JIACM 2006; 7(2): 136-44

REVIEW ARTICLE

Rheumatological Manifestations in HIV Infection

Annil Mahajan*, Vishal R Tandon**, S Verma***,

Abstract
The global epidemic of HIV infection has also affected the practice of rheumatologists. Reiters syndrome was the first reported
rheumatic disorder in patients of HIV infection, and since then, many other rheumatic manifestations have been reported. These
conditions include arthralgia, painful articular syndrome, Reiters syndrome, reactive arthritis, HIV-associated arthritis,
undifferentiated spondyloarthropathy, soft tissue rheumatism, septic arthritis, avascular bone necrosis, osteomyelitis, hypertrophic
osteoarthropathy, myalgias like polymyositis, dermatomyositis, Sjogrens like syndrome - DILS, vasculitis like Schonlein-Henoch
purpura, polyarteritis nodosa (PAN), giant cell arteritis(GCA), Wegeners granulomatosis (WG), Raynauds phenomenon and Behcets
syndrome. HIV-related neoplastic processes namely Kaposis sarcoma and non-Hodgkins lymphoma can also affect the
musculoskeletal system. Musculoskeletal manifestations can occur at any phase of the infection though they are much more
prevalent in late phases. There could be involvement of bone, joint, and muscle during the course of HIV infection. A number of
rheumatic manifestations have been described in HIV infection. The rheumatic manifestations can be attributed either to direct or
indirect effects of HIV virus with genetic and environmental factor also contributing a key role. One of the biggest paradoxes of HIV
infection is the finding of certain rheumatic diseases such as the diffuse infiltrative lymphocytosis syndrome (DILS), reactive arthritis,
Reiters syndrome, or inflammatory myopathy occurring in the face of immunodeficiency. Alternatively, other rheumatic diseases
such as rheumatoid arthritis and systemic lupus erythematosus have been reported as improving in the face of the CD4+ lymphocytes
depletion associated with HIV infection. Thus, an early understanding and treatment of rheumatic disease will go a long way in
reducing physical, mental, social, and economic burden in these miserable HIV infected patients.

Key words: HIV, Rheumatic, Manifestation.

Introduction prospective studies suggested that out of one hundred and

one patients with HIV infection, the musculoskeletal system
Human immunodeficiency virus (HIV-1) infection was
was involved in 72 patients. Thirty-five patients had
reported almost two decade ago. Since then the disease has
arthralgias, ten had Reiters syndrome, two had psoriatic
spread worldwide at an alarming rate. India already has the
arthritis and myositis respectively, and one had vasculitis.
second highest number of people estimated to be living
Also found were two previously unreported syndromes.
with HIV/AIDS in the world (5.1 million)1. The global epidemic
The first, occurring in 10 patients, consisted of severe
of HIV infection has affected the practice of almost every
intermittent pain involving less than four joints, without
clinician, and rheumatologists are no exception. Earliest reports
evidence of synovitis, of short duration (two to 24 hours),
of rheumatological associations of HIV infection were
and requiring therapy ranging from non-steroidal anti-
published in mid-19802-4, and since then much interest has
inflammatory drugs to narcotics. The second, occurring in
been aroused in this topic. Reiters syndrome was the first
12 patients, consisted of arthritis (oligoarticular in six
reported rheumatic disorder in HIV infection, and since then
patients, monoarticular in three patients, and polyarticular
many other rheumatic manifestations have been reported
in three patients) involving the lower extremities and lasting
ranging from 4 to 71.3% in their prevalence. Various aspects
from one week to six months. The synovial fluid studied in
of these rheumatic manifestations in HIV infected patients
five patients was sterile and inflammatory5.
are discussed in the present review.
Similarly, in another prospective study of 74 consecutive
Epidemiology HIV +ve patients, clinical and laboratory findings of rheumatic
The prevalence and characteristics of the rheumatic and manifestations were compared with 72 control HIV ve
extra-rheumatic manifestations of human immuno- subjects with similar risk factors for HIV. It was found that
deficiency virus (HIV) infection determined in one of the rheumatic manifestations were more frequently observed

* Assistant Professor, *** Postgraduate Student, Department of General Medicine,

** Senior Demonstrator, Department of Pharmacology and Therapeutics,
Government Medical College, Jammu - 180 001, J & K State, India.
in the HIV +ve group than the HIV -ve group: arthralgias Table I: Rheumatological consequences of HIV
were found in (45%), arthritis in (10%), and Reiters syndrome infection.
in (8%). Laboratory findings revealed rheumatoid factor in EventsinHIVinfection Rheumatologicalmanifestations
21% HIV +ve versus 2% in HIV -ve, antinuclear antibodies in
Directeffects Arthritis,myositis,vasculitis
17% HIV +ve vs 0 in HIV -ve, IgG anticardiolipin antibodies
Indirecteffects
in 94% HIV +ve vs 9% in HIV -ve. Hyperuricaemia was found
Chronicimmuneresponse .
1 B-cellhyperactivity,autoantibody
in 41% HIV +ve patients and hypouricaemia in 5%, compared toHIVantigens:Humoral productionandnon-specific
andcellmediated. symptomsofchronicimmune
with none in the HIV -ve group. Neoplasias were identified stimulation
in 13 HIV +ve patients, and in 7 these were associated with .
2 Lymphocyticinfiltrativesyndromes
hyperuricaemia, and in 3 with hypouricaemia. Of interest, 2 e.g.,DILS.
patients had urate abnormalities before the diagnosis of .
3 Vasculitis
neoplasia. Thus, the study suggests that rheumatic .
4 Inflammatorymyopathy

Mediatedbyintactcomponents Reiterssyndrome,psoriaticarthritis
manifestations and autoantibodies are more prevalent in (CD8cells)ofimmunesystem andotherundifferentiated
HIV +ve patients6. spondyloarthropathies

Selectiveimmunedeficiency .
1 Opportunisticinfectionofmusculo-
Natural course of the disease affectingCD4+helper skeletalsystem.
T-cells .
2 AmeliorationofCD4dependent
Rheumateiological manifestations can occur at any phase Rheumaticdiseasese.g.RA
of the infection, though they are much more prevalent in
late phases5, 7. There could be involvement of bone, joint, Direct effects
and muscle during the course of HIV infection.
Reports of isolation of HIV/detection of HIV RNA/p24 antigen
from synovial fluid, muscle cells and within intravascular
Rheumatic diseases associated with, or lesions have proven direct effects of virus in causation of
occurring in, patients with HIV infection arthritis, myositis, and polyarteritis nodosa (PAN)-like
A number of rheumatic manifestations have been described vasculitis14-16. Many symptoms are attributable to host
with HIV infection .These include arthralgia, painful articular immune response to infection, mediated by intact
syndrome, Reiters syndrome, reactive arthritis, HIV-associated components of immune system (CD8) or those arising due
arthritis, undifferentiated spondyloarthropathy, soft tissue to immunodeficiency.
rheumatism, septic arthritis, avascular bone necrosis,
osteomyelitis, hypertrophic osteoarthropathy, myalgias, Indirect effects
polymyositis, dermatomyositis, Sjogrens like syndrome DILS,
A. Early HIV infection:
vasculitis like Schonlein-Henoch purpura, polyarteritis nodosa
(PAN), giant cell arteritis (GCA), Wegeners granulomatosis (WG), Characterised by chronic activation of host cellular and
Raynauds phenomenon, and Behcets syndrome8-11. HIV- humoral responses.
related neoplastic processes such as Kaposis sarcoma and non- 1. Involvement of humoral arm is evidenced by presence
Hodgkins lymphoma can affect the musculoskeletal system12. of a plethora of antibodies in circulation occurring due
to spontaneous B-cell proliferation17.
Aetiopathogenesis of rheumatic
manifestations in HIV infection
The commonest laboratory abnormality is
polyclonal hyperglobulinaemia in 45% of HIV
The rheumatic manifestations can be attributed either to positive individuals18.
the direct effect of HIV infection or to host immune response
to the infection; those mediated by intact components of
Autoantibodies are more frequent in HIV positive
the immune system (CD8 cell), and those that arise because with rheumatoid factor and ANA being in low titre
of immunodeficiency13 with genetic and environmental in 17% of patients19. IgG anticardiolipin antibodies
factors also contributing a key role. seen in 95% patients with AIDS, more so in

Journal, Indian Academy of Clinical Medicine
Vol. 7, No. 2
April-June, 2006 137
 advanced cases in 20 - 30% HIV positive
individuals20, 21. ANCAs (both c-ANCA and p-ANCA)
present in approximately 43% of ELISA22.
2. Diffuse infiltrative lymphocytosis syndrome
(DILS): Sjogren-like syndrome is now a well established
manifestation of HIV infection with unrestricted
increase in number of CD8 T-cells directed against host
antigens bearing HLA-DR5 phenotype23.
3. Reiters syndrome (RS), psoriatic arthritis and
various undifferentiated spondyloarthropathies:
It has been postulated that the progressive CD4 cell
depletion occurring in HIV infection may permit
persistant gut infection and decreased clearance of
streptococcal and staphylococcal infection contributing
to the greater severity of spondyloarthropathies and
psoriasis respectively. The association between RS and
AIDS has been explained by the fact that the acquired
immunodeficiency heads to bacterial, viral, and parasitic
infections caused by micro-organisms with arthrogenic
potential24.
4. Vasculitis: Histopathological examination of HIV-
associated vasculitic lesions showed perivascular
infiltration by CD8+ T-cells25. Apart from the direct effect
of HIV infection, a host of opportunistic pathogens may
contribute to the vasculitis. Although antibodies to
neutrophil cytoplasmic antigens (ANCA) have been
described in HIV seropositive patients, these antibodies
do not appear to be associated with the HIV-associated
vasculitides.
5. Inflammatory myopathy: HIV infection is associated
with polymyositis like syndrome. The perivascular and
interstitial infiltrate chiefly comprises of CD8 cells26.
B. Advanced stage of HIV infection27
The rapid CD4 cell depletion occurring in this stage is
associated with infectious/septic arthritis and
osteomyelitis by conventional and opportunistic
pathogens.
Clinical presentation of rheumatological
manifestations in HIV patients
HIV-associated arthralgia
Frequency of arthalgias, unexplained in origin, in HIV +ve
138 Journal, Indian Academy of Clinical Medicine
subjects has been reported to be more than 45% and are
the most commonly observed manifestation in HIV
infection5. They are mild-to-moderate in severity, and may
be transient or intermittent, and are often oligoarticular
affecting large joints such as shoulder, elbow and knee
although any joint can be involved. A polyarticular
presentation is now also seen frequently28.The most
appropriate treatment alongwith a non-narcotic analgesic
such as acetaminophen or tramadol, is reassurance8, 9.
Painful articular syndrome
The painful articular syndrome is characterised by bone
and joint pain on movement, without evidence of synovitis29.
It is a self-limiting syndrome which lasts less than 24 hours.
This syndrome is usually observed in the late stage of HIV
infection. The exact aetiology of unclear, and treatment is
symptomatic8, 9.
HIV-associated arthritis8, 9
HIV associated arthritis occurs atleast as frequently, and
sometimes more commonly, than HIV indirectly associated
spondyloarthropathy. It is usually present as an oligoarthritis,
predominantly affecting lower extremities, which tend to
be self limiting, lasting for less than 6 weeks. Although early
reports in western communities reported asymmetrical
oligoarthritis as the usual pattern, polyarticular involvement
is now seen frequently30. The synovial fluid leucocyte count
is lower than seen in HIV-associated reactive arthritis (500 -
2,000/ l). Synovial fluid cultures are typically sterile. Isolation
of HIV from one synovial fluid sample, and electron
microscopy, show particles resembling retrovirus. No
mucocutaneous involvement is observed, and
enthesopathy is also absent. The treatment, by and large,
includes NSAIDs, and in more severe cases, low dose
corticosteroids. Patients may respond equally well to
hydroxychloroquine and sulphasalazine. Most of the patients
with HIV associated arthritis are in the late stage of infection.
The aetiology is still unclear, however recently both HTLV-I
and -II have been suggested to induce inflammatory or
autoimmune reactions which can increase significantly the
incidence of arthritis.
Reactive arthritis
Reactive arthritis occurs more commonly in the setting of
HIV infection and perturbation in the CD4 lymphocyte

Vol. 7, No. 2
April-June, 2006
count, and CD4 to CD8 ratios may be involved in the
pathogenesis of reactive arthritis. The most typical
presentation is that of a seronegative peripheral arthritis
predominantly involving the lower extremities, usually
accompanied by enthesitis and mucocutaneous features.
The diagnosis of reactive arthritis (RS) is based on the
combination of dermatological and articular alterations.
The patients cutaneous lesions are characterised by
exfoliation and the formation of crusts located on the face,
scalp, genitals, hands, and feet; onychodystrophy with
opacity; yellowish colouration; and hyperkeratosis of the
nails. Articular lesions lead to progressive deformity of
phalangeal joints of the hands, and intensive arthralgia,
mainly of the larger joints (shoulders, elbows, hips, and
knees). The synovial fluid white cell count rises to 2,000 -
10,000/ l, synovial fluid cultures are negative, and the
most common microorganism present in the synovial
membrane is Chlamydia. Unlike HIV-associated arthritis,
HLA-B27 association exists in 70% - 90% of patients8, 9, 31.
Jaccoud arthropathy is a non-erosive, deforming arthropathy
reported to occur in cases of chronic rheumatic fever and
systemic lupus erythematosus. Only two cases of HIV-
associated Jaccoud arthropathy have been reported in the
literature so far, both in patients with features of reactive
arthritis. Interestingly, a case of HIV-associated Jaccoud
arthropathy in a patient without features of reactive
arthropathy was presented recently, suggesting that
unpredictable presentation, are possible in HIV infection32.
Similarly, psoriasiform dermatitis can present in Reiters
syndrome associated with AIDS33.
NSAIDs are the mainstay of treatment 8, indomethacin, in
particular is recommended because of its additional
property to inhibit HIV replication, whereas rarely,
phenylbutazone is preferred in refractory cases.
Sulphasalazine like NSAIDs can ameliorate HIV infection to
a little extent. Methotrexate was initially considered
contraindicated because of its immunosuppressive action,
but recently it has been suggested to have a role in
treatment, if careful monitoring of HIV viral load and CD4
counts is done. Hydroxychloroquine also has been reported
to be very effective with in vitro reducing action on HIV
replication as well. Etretinate34 can be useful for both arthritic
and cutaneous manifestations. Research is also on to
evaluate the role of infliximab and other TNF blockers.
Journal, Indian Academy of Clinical Medicine
Vol. 7, No. 2
Psoriatic arthritis (PsA)
PsA is almost universally associated with HIV infection. It
occurs most commonly in the late stage, of HIV infection.
The psoriatic rash can be extensive especially in patients
not receiving anti-retroviral treatment. The arthritis is
predominantly polyarticular, involves lower limbs, and is
progressive. Amelioration is noted with onset of AIDS35.
The aetiologic mechanisms remain unclear, but most likely
represent a combination of genetic and environmental
factors36.
Antiretroviral treatment has been shown to be effective in
treating both HIV associated psoriasis and its associated
arthritis. Phototherapy, etretinate, and methotrexate can also
be useful. Etanercept37 may play an important role in
modulating the inflammatory activity and progression of
HIV-associated psoriasis and psoriatic arthritis. Although, both
cutaneous and joint manifestations of psoriasis improve
dramatically with its use, careful follow-up must be
exercised while prescribing etanercept in the setting of
HIV infection.
Undifferentiated spondyloarthopathy8, 9
Some HIV-infected patients fail to develop the entire
spectrum of clinical manifestations for disease to be called
as ankylosing spondylitis, Reiters syndrome, or psoriatic
arthritis, and are labelled as undifferentiated
spondyloarthopathy. The epidemic of HIV infection in sub-
SaharanAfrica in recent years, however, has been associated
with a dramatic upsurge in the prevalence of
spondyloarthropathies other than ankylosing spondylitis,
primarily reactive arthritis and undifferentiated forms of the
disease, and less often psoriatic arthritis. HLA-B27, because
of its rarity and virtual lack of association with the observed
cases of spondyloarthropathy in this population, cannot be
used as an aid in diagnosis of spondyloarthropathy in black
Africans. Conversely, HIV infection is increasingly showing
such a strong association with reactive arthritis, psoriatic
arthritis, and undifferentiated spondyloarthropathies in sub-
Saharan African populations that any patient with acute or
chronic inflammatory arthritis may need to be tested for
possible HIV infection38.
Enthesitis, dactylitis, oligoarthritis, sacroiliitis, nail changes, and
conjunctivitis are commonly seen in such patients and they

April-June, 2006 139
are usually negative for RA factor, ANA, and HLA B27. The
pathogenesis of HIV-associated spondyloarthropathy (SpA)
is poorly understood. On magnetic resonance imaging and
sonographic imaging, inflamed knees, extensive
polyenthesitis, and adjacent osteitis are the frequent findings.
The arthritis deteriorates despite conventional anti-rheumatic
treatment, but improves dramatically after highly active anti-
retroviral treatment, which is accompanied by a significant
rise in CD4 T-lymphocyte counts39. Otherwise, treatment is
symptomatic (NSAIDs); intralesional corticosteroids and
sulphasalazine may be used in more extensive disease8.
Avascular necrosis (Osteonecrosis)
Osteonecrosis, also known as avascular necrosis, is chiefly
characterised by death of bone caused by vascular
compromise. The true incidence of osteonecrosis in HIV-
infected patients is not well known and the pathogenesis
remains undefined. Hypothetical risk factors peculiar to HIV-
infected individuals that might play a role in the
pathogenesis of osteonecrosis include the introduction of
protease inhibitors and resulting hyperlipidaemia, the
presence of anticardiolipin antibodies in serum leading to
a hypercoagulable state, immune recovery, and vasculitis.
The most common presentation is arthralgia. The majority
of the patients will give history of receiving steroids, HAART
therapy, smoking, and alcoholism. This complication has
been reported mostly in adults, but recently, even the case
of a 5-year-old child with AIDS (stage 3) who developed
osteonecrosis related to the advanced stage of the illness
and to HAART is reported without any of the above risk
factors. Hence, it is believed that osteonecrosis should be
included as a differential diagnosis of every HIV-infected
patient who complains of pain of weight bearing joints.
Likewise, it seems prudent to rule out HIV infection in
subjects with osteonecrosis40, 41.
Myopathy
Skeletal muscle involvement can occur at all stages of HIV
infection, and may represent the first manifestation of the
disease. Myopathies in HIV-infected patients is classified as
follows: (1) HIV-associated myopathy and related conditions,
including HIV polymyositis, inclusion-body myositis,
nemaline myopathy, diffuse infiltrative lymphocytosis
syndrome (DILS), HIV-wasting syndrome, vasculitic
processes, myasthenic syndromes, and chronic fatigue; (2)
140 Journal, Indian Academy of Clinical Medicine
muscle complications of anti-retroviral therapy, including
zidovudine and toxic mitochondrial myopathy related to
other nucleoside-analogue reverse-transcriptase inhibitors
(NRTIs), HIV-associated lipodystrophy syndrome, and
immune restoration syndrome related to highly active anti-
retroviral therapy (HAART); (3) opportunistic infections and
tumour infiltrations of skeletal muscle; and (4)
rhabdomyolysis42, 43. Dermatomyositis, fibromyalgia, and
osteomyelitis complicating pyomyositis are a few other rare
presentations44.
Patients presenting with proximal muscle weakness can
show a normal or minor elevation of creatine phosphokinase
(CPK), and normal findings on electromyography. Whereas,
muscle biopsy can reveal CD8 polymyositis. This illustrates
the importance of muscle biopsy in identifying the
underlying pathology in HIV infected patients with muscle
weakness and little or no abnormality in laboratory
investigations45.
A severe neuromuscular weakness syndrome may occur in
HIV-infected individuals. The association with
hyperlactataemia and NRTI exposure supports
mitochondrial toxicity as a pathogenesis. In some, the onset
of neurological symptoms lag significantly after
discontinuation of anti-retroviral therapy, suggesting that
different aetiological mechanisms may underlie these
cases46. The management of HIV-associated polymyositis is
similar to that for other inflammatory myopathy9.
Diffuse infiltrative lymphocytosis syndrome (DILS):
Definite DILS is found in 3% of the patients, and possible
DILS in 3.4%. The prevalence of definite DILS is significantly
higher in African Americans (4.5%)47. Diffuse infiltrative
lymphocytic syndrome (DILS) is a rare manifestation of
human immunodeficiency virus (HIV) disease which is
characterised by a diffuse visceral CD8 lymphocytic
infiltration, a persistent CD8 lymphocytosis, bilateral parotid
swelling and cervical lymphadenopathy48. A role of Epstein-
Barr virus (EBV) and HIV, but not CMV, in the pathogenesis of
DILS, is suggested by our immunohistochemical findings49.
Evidence is also there suggesting that CD8 lymphocytosis
represents an immune response to viral infection rather
than a malignant disorder, i.e., it is a benign monoclonal
expansion50.
The following diagnostic criteria have been suggested:

Vol. 7, No. 2
April-June, 2006
a. Patient must be HIV seropositive by ELISA and Western been documented to be one of the presentations of DILS43.
blot;
Corticosteroids in moderate doses (30 - 40 mg prednisolone
b. Must have bilateral salivary gland enlargement or per day) might be useful in treating both glandular swelling
xerostomia persisting for more than 6 months; and and sicca symptoms of DILS, without adversely affecting
c. Must have histological confirmation of salivary or frequency of opportunistic infections, raising viral loads or
lacrimal gland lymphocytic infiltration in absence of depressing CD4 counts. Radiotherapy also has been
granulomatous or neoplastic enlargement. suggested to have a role, and besides, combination anti-
retroviral therapy is also effective. Cysts if refractory can
It is important to differentiate Sjogren syndrome and HIV be managed by aspiration and instillation of 1 ml of a depo
associated DILS; features similar and different are depicted steroid into the cyst8.
in Table II and III.
Vasculitis8,9,53
Table II: Comparison of clinical features of Sjogren
syndrome and HIV associated DILS8, 9, 51. The vasculitides associated with HIV are usually not life-
Features which are similar threatening, and present as a single flare rather than a
relapsing illness. A wide spectrum with inflammatory
a. Sicca symptoms
diseases has been described in patients of HIV infection.
b. Salivary gland swelling (often massive in DILS) Lesions included in these are hypersensitivity vasculitis,
c. Extraglandular involvement (hepatitis, renal tubular polyarteritis nodosa, and Henoch Schonlein purpura, others
acidosis) being Kawasaki disease, giant cell arteritis, Wegeners
d. Lymphocytic infiltration on salivary gland biopsy granulomatosis, and isolated angiitis of central nervous
e. Neutropenia and/or lymphopenia in peripheral blood system,small-vessel vasculitis, and inflammatory lung
f. Polyclonal hypergammaglobulinaemia. disease. Corticosteroids remain the mainstay of treatment,
although cytotoxic drugs also have been employed in
Table III: Comparison of clinical features of Sjogren
refractory cases.
syndrome and HIV associated DILS8, 9, 51.
Featureswhicharedifferent
Septic arthritis
Sjogrensyndrome DILS
In a prospective study among all new admitted patients
Sex 90%female 90%male
with septic arthritis (SA), 79% were HIV-1 seropositive.
Lymphadenopathy Common Massive
Gonococcal arthritis was found in four patients, all HIV
Extraglandularinvolvement Uncommon Common
positive. Non-gonococcal bacterial arthritis was established
Autoantibodies Anti-Ro,Anti-La Multiple,lowtitre
in 16 patients, of whom 13 were HIV positive. Causative
HLA-DR HLA-DR2,DR3 HLA-DR5,DR6
organisms involved in this group were: Staphylococcus
Infiltratinglymphocyte MainlyCD4+ MainlyCD8+
aureus, Streptococcus pneumoniae, Salmonella group B,
In addition, clinicians should be aware that the pulmonary Streptococcus group D, Klebsiella pneumoniae, and
process associated with DILS may mimic clinically and mycobacterium54. Among atypical mycobacterium species,
radiographically the pneumonic process caused by most commonly implicated are Mycobacterium avium-
Pneumocystis carinii. Other manifestations of DILS include intracellulare complex, M. kansasii, M. haemophilum, M.
a severe form of peripheral neuropathy; lymphocytic terrae and M. fortuitum. Septic arthritis due to Haemophilus
infiltration of the liver, evident as hepatitis; myositis; and influenzae has also been described in a HIV-infected
lymphocytic interstitial nephritis51. patient55. Fungal infections like Candida albicans also can
manifest with oligoarthritis or polyarthritis.
Such patients with the syndrome may also be seen in the
dental clinics. Recognition and appropriate referral are Thus, HIV-1 infection appears as a risk factor for SA patients,
responsibilities of the dental practitioner52. Myositis also has but SA cannot be used as a predictor for HIV-1 infection for

Journal, Indian Academy of Clinical Medicine
Vol. 7, No. 2
April-June, 2006 141
hospitalised patients. SA occurs infrequently, and may
present at any stage of HIV infection54.
Paradoxes of HIV infection
One of the biggest paradoxes of HIV infection is the finding
of certain rheumatic diseases such as the diffuse infiltrative
lymphocytosis syndrome (DILS), reactive arthritis, Reiters
syndrome, or inflammatory myopathy occurring in the face
of immunodeficiency. Alternatively, other rheumatic
diseases such as rheumatoid arthritis and systemic lupus
erythematosus have been reported as improving in the
face of the CD4 lymphocytes depletion associated with this
disease8.
Systemic lupus erythematosus
Systemic lupus erythematosus (SLE) in patients infected
with HIV due to transfusion of either blood or platelet
concentrate can show a near remission in the disease and
during the course of follow-up56. But contrary to previous
findings, it has been suggested that the features of both
HIV infection and connective tissue disease (SLE) can co-
exist57, 58. Systemic lupus erythematosus (SLE) may be
influenced by the treatment of HIV infection also. A person
with HIV infection was reported to develop SLE after the
initiation of highly active anti-retroviral therapy59.
Thus, generally, HIV-related immuno-suppression improves
SLE symptoms, but anti-retroviral therapy may lead to an
autoimmune disease flare subsequent to the increase of
circulating CD4 cell count60.
Rheumatoid arthritis (RA)
The effects of HIV infection on rheumatoid arthritis (RA) are
a matter of debate as there is no agreement on the influence
of HIV related immunodeficiency on this disease. Patients
with RA with symmetric joint erosions and positive
rheumatoid factor (RF) who develop classic acquired
immunodeficiency syndrome (AIDS) improve with
resolution of bony erosions and disappearance of RF, and
reach a complete clinical remission only in the paralytic
limbs61, 62.
Laboratory abnormalities associated with HIV
infection
The commonest laboratory abnormality is polyclonal
142 Journal, Indian Academy of Clinical Medicine
hyperglobulinaemia in 45%, whereas rheumatoid factor and
ANA occur in low titre in 17% of HIV patients. IgG
anticardiolipin antibodies are seen in 95% patients of AIDS,
moreso in advanced disease. ANCAs (both c-ANCA and p-
ANCA) are present in approximately 43% by ELISA. Similarly,
false positive results for HIV antibody by ELISA/Western blot
may be seen in SLE8.
Conclusion
As the epidemic of HIV is increasing, burden of rheumatic
disorders would also be a visible cause of morbidity in these
patients. The understanding of interface of HIV with the
immune system and clinical manifestations of rheumatic
and autoimmune disorders is important as HIV infection
can alter the clinical presentation and course of the disease.
Awareness regarding presence and interpretation of the
spectrum of auto-antibodies in these patients is important
as presence of auto-antibodies can lead to diagnotic
dilemma. One should entertain the possibility of HIV
infection in presence of polymyositis and vasculitis. Early
recognition and treatment of opportunistic infections is of
paramount importance as they can become the reasons
for rheumatological disorders. Anti-viral effects of drugs
like indomethacin and hydrochloroquine, and impact of
HAART in producing and affecting the clinical spectrum of
rheumatic disease has to be kept in mind while treating
HIV-infected patients. Early understanding and treatment
of rheumatic diseases will go a long way in reducing
physical, mental, social, and economic burden in these
unfortunate HIV-infected patients.
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NAGPUR 2006
National Conference on Pulmonary Diseases
1st November - 5th November, 2006, Nagpur.
th
8 Joint Conference of
National College of Chest Physicians (India) and Indian Chest Society
NC CP
INDIAN
CHEST SOCIETY
Prof. Dr. B.O. Tayade
Organising Secretary, NAPCON - 2006,
Head of Dept. - Chest Medicine Government Medical College,
Nagpur - 440 003, (Maharashtra) Ph.: 0712-2706189

Vol. 7, No. 2
April-June, 2006