Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 85-year-old man was admitted to our hospital for swollen and painful bilateral lower legs and a high fever. He was initially diagnosed with acute cellulitis and treated with antibiotics. Several days after the improvement of his swollen legs, he complained of both shoulder and arm pain. The laboratory data at this time were as follow: C-reactive protein 10.7 mg/dL, uric acid 8.7 mg/dL, and creatinine 1.07 mg/dL. Both rheumatoid factor and anti-CCP antibody were negative. Whole-body gallium scintigraphy showed a high pathological accumulation in both the shoulders and left wrist. As polymyalgia rheumatica was suspected, oral prednisolone (PSL) of 10 mg/day was started. The patient's shoulder pain improved and he was discharged. However, he was hospitalized twice in the next month because of left shoulder, left knee, right arm, and right wrist pain. During the third hospitalization, we found a subcutaneous nodule on right toe. Aspiration material from the nodule was a white paste, showing acicular crystals under the microscope. According to these findings, the nodule was diagnosed as a tophaceous nodule, and recurrent episodes of polyarthritis were diagnosed as chronic tophaceous gout. Low-dose PSL was continued and febuxostat was added. This patient had multiple risk factors for chronic tophaceous gout: obesity, a habit of drinking, diabetes mellitus, hyperlipidemia, congestive heart failure, and interruption of allopurinol treatment. We herein discuss the clinical course of the patient, the interruption of allopurinol treatment and polypharmacy in elderly patients.
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PMID:[An elderly man presenting polyarthritis diagnosed as chronic tophaceous gout]. 2670 Jul 82

Superficial bursitis most often occurs in the olecranon and prepatellar bursae. Less common locations are the superficial infrapatellar and subcutaneous (superficial) calcaneal bursae. Chronic microtrauma (e.g., kneeling on the prepatellar bursa) is the most common cause of superficial bursitis. Other causes include acute trauma/hemorrhage, inflammatory disorders such as gout or rheumatoid arthritis, and infection (septic bursitis). Diagnosis is usually based on clinical presentation, with a particular focus on signs of septic bursitis. Ultrasonography can help distinguish bursitis from cellulitis. Blood testing (white blood cell count, inflammatory markers) and magnetic resonance imaging can help distinguish infectious from noninfectious causes. If infection is suspected, bursal aspiration should be performed and fluid examined using Gram stain, crystal analysis, glucose measurement, blood cell count, and culture. Management depends on the type of bursitis. Acute traumatic/hemorrhagic bursitis is treated conservatively with ice, elevation, rest, and analgesics; aspiration may shorten the duration of symptoms. Chronic microtraumatic bursitis should be treated conservatively, and the underlying cause addressed. Bursal aspiration of microtraumatic bursitis is generally not recommended because of the risk of iatrogenic septic bursitis. Although intrabursal corticosteroid injections are sometimes used to treat microtraumatic bursitis, high-quality evidence demonstrating any benefit is unavailable. Chronic inflammatory bursitis (e.g., gout, rheumatoid arthritis) is treated by addressing the underlying condition, and intrabursal corticosteroid injections are often used. For septic bursitis, antibiotics effective against Staphylococcus aureus are generally the initial treatment, with surgery reserved for bursitis not responsive to antibiotics or for recurrent cases. Outpatient antibiotics may be considered in those who are not acutely ill; patients who are acutely ill should be hospitalized and treated with intravenous antibiotics.
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PMID:Common Superficial Bursitis. 2829 Jun 30

Cellulitis is a bacterial skin and soft tissue infection which occurs when the physical skin barrier, the immune system and/or the circulatory system are impaired. Diabetes, obesity and old age are associated with defects in all of these areas and as a result are major predisposing factors for cellulitis. In this review, we summarise current insights into the pathophysiology of cellulitis and place the Dutch guidelines on the clinical management of cellulitis of the lower extremities in perspective. Recent evidence on diagnostic strategies is discussed, the importance of which is underscored by findings that venous insufficiency, eczema, deep vein thrombosis and gout are frequently mistaken for cellulitis. Empiric antibiotic choices are designed against the background of a low prevalence of multi-resistant Staphylococcus aureus. Novel antimicrobial agents registered for cellulitis are also discussed. Relapses occur frequently due to a high prevalence of risk factors associated with cellulitis in combination with the ccurrence of persistent post-inflammatory lymphatic damage. Lastly, we identify knowledge gaps which, if addressed, will advance our understanding of the pathophysiology of cellulitis and improve its clinical management.
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PMID:Cellulitis: current insights into pathophysiology and clinical management. 2921 14

A 65-year-old Japanese man was admitted to our hospital with fever and inflammation of the right ankle. We initiated antibiotics on suspicion of cellulitis. After no clinical improvement, we performed magnetic resonance imaging, which showed a fluid collection in the flexor hallucis longus (FHL) tendon sheath. Synovial fluid analysis revealed monosodium uric crystals. Final diagnosis was FHL tendonitis secondary to gout proven by synovial fluid analysis. To our knowledge, this is the first case report of FHL tendonitis caused by gout. When ankle inflammation is examined in clinical situations, FHL tendonitis caused by gout should be considered.
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PMID:Gout in the Flexor Hallucis Longus Tendon Mimicking Cellulitis: A Case Report. 3207 28


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