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Journal of STD & AIDS

HIV and systemic lupus erythematosus: the clinical and diagnostic dilemmas of having dual diagnosis
J Burton, J H Vera and M Kapembwa
Int J STD AIDS 2010 21: 845
DOI: 10.1258/ijsa.2010.010062

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CASE REPORT

HIV and systemic lupus erythematosus: the clinical

and diagnostic dilemmas of having dual diagnosis

J Burton MRCPCH*, J H Vera MRCP† and M Kapembwa PhD BSc FRCP(Ed) FRCP(Lond)‡

*King’s College Hospital; †Imperial College London; ‡Northwick Park Hospital, London, UK

Summary: We present the case of a young black African woman living in the UK who presented with systemic lupus erythematosus
(SLE) and HIV. The reported coexistence of HIV and SLE is unusual with fewer than 30 published cases. We discuss some of the
clinical and diagnostic challenges that face clinicians when a patient presents with both conditions. In particular, we discuss the
overlap in symptoms, signs and laboratory findings, and the difficulties that this may pose in terms of making a diagnosis.
The implications that having a dual diagnosis may have for treating each condition are also discussed. With increased HIV testing
in a variety of clinical settings there is likely to be an increase in detection of similar cases. This case emphasizes the need for
careful diagnostic testing and judicious interpretation of the validity of laboratory results in order to reach an accurate diagnosis
in such patients.

Keywords: HIV, systemic lupus erythematosus (SLE), diagnosis

INTRODUCTION
Women account for half of all adults living with HIV world-
wide1 and systemic lupus erythematosus (SLE) is predomi-
nantly seen in young women of African or Asian ancestry.2
Surprisingly, coexistent HIV and SLE are unusual with fewer
than 30 published cases. Here, we describe the case of a black
African woman living in the UK who presented with both
HIV infection and SLE. We discuss some of the clinical and
diagnostic challenges posed by patients with coincidental SLE
and HIV infection.
CASE REPORT
A 36-year-old West African woman was referred to the rheuma-
tology clinic in 2006 with a nine-month history of fever, rash,
polyarthralgia, weight loss and Raynaud’s phenomenon. On
examination she had a maculopapular, non-photosensitive
rash on her trunk and arthralgia but with no evidence of arthri-
tis. Her investigations revealed a normocytic anaemia with no
evidence of haemolysis (haemoglobin 11.1 g/dL), white cell
count 3.8  109 (normal differential), normal platelet count,
urea and electrolytes (U&Es) and liver function tests (LFTs).
She had raised inflammatory markers (ESR 114 mm/hour;
CRP 77 mg/L), C3 complement level (1.94 g/L) and immuno-
globulin G and M (28.6 g/L and 3.1 g/L, respectively).
Immunological profiles showed positive antinuclear antibody
(ANA) 1:2560 and extractable nuclear antibody (ENA SS-A
[anti-Ro]; ENA SS-B [anti-La]; ENA nRNP). Anti double-
stranded DNA (anti-dsDNA) and rheumatoid factor were
Correspondence to: Dr J Burton, King’s College Hospital,
Denmark Hill, London SE5 9RS, UK
Email: jessicakb@hotmail.com
negative. An HIV test was not considered at this point. She
was born and brought up in Sierra Leone. However, she had
no other risk factors for HIV infection.
A diagnosis of SLE was made. However, it is important to
note that although she did have some clinical features of SLE,
she did not fulfil the American College of Rheumatology diag-
nostic criteria for the disease.3,4 She was commenced on daily
prednisolone (15 mg). One month later she commenced
weekly methotrexate (10 mg). Her rheumatological complaints
improved.
In her past medical history, she had been discovered to have
pancytopenia and seronegative hepatitis in 2004; these had
resolved spontaneously. An HIV test was negative both at
this time and again several months later in her early pregnancy.
In February 2007, she attended the rheumatology clinic with
fever, diarrhoea, abdominal pain, rash, mouth ulcers and sore
throat. On examination, she had a widespread maculopapular
rash, oral ulceration and 2 cm hepatomegaly. Laboratory tests
showed pancytopenia (neutrophils 1.29  109; platelets 124 
109; Hb 12.2 g/dL), normal U&Es and LFTs, sterile mid-stream
urine and blood cultures, and complement levels and immuno-
globulins within the normal range. The differential diagnoses
considered at this point were a flare-up of SLE, methotrexate-
related side-effects and possible infection. Methotrexate was
stopped and she received prednisolone and hydroxychloro-
quine. Over the next few weeks, she improved and predniso-
lone was gradually stopped. Again, HIV testing was not
considered at this point.
In September 2007, her husband was diagnosed HIV seropo-
sitive. The patient took an HIV test in December 2007, which
was also positive. The patient doubted the diagnosis and
undertook two further HIV tests at another hospital, both of
which gave equivocal results. She requested a repeat HIV test
in March 2008. This was again positive and her sample was

DOI: 10.1258/ijsa.2010.010062. International Journal of STD & AIDS 2010; 21: 845 –846
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846 International Journal of STD & AIDS Volume 21
................................................................................................................................................
sent to the reference laboratory. The reference laboratory con-
firmed HIV infection by the presence of HIV proviral DNA.
Her CD4 count at presentation in December 2007 was 1011
cells/mm3 (49%) with HIV viral load ,50 copies/mL. When
last seen in July 2009, she was clinically well although her
CD4 count had fallen to 836 (38%) and her HIV viral load
was detectable for the first time at 62 copies/mL. She remained
ANA positive (.1:640) and anti-dsDNA negative. She has
never been on antiretroviral therapy (ART).
DISCUSSION
The coexistence of SLE and HIV appears to be unusual with
fewer than 30 cases published in the literature. As far as diag-
nosis is concerned, this can be explained in a number of ways.
Firstly, there may be clinical confusion between the two enti-
ties. Rheumatological symptoms and signs are common in HIV
and overlap significantly with SLE.5 In our patient, the multi-
system manifestations of skin rash, weight loss, oral ulcers,
arthralgia, myalgia, anaemia, leucopenia and autoantibodies
were consistent with both SLE and HIV infection.
Secondly, one disease may suppress the laboratory manifes-
tations of the other. For example, lupus-related antibodies reac-
tive against retroviral Gag proteins have been reported.6,7 The
fact that our patient maintained low-level HIV viraemia in the
absence of ART may support this hypothesis.
Thirdly, some of the enzyme-linked immunosorbent assay
-based diagnostic tests for HIV have been associated with false-
positive results in patients with SLE.8 – 10 The reasons for this
are not clear but may be explained, in part, by similarities in
the repertoire of immune responses observed in both diseases.
HIV infection and SLE are characterized by dysfunctional
CD4/CD8 T-lymphocytes as well as polyclonal B-cell acti-
vation, which can result in autoantibody synthesis.11 Also,
among untreated HIV-infected individuals serological abnorm-
alities including hypergammaglobulinemia, positive rheuma-
toid factor, and antineutrophilic and cytoplasmic antibodies
are often found.12,13 While these immunological abnormalities
are rarely of clinical significance in HIV infection, they may
be pivotal in establishing the diagnosis of SLE. Vigilance is,
therefore, essential in the interpretation of these laboratory
markers in order to reach an accurate diagnosis.
Once treatment has been established there are further areas of
possible confusion. It appears that the treatment of one disease
may affect the course of the other. For example, treatment of
SLE using cyclophosphamide was associated with rapid CD4
cell depletion in a patient with concomitant HIV and SLE.14
In another case report, a patient with HIV infection had a recur-
rence of rheumatic disease after the initiation of ART.15
It seems likely that in the absence of treatment guidelines for
patients with active SLE and HIV infection, clinicians will con-
tinue to prescribe both immunosuppressive and antiretroviral
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December 2010
medications, the effects and safety of which are equally
unknown in patients with concomitant disease.
CONCLUSION
This case underscores the need for the dual diagnoses of HIV
and SLE to be considered by HIV physicians and also the
need for non-HIV physicians to consider HIV infection in
their differential diagnoses. The recent call by the chief
medical officer for England for increased HIV testing is likely
to lead to greater detection of similar cases. Confirmatory diag-
nostic testing and judicious interpretation of the validity of
laboratory results will be required to reach an accurate
diagnosis.
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(Accepted 7 September 2010)