Medical expert of the article
New publications
Syndrome of rapid decay of a tumor
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The syndrome of rapid decay of the tumor (CABP), or tumor-lysis syndrome (TLS) occurs with rapid death of a large mass of tumor cells.
Causes of the syndrome of rapid decay of the tumor
Most often, SBRs are observed at the beginning of cytostatic therapy in patients:
- with acute and chronic lymphoblastic leukemia and lymphomas (Berkit's lymphoma),
- with other tumors sensitive to chemotherapeutic, biotherapeutic and radiotherapy,
- sometimes the syndrome of rapid disintegration of the tumor develops spontaneously, even before the beginning of the anticancer treatment (Burkitt's lymphoma).
The mechanism of development of tumor-lysis syndrome
Severe metabolic disorders arise from the destruction of the cell membrane of tumor cells and the introduction of intracellular electrolytes (potassium, phosphates) and metabolic products (in particular, purine metabolism - uric acid) into the microcirculatory bed at a rate much higher than their plasma clearance.
Symptoms of the syndrome of rapid decay of a tumor
Symptoms of REDD vary:
- Short-term tonic convulsions and drowsiness due to hyperphosphatemia and secondary hypocalcemia.
- "Subclinical" arrhythmias.
- OPN is associated with hyperuricemia (uric acid or urate nephropathy) and / or hyperphosphatemia (phosphate nephropathy). In both cases, the renal tubules are primarily affected. The risk of developing acute renal failure is elevated in patients with a previous impairment of renal function (nephrotoxic chemotherapy, CRF of any etiology) and / or not corrected prior to chemotherapy by metabolic acidosis and dehydration.
- Severe respiratory failure.
- Stop cardiac activity due to fatal arrhythmia or hyperkalemia.
Treatment of the syndrome of rapid decay of the tumor
Treatment of REDD consists in vigorous hydration and correction of electrolyte disorders, using aluminum hydroxide, diuretics, GF and other methods of treatment.
- Aluminum hydroxide is used internally to bind phosphates
- Conservative treatment of hyperkalemia is to maintain a high diuresis, hydration and correction of the negative acidosis.
- Correction of hypocalcemia (secondary to hyperphosphataemia) is carried out only with the appearance of its symptoms and very cautiously. This is associated with a high risk of formation of insoluble calcium phosphate and calcification of soft tissues with a calcium phosphate product of more than 4.25 mmol 2 / L 2.
- Effective and relatively fast correction of metabolic disorders is possible with renal replacement therapy (HD or GF), using standard dialysate and substitutional regimens. The goal of DG / GF is the elimination of phosphates and uric acid. To carry out the procedure, it is necessary to select the filter and duration accordingly. Absolute indications for carrying out emergency GD (or GF), non-conservative treatment of hyperuricemia (uric acid level above 10 mg / dL), hyperkalemia (serum potassium above 6.5 mmol / l), hyperphosphataemia, severe renal failure arterial failure due to urate nephropathy in SBRO is reversible .
How to prevent the syndrome of rapid decay of the tumor?
Prevention of the rapid disintegration syndrome is well developed and not labor-consuming, its goal is to prevent renal failure (decreased uric acid production, non-renal phosphate binding) and an increase in renal excretion of potassium, phosphate and urate. Preventive measures are necessary for patients with a large mass of tumor tissue and predictable rapid cytolysis. Plasma biochemical markers of rapid cytolysis (potassium, phosphate, calcium, uric acid, lactate dehydrogenase) in patients with a high risk of developing RESB should preferably be examined 2-3 times a day for at least 2 days after the onset of cytostatic therapy. To prevent the syndrome of rapid decay of the tumor, intravenous administration of isotonic solutions and sodium carbonate, the intake of diuretics, allopurinol, and rasburicase are indicated.
Hydration of isotonic or hypotonic liquids (0.9% sodium chloride solution, Ringer's solution) in a daily volume of 3000 ml / m 2 (200-250 ml / h) begins several hours before the administration of cytostatics. Diuresis usually increases in response to water-salt loading, and after 2-4 h the rate of diuresis is equal to the infusion rate.
With severe fluid retention, low doses of loop diuretics (furosemide) or acetazolamide (diacarb) at a dose of 5 mg / kg per day are used.
To prevent the development of urate nephropathy, it is possible, by maintaining an alkaline urine reaction (pH> 7) by intravenous injection of sodium hydrogencarbonate (usually at a dose of 100-150 meq per liter of infusion solutions). However, the alkaline reaction of urine promotes the formation of an insoluble salt (calcium phosphate) in the tubules, so after the initiation of chemotherapy, the introduction of sodium hydrogencarbonate should be limited only to cases of decompensated negative acidosis.
Allopurinol inhibits the enzyme xanthine oxidase and prevents the conversion of xanthine to uric acid, prescribe the drug before the initiation of cytostatic therapy (if possible, for 1-2 days), taking allopurinol should continue after chemotherapy up to the normalization of the uric acid level (500 mg / m 2 per day for 1-2 days before and during the first 3 days of chemotherapy, in the following days 200 mg / m 2 per day). In rare cases (with renal insufficiency), the use of allopurinol is complicated by the development of hyperxanthinuria and xanthine nephropathy. Xanthine is soluble three times less than uric acid, and precipitates even with an alkaline reaction of urine.
Perspective in the prevention of urate nephropathy in the RAF is considered a new drug rasburikazu (modified recombinant uricase). Intravenous administration of drugs leads to a rapid metabolism of uric acid to a much more soluble allantoin, the latter is excreted in the urine. It is assumed that the Rasburicase promotes the dissolution of uric acid crystals and the resolution of already developed renal failure in the syndrome of rapid disintegration of the tumor, the results of the relevant studies have not yet been published.