An interesting case of ‘diabetic foot ulcer’ in an HIV-positive patient

Introduction

Kaposi sarcoma (KS) is a highly vascularised tumour caused by human herpesvirus-8 (HHV-8) affecting the skin, lymph nodes and viscera. ¹ It is classified into four types: epidemic AIDS-related, immune-compromised, classic or sporadic and endemic (African). This case report will focus on the epidemic AIDS-related type. More than 50% of people in Africa carry the virus, but this falls to 10% or less in Eastern Europe/Mediterranean and less than 1% in N. Europe. ² In 2010, it was estimated that 162 out of 172 cases of KS in the UK were caused by HIV/HHV-8 co-infection, with the remainder (10) due to HHV-8 alone. ³

Case presentation

We present here a 70-year-old white British male patient, who had long-term type II diabetes controlled with oral hypoglycaemic drugs. He came under the care of the podiatric team for diabetic foot ulcers in 2013. The lesion in his feet started as purplish nodules affecting the plantar aspect of the left foot; later the right foot was also involved. He was referred to the dermatologist who performed a punch biopsy which revealed KS, confirmed by immuno-cytochemistry (Figure 1). This prompted an HIV test which was positive; the patient was then referred to the sexual health clinic. Mr AB lived alone and claimed to have been sexually assaulted by an unknown male person 30 to 40 years earlier. He was previously investigated for dysphagia and weight loss in 2010 and later in 2011 for recurrent oral candida. He was also seen by his general practitioner for multi-dermatomal shingles in 2012. Clinical examination revealed foul smelling ulcers on both feet, with maggot infestation (Figure 2). Genital examination showed an ulcerated swollen glans penis with a partially stenosed meatus. The lesion was purplish, indurated and extending to the shaft. The baseline HIV viral load was 139,241 copies/ml and a CD4 count of 66. His hepatitis B (HBV) serology was positive with an HBV viral load of 1.3 × 10⁷IU/ml. His plasma was positive for HHV-8 (180 copies/ml). His syphilis serology was positive and he denied history of or treatment for syphilis. The patient was started on antiretroviral therapy (ART). The HIV and HHV-8 viral load became undetectable within three months of ART (Table 1). The tenofovir and emtricitabine in the ART regimen caused the HBV viral load to fall by four logs in five months. The lesions on his feet (Figures 2 and 3) and genitals disappeared within five months of ART. He also received three weekly doses of benzathine penicillin with the rapid plasma reagin titres falling at nine months. OPEN IN VIEWER

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Figure 2.

The left foot showing ulcerated purplish nodules covered with slough on the plantar aspect of the toes extending on to the dorsum area. (Appearance typical of diabetic foot ulcer).

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Figure 3.

The left foot showing complete healing of the ulcerated lesions 6 weeks after anti-retroviral therapy.

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Table 1.

Serial HIV viral loads and CD4 counts.

Dates	CD4	HIV viral load
21 June 2012	66	139,241
24 July 2012	92	297
30 August 2012	–	31
05 November 2012	–	Undetected
03 January 2013	60	Undetected
23 April 2013	87	Undetected

The patient was later reviewed by the oncology team. A whole body computed tomography (CT) scan showed non-specific nodules in the upper lobe of the left lung, hepato-splenomegaly and diffuse small bowel thickening. A CT scan, three months later whilst on ART, showed focal lesions in the right hilar region and broncho-pulmonary lymphadenopathy suggestive of metastatic KS. This could have been an immune reconstitution inflammatory syndrome phenomenon; however, further CT nine months later showed little change from the previous. Chemotherapy has been deferred on the advice of the oncologist, and he is being monitored by yearly CT and quarterly HHV-8 PCR, HIV viral load and CD4.

Discussion

The proportion of late diagnosis in HIV still remains high (47% in 2011) with an estimated economical burden to National Health Service (NHS) of £63,061 for every missed early diagnosis.^4,5 Our patient visited healthcare services with HIV-related issues at least three times before the final ‘late diagnosis’ was made. The skin is the common site of KS lesions, ⁶ ranging from small, painless nodules to macules. Extracutaneous lesions occur in the gastrointestinal tract and lungs. Pulmonary involvement is often associated with high mortality. ⁷ Although our patient has radiological evidence of pulmonary lesions, he has no chest symptoms. The genital lesions were clinically diagnosed as KS as were the lesions in the feet, by their vascular appearance and clinical clearance with ART. Our patient had a poor prognostic score on presentation, based on the modified AIDS Clinical Trials Group staging of Kaposi’s sarcoma,^8,9 with a CD4 count less than 150 and with suspected systemic lesions and a Karnovsky performance status of less than 70. However, after ART he made a significant clinical recovery.

Conclusion

The advent of effective antiretroviral therapy has substantially reduced the incidence of KS in the HIV population globally.^10,11 However, symptoms of KS caused by HIV can masquerade as diabetic foot ulcers as reported above. It is imperative to consider HIV testing for all patients seeking healthcare support with conditions described in the new National Institute of Clinical Excellence (NICE) guidance supporting the Health Protection Agency (HPA) advice and BHIVA/BASHH/BIS guidelines on expanding HIV testing. ¹² This would facilitate better management of patients with HIV with substantial savings for the tax-payer.