Tumor Lysis Syndrome
Urate Oxidase
Gout Suppressants
Allopurinol
Hyperuricemia
Leukemia, Lymphocytic, Chronic, B-Cell
Hematologic Neoplasms
Allopurinol: intravenous use for prevention and treatment of hyperuricemia. (1/55)
PURPOSE: To tabulate data obtained over a 21-year period to determine the efficacy and safety of an intravenous (IV) allopurinol preparation. PATIENTS AND METHODS: IV allopurinol was provided on a compassionate plea basis to patients of any age in whom xanthine oxidase inhibitor therapy was indicated as an adjunct to chemotherapy and for whom oral intake was restricted. Three hundred twenty-seven investigators at multiple hospitals in the United States treated 1,172 patients with IV allopurinol. The vast majority of these patients had a malignancy and were in danger of developing tumor lysis syndrome (TLS) and subsequent acute uric acid nephropathy (AUAN) and were unable to take oral allopurinol. Data referable to the time period of IV allopurinol administration were collected, collated, and analyzed retrospectively. There was no randomization. RESULTS: In patients initiating treatment for an elevated serum uric acid (SUA), the SUA normalized or improved in 87% of adult patients and normalized or improved in 95% of pediatric patients. IV allopurinol, administered prophylactically to patients at high risk of developing hyperuricemia and TLS, prevented an increase in SUA levels in 93% of adults and 92% of children. Toxicities caused by IV allopurinol were minimal and consisted of 10 instances of mild to moderate skin or allergic reactions. CONCLUSION: IV allopurinol is as efficacious and safe as oral allopurinol and will be of significant benefit to patients at risk of TLS and AUAN and unable to take oral medication. (+info)Syndrome of inappropriate antidiuretic hormone associated with chemotherapy-induced tumour lysis in small-cell lung cancer: case report and literature review. (2/55)
A patient with a small-cell lung cancer (SCLC) developed an asymptomatic hyponatremia, with all features of the syndrome of inappropriate antidiuretic hormone secretion (SIADH), two days after the start of his first cycle of chemotherapy with vindesine, ifosfamide and cisplatin. Progression of the tumour with an increase in paraneoplastic SIADH, or drug-induced causes of hyponatremia, could be ruled out by his further clinical course. The event was interpreted as a consequence of ADH release during the initial tumour cell lysis after effective chemotherapy. The occurrence of hyponatremia during the initial phase of chemotherapy for SCLC should be interpreted with caution. Although it is most commonly due to an increase in paraneoplastic ADH secretion reflecting ineffective therapy, it can also be due to release of ADH from malignant cells in the period of rapid tumour lysis, reflecting effective therapy. Based on this rare occurrence, a review of the aetiology, clinical findings, diagnosis, prognosis and treatment of SIADH in general is presented. (+info)Tumor lysis syndrome following hemi-body irradiation for metastatic breast cancer. (3/55)
Tumor lysis syndrome (TLS) is a rare serious acute complication of cancer therapy, reported mainly following chemotherapy in patients with large tumor load and chemosensitive disease. These are mainly patients with non-Hodgkin's lymphoma, leukemia and rarely in solid tumors. It is less frequently described after radiotherapy for lymphoid and hematological malignancies. TLS following radiotherapy for solid tumors is a very rare complication. In this report/review we describe a seventy-three-year-old male patient with progressive metastatic carcinoma of the breast to the lungs, liver and bone. He was referred for radiotherapy because of generalized bony pains. The patient was planned for sequential hemi-body irradiation starting with the more symptomatic upper half body. After premedication, he was given 8.5 Gy to the mid point at the maximum chest separation with anterior lung attenuator limiting uncorrected lung dose to 6.15 Gy. A further 3.5 Gy electron boost to the fungating breast tumor was given to the 100%. Forty-eight hours after irradiation he developed hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia and renal failure. These clinical and biochemical changes are typical of tumor lysis syndrome (TLS). Despite hydration, and treating the hyperuricemia, the patient developed coma and died eight days after irradiation. The prophylaxis and management of TLS and in high-risk patients are described to avoid this frequently fatal complication. (+info)Spontaneous acute tumor lysis syndrome with advanced gastric cancer. (4/55)
Acute tumor lysis syndrome (TLS) occurs frequently in hematologic malignancies such as high-grade lymphomas and acute leukemia, which are rapidly proliferating and chemosensitive tumors. It occurs rarely in solid tumors and has never been reported in gastric adenocarcinoma. Typical biochemical findings of acute tumor lysis syndrome are hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia in patients with a malignancy. Rapid changes of these electrolytes may cause cardiac arrhythmia, seizure, acute renal failure and sudden death. Therefore, as soon as it is detected, it should be taken care of immediately. Until now almost all cases of TLS associated with solid tumor have developed after cytoreductive therapy in chemosensitive tumors. We report here a case of spontaneous acute tumor lysis in a patient of advanced gastric cancer with hepatic metastases and multiple lymphadenopathy. The biochemical finding of TLS improved with the management and tumor burden also showed slight response to the one cycled combination chemotherapy but the patient died of progressive pneumonia. (+info)A randomized comparison between rasburicase and allopurinol in children with lymphoma or leukemia at high risk for tumor lysis. (5/55)
Standard therapy in the United States for malignancy-associated hyperuricemia consists of hydration, alkalinization, and allopurinol. Urate oxidase catalyzes the enzymatic oxidation of uric acid to a 5 times increased urine soluble product, allantoin. Rasburicase is a new recombinant form of urate oxidase available for clinical evaluation. This multicenter randomized trial compared allopurinol to rasburicase in pediatric patients with leukemia or lymphoma at high risk for tumor lysis. Patients received the assigned uric acid-lowering agent for 5 to 7 days during induction chemotherapy. The primary efficacy end point was to compare the area under the serial plasma uric acid concentration curves during the first 96 hours of therapy (AUC(0-96)). Fifty-two patients were randomized at 6 sites. In an intent-to-treat analysis, the mean uric acid AUC(0-96) was 128 +/- 70 mg/dL.hour for the rasburicase group and 329 +/- 129 mg/dL.hour for the allopurinol group (P <.0001). The rasburicase versus allopurinol group experienced a 2.6-fold (95% CI: 2.0-3.4) less exposure to uric acid. Four hours after the first dose, patients randomized to rasburicase compared to allopurinol achieved an 86% versus 12% reduction (P <.0001) of initial plasma uric acid levels. No antirasburicase antibodies were detected at day 14. This randomized study demonstrated more rapid control and lower levels of plasma uric acid in patients at high risk for tumor lysis who received rasburicase compared to allopurinol. For pediatric patients with advanced stage lymphoma or high tumor burden leukemia, rasburicase is a safe and effective alternative to allopurinol during initial chemotherapy. (+info)Oncologic emergencies for the internist. (6/55)
Most cancer patients experience at least one emergency during the course of the disease. This paper reviews the diagnosis and treatment of tumor lysis syndrome, hypercalcemia of malignancy, superior vena cava syndrome, spinal cord compression, strokes and seizures, and treatment-related emergencies. (+info)Urate-oxidase in the prevention and treatment of metabolic complications in patients with B-cell lymphoma and leukemia, treated in the Societe Francaise d'Oncologie Pediatrique LMB89 protocol. (7/55)
PURPOSE: To evaluate the frequency of metabolic complications and dialysis due to tumor lysis syndrome in patients with B-cell advanced-stage non-Hodgkin's lymphoma (NHL) and L3 leukemia at initiation of chemotherapy including the use of urate-oxidase. PATIENTS AND METHODS: Retrospective review of the clinical records of 410 patients with stage III and IV B-cell NHL and L3 leukemia treated in France and prospectively registered in the LMB89 protocol. RESULTS: During the first week of chemotherapy, only 34 of 410 patients recorded metabolic problems that included hypocalcemia (< 70 mg/dl) in 24 patients, hyperphosphatemia (> 6.5 mg/dl) in 28 and elevation of creatinine > or = 2 SD in 16. Six patients underwent dialysis for life-threatening problems and a seventh as a preventive measure. In the other 27 cases, metabolic problems were successfully resolved using urate-oxidase in combination with alkaline hyperhydration. Among the 410 patients, one case of hemolysis was reported and there was no severe allergic reaction to urate-oxidase. CONCLUSIONS: Only 1.7% of patients in our study receiving urate-oxidase during their induction chemotherapy needed renal dialysis. Urate-oxidase was well tolerated, and used as prophylaxis and/or treatment of hyperuricemia and tumor lysis syndrome consistently gave a lower rate of renal and metabolic complications than in other series of similar patients. (+info)Rasburicase (recombinant urate oxidase) for the management of hyperuricemia in patients with cancer: report of an international compassionate use study. (8/55)
BACKGROUND: Hyperuricemia and tumor lysis syndrome (TLS) are serious complications that can occur during chemotherapy for hematologic malignancies, even if standard management procedures, including administration of allopurinol, are undertaken. Rasburicase, a recombinant urate oxidase that converts uric acid (UA) into the soluble compound allantoin, has been shown to control hyperuricemia faster and more reliably than allopurinol.(1) METHODS: A compassionate use trial, running from January 1999 to December 2001, provided access to rasburicase for patients in nine countries who were at risk for TLS during the initiation of chemotherapy. Of the 280 patients enrolled in the study, 278 received rasburicase and were included in the analysis. A total of 166 pediatric patients who had leukemia (approximately 74%), lymphoma (approximately 24%), or solid tumors (approximately 3%) were treated with rasburicase. One hundred twelve adults with either leukemia (68%) or lymphoma (30%) also were treated. Rasburicase (0.20 mg/kg) was administered intravenously once a day for 1 to 7 days, at the investigator's discretion. Two doses daily could be administered during the first 3 days. A response was defined as a reduction in UA level or maintenance of a UA level less than 7.5 mg/dL (or less than 6.5 mg/dL, for children age < 13 years). RESULTS: UA levels at 24-48 hours after administration of the last dose of rasburicase were available for 122 pediatric patients and 97 adult patients. The mean UA level in 29 hyperuricemic children decreased from 15.1 mg/dL to 0.4 mg/dL, whereas in 27 hyperuricemic adults, the mean level decreased from 14.2 mg/dL to 0.5 mg/dL. Prophylactic administration of rasburicase to prevent TLS during chemotherapy reduced UA levels from a mean of 4.4 mg/dL to 0.8 mg/dL in 93 nonhyperuricemic children and from 4.8 mg/dL to 0.4 mg/dL in 70 nonhyperuricemic adults (for all reductions in UA levels, P < 0.001). The response rate was 100%. Rasburicase was very well tolerated. Serious adverse events related to rasburicase were observed in one patient. CONCLUSIONS: The results of the current study confirm that rasburicase is safe and highly effective in the prevention and treatment of chemotherapy-induced hyperuricemia in both children and adults. (+info)Tumor Lysis Syndrome (TLS) is a metabolic complication that can occur following the rapid destruction of malignant cells, most commonly seen in hematologic malignancies such as acute leukemias and high-grade non-Hodgkin lymphomas. The rapid breakdown of these cancer cells releases a large amount of intracellular contents, including potassium, phosphorus, and nucleic acids, into the bloodstream.
This sudden influx of substances can lead to three major metabolic abnormalities: hyperkalemia (elevated potassium levels), hyperphosphatemia (elevated phosphate levels), and hypocalcemia (low calcium levels). Hyperuricemia (elevated uric acid levels) may also occur due to the breakdown of nucleic acids. These metabolic disturbances can cause various clinical manifestations, such as cardiac arrhythmias, seizures, renal failure, and even death if not promptly recognized and treated.
TLS is classified into two types: laboratory TLS (LTLS) and clinical TLS (CTLS). LTLS is defined by the presence of abnormal laboratory values without any related clinical symptoms, while CTLS is characterized by laboratory abnormalities accompanied by clinical signs or symptoms. Preventive measures, such as aggressive hydration, urinary alkalinization, and prophylactic medications to lower uric acid levels, are often employed in high-risk patients to prevent the development of TLS.
Urate oxidase, also known as uricase, is an enzyme that catalyzes the oxidation of uric acid to allantoin. This reaction is an essential part of purine metabolism in many organisms, as allantoin is more soluble and easier to excrete than uric acid. In humans, urate oxidase is non-functional due to mutations in the gene encoding it, which leads to the accumulation of uric acid and predisposes to gout and kidney stones. Urate oxidase is found in some bacteria, fungi, and plants, and can be used as a therapeutic agent in humans to lower serum uric acid levels in conditions such as tumor lysis syndrome and gout.
Gout suppressants are a type of medication used to treat acute gout attacks and reduce the risk of future episodes. They work by decreasing the production of uric acid in the body or improving its elimination, thereby reducing the formation of uric acid crystals that cause inflammation and pain in the joints. Common examples of gout suppressants include:
1. Colchicine: This medication is often used to treat acute gout attacks by reducing inflammation and swelling in the affected joint. It should be taken as soon as possible after the onset of symptoms for best results.
2. Nonsteroidal anti-inflammatory drugs (NSAIDs): These medications, such as ibuprofen, naproxen, and celecoxib, can help alleviate pain and inflammation during an acute gout attack. They are usually more effective when taken at the first sign of an attack.
3. Corticosteroids: In some cases, corticosteroid medications like prednisone may be prescribed to treat severe gout attacks that do not respond to other treatments. These drugs can be administered orally or injected directly into the affected joint.
4. Allopurinol and febuxostat: These medications are called xanthine oxidase inhibitors, which reduce uric acid production in the body. They are typically used for chronic gout management to prevent future attacks and lower the risk of complications such as kidney stones and joint damage.
It is important to note that some gout suppressants may have side effects or interact with other medications, so it is crucial to discuss any concerns with a healthcare provider before starting treatment. Additionally, lifestyle changes such as maintaining a healthy weight, following a low-purine diet, and staying hydrated can help manage gout symptoms and lower the risk of future attacks.
Allopurinol is a medication used to treat chronic gout and certain types of kidney stones. It works by reducing the production of uric acid in the body, which is the substance that can cause these conditions when it builds up in high levels. Allopurinol is a xanthine oxidase inhibitor, meaning it blocks an enzyme called xanthine oxidase from converting purines into uric acid. By doing this, allopurinol helps to lower the levels of uric acid in the body and prevent the formation of new kidney stones or gout attacks.
It is important to note that allopurinol can have side effects, including rash, stomach upset, and liver or kidney problems. It may also interact with other medications, so it is essential to inform your healthcare provider of any other drugs you are taking before starting allopurinol. Your healthcare provider will determine the appropriate dosage and monitoring schedule based on your individual needs and medical history.
Hyperuricemia is a medical condition characterized by an excessively high level of uric acid in the blood. Uric acid is a waste product that's produced when the body breaks down purines, which are substances found in certain foods and drinks, such as red meat, seafood, and alcoholic beverages. Normally, uric acid is dissolved in the blood and then excreted by the kidneys through urine. However, if there's too much uric acid in the body or if the kidneys can't eliminate it efficiently, it can build up in the blood, leading to hyperuricemia.
Mild cases of hyperuricemia may not cause any symptoms and may not require treatment. However, high levels of uric acid can lead to the formation of uric acid crystals, which can accumulate in the joints and tissues, causing inflammation and pain. This condition is known as gout. Hyperuricemia can also increase the risk of developing kidney stones and kidney disease.
Hyperuricemia can be caused by several factors, including a diet high in purines, genetic factors, kidney disease, certain medications, and conditions that cause rapid cell turnover, such as cancer or psoriasis. Treatment for hyperuricemia typically involves lifestyle changes, such as reducing the intake of purine-rich foods and beverages, maintaining a healthy weight, and staying hydrated. Medications may also be prescribed to lower uric acid levels in the blood and prevent gout attacks.
Chronic lymphocytic leukemia (CLL) is a type of cancer that starts from cells that become certain white blood cells (called lymphocytes) in the bone marrow. The cancer (leukemia) cells start in the bone marrow but then go into the blood.
In CLL, the leukemia cells often build up slowly. Many people don't have any symptoms for at least a few years. But over time, the cells can spread to other parts of the body, including the lymph nodes, liver, and spleen.
The "B-cell" part of the name refers to the fact that the cancer starts in a type of white blood cell called a B lymphocyte or B cell. The "chronic" part means that this leukemia usually progresses more slowly than other types of leukemia.
It's important to note that chronic lymphocytic leukemia is different from chronic myelogenous leukemia (CML). Although both are cancers of the white blood cells, they start in different types of white blood cells and progress differently.
Hematologic neoplasms, also known as hematological malignancies, are a group of diseases characterized by the uncontrolled growth and accumulation of abnormal blood cells or bone marrow cells. These disorders can originate from the myeloid or lymphoid cell lines, which give rise to various types of blood cells, including red blood cells, white blood cells, and platelets.
Hematologic neoplasms can be broadly classified into three categories:
1. Leukemias: These are cancers that primarily affect the bone marrow and blood-forming tissues. They result in an overproduction of abnormal white blood cells, which interfere with the normal functioning of the blood and immune system. There are several types of leukemia, including acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL), acute myeloid leukemia (AML), and chronic myeloid leukemia (CML).
2. Lymphomas: These are cancers that develop from the lymphatic system, which is a part of the immune system responsible for fighting infections. Lymphomas can affect lymph nodes, spleen, bone marrow, and other organs. The two main types of lymphoma are Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL).
3. Myelomas: These are cancers that arise from the plasma cells, a type of white blood cell responsible for producing antibodies. Multiple myeloma is the most common type of myeloma, characterized by an excessive proliferation of malignant plasma cells in the bone marrow, leading to the production of abnormal amounts of monoclonal immunoglobulins (M proteins) and bone destruction.
Hematologic neoplasms can have various symptoms, such as fatigue, weakness, frequent infections, easy bruising or bleeding, weight loss, swollen lymph nodes, and bone pain. The diagnosis typically involves a combination of medical history, physical examination, laboratory tests, imaging studies, and sometimes bone marrow biopsy. Treatment options depend on the type and stage of the disease and may include chemotherapy, radiation therapy, targeted therapy, immunotherapy, stem cell transplantation, or a combination of these approaches.
Antineoplastic agents are a class of drugs used to treat malignant neoplasms or cancer. These agents work by inhibiting the growth and proliferation of cancer cells, either by killing them or preventing their division and replication. Antineoplastic agents can be classified based on their mechanism of action, such as alkylating agents, antimetabolites, topoisomerase inhibitors, mitotic inhibitors, and targeted therapy agents.
Alkylating agents work by adding alkyl groups to DNA, which can cause cross-linking of DNA strands and ultimately lead to cell death. Antimetabolites interfere with the metabolic processes necessary for DNA synthesis and replication, while topoisomerase inhibitors prevent the relaxation of supercoiled DNA during replication. Mitotic inhibitors disrupt the normal functioning of the mitotic spindle, which is essential for cell division. Targeted therapy agents are designed to target specific molecular abnormalities in cancer cells, such as mutated oncogenes or dysregulated signaling pathways.
It's important to note that antineoplastic agents can also affect normal cells and tissues, leading to various side effects such as nausea, vomiting, hair loss, and myelosuppression (suppression of bone marrow function). Therefore, the use of these drugs requires careful monitoring and management of their potential adverse effects.
Nitrogen compounds are chemical substances that contain nitrogen, which is a non-metal in group 15 of the periodic table. Nitrogen forms compounds with many other elements due to its ability to form multiple bonds, including covalent bonds with hydrogen, oxygen, carbon, sulfur, and halogens.
Nitrogen can exist in several oxidation states, ranging from -3 to +5, which leads to a wide variety of nitrogen compounds with different properties and uses. Some common examples of nitrogen compounds include:
* Ammonia (NH3), a colorless gas with a pungent odor, used in fertilizers, cleaning products, and refrigeration systems.
* Nitric acid (HNO3), a strong mineral acid used in the production of explosives, dyes, and fertilizers.
* Ammonium nitrate (NH4NO3), a white crystalline solid used as a fertilizer and explosive ingredient.
* Hydrazine (N2H4), a colorless liquid with a strong odor, used as a rocket fuel and reducing agent.
* Nitrous oxide (N2O), a colorless gas used as an anesthetic and laughing gas in dental procedures.
Nitrogen compounds have many important applications in various industries, such as agriculture, pharmaceuticals, chemicals, and energy production. However, some nitrogen compounds can also be harmful or toxic to humans and the environment if not handled properly.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.