Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute renal failure in Burkitt lymphoma is commonly the result of tumor lysis syndrome. We present a 15-year-old boy who developed hypertension, seizures, and acute renal failure due to extrinsic compression of the bladder and ureters by a large retrovesical Burkitt lymphoma. The causes of acute renal failure in Burkitt lymphoma and the incidence of acute urinary obstruction in this disease are reviewed.
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PMID:Acute renal failure due to obstruction in Burkitt lymphoma. 1035 13

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.
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PMID:Spontaneous acute tumor lysis syndrome with advanced gastric cancer. 1128 89

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.
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PMID:Oncologic emergencies for the internist. 1237 96

A 1.5-year-old ferret examined because of seizures was found to have low serum calcium, high serum phosphorus, and extremely high serum parathyroid hormone concentrations. Common causes of these abnormalities, including nutritional secondary hyperparathyroidism, chronic renal secondary hyperparathyroidism, tumor lysis syndrome, and hypomagnesemia, were ruled out, and a tentative diagnosis of pseudohypoparathyroidism was made. Pseudohypoparathyroidism is a hereditary condition in people that, to our knowledge, has not been identified in ferrets previously and is caused by a lack of response to high serum parathyroid hormone concentrations, rather than a deficiency of this hormone. The ferret improved after treatment with dihydrotachysterol (a vitamin D analog) and calcium carbonate. It was still doing well after 3.5 years of continued treatment.
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PMID:Suspected pseudohypoparathyroidism in a domestic ferret. 1271 Jul 72

Tumor lysis syndrome (TLS) is an important metabolic disorder frequently encountered in the management of a variety of cancers including lymphoma, leukemia, and neuroblastoma. Delayed recognition can result in a variety of biochemical abnormalities resulting in life-threatening complications such as renal failure, arrhythmias, and seizures. Identification of high-risk patients and early recognition of the syndrome is crucial in the early institution of appropriate prophylaxis and treatment. Recent advances in the understanding of urate metabolism, development of new urate-lowering drugs, and the application of biomarkers, calculation methods, and prognostic models to identify high-risk patients will pave the way in improving the management of TLS. We included in this review the new information regarding the urate transporters URAT-1, organic anion transporter 1/3, and MRP4; the urate elimination pathway; a comparison of the old- (allopurinol, native uricase) and new- (febuxostat, Y-700, PEG-uricase, rasburicase) generation urate-lowering agents; and application of new biomarkers (cystatin-C, neutrophil gelatinase-associated lipocalin, kidney injury molecule 1), estimated glomerular filtration rate and calculation methods (modification of diet in renal disease and prognostic model (Penn Predictive Score of Tumor Lysis Syndrome) in the identification of high-risk patients, and alternative unexplored mechanisms (asymmetric dimethylarginine and adenosine) to explain renal injury related to TLS.
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PMID:Tumor lysis syndrome. 1752 97

Seizure and epilepsy are common neurologic issues in cancer patients. Etiologies include structural abnormalities of the brain (eg, brain metastasis), cerebrovascular disease, reversible posterior leukoencephalopathy syndrome (RPLS), and radiation toxicity. Seizures associated with these etiologies often have focal features. Metabolic causes include hypoglycemia, electrolyte abnormalities, tumor lysis syndrome, thrombotic thrombocytopenic purpura (TTP), and medications used in cancer. A careful clinical evaluation can suggest the seizure etiology and guide subsequent work-up. Nonconvulsive status epilepticus should be suspected with persistent decreased level of consciousness following a seizure. Certain etiologies, such as RPLS and TTP, must be treated aggressively to minimize permanent neurologic injury. Routine prophylaxis with antiepileptic drugs (AEDs) is not recommended in patients with primary brain tumors or brain metastasis who have never had a seizure. Where indicated, the selection of AEDs should take into consideration side effects and interactions with chemotherapy. For this reason, non-enzyme-inducing AEDs are preferable in the cancer setting.
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PMID:Seizures and epilepsy in cancer: etiologies, evaluation, and management. 1836 62

Tumor lysis syndrome (TLS) is a potentially life-threatening metabolic disorder that occurs when tumor cells undergo rapid decomposition spontaneously or in response to cytoreductive therapy. Delayed recognition of the metabolic imbalances caused by the massive release of tumor cell contents may result in clinical complications such as acute kidney injury, seizures, and cardiac arrhythmias. Prevention, the key principle in TLS management, relies on the identification of patients at risk for developing TLS during chemotherapy or because of disease progression. TLS-related risk factors pertain to tumor type (particularly hematologic malignancies), specific tumor characteristics (e.g. bulky tumor, high cellular proliferation rate, sensitivity to cytoreductive therapy), and other host-related factors. A comprehensive grading system proposed by Cairo and Bishop classifies TLS syndromes into laboratory or clinical TLS, thus facilitating TLS prevention and management. The mainstays of TLS management include monitoring of electrolyte abnormalities, vigorous hydration, prophylactic antihyperuricemic therapy with allopurinol, and rasburicase treatment of patients at high TLS risk or with established hyperuricemia. Urine alkalinization and use of diuretics remain controversial clinical practices. In this review, we describe the incidence of, risk factors for, and diagnostic characteristics of TLS and summarize strategies for the prevention and management of TLS-associated metabolic abnormalities, particularly hyperuricemia. We specifically highlight recently published TLS management guidelines, which focus on the prevention of TLS and hyperuricemia based on a patient's level of risk, and the important role of nephrologists in the prevention and treatment of one of the most serious complications of TLS, acute kidney injury.
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PMID:An integrated clinical approach for the identification, prevention, and treatment of tumor lysis syndrome. 2003 31

Acute tumor lysis syndrome (ATLS) is characterized by severe metabolic abnormalities and organ dysfunction resulting from rapid destruction of neoplastic cells. Metabolic disturbances are thought to be the primary cause of clinical ATLS symptoms, which include renal dysfunction, seizures, and cardiac arrhythmias. The histopathologic lesions associated with organ dysfunction are largely unknown because of the low rate of mortality of ATLS in humans and the few cases of ATLS identified in laboratory animals. Here, we describe histologic, immunohistochemical, and electron microscopic analyses of thirty-one ATLS cases from a cohort of 499 mice that are prone to spontaneous lymphoblastic lymphoma owing to genetic defects in DNA replication fidelity. Seventy-three percent of our cohort died with lymphoblastic lymphoma, and 8% of affected mice died with diffuse microthromboemboli consistent with ATLS. Mice with ATLS had a high spontaneous mortality rate (>50%), a large tumor burden with disseminated disease, and evidence of leukemia. Blood vessels in the lung, kidney, and other organs were occluded by microthromboemboli composed of chromatin, cellular debris, fibrin, platelets, and entrapped erythrocytes and malignant cells. This case series suggests that ATLS can occur at high frequency in mice with disseminated lymphoblastic lymphoma and leads to a high rate of spontaneous death from microthromboemboli.
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PMID:Case series: acute tumor lysis syndrome in mutator mice with disseminated lymphoblastic lymphoma. 2019 Feb 1

Tumour lysis syndrome (TLS) is a life-threatening oncological emergency characterized by metabolic abnormalities including hyperuricaemia, hyperphosphataemia, hyperkalaemia and hypocalcaemia. These metabolic complications predispose the cancer patient to clinical toxicities including renal insufficiency, cardiac arrhythmias, seizures, neurological complications and potentially sudden death. With the increased availability of newer therapeutic targeted agents, such as rasburicase (recombinant urate oxidase), there are no published guidelines on the risk classification of TLS for individual patients at risk of developing this syndrome. We convened an international TLS expert consensus panel to develop guidelines for a medical decision tree to assign low, intermediate and high risk to patients with cancer at risk for TLS. Risk factors included biological evidence of laboratory TLS (LTLS), proliferation, bulk and stage of malignant tumour and renal impairment and/or involvement at the time of TLS diagnosis. An international TLS consensus expert panel of paediatric and adult oncologists, experts in TLS pathophysiology and experts in TLS prophylaxis and management, developed a final model of low, intermediate and high risk TLS classification and associated TLS prophylaxis recommendations.
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PMID:Recommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensus. 2033 65

Oncologic emergencies can occur at any time during the course of a malignancy, from the presenting symptom to end-stage disease. Although some of these conditions are related to cancer therapy, they are by no means confined to the period of initial diagnosis and active treatment. In the setting of recurrent malignancy, these events can occur years after the surveillance of a cancer patient has been appropriately transferred from a medical oncologist to a primary care provider. As such, awareness of a patient's cancer history and its possible complications forms an important part of any clinician's knowledge base. Prompt identification of and intervention in these emergencies can prolong survival and improve quality of life, even in the setting of terminal illness. This article reviews hypercalcemia, hyponatremia, hypoglycemia, tumor lysis syndrome, cardiac tamponade, superior vena cava syndrome, neutropenic fever, spinal cord compression, increased intracranial pressure, seizures, hyperviscosity syndrome, leukostasis, and airway obstruction in patients with malignancies. Chemotherapeutic emergencies are also addressed.
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PMID:Oncologic emergencies: Pathophysiology, presentation, diagnosis, and treatment. 2185 93


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