With increasing figure of persons acquiring HIV infection, the figure of HIV-infected patients with arthritic manifestations is bound to increase. HIV can show with myriad of presentations reactive arthritis, morbific arthritis, diffuse infiltrative lymphocytic syndrome ( DILS ) and myositis are some of the rheumatological conditions that can happen in a HIV-infected person. This reappraisal elaborates some of the more common arthritic jobs that are associated with HIV infection.
The purpose of this communicating is to give a brief reappraisal of the varied arthritic manifestations that occur in the class of HIV infection with peculiar accent on the impact of antiretroviral therapy on the altering clinical spectrum.[ 3 ]
Human immunodeficiency virus infection has been associated with protean clinical manifestations. The first study of association of HIV infection with reactive arthritis was published in 1987.[ 4 ]Since so a overplus of arthritic manifestations have been reported since the late 1880ss.[ 5 ],[ 6 ],[ 7 ],[ 8 ],[ 9 ],[ 10 ],[ 11 ].
The exact prevalence of arthritic manifestations is non known, it has been estimated that from retrospective analysis of patients with HIV infection rheumatologic characteristics occur in 30-40 % of HIV-infected patients. While in western literature, the prevalence of rheumatological ailments ranged from 10-45 % .[ 12 ],[ 13 ]In India the prevalence is low, upto 2-4 % in most instance series. The difference in prevalence could be due to different profile of presentation and sexual patterns in developing states like India as compared to the West.[ 14 ],[ 15 ],[ 16 ].
In one of the prospective surveies by Berman et al suggested that out of 101 patients with HIV infection, the musculoskeletal system was involved in 72 patients. Thirty-five patients had arthralgias, 10 had Reiter ‘s syndrome, 2 had psoriatic arthritis and myositis severally, and 1 had vasculitis. Besides found were 2 antecedently unreported syndromes. The first, happening in 10 patients, consisted of terrible intermittent hurting affecting less than four articulations, without grounds of synovitis, of short continuance ( 2-24 hours ) , and necessitating therapy runing from NSAIDs to narcotics. The 2nd, happening in 12 patients, consisted of arthritis ( oligoarticular in 6 patients, monoarticular in 3 patients, and polyarticular in 3 patients ) affecting the lower appendages and enduring from 1 hebdomad to 6 months.[ 17 ]
Another survey comparing 74 back-to-back HIV positive patients clinical and laboratory findings of arthritic manifestations were compared with 72 control HIV negative topics with similar hazard factors for HIV, the survey concluded that arthritic manifestations were more often observed in the HIV positive group than the HIV negative group: arthralgias were found in 45 % , arthritis in 10 % , and Reiter ‘s syndrome in 8 % patients.[ 18 ]
The arthritic manifestations ( Table 1 ) can be attributed either to the direct consequence of HIV infection or to host immune response to the infection ; those mediated by integral constituents of the immune system ( CD8 cell ) , and those that arise because of immunodeficiency with familial and environmental factors besides lending a cardinal function.
The arthritic manifestations of HIV consequences from a complex interplay of assorted immunologic, environmental, and familial factors in a background of HIV infection. A three cell theoretical account has been propagated in the causing of arthritic manifestations. In this theoretical account a dendritic cell presents a peptide from an immunogenic protein to both a CD4 and CD8 T-cell ringer. This interaction disrupts tolerance and consequences in the enlargement of the cytotoxic T-cells resulting in assorted clinical arthritic syndromes.[ 19 ]Human immunodeficiency virus itself may be implicated as a direct cause of arthritis diversely termed as HIV associated arthropathy or AIDS arthritis as amplified by the fact that HIV has been isolated from synovial fluid.[ 20 ]A broad assortment of systemic autoimmune arthritic diseases are besides associated with HIV infection. These include Sjogren’s-like syndrome, inflammatory myopathy, and systemic vasculitis. It has been postulated that antibodies against the 3rd hypervariable part ( V3 ) of HIV-1 gp120 ( V3-specific antibodies ) might hold a function in the autoimmune phenomena observed in HIV-infected individuals. In fact v3 antibodies have been detected from patients enduring from systemic autoimmune diseases.[ 21 ]As a corollary, a assortment of autoantibodies have been detected in patients with HIV infection.[ 22 ],[ 23 ],[ 24 ],[ 25 ],[ 26 ],[ 27 ].
Table 1 Classification as per the etiopathogenesis
Events in HIV infection
Arthritis, myositis, vasculitis
Chronic immune response to HIV antigens: humoral and cell mediated
B-cell hyperactivity, autoantibody production and non-specific symptoms of chronic immune stimulation
Lymphocytic infiltrative syndromes
e.g. , DILS
Mediated by integral constituents ( CD8 cells ) of immune system
Reiter ‘s syndrome, psoriatic arthritis
and other uniform
Selective immune lack impacting
CD4 + “ assistant ” T-cells
Opportunist infection of musculoskeletal
Amelioration of CD4 dependant
arthritic diseases e.g. RA
DILS: diffuse infiltrative lymphocytic syndrome
The assorted autoantibodies described in literature are given in Table 2
Polyclonal, IgG, IgA, IgM
dsDNA, Histone, Sm, U1RNP SSA
IgG, IgM AntiB2GP-1
PR3 and MPO
CLINICAL RHEUMATIC SYNDROMES
A figure of arthritic manifestations have been described in the class of HIV infections since the coming of this epidemic in the 80s. There are legion instance studies, instance series, and reviews in this respect. Therefore a simplified strategy of arthritic manifestations is warranted for easiness of understanding as given in Table 3.
Table 3 Arthritic upsets associated with or happening in HIV-infected patients
Unique to HIV infection
Found in HIV infected patients
Ameliorated by HIV infection
Diffuse infiltrative leucocytosis syndrome ( DILS )
HIV associated arthritis
HIV associated Reiter ‘s syndrome
Systemic lupus erythematosus ( SLE )
Zidovudine associated myopathy
Painful articular syndrome
Henoch Schonlein peliosis
Diffuse Infiltrative Leukocytosis Syndrome ( DILS )[ 28 ],[ 29 ]
The primary infective association in these persons is reflected as a distinguishable host immune response in persons with the HLA-DR5 phenotype.[ 30 ]The association with HLA-DRB1 allelomorphs showing the ILEDE amino acid sequence in the 3rd diverseness part, normally HLA-DRB1*1102, DRB1*1301, and DRB1*1302 has delayed patterned advance to AIDS in patients with DILS. This is due to detain in the development of the HIV-1 virus from the less aggressive M-tropic strain to the more quickly retroflexing T-tropic strain.[ 31 ]Pathologically, there is grounds of focal sialadenitis, similar to that seen in Sjogren ‘s syndrome, although there is less devastation of the salivary secretory organs. CD8+ lymphocytes constitute the prevailing inflammatory infiltrate, unlike that seen in non-HIV-associated Sjogren ‘s syndrome.[ 32 ]
The specifying presentation of DILS is a painless parotid expansion that is frequently monolithic. The average continuance between the find of HIV seropositivity and oncoming of symptoms in one survey was 3.4 old ages.[ 33 ]Submandibular and lachrymal secretory organ expansion frequently occurs together and is accompanied by sicca symptoms in more than 60 % patients. In add-on to glandular manifestations, there are a figure of extraglandular characteristics in these patients such as 7th cranial nervus paralysis, sterile lymphocytic meningitis, peripheral neuropathy, lymphocytic interstitial pneumonitis ( LIP ) , lymphocytic hepatitis, nephritic cannular acidosis, interstitial Bright’s disease, lymphoma, peripheral arthritis, and polymyositis. Significantly, the reported frequence of LIP was every bit high as 25-50 % in patients with DILS. Since the debut of peptidase inhibitors, this complication has become less frequent. The presence of nephritic cannular acidosis, lymphoma, and polymyositis in patients with DILS is associated with a hapless forecast.
The major characteristics separating this upset from Sjogren ‘s syndrome are shown in Table 4.
Table 4 Differences between diffuse infiltrative leucocytosis syndrome and Sjogren ‘s syndrome
Diffuse infiltrative leucocytosis syndrome
Sjogren ‘s syndrome
Sexual activity distribution
Chiefly work forces
Chiefly adult females
Autoantibodies antinuclear antibodies, anti-Ro/La )
Increased CD8+ T cells in blood
For the diagnosing of DILS a diagnostic standard[ 34 ]has been suggested, the patient must hold
( 1 ) HIV-seropositivity by ELISA and Western smudge
( 2 ) Bilateral salivary secretory organ expansion or dry mouth prevailing for more than 6 months, and
( 3 ) Histologic verification of salivary or lachrymal secretory organ lymphocytic infiltration in the absence of granulomatous or neoplastic expansion.
CT scanning has besides been used to find the extent of glandular puffiness and measure parotid cysts and possible salivary glandular malignance. Management depends on the extent of the manifestations. If the glandular puffiness does non worry patients, and the sicca symptoms are mild or even absent, so reassurance and observation are plenty. Pilocarpine in doses of 5-10 mg thrice daily may profit sicca symptoms. In add-on, regular alveolar consonant attention is needed.
There are some studies proposing that moderate doses of corticoids ( upto 30-40 milligram Pediapred per twenty-four hours ) might be utile in handling both the glandular puffiness and sicca symptoms of DILS without adversely impacting the frequence of timeserving infections, raising the viral tonss or dejecting the CD4 counts.[ 35 ]The consequence is normally transeunt. Lymphocytic interstitial pneumonitis may necessitate higher doses of corticoids ( upto 60 mg/day of Pediapred ) , sometimes for extended periods. Antiretroviral therapy may be good in glandular puffiness and sicca symptoms.
This occurs in more than 10 % patients in some studies. It was ab initio described as oligoarthritis, preponderantly impacting lower appendages that tended to be self-limiting, enduring less than 6 hebdomads. Although early studies in western communities reported asymmetrical oligoarthritis as the usual form, polyarticular engagement is now seen often.[ 36 ]No mucocutaneous engagement is observed, and enthesopathy is besides absent. There is no association with HLA-B27 or any other known familial factor. Synovial fluid civilizations are normally unfertile. The synovial fluid leucocyte count is lower than that seen in HIV-associated reactive arthritis ( 500-2,000/AµL ) . There may be a direct function of HIV as demonstrated by the isolation of HIV from a synovial fluid sample and negatron microscopy demoing atoms resembling retrovirus.[ 37 ]X raies of the affected articulations are normally normal.
Treatment includes non-steroidal anti-inflammatory drugs ( NSAIDs ) and in more terrible instances, low dose glucocorticoids. Patients may react every bit good to hydroxychloroquine and sulphasalazine. Most of the patients with HIV associated arthritis are in the late phase of infection. The etiology is still ill-defined, nevertheless late both HTLV-I and -II have been suggested to bring on inflammatory or autoimmune reactions which can increase significantly the incidence of arthritis.
Interferon-I± used in the intervention of Kaposi sarcoma is known to do arthralgia and myodynia. Rifabutin an anti-mycobacterial agent used may besides do arthralgia and myodynia. Indinavir, the peptidase inhibitor has besides been implicated in doing monoarthritis though the exact cause was non explained.
Painful Articular Syndrome
The painful articular syndrome is characterized by bone and joint hurting on motion, without grounds of synovitis.[ 38 ]It is a self-limiting syndrome which lasts less than 24 hours. This syndrome is normally observed in the late phases of HIV infection. The exact etiology is ill-defined, and intervention is diagnostic.[ 39 ],[ 40 ]
Muscle engagement in HIV infection covers a broad scope of upsets runing from unsophisticated myodynias and fibromyalgia to severe, disenabling HIV associated polymyositis or pyomyositis.[ 41 ],[ 42 ],[ 43 ]. In one series of skeletal musculus biopsies performed in 92 grownups with HIV infection at necropsy, there was wasting in 51, inflammatory infiltrates in 8, mortification in 8, and infection in 3.[ 44 ]HIV-associated polymyositis normally occurs early in HIV infection. The common presentation is of a subacute, progressive proximal musculus failing with an elevated creatine kinase.[ 45 ]
Electromyography shows myopathic motor unit potencies with early enlisting and full intervention forms, fibrillation potencies, positive crisp moving ridges, and complex repetitive discharges. Histopathology reveals interstitial inflammatory infiltrates of variable strength associated with degenerating and regenerating sarcostyles, like those seen in polymyositis without HIV-1. Concomitant vasculitis is rare. Like HIV-negative patients, the predominant cell populations are CD8+ T cells and macrophages occupying or environing healthy musculus fibres. It is controversial whether the virus straight leads to inflammatory myopathy. The intervention of HIV-associated polymyositis is similar to that for other inflammatory myopathies. Both the rise of creatine kinase and the musculus failing respond to glucocorticoids. Refractory instances might necessitate immunosuppressants such as amethopterin or Imuran. These should, nevertheless, be used with cautiousness.
Other musculus diseases in HIV-positive persons include myodynia in 1/3rd of the patients and fibromyalgia in 10 % .[ 46 ],[ 47 ]Nemaline rod myopathy has been seldom described in HIV-infected persons.[ 48 ]
Diffuse myopathy has been reported with antiretroviral drugs, particularly Retrovir.[ 49 ]Zidovudine causes reversible toxic mitochondrial myopathy manifested by myodynia, musculus tenderness, proximal musculus failing, and elevated creatine kinase degrees. The myopathy resolutenesss on discontinuance of the medicine. This status is comparatively rare in present epoch due to rareness of Retrovir usage in developed states. Even in developing states the incidence has decreased as high dose Retrovir is precluded and increased consciousness taking to early diagnosing of this status. It is characterized by insidious oncoming of myodynia, musculus tenderness, and proximal musculus failing after a average continuance of 11 months of therapy. It tends to be dose related, being associated with mitochondrial disfunction. Both clinically, by EMG and by musculus biopsy, it is hard to separate it from HIV-associated polymyositis, although the inflammatory infiltrates are less terrible or sometimes absent in Retrovir induced myopathy. Consequently, in any HIV-infected person who presents with an elevated CK and myodynia or musculus failing, the drug should be discontinued for 4 hebdomads and the patient re-evaluated before EMG or musculus biopsies are undertaken.[ 50 ]
Infective myositis ( pyomyositis ) can hold a important association with HIV infection.[ 51 ]Organisms implicated include staphylococci aureus, salmonella enteritidis, Microsporum, and toxoplasma.
HIV-associated Reiter ‘s Syndrome and Reactive Arthritis
Reiter ‘s syndrome, the first arthritic syndrome reported in patients with HIV infection, can be terrible, but whether it occurs more often in HIV-infected patients is controversial.[ 52 ]In two little retrospective surveies where cohorts of HIV-infected patients were studied, the prevalence of Reiter ‘s syndrome was between 5 % and 10 % , 100-200 times higher than the expected prevalence in the general population.[ 53 ],[ 54 ]Another survey of more than 1,000 homosexual work forces found the frequence of Reiter ‘s syndrome to be merely 0.3-0.5 % , and there was no difference in the frequence between HIV-positive and HIV-negative topics.[ 55 ]
The commonest clinical presentation is that of a seronegative peripheral arthritis chiefly affecting the lower appendages, normally accompanied by enthesitis ( sausaging of toes or fingers, Achilles tendonitis, and plantar fasciitis ) . Multidigit dactylitis, particularly in the upper appendages, is common and may be comparatively painless. Frank synovitis is less common but may happen at the mortise joint and the subtalar, metatarsophalangeal, and interphalangeal articulations of the pess. Knee engagement is common, frequently asymmetric, and without radiologic alterations. Hip engagement is uncommon. Synovitis of the carpus, cubitus, and shoulder is uncommon but consequence in contractures and joint merger. Enthesopathy may happen at the medial and sidelong epicondyles, rotator turnup, or flexor sinews of the figures.
The axial skeleton is normally non involved, and although radiogram may demo sacroiliitis, clinical sacroiliitis is uncommon. Mucocutaneous characteristics particularly keratoderma blennorrhagicum and circinate balanitis, are common. Psoriasiform skin roseolas are besides common and can be extended ; particularly in patients non having anti-retroviral intervention. It can be hard to separate HIV-associated Reiter ‘s syndrome from psoriatic arthritis. Urethritis occurs every bit frequently as in HIV-negative Reiter ‘s syndrome. Constitutional characteristics of Reiter ‘s syndrome, including weight loss, unease, lymphadenopathy, and diarrhoea, are hard to separate from characteristics of adrenal HIV disease. Amelioration is noted with oncoming of AIDS. Clinicians should urge HIV proving for patients with Reiter ‘s syndrome whose behaviour puts them at an increased hazard for HIV infection.
The intervention is similar to that of HIV-negative patients with Reiter ‘s syndrome. NSAIDs are the pillar of intervention. Indomethacin is frequently recommended, non merely for its efficaciousness, but besides for its alone suppression of HIV reproduction observed in vitro.[ 56 ]Phenylbutazone is seldom used now because of its high side consequence profile, but can be utile in furnace lining instances. Patients often have an unequal response to NSAIDs entirely. Second line agents like Sulfasalazine has been shown to be effectual in some surveies at doses of 1.5 to 2g/day[ 57 ]. Methotrexate was ab initio believed to be contraindicated because of its immunosuppressive consequence and because it was reportedly associated with the development of Pneumocystis carinii pneumonia and other timeserving infections. With careful monitoring of HIV viral tonss and CD4 counts, and the patient ‘s clinical position, more recent surveies have shown a function for amethopterin in the intervention of Reiter ‘s syndrome and psoriatic arthritis happening in the scene of HIV infection.[ 58 ]Hydroxychloroquine has besides been reported to be utile non merely in handling HIV-associated Reiter ‘s syndrome but besides in cut downing HIV reproduction as evidenced in assorted in vitro and in vivo surveies.[ 59 ]Etretinate[ 60 ]can be utile for both creaky and cutaneal manifestations. Research is besides been done to measure the function of Remicade and other TNF blockers.
Psoriatic arthritis, with or without psoriasis, occurs in HIV-infected individuals with prevalence likely the same as that in non-HIV septic individuals ( 1-2 % ) .[ 61 ]This seronegative arthropathy is encountered with increased frequence in the HIV-positive population. Psoriatic arthropathy nowadayss clinically with a figure of forms although there are no satisfactory diagnostic standards. Signs and symptoms include opposing hydrops of the tegument and hypodermic soft tissues, enthesitis, synovitis, condylitis, dactylitis and peritendinitis. The pes and mortise joint are the commonest and most terrible sites of redness.
Nail engagement is a common presenting symptom of psoriatic arthritis. Many patients with psoriatic tegument manifestations or onycholysis merely have these findings and do non run into the standards for the diagnosing of psoriatic arthritis. The beam phenomenon, a combination of dactylitis and peritendinitis impacting the sinews of the same figure, may happen. Sacroiliitis and spondylitis have besides been described. There is hence considerable convergence with Reiter ‘s syndrome and other connective tissue upsets and the descriptive term “ uniform spondylarthropathy ” ( described below ) may be appropriate.[ 62 ]
Unlike psoriatic arthropathy in the non-HIV septic population, which shows an association with HLA Cw6, B17, B7 Bw16 or Bw57, in HIV disease it is normally associated with HLA B27.[ 63 ],[ 64 ]The SAPHO syndrome is the accompaniment of synovitis, acne, unfertile tegument pustules, hyperostosis, and osteitis. This rare manifestation of psoriatic disease is seen with increased incidence in HIV disease.[ 65 ]The imagination characteristics depend on the spectrum of engagement. Non-specific puffiness and lymphedema of tissues is non uncommon and produces a reticulate form of increased denseness in hypodermic fat on CT, or signal hyperintensity on T2-weighted MRI sequences and hypoechogenicity on ultrasound. In dactylitis the inspissating impacting the soft tissues of a figure is associated with synovial thickener and peritendinitis.
Undifferentiated Spondyloarthopathy[ 66 ]
Some HIV-infected patients fail to develop the full spectrum of clinical manifestations for disease to be called as ancylosing spondylitis, Reiter ‘s syndrome, or psoriatic arthritis, and are labeled as uniform spondyloarthopathy. The epidemic of HIV infection in sub-Saharan Africa in recent old ages, nevertheless, has been associated with a dramatic rush in the prevalence of spondyloarthropathies other than ancylosing spondylitis, chiefly reactive arthritis and uniform signifiers of the disease, and less frequently psoriatic arthritis. HLA-B27, because of its rareness and practical deficiency of association with the ascertained instances of spondyloarthropathy in this population, can non be used as an assistance in diagnosing of spondyloarthropathy in black Africans.
Conversely, HIV infection is progressively demoing such a strong association with reactive arthritis, psoriatic arthritis, and uniform spondyloarthropathies in sub-Saharan African populations that any patient with ague or chronic inflammatory arthritis may necessitate to be tested for possible HIV infection.[ 67 ]Enthesitis, dactylitis, oligoarthritis, sacroiliitis, nail alterations, and pinkeye are normally seen in such patients and they are normally negative for RA factor, ANA, and HLA-B27. The pathogenesis of HIV-associated spondyloarthropathy ( SpA ) is ailing understood. On magnetic resonance imagination and sonographic imagination, inflamed articulatio genuss, extended polyenthesitis, and next osteitis are the frequent findings.
The arthritis deteriorates despite conventional anti-rheumatic intervention, but improves dramatically after extremely active antiretroviral intervention, which is accompanied by a important rise in CD4 T-lymphocyte counts.[ 68 ]Otherwise, intervention is diagnostic ( NSAIDs ) ; intralesional corticoids and sulphasalazine may be used in more extended disease.
The intervention is similar to that for non-HIV septic patients. NSAIDs, such as Indocin can be used ab initio for the joint symptoms, but consequences have been dissatisfactory. There are studies that Butazolidin ( 100 mg 3 times per twenty-four hours ) is an effectual drug and neutropenia is non a job even in patients having Retrovir. Patients, in whom psoriatic joint disease does non react to NSAIDs, may be treated with Butazolidin or sulfasalazine ( 1-2 g/day ) . There is some informations on second-line agents such as gold, amethopterin, and Imuran.[ 69 ]Etretinate may besides be helpful. The usage of psoralen and pulsed UV-A phototherapy ( PUVA ) has helped the tegument and articulations of some HIV-infected persons with psoriatic arthritis. Antiretroviral intervention has besides been found to be helpful.
In a prospective survey among all new admitted patients with infected arthritis, 79 % were HIV-1 seropositive. Gonococcal arthritis was found in 4 patients, all HIV positive. Non-gonococcal bacterial arthritis was established in 16 patients, of whom 13 were HIV positive. Causative beings involved in this group were: Staphylococcus aureus, Streptococcus pneumoniae, Salmonella group B, Streptococcus group D, Klebsiella pneumoniae, and mycobacteria. Among untypical mycobacteria species, most normally implicated are Mycobacterium avium intracellulare complex, M. kansasii, M. haemophilum, M. terrae, and M. fortuitum. Septic arthritis due to Haemophilus influenzae has besides been described in a HIV-infected patient.[ 70 ]Fungal infections like Candida albicans besides can attest with oligoarthritis or polyarthritis. Therefore, HIV-1 infection appears as a hazard factor for infected arthritis patients, but it can non be used as a forecaster for HIV-1 infection for hospitalized patients. Septic arthritis occurs infrequently, and may show at any phase of HIV infection.[ 71 ]
Avascular mortification or osteonecrosis normally affecting the femoral caput, has been reported in patients with HIV infection with or without other hazard factors like steroid therapy or radiation therapy. The exact incidence is non known. It is postulated that either HIV-induced vasculopathy or HIV-associated antiphospholipid antibodies may be causal factor ensuing in this status. Typically patient nowadayss with hip hurting. But increasing usage of MRI has revealed symptomless subclinical instances besides.[ 72 ],[ 73 ]
A whole spectrum of vasculitides has been described in patients with HIV infection. In one survey, 23 % patients with diagnostic disease had vasculitis.[ 74 ]The vasculitides associated with HIV are normally non dangerous, and present as a individual flair instead than a relapsing unwellness. A broad spectrum with inflammatory diseases has been described in patients of HIV infection.
Lesions included in these are hypersensitivity vasculitis, polyarteritis nodosa, and Henoch Schonlein peliosis, others being Kawasaki disease, elephantine cell arteritis, Wegener ‘s granulomatosis, and isolated angiitis of cardinal nervous system, small-vessel vasculitis, and inflammatory lung disease.[ 75 ],[ 76 ],[ 77 ]. Corticosteroids remain the pillar of intervention, although cytotoxic drugs besides have been employed in furnace lining instances.
Vasculitis ensuing from CMV ( CMV ) infection can ensue in outstanding GI and cutaneal manifestations and its inclusion organic structures can be demonstrated microscopically. In such instances, ganciclovir or foscarnet should be started and any attendant immunosuppressive therapy reduced.[ 78 ]
Natural Course of Other Rheumatological Diseases in HIV Infection
One of the biggest paradoxes of HIV infection is the determination of certain arthritic diseases such as the DILS, reactive arthritis, Reiter ‘s syndrome, or inflammatory myopathy happening in the face of immunodeficiency. Alternatively, other arthritic diseases such as arthritic arthritis and systemic lupus erythematosus have been reported as bettering in the face of the CD4 lymphocytes depletion associated with this disease.
Initial surveies indicated that rheumatoid arthritis underwent a remittal with progressing HIV infection.[ 79 ],[ 80 ]Subsequently, surveies have indicated that active rheumatoid arthritis can coexist with HIV infection.[ 81 ]Systemic lupus erythematosus has been reported to coexist with HIV infection.[ 82 ],[ 83 ]Initially, it was suggested that HIV infection could cut down lupus activity. Other surveies have demonstrated that certain subsets of patients have a more rapid diminution in the CD4 counts with rapid patterned advance to clinical AIDS.[ 84 ]
Last the undermentioned arthritic conditions have besides been associated with intervention with protease inhibitors: adhesive capsulitis, Dupuytren ‘s contracture, and tendosynovitis of manus and pess.[ 85 ]
Immune Reconstitution Inflammatory Syndrome
Immune reconstitution inflammatory syndrome ( IRIS ) is a aggregation of inflammatory upsets doing with self-contradictory deterioration of preexistent infective procedures following the induction of antiretroviral therapy in HIV patients.[ 86 ],[ 87 ],[ 88 ],[ 89 ]. A figure of autoimmune and musculoskeletal manifestations have been reported to happen during IRIS. These include ego restricting musculoskeletal characteristics like arthralgia and myodynia and sometimes transeunt synovitis. Sometimes flair of systemic arthritic diseases like SLE, RA, polymyositis have besides been reported to happen.[ 90 ],[ 91 ],[ 92 ].
ROLE OF DMARDs AND IMMUNOSUPPRESSIVES IN THE MANAGEMENT OF INFLAMMATORY RHEUMATIC DISEASES ASSOCIATED WITH HIV INFECTION
As mentioned above disease modifying antirheumatic drugs and other biological response qualifiers are non contraindicated in intervention of systemic arthritic diseases associated with HIV infection. But the same are to be used with cautiousness in position of hazard of immunosuppression, attendant timeserving infections and hazard of patterned advance of HIV infection.[ 93 ]A figure of studies of successful usage of sulfasalazine, amethopterin, and cyclosporine in HIV associated arthritic diseases have led to increasing and earlier usage of disease agents.[ 94 ],[ 95 ],[ 96 ],[ 97 ]. In add-on Remicade and Enbrel which are anti-TNF biologic response qualifiers have been found to be safe in HIV associated arthritic arthritis and spondyloarthropathies. However, in developing states like India utmost cautiousness is to be exercised due to high prevalence of TB in the community and due to the fact that incidence of TB is increased multiplex both due to HIV infection and anti-TNFI± usage ( dual hazard ) .[ 98 ],[ 99 ],[ 100 ].
HIV infection is associated with a figure of musculoskeletal diseases both inflammatory and non-inflammatory. Extensive and earlier usage of antiretroviral therapy has altered the profile of arthritic manifestations. While there has been important lessening in inflammatory spondyloarthropathies and other inflammatory arthritis, certain arthritic diseases like osteonecrosis, osteopenia and immune reconstitution inflammatory syndrome are progressively being recognized. Due to better endurance and increasing prevalence of HIV infections, the profile of arthritic diseases will go on to germinate and rheumatologists need to be cognizant of this in future.