Abstract

Tumour lysis syndrome (TLS) is a group of pathophysiological processes caused by rapid degradation of tumour cells with subsequent release of intracellular contents into the extracellular space. It is characterized by the development of systemic metabolic disturbances with or without clinical manifestations. The process usually occurs in highly proliferative, large tumours after induction of cytotoxic therapy. Rarely, however, spontaneous TLS can develop, as well as signs of multiorgan failure triggered by an excessive metabolic load and sterile inflammation. The combination of the aforementioned is thus quite unique. Here, we present a 63-year-old male in which spontaneous TLS was accompanied with acute liver failure and delineated underlying nonHodgkin lymphoma. Initial laboratory findings included hyperkalaemia, hyperphosphataemia, hypocalcaemia, uraemia, and increased creatinine levels indicating the onset of TLS with acute kidney injury. Moreover, the patient showed signs of jaundice, coagulopathy, and hepatic encephalopathy. Development of TLS with multiorgan failure prompted rapid initiation of critical care management, including vigorous intravenous fluid therapy, allopurinol treatment, high flow continuous venovenous haemodiafiltration, and commencement of chemotherapy. The case highlights the possibility of TLS as a differential diagnosis in patients presenting with multiorgan failure and the importance of early detection of this potentially challenging and fatal diagnosis.

Highlights

  • Tumour lysis syndrome (TLS) is a group of pathophysiological processes that occur when tumour cells start to rapidly degrade [1,2,3]. e subsequent release of intracellular contents into the extracellular space and blood typically leads to systemic metabolic disturbances with or without clinical manifestations [1,2,3]. e syndrome usually develops in patients with highly proliferative tumours, a relatively large tumour burden, and a high sensitivity to cytotoxic therapy, such as haematologic malignancies [1,2,3,4]

  • Hyperkalaemia and hyperphosphataemia are a result of their release from rapidly lysed tumour cells, hypocalcaemia is related to hyperphosphataemia with precipitation of calcium phosphate in so tissues, and uric acid represents the end-metabolic product of purines from nucleic acids [2, 7,8,9]

  • In the case presented here, the patient did not have a diagnosed malignancy at the presentation. It was a specific laboratory pattern consisting of hyperkalaemia, hypocalcaemia, upper limit values of phosphates, and high Lactate dehydrogenase (LDH) levels together with a retroperitoneal mass of undetermined characteristics, (a)

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Summary

Case Report

Acute Liver Failure as the Leading Manifestation of Spontaneous Tumour Lysis Syndrome in a Patient with NonHodgkin Lymphoma: Do Current Diagnostic Criteria of Tumour Lysis Syndrome Need Re-Evaluation?. Tumour lysis syndrome (TLS) is a group of pathophysiological processes caused by rapid degradation of tumour cells with subsequent release of intracellular contents into the extracellular space. It is characterized by the development of systemic metabolic disturbances with or without clinical manifestations. Development of TLS with multiorgan failure prompted rapid initiation of critical care management, including vigorous intravenous uid therapy, allopurinol treatment, high ow continuous venovenous haemodia ltration, and commencement of chemotherapy. Development of TLS with multiorgan failure prompted rapid initiation of critical care management, including vigorous intravenous uid therapy, allopurinol treatment, high ow continuous venovenous haemodia ltration, and commencement of chemotherapy. e case highlights the possibility of TLS as a di erential diagnosis in patients presenting with multiorgan failure and the importance of early detection of this potentially challenging and fatal diagnosis

Introduction
Conjugated bilirubin
Coagulation tests
Findings
Discussion
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