This site is intended for healthcare professionals

Go to /sign-in page

You can view 5 more pages before signing in

Tumour lysis syndrome

Authoring team

Acute tumour lysis syndrome (ATLS) can be described as a group of metabolic abnormalities which include hyperuricaemia, hyperphosphataemia, hyperkalaemia, hypocalcaemia and renal failure (1).

  • can be due to spontaneous or treatment-mediated cell destruction (2)

The tumour lysis syndrome:

  • generally occurs in patients with lymphoproliferative malignancies, most often after initiation of treatment

  • pathophysiology of tumour lysis syndrome involves massive tumor cell lysis - this leads to the release of large amounts of potassium, phosphate, and uric acid

  • deposition of uric acid and calcium phosphate crystals in the renal tubules may cause acute renal failure, which is often exacerbated by concomitant intravascular volume depletion. These products are normally renally excreted - therefore preexisting renal failure exacerbates the metabolic derangements of tumor lysis syndrome

  • most commonly occurs after initiation of cytotoxic chemotherapy in patients with acute lymphoblastic leukemia and high-grade lymphomas like Burkitt’s lymphoma (4)

Reference:


Create an account to add page annotations

Annotations allow you to add information to this page that would be handy to have on hand during a consultation. E.g. a website or number. This information will always show when you visit this page.

The content herein is provided for informational purposes and does not replace the need to apply professional clinical judgement when diagnosing or treating any medical condition. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions.

Connect

Copyright 2024 Oxbridge Solutions Limited, a subsidiary of OmniaMed Communications Limited. All rights reserved. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions receives funding from advertising but maintains editorial independence.