Spontaneous Tumour Lysis Syndrome Following Untreated Metastatic Colorectal Adenocarcinoma, a Case Report


Benjamin Reardon*1, Andrea Knox1, Cecily Forsyth1, Syapiq Long2
1 Haematology Department, Central Coast Local Health District NSW Australia, University of Newcastle
2 Haematology Department, Hunter New England Health District NSW Australia

Article Information

*Corresponding Author: Benjamin Reardon, Haematology Department, Central Coast Local Health District NSW Australia, University of Newcastle.

Received: April 20, 2021
AcceptedApril 30, 2021
Published: May 10, 2021

Citation: Benjamin Reardon, Andrea Knox, Syapiq Long, Cecily Forsyth. (2021) “Spontaneous tumour lysis syndrome following untreated metastatic colorectal adenocarcinoma, a case report”, J Oncology and Cancer Screening, 2(5); DOI: http;//doi.org/04.2021/1.1021.
Copyright: © 2021 Benjamin Reardon. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We report a case of the spontaneous tumour lysis syndrome in untreated metastatic colorectal adenocarcinoma. Tumour lysis syndrome is normally associated with haematological malignancies. A previously well 65-year-old Caucasian male presented with confusion after a recent diagnosis of metastatic colorectal cancer. He was found to have clinical and laboratory findings consistent with tumour lysis syndrome, and was managed aggressively as such. The recognition of spontaneous tumour lysis syndrome in solid tumours is important to prevent diagnostic delays and ensure appropriate therapy


tumour lysis syndrome, colorectal, metastasis, solid tumour, adenocarcinoma


Tumour lysis syndrome (TLS) is a group of metabolic derangements resulting from the release of large amounts of cellular components into the circulation due to the rapid lysis of malignant cells [1]. It is frequently observed following treatment of high-grade haematological malignancies, but only rarely associated with treatment of non-haematological solid tumours [2,3]. Spontaneous TLS prior to the initiation of therapy has been described in solid organ malignancies, although rare [4]. We report a case of spontaneous laboratory and clinical TLS in a patient who presented with untreated metastatic colorectal cancer.

Case Report/Case Presentation:

A 65-year-old Caucasian male presented to the emergency department with a history of increasing confusion. Two weeks prior, abnormal liver function tests (LFTs) were noted on blood tests performed to investigate lethargy. This was followed by an abdominal ultrasound which showed hepatic lesions suspicious for malignant metastases. A CT abdomen and pelvis suggested likely metastatic colorectal cancer with irregular mural thickening of the sigmoid colon and multiple heterogenous deposits in an enlarged liver (Figure 1).

Figure Legends:

Figure 1: Non-obstructive irregular focal thickening of the sigmoid colon.

Prior to further investigation, he presented to hospital with worsening confusion over three days. His initial investigations demonstrated significant metabolic and hepatic derangement with no intracranial abnormalities. Blood results showed hyperphosphataemia 2.42 mmol/L (normal range 0.75-1.5), hyperkalaemia 5.7 mmol/L (3.5-5.2), hyperuricaemia 1.03 mmol/L (0.24-0.48), hypocalcaemia 1.48 mmol/L (corrected 1.96 mmol/L, 2.10-2.60) and a raised LDH 4716 U/L (120-250) and creatinine 221 umol/L (60-110). The patient’s tumour markers were also deranged including CEA 2990.8 ug/L (<5); CA19-9 7027 kU/L (<37); CA125 164 kU/L (<35). LFTs continued to be deranged with a predominantly obstructive pattern (bilirubin 56 μmol/L [3-20]; albumin 16 g/L [35-52]; protein 41 g/L [60-80]; ALP 310 U/L (30-110); GGT 283 U/L [9-36]; AST 114 U/L [12-36], ALT 13 U/L [<55]). He also had a significant leucocytosis of 36.2 x 10^9/L (4.0-11.0) with a neutrophilia 33.2 x 10^9/L (2.0-8.0) and normocytic anaemia Hb 122 g/L (130-180). Two months prior his baseline creatinine and potassium were 70 umol/L and 3.9 umol/L, respectively.

Sigmoidoscopy revealed an ulcerated, partially circumferential non-obstructing mass in the sigmoid colon. Histopathology confirmed this as adenocarcinoma of colorectal origin (KRAS, CK20, CDX2 and BER-EP4 stain positive; patchy positive for CEA; and negative for P40, CK5/6, p63). Molecular testing and cytogenetics were unsuccessful due to inadequate yield. The immunohistochemistry of this patient’s adenocarcinoma was negative for the BRAF V600E mutation, and RAS gene mutation analysis showed a KRAS missense mutation.

The patient was diagnosed with spontaneous tumour lysis syndrome and admitted to the high dependency unit. He received aggressive diuresis and measures to correct his electrolyte and acid-base abnormalities. Rasburicase followed by allopurinol was used to manage hyperuricaemia. The patient’s hyperkalaemia improved, however his acute kidney injury and hepatic dysfunction continued to worsen despite treatment. Unfortunately the patient continued to deteriorate, both clinically and biochemically, and it was decided he was not for further intervention. The patient died in peace and dignity surrounded by his immediate family 9 days after hospital presentation.

Discussion and Conclusion:

This patient fulfilled the Cairo-Bishop criteria for spontaneous laboratory and clinical TLS with the diagnosis of metastatic colorectal cancer [5,6]. There was no evidence of risk factors for TLS including haemolysis, haematological malignancy, or metastatic renal invasion. Additionally he had no previous history of gout, thyroid or parathyroid disease, pre-existing kidney disease, diabetes or alcohol abuse.

TLS has been described as a rare complication of solid tumours, predominantly after therapy has been commenced [3]. We have found one report of untreated colorectal cancer presenting with spontaneous TLS [7], and one of adenocarcinoma of likely gastrointestinal origin [8]. The first documents a widespread mucinous adenocarcinoma in a young patient who presented in TLS and received one cycle of lymphoma-directed immunochemotherapy prior to the diagnosis of adenocarcinoma being established. The second, in 1977, describes a post-mortem diagnosis of TLS in a male with untreated anaplastic adenocarcinoma of likely gastrointestinal tract primary, who presented with acute renal failure. Within gastrointestinal malignancies there are other case reports, including two of gastric adenocarcinoma [9,10], and one of hepatocellular carcinoma [3]. This supports the notion that haematological malignancy is certainly not the only cause of TLS. The other reports of spontaneous solid tumour TLS have common the themes of a large burden of disease and an extremely poor prognosis [11]. Reports in cases where patients survived either did not met the criteria for laboratory TLS or were clearly associated with chemotherapy [3,12].

TLS is commonly associated with high-grade haematological malignancies, either occurring spontaneously or most frequently following treatment. There are only infrequent reports of TLS in association with non-haematological solid tumours and the majority of these describe post-therapy TLS rather than spontaneous TLS. The outlook for patients who present with spontaneous TLS due to a non-haematological solid tumour is dire but might improve if the diagnosis is made early and appropriate corrective measures introduced. Understanding that TLS can be due to solid tumours will aid correct diagnosis and cancer-specific therapy.


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