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Seronegative spondyloarthropathy has been described in association with HIV infection.
It appears to be more severe and more resistant to therapy than spondyloarthropathies in persons
without HIV infection. This spondyloarthropathy is oligoarticular, mainly involves the lower
extremities, and can be accompanied by enthesitis (at tendinous insertions on bones), skin rashes,
and mucus membrane involvement. It may become quiescent with antiretroviral therapy. In
Caucasians with HIV infection, HLA-B27 is found in 80 to 90% of patients with this form of
reactive arthritis, but Africans are likely to be HLA-B27 negative.[1020,1026]
Osteomyelitis most often affects younger persons with AIDS with low CD4 counts. The
mortality rate is high.[1032] The most common organism cultured is Staphylococcus aureus;
other bacterial organisms cultured may include streptococci and Enterobacter.[1027] Some
cases may be due to atypical mycobacteria, particularly with low CD4 counts. Skeletal lesions
from infection with atypical mycobacteria are often multiple, and concomitant skin lesions are
frequent.[1028]
Osteolytic bone lesions may appear with bacillary angiomatosis, caused by the
Rickettsia-like organism Bartonella henselae. Such lesions can appear in the distal extremities
and cause local pain. Radiographically, these lesions appear as circumscribed lytic areas that
may cause cortical destruction with a periosteitis or may permeate the marrow cavity.[510]
Osteonecrosis has been observed more frequently since the 1990’s with HIV infection,
and is 100-fold more likely to occur in HIV-infected persons than the general population. The
hip is most commonly affected area and often bilaterally.[1029] Risk factors include
corticosteroid therapy, hyperlipidemia, alcoholism, hypercoagulability, and megestrol acetate
use. Plain film radiographs and magnetic resonance imaging are used for diagnosis.[1030]
Osteonecrosis appears to be more prevalent in HIV-positive patients undergoing primary total
hip arthroplasty than in HIV-negative control patients. Compared to HIV-negative patients,
osteonecrosis in HIV-infected persons develops at an earlier age, and is accompanied by a lower
prevalence of osteoarthrosis in HIV-positive patients. The duration of HIV infection is
significantly shorter in patients with osteonecrosis.[1031]
Bone demineralization with osteopenia and osteoporosis is observed more frequently in
HIV infected persons with long survival. Risk factors for the development of osteopenia include
antiretroviral therapy (ART), older age, longer duration of HIV infection, high viral load,
lipoatrophy, poor nutrition, and lower body weight. A decrease in bone mineral density of 2 to
6% per year in the first two years following initiation of ART is similar to that of the first two
years following menopause, particular when tenofovir is part of the regimen. Both tumor
necrosis factor and interleukin-6 are cytokines produced in increased amounts in persons infected
with HIV, and these cytokines may affect osteoclast activation and resorption of bone.[306].
Soft tissue and osteoarticular infections with HIV infection are not common overall.
Findings may include septic arthritis, soft tissue abscesses, osteomyelitis, pyomyositis, and
cellulitis. The most common pathogen is Staphylococcus aureus. Risk factors include a low
CD4 count, presence of intravascular indwelling catheters, extra-articular infection and trauma,
and history of injection drug use. The course and treatment of these conditions is similar to that
of non-HIV infected persons.[1032]
Soft tissue infections with methicillin-resistant Staphylococcus aureus (MRSA) are
becoming increasingly common in HIV-infected persons. In one study of men having sex with
men, the MRSA carriage rate was 8.2%, over half of colonized persons subsequently developed
infection, and the incidence of community-associated MRSA soft-tissue infections was over 6-
fold higher in the HIV-infected persons than among the non-HIV-infected persons. Soft-tissue