A pilot multifaceted gout management program can significantly improve primary care gout management performance.
A 71-year-old male presented to the emergency department (ED) for worsening right knee pain for the prior 3–4 weeks. Point-of-care ultrasound (POCUS) of the right knee showed a pseudo-double contour sign. Subsequent ultrasound-guided arthrocentesis of the knee joint was performed, and fluid studies showed the presence of calcium pyrophosphate crystals, which was consistent with pseudogout. Ultrasound for detection of calcium pyrophosphate crystals in pseudogout and chondrocalcinosis has sensitivity of 86.7% and specificity of 96.4% making POCUS a valuable tool for diagnosing crystalline-induced arthropathy in the ED.
Drug-induced antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) has been increasingly recognized in the literature with numerous medications listed as causative agents in disease pathology. Doxycycline is a commonly prescribed medication within the United States which is a synthetic, broad-spectrum antibiotic with antimicrobial properties and at low doses exhibits anti-inflammatory effects. In this report, we describe a case of doxycycline-induced ANCA-associated vasculitis with laboratory and biopsy findings supporting the diagnosis, which to the best of our knowledge is the first described case of doxycycline-induced AAV in the literature. The patient was started on doxycycline for treatment of potential Lyme disease. She began to develop progressively worsening myasthenia, erythematous macular rash, anorexia, anemia, and fatigue for several weeks following the course of doxycycline with initial concern of a paraneoplastic process. Ultimately, the patient was discovered to be positive for antinuclear antibody (ANA), perinuclear antineutrophil cytoplasmic antibody (pANCA), and myeloperoxidase (MPO) antibody for which she was treated with a course of prednisone leading to complete remission of disease. A brief review of the pathogenesis of ANCA vasculitides will also be discussed within this article.
A 45-year-old Asian man with a 20-year history of gout is seen in clinic after lost to follow up for 10 years. He was previously treated with allopurinol but had been off therapy for many years. He describes several weeks of nasal bridge swelling with new episodes of snoring and apnea. On exam, he has a tender, erythematous mass over dorsum of nose with bulky tophi of multiple joints on hands, elbows, knees, and feet. Point-of-care ultrasound of his nasal bridge shows an area of inhomogeneous, hyperechoic aggregation with a hypoechoic rim consistent with gouty tophus [1]. Sinus CT without contrast shows a soft tissue partially calcified mass with bilateral nasal bone erosions. His uric acid was 12.6 mg/dl. This case is a rare presentation of gouty tophi causing nasal bone erosions. The patient tested negative for hereditary enzyme deficiencies. He did test positive for HLA-B*5801 putting him at risk for allopurinol hypersensitivity syndrome. He was treated with febuxostat and eventually pegloticase infusions. With urate lowering therapy, his nasal mass size decreased, and apnea improved without need for surgical intervention (Fig. 1).
Introduction: Gout is an inflammatory, metabolic disease associated with a high comorbidity burden including cardiovascular disease, hypertension, type 2 diabetes, hyperlipidemia, renal disease, and metabolic syndrome. Approximately 9.2 million Americans have gout, making prognosis and treatment outcome predictors highly important. About 600,000 Americans have early-onset gout (EOG), generally defined as first gout attack at B 40 years of age. However, data on EOG clinical features, comorbidity profile, and treatment response are sparse; this systematic literature review provides insight. Methods: PubMed and American College of Rheumatology (ACR)/European Alliance of the Associations for Rheumatology (EULAR) abstract archives were searched for early-onset gout, ''early onset gout,'' and (''gout'' AND ''age of onset''). Duplicate, foreign language, single case report, older (before 2016), and irrelevant/data insufficient publications were excluded. The age of diagnosis categorized patients as having common gout (CG, generally [ 40 years) or EOG (generally B 40 years). Applicable publications were extensively reviewed/discussed among authors for inclusion/exclusion consensus. Results: A total of 283 publications were identified, with 46 (35 articles, 10 abstracts) reviewed and 17 (12 articles, 5 abstracts) ultimately included. Eleven reported clinical characteristics, with 6 EOG-CG retrospective/crosssectional comparisons. Gout diagnosis preceded cardiometabolic comorbidity and renal comorbidities were less prevalent in EOG than CG patients. EOG patients had more severe disease (more gout flares, polyarticular disease), higher pre-therapy serum urate (SU), and worse oral urate-lowering therapy response. Genetics-focused publications reported higher incidences of dysfunctional urate transporter mutations in EOG patients. Conclusions: This review suggests that EOG is more recalcitrant to urate-lowering therapy, is associated with urate transporter defects, and carries heavy disease burden. Therefore, early rheumatology referral and urate-lowering in a treat-to-target fashion may benefit EOG patients. Interestingly, EOG patients had fewer cardiometabolic comorbidities at diagnosis than CG patients, presenting a potential ''window of opportunity'' to attenuate cardiometabolic comorbidity development with SU control. Preventing gout-related suffering
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