Radiotherapy-induced tumor lysis syndrome in a dog with thymoma.

A 13-year-old, female, mixed-breed dog with a huge cranial mediastinal mass underwent radiotherapy (RT). On the following day, the dog presented with lethargy and anorexia. Hematological examination revealed elevated levels of blood urea nitrogen, creatinine, inorganic phosphorus, potassium, lactate dehydrogenase, creatine phosphokinase and aspartate aminotransferase, decreased calcium level, and metabolic acidosis. Urine output markedly decreased. The patient recovered with fluid therapy and diuretic therapy; however, died suddenly from an unknown cause 11 days after RT completion. Histopathological examination after necropsy showed thymoma in the cranial mediastinum and extensive tubular necrosis of both kidneys which may be due to RT-induced tumor lysis syndrome (TLS). This report suggests that the risk of TLS should be evaluated in dogs with thymoma who undergo RT.

Feline anaplastic oligodendroglioma: long-term remission through radiation therapy and chemotherapy.

A 10-year-old spayed female Abyssinian cat was presented with cluster limbic focal seizures with secondary generalisation. From magnetic resonance imaging (MRI) findings, the cat was diagnosed clinically as having a glioma in the left piriform lobe, and hypofractionated radiation therapy (RT) was performed using a linear accelerator. Although the tumour size had reduced significantly at 4 months after RT, recurrence was observed at 11 months after RT. Additional RT was performed and was effective; however, recurrence was observed at 11 months after the additional RT. Chemotherapy was started using nimustine (ACNU; 30 mg/m(2), every 6 weeks). Tumour regression was confirmed by follow-up MRIs from 2 to 5 months after starting chemotherapy. Four years and 2 months after the first presentation the cat died as a result of tumour lysis syndrome following treatment of a high-grade lymphoma. Histopathological diagnosis of the brain tumour confirmed anaplastic oligodendroglioma.

Case series: acute tumor lysis syndrome in mutator mice with disseminated lymphoblastic lymphoma.

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.

Diagnostic exercise: sudden death in a mouse with experimentally induced acute myeloid leukemia.

A 22-week-old female 129/SvEv mouse suddenly died in the context of an experiment aimed at defining the efficacy of valproic acid in a mouse model of PML/RARalpha-induced acute myeloid leukemia. Histologic analysis confirmed the mouse as being affected by a progressive myeloid leukemia, with infiltration of the spleen, bone marrow, liver, kidneys, and lungs. Variably sized intravascular clumps (emboli) of dense basophilic material admixed with necrotic or lytic neoplastic cells were also observed in multiple organs. A positive reaction to Feulgen and Hoechst stain confirmed the high content in chromatin of these basophilic emboli. Cleaved caspase-3 activity was demonstrated both in the leukemic infiltrates and among the intravascular necrotic or lytic neoplastic cells accompanying the basophilic emboli. A diagnosis of acute tumor lysis syndrome related to therapy-induced massive necrosis and/or apoptosis of leukemic cells with subsequent dissemination of emboli of chromatin was proposed.

Acute tumour lysis syndrome in a dog with B-Cell multicentric lymphoma.

A 5-year-old, spayed female German Shepherd dog was admitted to hospital with marked generalised lymphadenomegaly and splenomegaly. A stage Va B-cell multicentric lymphoma was diagnosed on clinical, cytological (lymph node, bone marrow), histological-immunohistochemical (lymph node excision) and imaging grounds. Since no satisfactory remission was achieved using a multi-drug chemotherapy protocol that included cyclophosphamide, vincristine, cytosine arabinoside, prednisolone, and subsequently supplemented by L-asparaginase, it was replaced by another protocol combining vincristine, L-asparaginase, prednisolone, cyclophosphamide and doxorubicin. Soon after the third weekly session of the second protocol, the clinical status of the animal deteriorated suddenly and severely, with a bleeding tendency, jaundice, hyperuricaemia, hyperphosphataemia, azotaemia, hyperbilirubinaemia and, presumptive disseminated intravascular coagulation. There was also complete regression of lymphadenomegaly. This report emphasises the clinicopathological features and the diagnostic peculiarities of the acute tumour lysis syndrome, which occurs uncommonly in dogs.

Spontaneous acute tumor lysis syndrome in a DBA/1J mouse: a case report and review.

Spontaneous acute tumor lysis syndrome (ATLS) was diagnosed in a 10-month-old female DBA/1J sentinel mouse with leukemic lymphoma. The mouse was unable to maintain balance and died shortly after being observed rolling around in its cage. Disseminated neoplastic disease, including a large cranial mediastinal mass, enlarged lymph nodes and splenomegaly, was present at necropsy. Histopathologic examination revealed widespread massive necrosis of lymphoblastic tumor cells, and widely disseminated microemboli composed of nuclear and cytoplasmic cell debris. Although ATLS is widely recognized as an oncologic emergency in humans, acute lesions of ATLS have not been described. The mechanical obstruction of capillary beds by microemboli originating from disintegrating necrotic tumor cells was the likely cause of clinical signs and death in this mouse. We propose that similar microemboli may contribute to the pathogenesis of the acute renal failure and other clinical signs associated with ATLS in humans. Recognition of spontaneous ATLS in laboratory animals is especially important in studies that assess the efficacy and/or toxicity of anticancer treatments, where early deaths due to ATLS might mistakenly be attributed to a direct test article effect.

Oncologic emergencies.

Cancer can lead to emergencies either due to the primary disease, or as a result of therapy. Appropriate diagnosis and rapid treatment of these conditions can result in survival of the patient. Whether chemotherapy is implemented or not, the clinician may be presented with a patient in need of emergency stabilization. Common occurring emergencies are related to effects of the cancer, ranging from immune dysfunction due to marrow infiltration to brain herniation due to increased intracranial pressure from neoplasia. Often adverse effects secondary to chemotherapy can cause emergency situations such as sepsis. Prompt diagnosis and treatment may result in a favorable outcome. Addressed in this chapter are commonly occurring emergencies and specific stabilizing treatments.

Transient hypoparathyroidism following successful treatment of hypercalcaemia of malignancy in a dog.

A 4-year-old, entire female, English Cocker Spaniel was presented for treatment of lymphosarcoma and secondary hypercalcaemia. After induction chemotherapy the dog became severely hypocalcaemic and showed signs of weakness, muscle fasciculation and facial pruritus. Hormone analysis confirmed inadequate production of parathyroid hormone. Although hypocalcaemia has been previously reported as a component of tumour lysis syndrome, it has not been associated with transient parathyroid hormone deficiency.

[Tumor lysis syndrome in a dog]. / Tumor lysis syndroom bij een hond.

The acute tumour lysis syndrome in humans as well as in dogs is caused by the acute lysis of tumour cells following chemotherapy. The release of intracellular products and their metabolites result in hyperkalemia, hyperphosphatemia, and hyperuricemia. The precipitation of uric acid and calciumphosphate in the kidneys can lead to hypocalcemia and acute renal failure which leads to fatal azotemia and arrhythmia's due to electrolyte disturbances. In this article the occurrence of the acute tumour lysis syndrome in a dog with malignant lymphoma is described. Suggestions to prevent the tumour lysis syndrome are made.