Tumor Lysis Syndrome

Etiology

The risk of tumor lysis syndrome is the highest in patients undergoing treatment for hematologic malignancies. Tumors most commonly associated with tumor lysis syndrome include clinically aggressive non-Hodgkin lymphomas, acute lymphoblastic leukemia, acute myeloid leukemia, and Burkitt lymphoma or Burkitt leukemia. These tumors have a high proliferative rate and demonstrate significant sensitivity to chemotherapy.[6] Other hematologic malignancies are less commonly associated with tumor lysis syndrome.

Solid tumors that can cause tumor lysis syndrome are small cell carcinoma of the lung, breast cancer, and neuroblastoma.[7][8][9][10] International panels of experts have stratified tumors based on the risk of developing tumor lysis syndrome.[11][12] Patients are generally categorized into 3 risk levels—high risk, where greater than 5% of patients develop tumor lysis syndrome; intermediate risk, with 1% to 5% of patients developing tumor lysis syndrome; and low risk, with fewer than 1% of patients developing tumor lysis syndrome. The tumors associated with each risk category include:

• High-risk tumors
  • Advanced Burkitt lymphoma
  • Acute lymphoblastic leukemia with a white blood cell count exceeding 100,000/µL or a lactate dehydrogenase level that is twice the upper limit of normal
  • Diffuse large B-cell lymphoma with bulky disease (>10 cm) and a baseline lactate dehydrogenase level greater than twice the upper limit of normal
  • Acute myeloid leukemia with a white blood cell count of 100,000/µL or more
  • Early-stage leukemia or Burkitt lymphoma with elevated lactate dehydrogenase

• Intermediate-risk tumors
  • Acute myeloid leukemia with a white blood cell count ranging from 25,000 to 100,000/µL
  • Acute lymphoblastic leukemia with a white blood cell count below 100,000/µL and lactate dehydrogenase levels less than twice the upper limit of normal
  • Diffuse large B-cell lymphoma with lactate dehydrogenase levels twice the upper limit of normal but without bulky disease
  • Early-stage leukemia or Burkitt lymphoma with lactate dehydrogenase levels below twice the upper limit of normal

• Low-risk tumors
  • Solid cancers
  • Multiple myelomas
  • Indolent lymphomas
  • Chronic lymphocytic leukemia
  • Chronic myeloid leukemia 
  • Acute myeloid leukemia with a white blood cell count of less than 25,000/µL and a lactate dehydrogenase elevated to less than twice the upper limit of normal

Tumors that exhibit greater sensitivity to chemotherapy agents are associated with an increased risk of tumor lysis syndrome. However, tumor lysis syndrome can also be associated with administering steroids, biological immunomodulators, and monoclonal antibodies.[13] Agents that are associated with the development of tumor lysis syndrome include thalidomide, bortezomib, hydroxyurea, paclitaxel, fludarabine, etoposide, venetoclax, rituximab, obinutuzumab, and chimeric antigen receptor T-cell therapy for hematologic malignancy.[14]

Several reports of tumor lysis syndrome occurring spontaneously before the initiation of chemotherapy have been documented in patients with non-Hodgkin lymphomas, acute leukemias, and breast cancer.[15] Unlike postchemotherapy tumor lysis syndrome, spontaneous tumor lysis syndrome is not associated with hyperphosphatemia. This distinction may be attributed to the high cell turnover rate in tumors, which increases uric acid levels while the tumor reutilizes the released phosphate to grow new cells. In contrast, postchemotherapy tumor lysis syndrome involves the destruction of tumor cells without the synthesis of new cells.[16] 

Certain patient factors can also predispose to an increased risk of tumor lysis syndrome. Patients at higher risk for tumor lysis syndrome include those with pretreatment hyperuricemia, preexisting renal issues, oliguria, and volume depletion. Impaired renal function significantly increases tumor lysis syndrome risk, necessitating close monitoring and managing fluid status and uric acid levels before and during treatment.[12][11]

Epidemiology

The exact incidence of tumor lysis syndrome remains undetermined. In a retrospective study involving 102 patients with high-grade non-Hodgkin lymphoma, the overall incidence of tumor lysis syndrome was reported as 42%. However, only 6% of these cases were clinically significant.[17] Susceptibility to tumor lysis syndrome does not appear to be influenced by ethnicity or sex. Analysis of the National Inpatient Sample database reveals that the malignancies most frequently associated with tumor lysis syndrome are non-Hodgkin lymphoma (30%), solid tumors (20%), acute myeloid leukemia (19%), and acute lymphoblastic leukemia (13%). The overall in-hospital mortality rate for tumor lysis syndrome is approximately 21%.[18] 

A retrospective study involving 951 newly diagnosed cancer patients at a tertiary care center in the United States showed that the incidence of laboratory tumor lysis syndrome was 9.3% and clinical tumor lysis syndrome was 6.7% (Cairo et al, Blood, 2012). Hematologic cancers, particularly acute leukemia and multiple myeloma, exhibited the highest rates of tumor lysis syndrome, with laboratory tumor lysis syndrome occurring in 21.1% of cases and clinical tumor lysis syndrome in 15.1% of cases. Laboratory tumor lysis syndrome was often marked by hyperuricemia (52% of patients), whereas clinical tumor lysis syndrome commonly involved renal insufficiency (62.5%) and cardiac arrhythmias (35.9%).

A study involving 788 adult and pediatric patients with acute leukemia or non-Hodgkin lymphoma in 4 European countries revealed that the incidence of tumor lysis syndrome differed between laboratory and clinical tumor lysis syndrome, with rates of 18.9% and 5%, respectively. The incidence rates for laboratory and clinical tumor lysis syndrome were 21.4% and 5.2% in acute lymphoblastic leukemia, 14.7% and 3.4% in acute myeloid leukemia, and 19.6% and 6.1% in non-Hodgkin lymphoma, respectively.[19]

Pathophysiology

Electrolyte Imbalances in Tumor Lysis Syndrome

Tumor lysis syndrome is caused by the massive release of intracellular ions such as potassium, phosphorus, and nucleic acids metabolized to uric acid. The main organ responsible for the excretion of these substances is the kidney. When renal compensatory mechanisms are exhausted, uric acid obstructive uropathy may develop, potentially progressing to acute kidney injury.[20][21]

Hyperuricemia: DNA is composed of smaller units called nucleotides, which are the building blocks of the DNA molecule. Each nucleotide consists of 3 main components—a phosphate group, a sugar group, and a nitrogen base (adenine, thymine, guanine, or cytosine). Adenine and guanine are purines, whereas thymine and cytosine are pyrimidines. In RNA, the sugar is ribose, and the nitrogen bases include adenine, thymine, and uracil. The stepwise metabolism of adenine and guanine produces xanthine; adenine converts to hypoxanthine, whereas guanine converts to xanthine. Xanthine is further metabolized into uric acid by xanthine oxidase. Most mammals possess urate oxidase, which converts uric acid into the more soluble allantoin for renal excretion. Humans lack this enzyme. Due to the rapid turnover of tumor cells, excessive uric acid crystallizes in the renal tubules, causing obstructive uropathy and reduced glomerular filtration rate. Animal models demonstrate that urate nephropathy increases proximal and distal tubule pressure, peritubular capillary pressure, and vascular resistance. Uric acid also scavenges nitric oxide, a potent vasodilator, leading to vasoconstriction and kidney ischemia.[22] In addition, uric acid acts as a pro-inflammatory agent, triggering cytokine release such as tumor necrosis factor-α, exacerbating renal injury.[23][24][17]

Hyperkalemia: Intracellular potassium concentrations are approximately 120 to 130 meq/L. The lysis of tumor cells releases substantial amounts of potassium into the bloodstream, which is typically absorbed by the liver and skeletal muscles, with the remainder excreted through the gastrointestinal tract or kidneys. However, uric acid obstructive uropathy can impede potassium excretion, leading to potentially life-threatening hyperkalemia and the risk of cardiac arrest due to arrhythmias.

Hyperphosphatemia: Tumor lysis syndrome–related hyperphosphatemia is caused by phosphate release from the nucleic acids of lysed tumor cells. The phosphorus concentration in malignant cells can be up to 4 times higher than in normal cells; thus, rapid tumor cell breakdown frequently results in hyperphosphatemia. Normally, the kidneys excrete phosphorus; however, this process can be hindered by acute or chronic kidney injury. Although less common in spontaneous tumor lysis syndrome compared to chemotherapy-induced tumor lysis syndrome, hyperphosphatemia can still cause calcium chelation, resulting in hypocalcemia. Calcium-phosphorus salt deposits can form in the kidneys and soft tissues, with precipitation in the heart potentially causing cardiac arrhythmias.[25][26]

Hypocalcemia: Hypocalcemia in tumor lysis syndrome is mainly due to phosphorus chelation. This condition is more hazardous than hyperphosphatemia, with potential complications including arrhythmias, tetany, seizures, and death.[27][28] Hypocalcemia may persist after normalizing phosphorus levels due to 1,25-dihydroxyvitamin D deficiency.[29]

Histopathology

The histopathological characteristics of tumor lysis syndrome include the deposition of uric acid, calcium phosphate, and xanthine crystals in the lamina of the distal kidney tubules.[30] In addition, uric acid crystals may accumulate within kidney tubular epithelial cells and the medulla. Low urine flow, low solubility, and high solute concentrations contribute to crystal formation. Crystal deposition in the renal pelvis, calyces, and ureter can cause inflammation, leading to urinary flow obstruction. Prolonged obstruction can result in hydroureter, hydronephrosis, and eventually acute kidney injury.

History and Physical

In the context of tumor lysis syndrome, a range of clinical signs and symptoms can emerge either before the onset of chemotherapy or, more frequently, within 72 hours after the administration of cytotoxic agents. Key areas to focus on while obtaining the medical history include the timing of symptom onset relative to the malignancy, abdominal pain and distension, and urinary symptoms such as dysuria, oliguria, flank pain, and hematuria. In addition, symptoms indicative of hypocalcemia, including anorexia, vomiting, cramps, seizures, spasms, altered mental status, and tetany, should be thoroughly assessed.[31]

Symptoms associated with hyperkalemia, such as weakness and paralysis, are also pertinent. Tumor lysis syndrome may present with various other clinical manifestations, including lethargy, edema, and signs of fluid overload. Further complications may include heart failure, cardiac dysrhythmias, syncope, and, in severe cases, sudden death.

Physical Examination

The physical examination should focus on the electrolyte abnormalities associated with tumor lysis syndrome. The physical findings associated with these abnormalities include:

• Hypocalcemia
  • Carpal spasm
  • Pedal spasm
  • Tetany
  • Chvostek sign
  • Trousseau sign
  • Wheezing associated with bronchospasm
  • Seizure

• Acute kidney injury and uremia from hyperuricemia and obstructive uropathy
  • Weakness
  • Lethargy
  • Malaise
  • Nausea
  • Vomiting
  • Metallic taste in the mouth
  • Irritability
  • Generalized pruritis
  • Rales and Ronchi from volume overload
  • Muffled heart sound from pericarditis secondary to uremia
  • Joint pain
  • Renal colicky pain
  • Calcium phosphate crystal deposits in the skin
  • Pruritis
  • Gangrene

The clinical presentation can be quite diverse, encompassing a range of symptoms from electrolyte disturbances to signs of fluid overload and uremia. Monitoring for these manifestations as part of the comprehensive evaluation of tumor lysis syndrome is crucial to ensure timely and appropriate management. The early identification of these clinical signs can significantly impact patient outcomes by guiding prompt intervention and treatment strategies.

Evaluation

Diagnostic Evaluation

Various studies are used in the evaluation of tumor lysis syndrome. 

Imaging: Chest radiography and computed tomography (CT) imaging are essential for assessing mediastinal masses and associated pleural effusions. A CT scan or abdominal ultrasound is recommended to determine if a mass is located in the abdomen or retroperitoneum. Clinicians should exercise caution with intravenous (IV) contrast administration due to the risk of acute kidney injury associated with tumor lysis syndrome.

Electrocardiography: Electrocardiography (ECG) is essential for evaluating patients with tumor lysis syndrome to identify abnormalities related to hyperkalemia and hypocalcemia. Hyperkalemia, in particular, poses a risk of life-threatening arrhythmias, making ECG monitoring crucial for managing tumor lysis syndrome.

Laboratory assessments: The complete blood count is used to diagnose hematologic malignancies associated with tumor lysis syndrome, with typical findings including leukocytosis, anemia, and thrombocytopenia. The comprehensive metabolic panel is used to monitor metabolic abnormalities associated with tumor lysis syndrome, such as hyperkalemia, hypocalcemia, hyperphosphatemia, and hyperuricemia. Elevated levels of blood urea nitrogen, creatinine, and lactate dehydrogenase may indicate the onset of tumor lysis syndrome and require close monitoring, ideally 2 to 3 times daily before and after the initiation of therapy. In addition, urinalysis is crucial for detecting uric acid precipitation and obstructive uropathy, with urine pH, specific gravity, and urine output assessed regularly. Urine alkalinization with sodium bicarbonate is standard practice in managing tumor lysis syndrome.

Diagnostic Criteria for Tumor Lysis Syndrome

The diagnosis of tumor lysis syndrome relies on criteria developed by Cairo and Bishop.[32][7][33] Established in 2004, the Cairo-Bishop definition outlined specific laboratory criteria for diagnosing tumor lysis syndrome at the time of presentation and within 7 days following treatment. These criteria also categorize the severity of tumor lysis syndrome, ranging from grade 0 (asymptomatic) to 5 (death), based on factors such as the extent of serum creatinine elevation, the type and presence of cardiac arrhythmias, and the occurrence and severity of seizures.

Laboratory diagnostic criteria: Tumor lysis syndrome diagnosis requires the presence of 2 or more of the following criteria within the same 24-hour period from 3 days before to 7 days after chemotherapy initiation:

• Uric acid 25% increase from baseline or ≥8.0 mg/dL
• Potassium 25% increase from baseline or ≥6.0 mEq/L
• Phosphorus 25% increase from baseline or ≥4.5 mg/dL (≥6.5 mg/dL in children)
• Calcium 25% decrease from baseline or ≤7.0 mg/dL

Clinical diagnostic criteria: Clinical tumor lysis syndrome is defined by the presence of laboratory tumor lysis syndrome plus one or more of the following:

• Creatinine greater than 1.5 times the upper limit of normal of an age-adjusted reference range
• Seizure
• Cardiac arrhythmia or sudden death

In addition, other causes of acute kidney injury should be ruled out. The criteria established by Cairo and Bishop have several limitations. The most significant drawback is that the definition of tumor lysis syndrome requires the initiation of chemotherapy, whereas, in clinical practice, tumor lysis syndrome can develop spontaneously without initiating chemotherapy. Another limitation is the use of creatinine levels >1.5 times the upper limit for a patient's age and gender. However, this approach is not standard, as patients with chronic kidney disease have elevated levels of creatine in the absence of acute kidney injury.[34]

Treatment / Management

Prevention of Tumor Lysis Syndrome

The most important factor considered for the management of tumor lysis syndrome is the ability to prevent its development based on anticipation. The main goal of prophylaxis is to ensure sufficient urine production and to lower uric acid, potassium, and phosphate blood concentrations. The primary prophylactic strategies are IV hydration and hypouricemic agents such as allopurinol and rasburicase. Avoiding substances that can cause vasoconstriction of the renal vasculature, including but not limited to nonsteroidal anti-inflammatory drugs and iodinated contrast, is advisable. Multiple clinical trials have failed to demonstrate the superiority of any particular prophylactic regiment for tumor lysis syndrome. Monitoring biological values every 4 to 6 hours after starting antitumor therapy for high-risk patients, every 8 to 12 hours for those at intermediate risk, and daily for low-risk patients is recommended.[35]

Rapid Expansion of Intravascular Volume

Aggressive IV hydration is crucial for preventing tumor lysis syndrome in high-risk patients, aiming to improve renal perfusion, glomerular filtration, and urine output.[11] For tumors with a high risk of releasing a large amount of intracellular substances after the initiation of chemotherapy, aggressive hydration should be started before the initiation of treatment. In patients with preexisting kidney or cardiac conditions, careful fluid management and monitoring are essential to avoid fluid overload, with diuretics potentially used to support urine output.

Crystalloids are recommended for volume expansion to rapidly enhance the glomerular filtration rate, thereby facilitating the elimination of solutes associated with tumor lysis syndrome. IV fluid administration should commence 48 hours before the initiation of chemotherapy and continue for 48 hours following chemotherapy. Adequate hydration, typically around 3 to 3.5 L/m² daily or 4 to 5 L/d, may be required to achieve optimal hydration and to target a urine output of approximately 2 mL/kg/h.[36][37] Diuretics, such as furosemide, may be used to sustain urine output but are not recommended for patients with hypovolemia or obstructive uropathy. Hydration fluids should initially be free of potassium and calcium to prevent the complications of hyperkalemia and hyperphosphatemia.

Sodium Bicarbonate for Urine Alkalinization

Alkalinizing the urine increases the solubility of uric acid by about 10-fold. Urine alkalinization can be achieved by adding 40 to 50 mEq of sodium bicarbonate per liter of hydration fluid in tumor lysis syndrome. However, a potential drawback of urine alkalinization is the reduction in ionized calcium levels, which may decrease calcium-albumin binding and exacerbate hypocalcemia associated with tumor lysis syndrome, potentially resulting in arrhythmias or tetany. In addition, urine alkalinization may promote the precipitation of calcium and phosphate salts in renal tubules, worsening acute kidney injury in tumor lysis syndrome. Therefore, sodium bicarbonate should be used for urine alkalinization only in patients with metabolic acidosis when rasburicase is unavailable, and calcium levels should be monitored serially.[11][38]

Allopurinol

Allopurinol is a structural isomer of hypoxanthine and is converted to its active metabolite, oxypurinol, by xanthine oxidase. Allopurinol competitively inhibits xanthine oxidase and blocks the conversion of xanthine to uric acid, thereby reducing the formation of uric acid and decreasing the incidence of obstructive uropathy.[39] Although allopurinol effectively reduces uric acid production in tumor lysis syndrome, it does not treat hyperuricemia once it has developed. Allopurinol is recommended for tumor lysis syndrome prevention, provided pretreatment uric acid levels are below 8 mg/dL (476 μmol/L).

Adverse effects of allopurinol include skin rash, eosinophilia, and acute hepatitis, collectively known as allopurinol hypersensitivity syndrome. Clinicians should also be cautious of potential drug interactions with azathioprine, particularly in patients with solid organ transplants or autoimmune disorders. Allopurinol use can lead to elevated levels of xanthine in urine and serum. Xanthine has limited solubility and can crystallize in renal tubules, aggravating obstructive uropathy associated with tumor lysis syndrome. 

Allopurinol is generally administered at a dosage of 100 mg/m² every 8 hours for adults, with a maximum daily dose of 800 mg, and should be adjusted for renal impairment. In children, the dosage ranges from 50 to 100 mg/m² every 8 hours or 10 mg/kg/d.[11] IV administration can be used for those who cannot take oral medication, with a maximum dose of 600 mg/d.[40] Treatment should start 24 to 48 hours before induction chemotherapy and continue for up to 7 days, depending on serum uric acid levels and other markers of tumor lysis. Screening for the HLA-B*58:01 allele is recommended for specific high-risk populations to avoid severe cutaneous reactions, particularly in patients of Asian ancestry.[41]

Rasburicase

Rasburicase is recommended over allopurinol for the prevention and treatment of tumor lysis syndrome in high-risk adult and pediatric patients, particularly those with compromised renal or cardiac function. Rasburicase is a recombinant urate oxidase derived from Aspergillus flavus and catalyzes the conversion of uric acid to allantoin, carbon dioxide, and hydrogen peroxide. This approach contrasts with allopurinol, which inhibits uric acid formation but does not rapidly reduce serum uric acid levels.

Rasburicase dosing typically starts at 0.2 mg/kg daily, with adjustments based on risk stratification and baseline uric acid levels; it can be administered intramuscularly or IV. Caution is necessary for patients with glucose-6-phosphate dehydrogenase deficiency, as hydrogen peroxide produced with rasburicase can cause severe methemoglobinemia or hemolytic anemia in these patients.[42](B3)

The United States Food and Drug Administration approved rasburicase in 2009. In children, rasburicase has demonstrated superior efficacy compared to allopurinol. In a phase 1/2 trial involving 131 pediatric patients undergoing chemotherapy for high-risk hematologic malignancies, rasburicase effectively reduced serum uric acid levels and improved clinical outcomes without necessitating dialysis.[43] A randomized trial further demonstrated rasburicase's superiority, showing more significant reductions in uric acid levels and a faster onset of action compared to allopurinol.[24] In adults, rasburicase has demonstrated effectiveness in managing tumor lysis syndrome with less data compared to pediatric studies. Trials have reported that rasburicase achieves faster normalization of uric acid levels and lowers the incidence of laboratory tumor lysis syndrome more effectively compared to allopurinol. However, the evidence is less robust for clinical tumor lysis syndrome outcomes and mortality benefits, partly due to study design limitations and patient heterogeneity.[44](A1)

Febuxostat

Febuxostat is a newer xanthine oxidase inhibitor that is more expensive than allopurinol but does not cause the hypersensitivity reactions associated with allopurinol. Febuxostat requires no dose adjustment for mild-to-moderate renal impairment and has fewer drug-drug interactions.[45] Febuxostat can also be used in situations where rasburicase is unavailable or contraindicated. In the clinical trial, Febuxostat for TLS Prevention in Hematologic Malignancies (FLORENCE), febuxostat demonstrated superior control of tumor lysis syndrome–related hyperuricemia with a favorable safety profile and preservation of renal function.[46] Caution is advised against concurrent use with azathioprine or mercaptopurine due to the risk of severe toxicity from increased plasma concentrations. (A1)

Treatment of Tumor Lysis Syndrome

For individuals who develop tumor lysis syndrome during cancer treatment or spontaneously before chemotherapy, intensive supportive care is essential, including continuous urine output monitoring, cardiac monitoring, and regular measurements of electrolytes, creatinine, and uric acid. Management involves correcting specific electrolyte abnormalities, administering rasburicase if not previously given, hydrating to flush uric acid crystals, and considering renal replacement therapy if necessary. Early consultation with a renal specialist is recommended.[11]

Management of Electrolyte Abnormalities

Hyperkalemia poses a significant risk due to the potential for cardiac dysrhythmias. Managing it requires restricting potassium and phosphate intake, frequent serum potassium monitoring, and if necessary, using potassium-lowering agents or dialysis. Calcium chloride and calcium gluconate can be administered parenterally to manage hypocalcemia. In tumor lysis syndrome, hypocalcemia often results from hyperphosphatemia, and calcium administration may exacerbate the deposition of calcium-phosphate crystals in soft tissues and kidneys, worsening acute kidney injury. Hyperphosphatemia may occasionally require hemodialysis, but management primarily involves aggressive hydration and phosphate binder therapy.

Hemodialysis: Hemodialysis may be necessary in severe cases where potassium and phosphorus levels are excessively high due to tumor lysis syndrome–associated acute kidney injury. Indications for renal replacement therapy include severe oliguria or anuria, fluid overload, persistent hyperkalemia, symptomatic hypocalcemia due to hyperphosphatemia, and a calcium-phosphate product ≥70 mg²/dL².[47][11] The release of intracellular ions during tumor lysis syndrome can lead to rebound hyperkalemia or hyperphosphatemia with intermittent hemodialysis. Continuous renal replacement therapy, with a high dialysate or replacement fluid flow rate, is preferred for effective solute removal.

Peritoneal dialysis is insufficient due to its lower effectiveness in clearing uric acid and phosphate. In addition, patients might experience abdominal complications related to tumors, such as peritoneal carcinomatosis or compartment syndrome. For life-threatening hyperkalemia, early hemodialysis is advised, whereas continuous renal replacement therapy may be the optimal approach for severe hyperphosphatemia.

Differential Diagnosis

Tumor lysis syndrome should be differentiated from other clinical conditions that can cause hyperkalemia, hyperphosphatemia, and hyperuricemia. The differential diagnosis of these electrolyte abnormalities includes:

• Hyperkalemia
  • Hypocalcemia
  • Metabolic acidosis
  • Congenital adrenal hyperplasia
  • Toxicity from digitalis
  • Acute tubular injury
  • Electrical burn
  • Head trauma
  • Rhabdomyolysis
  • Thermal burns

•  Hyperphosphatemia
  • Monoclonal gammopathy
  • Waldenström macroglobulinemia
  • Multiple myeloma
  • Pseudohypoparathyroidism
  • Rhabdomyolysis
  • Vitamin D intoxication
  • Oral saline laxative (Phospho-soda) abuse
  • Pseudohyperphosphatemia

• Hyperuricemia
  • Hyperparathyroidism
  • Hypothyroidism
  • Nephrolithiasis
  • Alcoholic ketoacidosis
  • Diabetic ketoacidosis
  • Gout
  • Pseudogout
  • Type 1a glycogen storage disease
  • Hemolytic anemia
  • Hodgkin lymphoma
  • Uric acid nephropathy

Prognosis

Tumor lysis syndrome poses significant clinical risks, particularly in patients with high or intermediate risk undergoing treatments such as induction chemotherapy for acute myeloid leukemia. A retrospective study involving 772 acute myeloid leukemia patients found that tumor lysis syndrome developed in 17% of cases, with clinical tumor lysis syndrome occurring in 5% of those affected. Clinical tumor lysis syndrome significantly raised the risk of death during induction therapy, with 79% of patients with clinical tumor lysis syndrome experiencing fatal outcomes.[6] The need for immediate intervention when tumor lysis syndrome is diagnosed underscores the importance of preventive strategies, particularly in high-risk populations.

Complications

Tumor lysis syndrome can lead to severe complications, including acute kidney injury, cardiac arrhythmias, and metabolic disturbances. The rapid release of intracellular contents from lysed tumor cells results in hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia, which can precipitate life-threatening conditions. The resultant electrolyte imbalances and kidney dysfunction necessitate intensive monitoring and management to prevent progression to multiple-organ failure. Clinical tumor lysis syndrome, characterized by these severe manifestations, significantly increases mortality rates and complicates treatment regimens, underscoring the critical need for early recognition and proactive prophylaxis in high-risk patients.