{"id":9970,"date":"2022-01-08T12:30:32","date_gmt":"2022-01-08T10:30:32","guid":{"rendered":"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/metabolism\/hyperuricemia-and-gout\/"},"modified":"2022-01-08T13:47:43","modified_gmt":"2022-01-08T11:47:43","slug":"hyperuricemia-and-gout","status":"publish","type":"page","link":"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/metabolism\/hyperuricemia-and-gout\/","title":{"rendered":"Hyperuricemia and gout"},"content":{"rendered":"<span class=\"block-heading\" id=\"header_1\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Hyperuricemia<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_1\">\n\n\n<p class=\"wp-block-paragraph\">Hyperuricemia is an elevated uric acid level in the blood (>7mg\/dL).<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Uric acid is a product of pruine metabolism.<\/li><li>Hyperurecemia is manifested as <strong>gout<\/strong>, <strong>urate nephropathy<\/strong>, and <strong>nephrolithiasis<\/strong>.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_2\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Etiology<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_2\">\n\n\n<p class=\"wp-block-paragraph\">Hyperuricemia can be due to increased production, decreased excretion, or both.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Increased production<\/strong> <ul><li>Tumor lysis syndrome<\/li><li>Hemolysis<\/li><li>Rhabdomyolysis<\/li><li>HPRT deficiency<\/li><li>Purine-rich diet (meat, seafood, alcohol)<\/li><\/ul><\/li><li><strong>Decreased excretion<\/strong><ul><li>Acute\/chronic renal disease<\/li><li>Metabolic acidosis (keto\/lactic acidosis)<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_3\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Gout<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_3\">\n\n\n<p class=\"wp-block-paragraph\">Discussed below.<\/p>\n\n\n<\/span><span class=\"block-heading\" id=\"header_4\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Urate nephropathy and nephrolithiasis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_4\">\n\n\n<p class=\"wp-block-paragraph\">Urate excretion occurs mainly in the kidneys; uric acid crystals can be deposited in the tubular system, leading to urate nephropathy, and nephrolithiasis.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Acute urate nephropathy<\/strong>. Sudden uric acid deposition may cause occlusion and lead to acute kidney injury. <ul><li><strong>Etiology<\/strong>. Occurs predominantly due to <strong>tumor lysis syndrome<\/strong>.<\/li><li><strong>Treatment<\/strong>. IV fluids and allopurinol.<\/li><li><strong>Prevention<\/strong>. Use rasburicase prophylactically in case of treating tumors.<\/li><\/ul><\/li><li><strong>Chronic urate nephropathy<\/strong>. Chronic deposition of uric acid crystals due to chronic hyperuricemia leads to chronic tubulointerstitial nephritis.<ul><li>Presents with chronic inflammation and fibrosis, leading to renal insufficiency.<\/li><li><strong>Treatment<\/strong>. Uric acid reducing therapy (see <strong>Gout: treatment<\/strong> below).<\/li><\/ul><\/li><li><strong>Nephrolithiasis<\/strong>. Uric acid calculi are typically the result of acidic urine (pH &lt;5.5) due to chronic dehydration and diarrhea, or more rarely, <strong>hyperuricosuria<\/strong>, caused by excessive intake of purines.<ul><li>Uric acid calculi are radiolucent, meaning that they generally do not show up on x-ray or CT scans; they can be, however, visualized by using ultrasound.<\/li><li><strong>Treatment<\/strong>. Urinary stone treatment (analgesics, antispasmotics, opioids), and alkalization of the urine using potassium citrate.<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_5\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Gout<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_5\">\n\n\n<p class=\"wp-block-paragraph\">Gout is an inflammatory disease in which <strong>monosodium urate<\/strong> (MSU) crystals are deposited within joints and other extra-articular tissues.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Gout can be <strong>primary <\/strong>(most cases, appears in adult men) or <strong>secondary<\/strong> to metabolic or systemic disease, and certain drugs (thiazides, cyclosporin).<\/li><li><strong>Lesh-Nyhan syndrome <\/strong>is a rare, X-linked disorder caused by HPRT deficiency leading to the excessive degradation of purines into urate. Presents with mental retardation, and the consequences of hyperuricemia (gout, nephropathy).<\/li><li>Renal damage is a major complication of gout (urate nephropathy and nephrolithiasis).<\/li><li>Cold temperature, low pH, dehydration and injury can contribute to gouty inflammation. <\/li><li>Gout can manifest in sites of previous fractures.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_6\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Stages<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_6\">\n\n\n<ul class=\"wp-block-list\"><li><strong>Asymptomatic hyperuricemia<\/strong>. Urate level of &gt;8mg\/dL, clinically silent.<\/li><li><strong>Acute gouty arthritis<\/strong>. Presents as an inflammation of a single joint, typically of the 1st MTP joint. Sudden, severe pain and disability, reddening and swelling. Most frequently, associated with alcohol consumption. Resolves within days to weeks.<ul><li><strong>Intercritical gout<\/strong>. Refers to the symptom-free period in-between the gouty attacks. With time, these periods become shorter, as attacks become more frequent.<\/li><\/ul><\/li><li><strong>Chronic gout<\/strong>. Long-lasting, low-grade inflammation and structural changes, often involving the joints of the upper limb as well. Characterized by the formation of urate-containing masses (tophi) in the fingers, feet, external ear, and around tendons, but may also appear within organs (kidneys) and the skin.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_7\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_7\">\n\n\n<p class=\"wp-block-paragraph\">The ACR\/EULAR classification criteria use clinical, laboratory, and imaging investigations as a scoring system for the determination of gout.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Entry criteria: at least 1 episode of peripheral joint swelling, pain, or tenderness.<\/li><li>Complaints fitting the diagnosis of gout.<\/li><li>Serum urate, and synovial fluid analysis (gold standard).<\/li><li>US\/x-ray\/CT<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_8\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_8\">\n\n\n<ul class=\"wp-block-list\"><li>Lifestyle modification (avoid red meat, seafood, alcohol, sugary drinks) and control of co-morbidities (DM, HTN, CKD).<\/li><li>Acute attacks should be treated with <strong>colchicine <\/strong>(microtubule dimerization and neutrophil migration inhibitor) as soon as possible, along with an NSAID, systemic or local corticosteroids.<\/li><li><strong>Urate-lowering therapy<\/strong>, increasing the dose until the desired serum urea level is reached (see Table 1).<\/li><\/ul>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"pure-table\"><thead><tr><th>Group<\/th><th>Mechanism<\/th><th>Examples<\/th><\/tr><\/thead><tbody><tr><td>Xanthine oxidase inhibitors<\/td><td>Inhibit the synthesis of purine bases.<\/td><td>Allopurinol<br>Febuxostat (non-purine-based, safer)<\/td><\/tr><tr><td>Reabsorption inhibitors<\/td><td>Inhibit the reabsorption of uric acid in the kidney.<\/td><td>High-dose sulfinpyrazone<br>Probenecid<\/td><\/tr><tr><td>Recombinant uricases<\/td><td>Convert urate into allantoin, which is excreted in the stool. <br>Can only be used short-term in severe gout, as their efficacy decreases due to the production of antibodies.<\/td><td>Rasburicase<br>Pegloticase (longer half-life)<\/td><\/tr><\/tbody><\/table><figcaption><strong>Table 1. Treatment of gout<\/strong><\/figcaption><\/figure>\n\n\n<\/span><span class=\"block-heading\" id=\"header_9\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">References<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_9\">\n\n\n<p class=\"wp-block-paragraph\"><a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK459218\/\">https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK459218\/<\/a><\/p>\n<\/span><div id=\"the_titles\" style=\"display:none;\"><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Hyperuricemia<\/h3><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Etiology<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Gout<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Urate nephropathy and nephrolithiasis<\/h4><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Gout<\/h3><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Stages<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Diagnosis<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Treatment<\/h4><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">References<\/h3><\/div>","protected":false},"excerpt":{"rendered":"<p>Hyperuricemia Hyperuricemia is an elevated uric acid level in the blood (>7mg\/dL). Uric acid is a product of pruine metabolism. Hyperurecemia is manifested as gout, urate nephropathy, and nephrolithiasis. Etiology Hyperuricemia can be due to increased production, decreased excretion, or both. Increased production Tumor lysis syndrome Hemolysis Rhabdomyolysis HPRT deficiency Purine-rich diet (meat, seafood, alcohol) [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":9852,"menu_order":11,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-9970","page","type-page","status-publish","hentry"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.9 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Hyperuricemia and gout &#8211; Meddists<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/metabolism\/hyperuricemia-and-gout\/\" \/>\n<meta name=\"twitter:label1\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data1\" content=\"3 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/metabolism\\\/hyperuricemia-and-gout\\\/\",\"url\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/metabolism\\\/hyperuricemia-and-gout\\\/\",\"name\":\"Hyperuricemia and gout &#8211; 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