions by bone biopsy in patient B (3 months after KS diagnosis), as the differential diagnosis is wide, and include bacillary angiomatosis, cancers or metastasis. Chemotherapy and antiretroviral treatment did not affect bone lesions using CT scan despite a good response on other KS‐affected sites. Prognostic factors are well established in AIDS‐associated KS [2]; however disseminated bone disease does not seem to have an impact on disease evolution. A larger sample size is needed to confirm this hypothesis.
Patient with 10yr follow up, lumbar vertebre after 6 (2002) and 13 (2012) sycles of chemotherapy with Liposomal Doxorubicin.
1
Baseline characteristics for all four patients with AIDS‐related KS and osseous lesions. Staging classification is based on Known SE et al. J Clin Oncol 1989; 7: 1201–7 and includes the following parameters: T for Tumor (T0 = KS confined to skin and minimal oral disease, T1 = all other manifestations), I for Immune system (I0 = CD4 cells >200/ µL and I1 = CD4 cells <200 µL) and S for systemic illness (S0 = no history of opportunistic infections, S1 = history of opportunistic infections and thrush)
Patient
Sex
Age
Ethnicity
Kaposi stage (TIS)
Follow‐up time since KS diagnosis
Visceral involvement
Bone lesion (imaging)
HHV8 viremia at KS diagnosis (full blood c/mL)
Chemotherapy (first line, number of cycles, time period)
Last HIV‐RNA (c/µL)
ART including PI (y/n)
Special comment
A
M
47 (1965)
CAU
1/1/1
10 years
yes
Axial skeleton, disseminated, hypodense (CT scan)
n.a.
Liposomal Doxorubicin (13, 1999–2004)
< 20
yes
DXA‐scan BMD within normal range
B
M
45 (1969)
SSA
1/1/1
8 months
Yes
Axial skeleton, disseminated, hypodense (CT scan)
2200
Paclitaxel (4, 2012–ongoing)
45
yes
KS confirmation by bone biopsy
C
M
41 (1971)
SSA
1/0/1
5 years
Yes
Axial skeleton, disseminated, hypodense (CT scan)
Not done
none
94
no
D
M
39 (1973)
SSA
1/1/1
6 months
Yes
Axial skeleton, single lesions, hypodense (CT scan)
62200
Paclitaxel (3, 2012–ongoing)
< 20
yes (but stop May 2012)
(Abbreviations: SSA = Sub Saharan Africa; CAU = Caucasian; n.a.=not available DXA = Dual‐energy X‐ray absorptiometry; BMD = bone mineral density)