Clinical manifestations

Cure Arthritis Naturally

Cure Arthritis Naturally

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Arthritis can occur at any stage of HIV infection, but the true prevalence of arthritic syndromes and the nature of their association with HIV infection remain unclear. The pattern of HIV-associated arthritis is similar to that of other viral disorders: acute onset, short duration, no recurrences, and no erosive changes [11]. Prospective studies have shown a high prevalence of rheumatic complaints in 30% to 40% of HIV-infected patients, with arthralgias the most common rheumatic manifestation in approximately 25% to 40% of cases [12-14]. Knees, shoulders, and elbows are more frequently involved, although any joint can be affected. Transient but sometimes severe arthralgias also occur [12,13,15]. Arthralgias and myalgias are common in advanced stages of HIV infection, suggesting they are reactive in nature [12]. Jaccoud's arthropathy, a nonerosive deforming arthropathy reported to occur in cases of chronic rheumatic fever and systemic lupus erythemato-sus (SLE), has also been reported in HIV-infected patients [16].

Seronegative spondyloarthritides

Spondyloarthritis are frequently seen in HIV-positive patients, and initial descriptions uniformly reported seronegative spondyloarthritides including ReA, PsA, and undifferentiated spondyloarthritis as the most common rheumatic diseases associated with HIV infection. Early descriptions also reported a very low incidence of osteoarticular septic complications in HIV patients from the Western world in whom homosexual behavior was the most common risk factor [1-4,17-21]. At variance with these findings were the Spanish reports describing osteoarticular infection, including septic arthritis and pyomyositis as the most common osteoarticular manifestations associated with HIV infection [15,16,20]. This difference was attributed to geographic differences and differences in risk factors with a high prevalence of intravenous drug use [22].

The pandemic of HIV infection in Africa has resulted in an increased awareness of the different types of arthritis that can accompany HIV infection and AIDS. HIV-positive patients have an increased prevalence of ReA [17,19-21,23]. These arthritides are similar to those reported in other parts of the world, although risk factors are different in Africa where heterosexual transmission is a more common cause than homosexual transmission or intravenous drug usage. The changing epidemiology of spondyloarthritides in this region of the world has important practical and educational implications. In Zambia, the prevalence of spondyloarthritis is calculated at approximately 180 per 100,000 in HIV-positive versus 15 per 100,000 in HIV-negative individuals in the general population [24]. ReA was the most common inflammatory joint disorder in black Zambians (272 of 595 newly seen patients), and was closely linked to HIV infection but not with HLA-B27, with clinical and radiologic characteristics similar to those reported in HLA-B27-positive whites.

HLA-B27 is less common among blacks with idiopathic spondylo-arthritis. In HIV-positive African AIDS patients, clinical, diagnostic, and radiographic features of seronegative spondyloarthropathies are indistinguishable from those of conventional (HLA-B27 related) disease, but with a higher overall frequency of uveitis, keratoderma, and onycholysis [25-28].

Conventional treatment of rheumatic lesions, including intra-articular steroids, seems to be safe and reasonably effective, even in AIDS patients. Anecdotal evidence suggests that treatment with methotrexate and azathioprine leads to exacerbation of HIV disease and should be avoided [29-31]. In a patient with severe HIV-associated ReA, MRI and sonographic imaging of inflamed knees had extensive polyenthesitis and adjacent osteitis. The arthritis deteriorated despite conventional antirheumatic treatment, but improved dramatically after highly active antiretroviral therapy (HAART), which was accompanied by a significant rise in CD4 T-lymphocyte counts [32].

ReA in HIV-positive patients has been widely documented. Some authors consider that CD4-positive lymphocyte subpopulation does not play a determinant role in ReA [33]. The pathogenesis of ReA seems to be linked to HLA-B27, which has been described as the major susceptibility factor for the disease [34]. The association between AIDS and ReA could be explained by the severe immunosuppression, which predisposes to the invasion by ar-thritogenic microorganisms. Furthermore, AIDS patients have a wide spectrum of gastrointestinal and genitourinary infections (Shigella sp, Chlamydia trachomatis, Entamoeba histolytica, Giardia lamblia, Cryptosporidium sp, Isospora belli, Candida sp, and cytomegalovirus). Some of these infections have been related to the pathogenesis of ReA, and are usually asymptomatic even in HIV-positive patients [20], although other studies suggest the direct or reactive role of retrovirus in the genesis of ReA [15,35,36]. Only limited data are available, however, on synovial immunopa-thology. Nonspecific chronic synovial inflammation and high synovial fluid cell counts are present in some patients. In other patients, the evidence of inflammatory changes is minimal. The course of ReA in HIV infection may be more severe, progressive, and refractory to treatment than in non-HIV-positive patients [37]. The presence of malar rash in these patients has been reported as the clue for early diagnosis of HIV infection [38]. In an HIV-positive patient with active Reiter's syndrome despite HAART and un-detectable plasmatic viral load, acitretin without nonsteroidal anti-inflammatory drugs was effective [39].

In sub-Saharan Africa a dramatic upsurge in the prevalence of rheumatic complaints, directly related to increase of HIV infection, has been observed. These manifestations are mostly spondyloarthritides, primarily ReA and un-differentiated forms of the disease, and less often PsA. HLA-B27 is virtually absent in most of the sub-Saharan Africa populations, and ankylosing spondylitis is rare; only a few cases have been reported from central and southern Africa [40]. The prevalence of HLA-B27 in African blacks is 10 times lower than in white populations. There is also a virtual absence of ankylosing spondylitis even in the West African countries of Gambia and Senegal, where 3% to 6% of the general population is HLA-B27 positive. The clinical features of the disease are similar to those in white HLA-B27-positive patients with ankylosing spondylitis. Acute anterior uveitis and familial occurrence are rare. In Togo, spondyloarthritis was diagnosed in 31 of 2030 patients. Of these 31 patients, eight were HIV-positive patients and had no sacroiliitis [41]. The same authors reported 44 patients with spondyloar-thritides; 15 had ankylosing spondylitis and 11 of these were HIV-positive [42]. The symptoms of ankylosing spondylitis in these patients were comparable with those of European patients. The results of these studies contradict the reputed scarcity of ankylosing spondylitis in black Africa [43]. The epidemiology of spondyloarthritides in sub-Saharan Africa has changed by the expanding HIV epidemic, despite the low prevalence of HLA-B27 [44]. More studies are needed to evaluate risk and protective factors for seronegative spondyloarthritis in sub-Saharan African populations and better dissect the relative importance of genetic and environmental factors in the pathogenesis of spondyloarthritis [45].

An increased prevalence of PsA has been clearly established with HIV infection, mostly in AIDS patients [13,30,46]. A variety of psoriatic manifestations may accompany HIV infection, with nail involvement present in most HIV-positive patients with inflammatory articular involvement. The articular pattern most frequently observed is polyarticular and symmetric with enthesopathy and dactylitis, but sacroiliac or spinal affection can also occur [46,47]. Of 702 new Zambian patients with inflammatory arthritis, 28 had PsA and 27 of these were HIV positive. At first consult, 16 patients (60%) were in WHO clinical stage I. PsA is almost universally associated with HIV infection in black Zambians. The clinical features are similar to those described for whites with AIDS-associated PsA [48]. The course of psoriatic arthropathy during HIV infection is variable but tends to progress together with the decrease of CD4+ cell count and to be refractory to conventional treatment. In this regard, the presence of psoriasis can be considered a sign of poor prognosis in HIV infection [47,49].

Infectious rheumatic diseases

In contrast, in HIV-infected patients addicted to intravenous drugs and hemophiliacs, there was an absence of ReA, and a low frequency of symptoms of articular swelling, and a marked presence of septic arthritis. Skeletal infections were caused predominantly by Staphylococcus aureus (60%) and Candida albicans (20%), although uncommon pathogens, such as septic arthritis by Stenotrophomonas maltophilia, Prototheca wickerhamii [50], and so forth have been reported in HIV-infected patients.

The practices that lead to HIV infection (the route of entry) seem to play a more decisive role in the appearance of rheumatic manifestations in these patients than the presence of the virus itself or the immunologic alterations thereby produced [51-53]. This suggests that the relative prevalence of associated infections for the routes of entry have a major influence in the types of rheumatic manifestations associated with HIV infection and provide clues to the ethiopathogenesis of the particular syndromes even in HIV-negative individuals.

In a study of 43 cases of hemophiliacs with AIDS and septic arthritis, the spectrum of pathogen microorganisms was somewhat different than in other risk groups. The clinical picture mimics that of hemarthrosis, with high erythrocyte sedimentation rate and fever, often causing a delay in diagnosis, exclusively affecting joints with hemophilic arthropathy, with absence of peripheral leukocytosis, varying CD4+ cell counts. Treatment with systemic antibiotics is often sufficient, obviating the need for ar-throtomy and open drainage. Prognosis regarding joint function is relatively good, but the prognosis for the medium- to long-term survival of the patient is poor [54-57].

Soft tissue infections are rarely seen in patients with HIV infection. When present, they tend to occur in the presence of low CD4+ cell counts (<200 cells/mm3) [58]; intravascular indwelling catheters; extra-articular infection; intravenous drug users; hemophiliacs; and trauma. A wide spectrum of clinical manifestations, however, ranging from cellulitis and soft tissue abscesses to pyomyositis are seen in these patients. In general, the clinical picture, causal microorganisms, and response to therapy are similar to that of HIV-negative patients. Tropical pyomyositis is an acute bacterial infection of skeletal muscles characterized by rapid formation of abscesses. Occurrence of tropical pyomyositis is a criterion for classification of HIV-infected patients in WHO disease stage III; tropical pyomyositis in HIV-infected patients may simulate septic arthritis of the hip and knee, respectively [59]. The most common infectious agent is S aureus [60], although Salmonella enter-itidis [61] has been found. Musculoskeletal manifestations caused by congenital and secondary syphilis usually subside completely after diagnosis and antibiotic therapy in HIV-positive and AIDS patients [62].

Autoimmune diseases

Infection with HIV-1 continues to provide important insights into autoimmunity and rheumatic diseases [63]. Sjogren's-like syndrome, inflammatory myopathy, and systemic vasculitis are associated with HIV infection. HIV-positive patients share a number of clinical and serologic features with SLE. Whether this is true SLE or not is controversial and discussed later. Nevertheless, for the unaware, these similarities may lead to diagnostic confusion [64].

There are few reported cases of concomitant HIV and SLE, generally in patients with long-standing HIV infection that presents with fever, arthral-gias and arthritis, photosensitive rash, oral ulcers, alopecia, headache, pleuritic chest pain, and lymphadenopathy. Laboratory tests show leukopenia, thrombocytopenia, nephropathy and diverse autoantibodies against antinuclear antibodies, antiribonucleoprotein, anti-Smith, anti-ribosomal-P protein, and anticardiolipin (aCL). Review of the literature revealed less than

40 cases of concomitant SLE and HIV; in these patients, rheumatologic signs and symptoms were common and overlapped significantly with SLE. Nevertheless, regardless of whether there is an increased prevalence of SLE among HIV-positive patients, autoantibodies, such antinuclear antibodies, anti-DNAds, anti-Smith, anti-smooth muscle, anti-parietal cell, antiglomeruli, antithyroid, and anti-neutrophil cytoplasm antibodies seem to be increased in AIDS [65].

Although it has been suggested that these diseases can be mutually exclusive, distinguishing between the two of them can be difficult because of the high degree of rheumatic complaints and autoantibodies in HIV-positive patients. SLE should be considered in HIV-positive patients with rheumato-logic complaints [66].

Moreover, false-positive syphilis tests and the lupus anticoagulant have been reported in 40% to 50% of HIV-positive patients in advanced stages. High-titers of aCL have been detected in a significant proportion of HIVpositive patients without any known clinical relationship. In acute infectious episodes with Pneumocystis carinii aCL may be present, and may become negative when the infection is cleared. The IgG aCL isotype has been found in 85% to 95% of patients with advanced HIV infection [67]. In one study, aCL were detected in 17 (50%) of 34 HIV-positive patients, and their presence was significantly associated with the detection of cerebral perfusion abnormalities by Tc 99m hexamethylpropyleneamine oxime single-photon emission CT [68]. Identification of the epitopes recognized by antiphospho-lipid antibodies induced by HIV-1 will offer insight into the mechanism of thrombosis associated with antiphospholipid antibodies found in the rheumatic diseases.

Muscular complications of HIV infection are classified as follows: (1) HIV-associated myopathy and related conditions including polymyositis, inclusion-body myositis, nemaline myopathy, diffuse infiltrative lymphocyto-sis syndrome, HIV-wasting syndrome, vasculitis, myasthenic syndromes, and chronic fatigue; (2) iatrogenic conditions including mitochondrial my-opathy, HIV-associated lipodystrophy syndrome, and immune restoration syndrome; (3) tumor infiltrations of skeletal muscle; and (4) rhabdomyolysis [69].

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