Hyperuricemia

Changed by Hamish Smith, 30 Apr 2018

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HyperuricemiaHyperuricaemia
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HyperuricemiaHyperuricaemia is defined as elevated levels of uric acid (≥7 mg/dL) in the blood and may be caused by either urate over production or under excretion.

Clinical presentation

Patients with hyperuricemia may be asymptomatic or have symptoms and signs relating to one of the complications of hyperuricemiahyperuricaemia (eg. gout, nephrolithiasis).

Pathology

Uric acid is produced as the end product of purine nucleotide degradation. Hypoxanthine and xathine are the intermediates which are converted to uric acid via the enzyme xanthine oxidase. Uric acid is mostly excreted via the kidneys with the rest being excreted intestinally, but up to 90% is resorbed via the transporters URAT1 and GLUT9 in the kidneys 1,2. HyperuricemiaHyperuricaemia may result from urate under excretion, overproduction or a combination of both.

Causes:

Radiological features

No radiological features are specific for hyperuricemiahyperuricaemia. Signs of complications of hyperuricemiahyperuricaemia may be visible (eg. gout, nephrolithiasis).

Treatment and prognosis 

HyperuricemiaHyperuricaemia is treated by addressing the underlying cause of urate overproduction or under excretion, xanthine oxidase and URAT1 inhibitors are also commonly used 2. HyperuricemiaHyperuricaemia is a risk factor for cardiaccardiovascular disease and gout 2,3.

  • -<p><strong>Hyperuricemia </strong>is defined as elevated levels of uric acid (≥7 mg/dL) in the blood and may be caused by either urate over production or under excretion.</p><h4>Clinical presentation</h4><p>Patients with hyperuricemia may be asymptomatic or have symptoms and signs relating to one of the complications of hyperuricemia (eg. <a title="Gout" href="/articles/gout">gout</a>, <a title="Nephrolithiasis" href="/articles/urolithiasis">nephrolithiasis</a>).</p><h4>Pathology</h4><p>Uric acid is produced as the end product of purine nucleotide degradation. Hypoxanthine and xathine are the intermediates which are converted to uric acid via the enzyme xanthine oxidase. Uric acid is mostly excreted via the kidneys with the rest being excreted intestinally, but up to 90% is resorbed via the transporters URAT1 and GLUT9 in the kidneys <sup>1,2</sup>. Hyperuricemia may result from under excretion, overproduction or a combination of both.</p><h5>Causes:</h5><ul>
  • +<p><strong>Hyperuricaemia </strong>is defined as elevated levels of uric acid (≥7 mg/dL) in the blood and may be caused by either urate over production or under excretion.</p><h4>Clinical presentation</h4><p>Patients with hyperuricemia may be asymptomatic or have symptoms and signs relating to one of the complications of hyperuricaemia (eg. <a href="/articles/gout">gout</a>, <a href="/articles/urolithiasis">nephrolithiasis</a>).</p><h4>Pathology</h4><p>Uric acid is produced as the end product of purine nucleotide degradation. Hypoxanthine and xathine are the intermediates which are converted to uric acid via the enzyme xanthine oxidase. Uric acid is mostly excreted via the kidneys with the rest being excreted intestinally, but up to 90% is resorbed via the transporters URAT1 and GLUT9 in the kidneys <sup>1,2</sup>. Hyperuricaemia may result from urate under excretion, overproduction or a combination of both.</p><h5>Causes:</h5><ul>
  • -<li>Preeclampsia and eclampsia</li>
  • -<li>Sarcoidosis</li>
  • +<li>Preeclampsia and <a href="/articles/eclampsia">eclampsia</a>
  • +</li>
  • +<li><a href="/articles/sarcoidosis-1">Sarcoidosis</a></li>
  • -<li>Tumor lysis syndrome</li>
  • -<li>Haematological diseases (eg. hemolytic anaemia, lymphoma, leukemia)</li>
  • +<li><a href="/articles/tumor-lysis-syndrome">Tumor lysis syndrome</a></li>
  • +<li>Haematological diseases (eg. <a href="/articles/haemolytic-anaemia">hemolytic anaemia</a>, <a href="/articles/lymphoma">lymphoma</a>, leukemia)</li>
  • -</ul><h4>Radiological features</h4><p>No radiological features are specific for hyperuricemia. Signs of complications of hyperuricemia may be visible (eg. gout, nephrolithiasis).</p><h4>Treatment and prognosis </h4><p>Hyperuricemia is treated by addressing the underlying cause of urate overproduction or under excretion, xanthine oxidase and URAT1 inhibitors are also commonly used <sup>2</sup>. Hyperuricemia is a risk factor for cardiac disease and gout <sup>2,3</sup>.</p>
  • +</ul><h4>Radiological features</h4><p>No radiological features are specific for hyperuricaemia. Signs of complications of hyperuricaemia may be visible (eg. gout, nephrolithiasis).</p><h4>Treatment and prognosis </h4><p>Hyperuricaemia is treated by addressing the underlying cause of urate overproduction or under excretion, xanthine oxidase and URAT1 inhibitors are also commonly used <sup>2</sup>. Hyperuricaemia is a risk factor for cardiovascular disease and gout <sup>2,3</sup>.</p>

References changed:

  • 1. Enomoto A, Kimura H, Chairoungdua A, Shigeta Y, Jutabha P, Cha SH, Hosoyamada M, Takeda M, Sekine T, Igarashi T, Matsuo H, Kikuchi Y, Oda T, Ichida K, Hosoya T, Shimokata K, Niwa T, Kanai Y, Endou H. Molecular identification of a renal urate anion exchanger that regulates blood urate levels. (2002) Nature. 417 (6887): 447-52. <a href="https://doi.org/10.1038/nature742">doi:10.1038/nature742</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/12024214">Pubmed</a> <span class="ref_v4"></span>
  • 2. Gliozzi M, Malara N, Muscoli S, Mollace V. The treatment of hyperuricemia. (2016) International journal of cardiology. 213: 23-7. <a href="https://doi.org/10.1016/j.ijcard.2015.08.087">doi:10.1016/j.ijcard.2015.08.087</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/26320372">Pubmed</a> <span class="ref_v4"></span>
  • 3. Erick Prado de Oliveira, Roberto Carlos Burini. High plasma uric acid concentration: causes and consequences. (2012) Diabetology & Metabolic Syndrome. 4 (1): 12. <a href="https://doi.org/10.1186/1758-5996-4-12">doi:10.1186/1758-5996-4-12</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/22475652">Pubmed</a> <span class="ref_v4"></span>

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  • Musculoskeletal

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  • hyperuricaemia

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