To the Editor,

Kaposi’s sarcoma (KS) is associated with human herpes virus 8 (HHV-8), although, alone, HHV-8 is not a major risk factor. Situations that affect immunity, such as infection from human immunodeficiency virus (HIV) or immunosuppressant treatment in solid organ transplant (SOT) patients, markedly increase risk.1,2 KS in SOT patients tends to occur within the first few months post-transplant.1,3 A high CD4 lymphocyte count and high-activity anti-retroviral therapy (HAART) both significantly reduce the risk in patients with HIV.2,3

Proliferation signal inhibitors (PSI) inhibit tumour angiogenesis by reducing the production of vascular endothelial growth factor (VEGF) and its Flk-1/KDR receptor. The VEGF system plays a central role in the development of KS, and so the effect of PSI is particularly relevant. The results observed in SOT with KS after converting to PSI demonstrate this relationship, and these drugs are currently the primary therapeutic option.1 In KS associated with HIV, the first line of treatment is controlling the HIV with HAART, and the usefulness of PSI is still being researched.2 Here we present the case of an HIV patient with a kidney transplant (KT) that developed KS.

A 59-year old male infected with HIV (by sexual transmission) that was well controlled with HAART received a KT in May 2001. He then continued treatment with HAART, always maintaining a negative viral load and CD4>200 cells/µl. The immunosuppressant treatment consisted of steroids, mycophenolate, and tacrolimus. The mycophenolate was suspended in January 2003 due to haematological intolerance. In august 2003, we performed a biopsy due to progressive deterioration of renal function and the patient was diagnosed with chronic nephropathy.

In February 2010, purple nodular lesions appeared on the patient’s left arm, leading to the histopathological diagnosis of KS with intense immunohistochemical expression for CD31, CD34, and HHV-8. An analysis of the extent of the disease ruled out visceral involvement. Blood PCR analysis was negative for cytomegalovirus (CMV), Epstein-Barr virus HHV-6, HHV-7, and HHV-8, with positive HHV-8 serology (IgG-IFI). At this moment the patient already had creatinine levels nearing 4.5mg/dl due to the chronic nephropathy. We decided to significantly reduce the tacrolimus prescription (to 3-4ng/ml) and start treatment with sirolimus (at 4-6ng/ml. We did not completely remove the tacrolimus treatment for fear of poor tolerance to PSI due to renal failure. Renal function continued to deteriorate, and we recommenced dialysis in November 2010, suspending tacrolimus. We continued sirolimus treatment at low doses until the KS was resolved in Match 2011. The patient currently continues on dialysis with a complete remission of all lesions.

Our patient developed KS very late (9 years post-KT) and in spite of a good control of the HIV infection. He had several different risk factors (HHV-8, HIV, immunosuppressant treatment) that were able to act synergistically, favouring the development of the tumour with an atypical epidemiological pattern. Given the experience published regarding HIV-negative SOT, we believe that it was the conversion to sirolimus rather than the decreased tacrolimus levels that caused the favourable evolution of the KS. Only three other cases of KS in HIV-positive SOT (two KT, one live transplant) have been communicated with a positive response following conversion to PSI.4,5 However, these cases were not described in detail since they made up part of a general series on SOT in patients with HIV.

Although the most extensive treatment in HIV-positive SOT is the combination of MMF and anti-calcineurinics, good results have also been obtained with protocols based on PSI.5,6 Additionally, PSI appear to have beneficial effects on the replication of HIV.5 We believe that a treatment regimen based on PSI could be the therapy of choice as the primary immunosuppressant following KT in transplant recipients with HIV infection and risk factors for KS (male, sexual practices, ethnicity, HHV-8 positive), as long as contraindications do not exist.

Conflicts of interest

The authors have no conflicts of interest to declare.