A 66-year-old Caucasian female presented to the emergency room with a history of vomiting, diarrhea, worsening shortness of breath, and decreased oral intake. She was previously diagnosed with stage IV non-small cell lung carcinoma. She has a 20 pack-year history of cigarette smoking (1/2 a pack per day for 40 years) prior to diagnosis. On examination she had positive rhonchi bilaterally and decreased breath sounds in the right lower lobe. She had a right pleural effusion on chest X-ray. Her initial biochemical and hematology results are: serum chemistry -sodium 138 mmol/L, potassium 6.9 mmol/L, chloride 89 mmol/L, CO 2 15 mmol/L, glucose 8.1 mmol/L, blood urea nitrogen (BUN) 35.3 mmol/L, creatinine 301 μmol/L, phosphate 1.91 mmol/L, total calcium 2.2 mmol/L, albumin 26 g/L, alanine aminotransferase (ALT) 117 IU/L, alkaline phosphatase (ALP) 431 IU/L, lactate dehydrogenase (LD) 4,477 IU/L, total bilirubin 65 μmol/L, white blood cell (WBC) count 21.6 × 10 9 /L, hemoglobin 143 g/L, mean cell volume (MCV) 98.4 fL, platelets 169 × 10 9 /L, lymphocytes 5%, granulocytes 89.7%, monocytes 3.0%, basophils 1.9%, eosinophils 0.4%.
DiscussionThis patient was found to have advanced carcinoma of the lungs and was admitted with a diagnosis of acute renal failure and metabolic acidosis secondary to vomiting and diarrhea. She also had pleural effusion for which she had a chest tube placed. Her liver enzymes showed that LD activity was increased to a greater degree compared with ALT and aspartate aminotransferase (AST) activities. The tumor cells were most likely the main source of LD. Some rapidly growing cancer cells depend on anaerobic glycolysis to generate ATP, even in the presence of adequate oxygen (the Warburg effect), thereby producing more lactate via LD [1]. Adenocarcinoma of the lung is strongly associated with cigarette smoking. A very high total LD, which can be as high as 20 times the upper reference limit, has been reported to be associated with poor outcome and a low survival rate [2]. Increased LD in lung carcinoma has been mainly attributed to LD 3 , LD 4 , and LD 5 isoenzymes [3,4]. In this case, LD isoenzymes were not measured. The renal function of this patient was compromised, as indicated by abnormal BUN and creatinine concentrations. In addition, leukocytosis suggests that this patient has an underlying infection. All these processes would result in tissue destruction and contribute to the circulating pool of LD. Patients who have