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Abstract
A HIV positive man with a CD4 count of 777×106/l and suppressed viral load on antiretroviral medication had a delayed diagnosis of Kaposi's sarcoma (KS) affecting his left leg. He was diabetic and on a controlled diet and had a previous deep vein thrombosis affecting the same leg. Factors that have been studied in HIV-related KS as well as classical KS, such as diabetes mellitus, not smoking and previous deep vein thrombosis, may have increased our patient's risk for the development of this disease. Clinicians should consider KS as a possible diagnosis even in patients with well-controlled HIV.
- HIV
- Kaposi's sarcoma
- diabetes mellitus
- deep vein thrombosis
- HIV testing
- HIV skin disease
- sexual behaviour
- information tech
- gum services
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- HIV
- Kaposi's sarcoma
- diabetes mellitus
- deep vein thrombosis
- HIV testing
- HIV skin disease
- sexual behaviour
- information tech
- gum services
Case
A 46-year-old UK born Caucasian man presented to his general practitioner with three painful, pigmented raised lesions, which blanched on pressure (figure 1), affecting his left lateral leg and causing pitting oedema from his foot to his knee. He was a non-smoker who had been diagnosed with diet-controlled diabetes mellitus (DM) 2 years previously. He had also developed a left leg proximal deep vein thrombosis (DVT) treated with warfarin for 6 months just prior to the onset of this lesion. His general practitioner referred him to his HIV clinic as he felt that there was a low index of suspicion for Kaposi's sarcoma (KS), because the lesions did not look typical of KS and because his latest viral load was <40 copies/ml. He was stable on Kivexa and Efavirenz with a viral load <40 copies/ml for 6 years and a current CD4 count of 777×106/l (32%). His lowest CD4 count was 164×106/l (9%). He had no prior HIV-related illness. His serum PCR for human herpes virus 8 (HHV-8) DNA was negative.
One raised lesion.
He was referred to a vascular surgeon to exclude an arteriovenous malformation. The vascular surgeon referred him on to a dermatology clinic where he underwent skin biopsy; the histology was reported as consistent with KS and was verified by an expert in HIV-related histopathology. A CT scan showed no visceral involvement. There was a considerable delay of 12 months in the diagnosis of KS in this patient; during this time, some lesions became smaller and others enlarged. He was referred to oncology 14 months after presentation where he underwent chemotherapy with liposomal doxorubicin.
Discussion
KS is the most common AIDS-related cancer; however, the use of highly active antiretroviral therapy has greatly decreased its incidence.1 There are four types of KS, which are classical, endemic, iatrogenic (following a transplant) and HIV related.2
HIV-related KS is most common in people with a CD4 count <200×106/l and treatment with highly active antiretroviral therapy frequently leads to regression. However, patients with HIV can develop KS with higher CD4 counts and suppressed viral loads. Our patient developed KS with a CD4 count of 777×106/l, but a literature search did not find many cases with CD4 counts at this level.
A study in 2007 reported some patients with a median CD4 count of 340×106/l and no other AIDS defining conditions; their KS was indolent with none having visceral involvement.3 A further letter in 2008 reported KS in 96 patients who had a CD4 count of >300×106/l and undetectable viral loads.4
The main cause of KS is HHV-8. However, HHV-8 DNA is not detected in all patients with KS as with our patient.5 Previous research has identified other cofactors for KS. Our patient had been diagnosed with DM 2 years earlier and this may have led to a higher risk of KS due to additional immunosuppression. A study of KS in 28 HIV negative men who have sex with men and who had no evidence of immunosuppression found that 4 (14%) out of 28 had been diagnosed with DM, although the background frequency of DM was not mentioned.6 A case–control study of 142 cases of classical KS in Sicily in 2008 showed an increased risk with DM (OR 4.73; 95% CI 2.02 to 11.1).7 Non-smoking was also found to be associated with an increased risk of developing classical KS in the same study. A cohort study from the USA showed similar results for HIV-related KS (RR=0.6; 95% CI 0.5 to 0.9).8 Our patient had no Mediterranean origins but HIV infection is associated with immunosenescence, which may be the reason this case resembles classical (elderly) KS,9 even though the patient was not an elderly man. Is DVT associated with KS? In the literature, there are two case reports where a DVT preceded the development of KS as with our patient.10 In conclusion, our patient presented with KS despite having a high CD4 count and suppressed viral load, which may have been explained by cofactors such as DM, not smoking and a previous DVT.
Key messages
There was a considerable delay in the diagnosis of Kaposi's sarcoma (KS) in our patient.
Factors such as diabetes mellitus, not smoking and a previous deep vein thrombosis may have increased our patient's risk for KS.
Clinicians should continue to have a high index of suspicion for KS even in patients with high CD4 counts and suppressed viral loads.
Footnotes
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.