Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lactic acidosis has been described in patients with leukemia and lymphoma, but its occurrence in other malignant diseases is not documented. We treated two patients with oat cell carcinoma of the lung and extensive liver metastases in whom lactic acidosis developed. Tumor-induced hepatic dysfunction appeared to be a major factor in the pathogenesis of the lactic acidosis observed in these patients.
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PMID:Lactic acidosis in oat cell carcinoma with extensive hepatic metastases. 21 48

In this article, the acid-base disturbances encountered in hematologic diseases are discussed. Occurrence of lactic acidosis (LA) without obvious clinical tissue hypoxia has been reported in patients with leukemia and lymphoma. Most of the patients with LA had liver involvement and clinical evidence of impaired hepatic function, suggesting that both increased production and decreased lactate metabolism are necessary for the development of LA in leukemia and lymphoma. Acute tumor lysis syndrome consists of hyperuricemia, hyperpotassemia, and hyperphosphatemia with hypocalcemia following neoplastic cell lysis, particularly in lymphoproliferative disorders. In patients with multiple myeloma (MM), proximal renal tubular acidosis (Fanconi syndrome) associated with Bence Jones proteinuria has been reported. In addition, MM is one of the first conditions recognized to be associated with lower anion gap.
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PMID:[Acid-base disturbances in hematologic diseases]. 143 14

We report a patient with myelomonocytic leukaemia, persistent hypokalaemia and lactic acidosis. Cytotoxic chemotherapy induced a short remission with normalisation of the potassium concentration; death resulted from lactic acidosis. These two uncommon complications of leukaemia are discussed briefly.
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PMID:Hypokalaemia and lactic acidosis in a patient with myelomonocytic leukemia. 231 22

Lactic acidosis or hypoglycemia occasionally occurs in patients with neoplastic diseases. We have described a patient with monocytic leukemia who had both, apparently as a result of marked leukemic infiltration of the liver. These metabolic anomalies were greatly ameliorated by chemotherapy. Thus, in leukemia and other malignant disorders in which significant liver infiltration is present, these metabolic derangements should be looked for, as their presence may call for a prompt and intensive treatment.
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PMID:Prolonged and concurrent lactic acidosis and hypoglycemia in a patient with monocytic leukemia. 693 23

Occurrence of lactic acidosis with adequate tissue oxygenation (type B lactic acidosis) has been described in association with leukemia, lymphoma and a single case of Hodgkin's disease. No cases of this type have been reported in association with solid tumors. A case of type B lactic acidosis in a woman with rapidly progressing metastatic breast carcinoma is described.
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PMID:Lactic acidosis associated with metastatic breast carcinoma. 747 Nov 17

A patient with an intermediate grade B-cell non-Hodgkin's lymphoma who presented with severe dyspnea caused by lymphoma-related lactic acidosis is described. The serum lactate and pyruvate levels paralleled the disease activity. Although oncologists are familiar with the relationship between bulky solid tumors and lactic acidosis, well-documented lymphoma cases are extremely rare.
Leukemia 1994 Jun
PMID:Lactic acidosis in a patient with B-cell non-Hodgkin's lymphoma. 820 79

Acute tumour-lysis syndrome (ATLS) is a frequently fatal complication after cytoreductive leukaemia therapy. Lactic acidosis is associated with ATLS and its extent is correlated with the severity of ATLS. In the course of cytoreductive therapy, apoptosis is induced in tumour cells, which results in loss of mitochondrial function. We hypothesize that loss of mitochondrial function leads to compensatory glycolysis, which is the main cause of lactate accumulation and acidosis. We tested this hypothesis using the model of glucocorticoid-induced apoptosis in the human acute lymphoblastic leukaemia cell line CCRF-CEM. After induction of glucocorticoid-induced apoptosis, a biphasic course of lactate production was observed. Prior to the onset of apoptosis, i.e. prior to the loss of membrane potential, lactate production was reduced. However, subsequent to loss of mitochondrial membrane potential a massive increase in lactate production was observed (15.5 +/- 0.5 versus 10.17 +/- 0.09 mmol/10(6) cells, P = 0.001). We also demonstrated that inhibition of respiratory chain activity by antimycin A resulted in excess lactate production. In the model cell line used, conditional bcl-2 expression delayed glucocorticoid-induced apoptosis by protecting against loss of mitochondrial membrane potential; bcl-2 expression delayed the increase in lactate production and had no effect on the pre-apoptotic drop in lactate production. Apoptosis-induced lactate production was also observed in other cell lines (HL60, THP1 and OPM2) with various cytotoxic agents [doxorubicin, gemcitabine and vumon (VM26)]. Thus, the data suggest that lactate acidosis can be caused by apoptotic loss of mitochondrial function and massive apoptosis of a tumour mass via lactic acidosis may be the essential pathological event in ATLS.
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PMID:Increased lactate production follows loss of mitochondrial membrane potential during apoptosis of human leukaemia cells. 1155 82

Type B lactic acidosis is rare among patients with malignant diseases. To date only one case report has documented lactic acidosis occurring in a patient with multiple myeloma (MM). Our patient, a 55-year-old black man, was diagnosed with stage IIIA immunoglobulin G-kappa (IgG-kappa) MM in September 1995. He was found to have severe lactic acidosis at the time of second relapse. During the terminal phase of his disease, he required multiple hospitalizations for management of lactic acidosis and other complications of his MM. No other cause of his elevated lactate levels was identified. Although type B lactic acidosis may more commonly occur in patients with leukemia or lymphoma, it may rarely present in patients with rapidly progressive and refractory MM.
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PMID:Multiple myeloma associated with lactic acidosis. 1261 30

An 11-month-old girl with B-cell leukemia/lymphoma developed profound lethargy due to severe lactic acidosis during chemotherapy and total parenteral nutrition (TPN). Initial treatment with NaHCO3 was ineffective. Treatment with a vitamin cocktail (OH-cobalamin, pyridoxine, thiamine, riboflavine, biotin, carnitine) at pharmacologic doses rapidly improved the child's clinical and laboratory status. Lactic acidosis was caused by an impairment of pyruvate dehydrogenase complex, which was due to lack of its necessary cofactor thiamine in the TPN. This case report indicates that lactic acidosis may be a front-line diagnosis in patients on TPN with lethargy and outlines the need for monitoring thiamine supply in TPN.
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PMID:Severe lactic acidosis due to thiamine deficiency in a patient with B-cell leukemia/lymphoma on total parenteral nutrition during high-dose methotrexate therapy. 1466 73

Lactic acidosis (LA) associated with hematologic malignancies is uncommon, life-threatening, and generally occurs in adults. Its pathogenesis is poorly understood. This is a case report of LA due to leukemic transformation that occurred in a patient with non-Hodgkin's lymphoma (NHL). A 24-year-old man with NHL was admitted to the hospital with dyspnea. Venous blood gas analysis revealed metabolic acidosis (pH 7.05; HCO3 6 mEq/L; BE 22 mmol/L; anion gap 28 mEq/L); the patient had an elevated plasma lactate concentration (12 mmol/L) and low glucose concentration (38 mg/dL). There was no reason other than leukemia-such as infection, circulatory failure, or drug use-for the development of severe LA. This case report shows that in patients with NHL, leukemic transformation may give rise to LA.
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PMID:Fatal lactic acidosis due to leukemic transformation in a patient with non-Hodgkin's lymphoma: case report. 1641 52


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