Severe Lactic Acidosis and Renal Involvement in a Patient with Relapsed Burkitt's Lymphoma

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Title: Severe Lactic Acidosis and Renal Involvement in a Patient with Relapsed Burkitt's Lymphoma
Authors: Revesz, T.; Obeid, K.; Mpofu, C.
Publisher: Pediatric Hematology and Oncology
Date Published: May 1995 - June 1995
Reference Number: 69
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We describe an 8-year-old patient with relapsed Burkitt's lymphoma who developed complex metabolic problems, including renal diabetes insipidus and severe lactic acidosis. The lactic acidosis responded temporarily to chemo- and radiotherapy but not to bicarbonate or thiamine administration. These metabolic changes were most likely due to the lymphomatous infiltration of the kidneys. Severe lactic acidosis, without evidence of thiamine deficiency, seems to be a very rare event in children with cancer.

This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)

Revesz, et al. report on an 8-year-old male patient suffering from a type of cancer called Burkitt's lymphoma. He developed complex metabolic problems including lactic acidosis and kidney-related diabetes insipidus. Lactic acidosis is a rarely documented complication of malignant cancers. In children with cancer, it is often due to a diet-induced thiamin deficiency and is easily remedied. This patient's lactic acidosis did not respond to thiamin treatment.

At the initial diagnosis, the patient's kidneys were functioning normally, though they were larger than normal. He was placed on chemotherapy, but continued to decline and the cancer spread into the testes. At this time, a month into the chemotherapy, the patient's kidneys, though larger than normal, still functioned normally. After five months of intensive chemotherapy, the patient's condition improved considerably. Two months later, while still on chemotherapy, his condition deteriorated. He had two seizures and developed diabetes insipidus related to the kidney. His kidneys were still enlarged. This enlargement was due to the spread of the cancer to these organs. The patient developed severe metabolic acidosis that could not be controlled. During his last few weeks of life, his kidneys' ability to filter bodily fluid declined as the cancerous tumor continued to infiltrate the kidneys.

The nature of the process by which lactic acidosis occurs in malignancy is unclear. It occurs in only a very small percentage of patients and often without any identifiable precipitating event. Plasma lactate is regulated by the balance between lactate production and its use. The liver is responsible for removing up to 70% of plasma lactate, and the kidney removes the rest. The lymphomatous infiltration of the kidneys in the patient could have indicated both an overproduction of lactic acid by the tumor cells and an impaired kidney uptake of lactate. This could account for the severe lactic acidosis.