Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gouty arthritis, one of the most painful and common forms of adult arthritis, is caused by monosodium urate crystal deposits in joints, most often in the lower extremities. Crystals trigger an inflammatory response leading to acute flares characterized by a rapid onset of pain, warmth, swelling, and redness in involved joints. Over time, continued monosodium urate crystal deposits and inflammation can lead to chronic tophaceous gout that result in bone erosion, progressing to joint destruction and significant disability. The goal of therapy in an acute gout flare is prompt and safe termination of pain and inflammation. Acute gouty arthritis is usually treated with nonsteroidal anti-inflammatory drugs, colchicine, or corticosteroids. However, for a growing number of patients, current standard treatments are ineffective or are contraindicated, largely due to the presence of comorbidities. Gouty arthritis can have a major negative impact of health-related quality of life, especially in patients with difficult-to-treat disease, as revealed by recent studies comparing health-related quality of life with that of the general population. Additionally, gouty arthritis also constitutes an important economic burden through absence from work and medical costs. This burden is even greater in patients with difficult-to-treat disease.
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PMID:The Human and Economic Burden of Difficult-to-Treat Gouty Arthritis. 2671 99

We present an elderly diabetic man with left hallux pain and drainage who was initially diagnosed with acute gouty arthritis using the diagnostic rule for acute gout and monosodium urate crystals presented on synovial fluid analysis. Further investigation with surgical debridement, plain X-ray, MRI and wound culture revealed concomitant Citrobacter koseri septic arthritis with osteomyelitis. C. koseri is considered an opportunistic infection that rarely causes musculoskeletal infections. Acute gouty arthritis and septic arthritis are rarely seen occurring concomitantly in the same joint and are often difficult to differentiate due to similar findings on exam and imaging. The present case illustrates that osteomyelitis with an opportunistic organism can present concomitantly with acute gouty arthritis, and the diagnosis of one should not exclude the other.
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PMID:Citrobacter koseri causing osteomyelitis in a diabetic foot with concomitant acute gouty arthritis successfully treated with ertapenem. 3135 98

Acute gouty arthritis is an auto-inflammatory disease caused by the deposition of monosodium urate (MSU) crystals in joints or tissues. Excessive neutrophil recruitment into gouty lesions is a general clinical sign and induces a pain phenotype. Attenuation of successive periods of neutrophil infiltration might be a beneficial approach to achieve therapeutic efficacy. In this study, the activity of 1-palmitoyl-2-linoleoyl-3-acetyl-rac-glycerol (PLAG) in attenuation of excess neutrophil infiltration was assessed in gout-induced lesions of BALB/c mice. Neutrophil infiltration in MSU-induced gouty lesions was analyzed using immunohistochemical staining. ELISA and RT-PCR were used to measure attenuation of expression of the major neutrophil chemoattractant, CXC motif chemokine ligand 8 (CXCL8), in a PLAG-treated animal model and in cells in vitro. The animal model revealed massive increased neutrophil infiltration in the MSU-induced gouty lesions, but the PLAG-treated mice had significantly reduced neutrophil numbers in these lesions. The results also indicated that the MSU crystals stimulated a damage-associated molecular pattern that was recognized by the P2Y6 purinergic receptor. This MSU-stimulated P2Y6 receptor was destined to intracellular trafficking. During intracellular endosomal trafficking of the receptor, endosome-dependent signaling provided expression of CXCL8 chemokines for neutrophil recruitment. PLAG accelerated initiation of the intracellular trafficking of the P2Y6 receptor and returning the receptor to the membrane. This process shortened the intracellular retention time of the receptor anchoring endosome and subsequently attenuated endosome-dependent signaling for CXCL8 expression. These study results suggested that PLAG could be used for resolution of acute inflammation induced in gout lesions.
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PMID:1-Palmitoyl-2-Linoleoyl-3-Acetyl-rac-Glycerol (PLAG) Mitigates Monosodium Urate (MSU)-Induced Acute Gouty Inflammation in BALB/c Mice. 3239 18