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132 STEROID-INDUCED LACTIC ACIDOSIS IN LYMPHOMA.
  1. A. Sequeira1,
  2. B. Nair1,
  3. P. Isaac1,
  4. V. Vachharajani1,
  5. L. Slay1
  1. 1Louisiana State University Health Sciences Center, Shreveport, LA.

Abstract

Introduction Lactic acidosis may occur in lymphoma from various mechanisms. We describe a case of lymphoma-associated lactic acidosis that may have been precipitated by corticosteroid therapy.

Case A 50-year-old woman was admitted with a 3-week history of fatigue, anorexia, headaches, and fever. Physical examination was remarkable for a blood pressure of 90/70 mm Hg, pulse 120/min, and dry mucus membranes. No lymphadenopathy or hepatosplenomegaly were noted. Pertinent laboratory data: Hgb 13.6 g/dL, WBC 4,500/mm3, Na+ 132 mEq/L, K+ 3.4 mEq/L, BUN 31 mg/dL, and creatinine 2.1 mg/dL. She was hydrated aggressively, with marked improvement in blood pressure and creatinine (1.3 mg/dL). Bilateral suprarenal masses on ultrasonography led to CT of the chest, abdomen, and pelvis. Multiple pulmonary nodules, mediastinal lymphadenopathy, and nonenhancing bilateral adrenal masses (right 10 × 7.3 cm; left 9 × 7.9 cm) were found. Subsequent evaluation revealed adrenal insufficiency. MRI of the brain revealed a 19 mm pituitary mass compressing the optic chiasm. Visual fields were intact. Hydrocortisone 30 mg po bid was initiated. Prior to percutaneous mediastinal lymph node biopsy, she received hydrocortisone 100 mg IV for 2 days. Four days later, she developed worsening renal failure, lactic acidosis (10 mmol/L), and drowsiness. Hydrocortisone was increased to 100 mg IV q8h. Because of a nondiagnostic mediastinal biopsy, mediastinoscopy was performed, which revealed malignant lymphoma. Bone marrow biopsy and immunophenotyping led to a diagnosis of disseminated T-cell lymphoma. Following mediastinoscopy, severe lactic acidosis persisted, and she developed multiorgan failure, from which she succumbed.

Discussion Lactic acidosis is a rare but fatal complication of lymphoproliferative malignancies. It characteristically develops suddenly, in association with extensive disease. Proposed mechanisms include increased glycolysis by tumor cells, impaired hepatic and renal clearance, local hypoxia in large tumors, and thiamine deficiency. Recent studies suggest that during apoptosis, tumor cells produce large amounts of lactate. This may occur with cytoreductive chemotherapy or corticosteroid monotherapy. This patient receive no specific therapy for lymphoma. We postulate that the large doses of steroids she received prior to the diagnostic procedures contributed to the propagation of lactic acidosis by causing tumor apoptosis.

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