Texas Tech University Health Sciences Center Lubbock, TX
Genanew D. Bedanie, MD1, Alay G. Tikue, MD1, Thanita Thongtan, MD1, Sara Mousa, MD2, Sameer Islam, MD1; 1Texas Tech University Health Sciences Center, Lubbock, TX; 2University Medical Center, Lubbock, TX
Introduction: Type B lactic acidosis secondary to GI solid tumor is very rare though can be seen in patients with leukemia. It occurs when excess lactate is produced despite normal systemic perfusion. Its presence indicates poor outcome. We present a patient who developed type B lactic acidosis due to advanced adenocarcinoma of the colon with liver metastasis.
Methods: A 61-year-old man with stage IV adenocarcinoma of the colon was admitted with fatigue, nausea, shortness of breath and abdominal pain. He was afebrile and no source of infection was identified. On examination he was emaciated, blood pressure 130/77mmHg, heart rate 116 beat/min, respiratory rate 24 breath/min, and temperature of 36F. Chest was clear and normal heart sounds. Abdominal exam showed right upper quadrant tenderness and an enlarged liver.
Laboratory test revealed white blood cell count 12K, hemoglobin 13gm/dL, and platelet 346K. Alanine transferase 74units/L, aspartate transaminases 111units/L, alkaline phosphatase 724units/L and total bilirubin 2.0mg/dl. PH 7.2, bicarbonate 5.9, Lactate went up from 14- >24mmol/L despite appropriate fluid resuscitation and bicarbonate infusion. The patient was covered with antibiotics for possible sepsis. Computed tomography of the abdomen/pelvis revealed rectal mass and likely liver metastasis (Figure 1,2). Colonoscopy showed a partially obstructing mass in the recto-sigmoid colon. Colon and liver biopsy confirmed invasive adenocarcinoma. Discussion: Type B lactic acidosis is very rare, but it is a life threatening complication of malignancy. It was first described by Field et al in 1963 in a patient with hematologic malignancy. Exact pathogenesis is unclear, but absence of systemic hypo-perfusion is the hallmark. The cancer cells switch their metabolism to lactic acid pathway for tumor cell proliferation (Warburg effect), this leads to anaerobic glycolysis due to overexpression of glycolytic enzymes and over production of lactate by the tumor cells. Local hypoxia related to extensive tumor infiltration and ischemic damage is also contributory. About 80% of lactate is metabolized by liver, and metastasis can derange liver function, however, type B lactic acidosis was reported in multiple patients with normal liver function. This indicates pathogenesis is multifactorial. It is recommended to treat patient as type A lactic acidosis until the cause is identified. Chemotherapy is a corner stone to lower lactate level in hematologic malignancy, but response is slow in other solid tumors.
Figure 1: Mild enlargement of innumerable hepatic metastases resulting in overall enlargement of the liver and elevation of the right hemidiaphragm. Enlarging retroperitoneal nodal metastases.
Figure 2: Computed tomography of abdomen/pelvis revealed moderate-sized peri-colonic mass in the pelvis with enlarging satellite nodules. Interval placement of a stent in the recto-sigmoid colon with mild mural thickening of the colon.
Disclosures: Genanew Bedanie indicated no relevant financial relationships. Alay Tikue indicated no relevant financial relationships. Thanita Thongtan indicated no relevant financial relationships. Sara Mousa indicated no relevant financial relationships. Sameer Islam indicated no relevant financial relationships.