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Cure Arthritis Naturally

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2 vs 1 < .05

Osteoporosis

0/25

17/75

2 vs 1 .000

Osteonecrosis

0/50

7/96

2 vs 1 .000

Data from Medina F, Perez-Saleme L, Fuentes J, et al. Impact of highly active antiretroviral therapy on rheumatic manifestations in human immunodeficiency virus infected patients. Arthritis Rheum 2004;48:S185.

Data from Medina F, Perez-Saleme L, Fuentes J, et al. Impact of highly active antiretroviral therapy on rheumatic manifestations in human immunodeficiency virus infected patients. Arthritis Rheum 2004;48:S185.

the advent of HAART, the spectrum of rheumatic manifestations in HIV infection changed. ReA, PsA, and myopathies have fallen, maybe as a result of immune restoration, and osteonecrosis, urate abnormalities, and chronic infections (tuberculosis [TB]) started to report, maybe as a result of metabolic shifts (Table 1). HAART itself, however, is associated with rheumatic complications whose pathogenesis is poorly understood. Indinavir has been associated with case reports of monoarthritis [87,88], frozen shoulder, temporomandibular dysfunction, and Dupuytren's disease [89]. New HIV treatments also may ameliorate these rheumatic conditions; the impact of changes in HIV treatment on these disorders requires further assessment [90].

Earlier studies failed to detect a higher presence of osteoporosis or excessive loss in bone mineral density in HIV-positive patients [91]. Subsequently, however, combined antiretroviral therapy, mainly HAART, has been associated with significant osteopenia and osteoporosis associated in HIV infection. Dual-energy radiographic absorptiometry was performed in 112 men. Those receiving protease inhibitor had a higher incidence of osteopenia and osteoporosis according to WHO definitions (relative risk, 2.19; 95% confidence interval, 1.13-4.23; P = .02) and the authors concluded that osteope-nia and osteoporosis are independent side effects of HAART associated with protease inhibitor-containing regimens that seem to be independent of adipose tissue maldistribution [92]. Nonexclusive risk factors for osteope-nia and osteoporosis could be drug interactions, cytokine activation, and liver dysfunction, in addition to decreased physical activity and hypogonad-ism [93]. Because the use of HAART is increasing, it is important to establish the meaning of these findings. Moreover, calcium and antiresorptive therapy should be considered in HIV-positive patients on this therapeutic regimen.

Osteonecrosis of the femoral head has been observed in HIV-positive patients receiving protease inhibitor-containing HAART, in the absence of classic risk factors for osteonecrosis [94,95]. Recently, it has been reported that 4% of HIV-positive patients may unknowingly have the bone disorder osteonecrosis [96], and the authors suggest that avascular osteonec-rosis should be considered as a late complication of HIV infection.

As a possible explanation of these findings, osteoprotegerin ligand (OPGL, TNFS11) and its receptor RANK (TNFRS11A) are essential for the development and activation of osteoclasts and are critical regulators of physiologic bone remodeling and osteoporosis. Production of osteoprote-gerin ligand by activated T cells can directly regulate osteoclastogenesis and bone remodeling. This process may explain why autoimmune diseases and chronic viral infections, such as hepatitis and HIV, result in systemic and local bone loss. Inhibition of osteoprotegerin ligand binding to RANK by the natural decoy receptor osteoprotegerin prevents bone loss in postmeno-pausal osteoporosis and cancer metastases and completely blocks crippling in a rat model of arthritis [97].

Hypouricemia and hyperuricemia may be considered markers of neopla-sia. Urate abnormalities have been detected in HIV-positive patients, with hyperuricemia in 41% and hypouricemia in 5% of these patients, compared with none in the HIV-negative group (P < .001) [15]. Acute gout attacks in HIV-positive patients also have been described. Another possibility may be related to therapy, because asymptomatic hyperuricemia has been associated with ritonavir, but gout has rarely been reported. In a retrospective cohort of 1825 HIV-positive patients, 18 patients had gout, of whom 15 were on HAART. Seven of the 18 patients had lipodystrophy and dyslipidemia. Gout was seen in patients with known risk factors for gout or who were receiving ritonavir as a boosted protease inhibitor and who also had lipodys-trophy [98]. Properly conducted epidemiologic studies are needed to confirm these preliminary reports. African countries are a valuable source of clinical material for comparative studies to help elucidate factors that influence the development of rheumatic diseases.

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