Joint, bone, spine : revue du rhumatisme
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Many medications have been evaluated for the treatment of nonspecific low back pain. The only medications proven to be more effective than a placebo in chronic low back pain are nonsteroidal antiinflammatory drugs (NSAIDs), the acetaminophen-tramadol combination, antidepressants other than selective serotonin reuptake inhibitors, and some types of spinal applications of glucocorticoids or local anesthetics. However, the efficacy of these drugs in inducing pain relief is limited, and NSAIDs are the only drugs that also improve function. ⋯ In addition, treatment effects vary dramatically across studies. One factor in this variability is the heterogeneity of patient populations. To improve the uniformity of patient populations enrolled in therapeutic trials, the selection criteria should take into account the nociceptive, dysfunctional, and possible neuropathic components of the pain syndrome.
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TNF-α antagonist therapy is associated with a risk of severe, extrapulmonary, disseminated tuberculosis, which is fatal in 10% of cases. The risk of tuberculosis is increased four-fold in patients on TNF-α antagonist therapy. The main risk factors are a history of untreated or inadequately treated primary tuberculosis, recent contact with a tuberculosis patient, and residence in or travel to a high-endemicity region. ⋯ However, the accuracy of IGRAs for diagnosing latent tuberculosis remains unknown, because no reference standard is available. In addition, patients taking immunosuppressant agents to treat systemic disease may exhibit anergia, which complicates the interpretation of IGRAs. Until additional data become available, caution requires that IGRAs be used only when a positive or negative result, as assessed on a case-by-case basis, will help to decide whether tuberculosis chemoprophylaxis is in order.
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Review Case Reports
Paradoxical exacerbation of tuberculosis after TNFα antagonist discontinuation: beware of immune reconstitution inflammatory syndrome.
Paradoxical worsening of tuberculosis associated with immune reconstitution during antiretroviral therapy in patients with HIV infection is known as the immune reconstitution inflammatory syndrome (IRIS). Here, we report a case of paradoxical worsening of IFN-alpha induced tuberculosis in a patient experiencing reconstitution of pathogen-specific immune responses after discontinuing TNFα antagonist therapy. This case serves to alert clinicians that complications such as tuberculosis may worsen after TNFα antagonist discontinuation. This situation may paradoxically require readministration of the immunosuppressive drug in some patients.
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Gout results from elevated urate concentrations in the blood (hyperuricaemia). When super-saturation of urate is reached, monosodium urate crystals form within the joint. In some individuals, these crystals elicit a painful self-limiting inflammatory response that is characteristic of acute gouty arthritis. ⋯ Genome-wide association scans for genes regulating serum urate concentrations have identified two major regulators of hyperuricaemia- the renal urate transporters SLC2A9 and ABCG2. The risk variants at each gene approximately double the risk for gout in people of Caucasian ancestry, with SLC2A9 also resulting in higher risk for gout in people of Polynesian ancestry, a diverse population characterized by a high prevalence of gout. Ongoing genetic association studies are identifying and confirming other genes controlling serum urate concentrations; although genome-wide association studies in gout per se await recruitment of suitable case sample sets.