PMC3368228_01
Etiology of tumor lysis syndrome. TACE: transarterial chemoembolization. Others include surgery, bisphosphonates, radiofrequency, combination of different cancer therapies.
CRIM2012-468452.001.jpg
PMC3368228_01_CRIM2012-468452.001.jpg
fig1
In the setting of a malignancy with a high proliferation rate, large tumor burden, and/or high sensitivity to treatment, initiation of anticancer treatment, such as chemotherapy, radiotherapy, resective surgical procedures, immunotherapy, hormonotherapy, radiofrequency ablation, or sometimes glucocorticoid therapy alone may result in the rapid lysis of tumor cells (Table 1) (Figure 1). In addition, TLS can occur spontaneously from the tumor necrosis prior the onset of anticancer therapy (Table 1) (Figure 1).  TLS in solid tumors were chemotherapy-induced, even though various other causes were pointed out for TLS in solid tumors as well (Table 1) (Figure 1). The dominant factor for developing TLS in solid tumors, which occurred in all 100 cases, was having a large tumor burden.
Reported cases of tumor lysis syndrome in solid tumors.
CRIM2012-468452.002.jpg
PMC3368228_01_CRIM2012-468452.002.jpg
fig2
According to the literature review, there have been 100 reported cases of TLS in patients with solid tumors from the first report in 1977 to 2011 (Table 1) (Figure 2), including small cell carcinomas, squamous cell carcinomas, adenocarcinomas of the lung, mixed small cell and nonsmall cell lung carcinoma, gastrointestinal carcinomas, hepatoblastomas, hepatocellular carcinomas, renal carcinomas, transitional cell carcinoma, prostate carcinomas, breast carcinomas, ovarian carcinomas, endometrial carcinoma, vulva carcinomas, thymomas, melanomas, gestational trophoblastic neoplasia, germ cell tumors, neuroblastomas, medulloblastomas, and sarcomas.
EKG from the patient's admission showing atrial fibrillation with rapid ventricular response and peaked T waves.
CRIM2012-468452.003.jpg
PMC3368228_01_CRIM2012-468452.003.jpg
fig3
An EKG demonstrated atrial fibrillation with rapid ventricular response, left anterior fascicular block, and peaked T waves (Figure 3).
Mechanism of action of hypouricemic agents. Hyperuricemia is a consequence of the catabolism of purine nucleic acids to hypoxanthine and xanthine and then to uric acid via the enzyme xanthine oxidase. Allopurinol is a competitive inhibitor of the enzyme xanthine oxydase. Rasburicase (exogenous urate oxidase) leads uric acid to a more soluble compound, allantoin.
CRIM2012-468452.004.jpg
PMC3368228_01_CRIM2012-468452.004.jpg
fig4
Allopurinol is a competitive inhibitor of xanthine oxidase (Figure 4), and it has been successfully prescribed for the treatment of hyperuricemia. TLS who have been prescribed allopurinol may develop xanthine precipitation leading to acute renal failure. This can be avoided by replacing allopurinol with urate oxidase, which catabolizes uric acid to the more soluble compound allantoin (Figure 4).