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B-cell lymphoma, thiamine deficiency, and lactic acidosis
Umair Masood, MD, Anuj Sharma, MD, Sonny Nijjar, MD, and Karthikeyan Sitaraman, MD
Type B lactic acidosis is found in the absence of tissue hypoperfusion,
can be associated with malignancies, and can be caused by thiamine
deficiency. We present a patient who presented with an abdominal mass
that biopsy disclosed to be a diffuse large B-cell lymphoma. Because
thiamine deficiency is a rare cause of lactic acidosis in cancer, the patient
was treated with intravenous thiamine with rapid normalization of the
lactic acid level. The level prior to treatment was low. The case emphasizes a rare cause of lactic acidosis.
T
ype A lactic acidosis is commonly due to marked tissue
hypoperfusion, whereas type B lactic acidosis is found
without tissue hypoperfusion (1). Rarely, lactic acidosis
is associated with aggressive solid tumors such as lymphomas. It can be due to various causes including thiamine
deficiency. We present a patient with type B lactic acidosis due
to deficiency of thiamine in the setting of a B-cell lymphoma.
CASE DESCRIPTION
A healthy 72-year-old man presented to the emergency
department with vague abdominal discomfort and swelling of
his left lower extremity. He had a left lower quadrant palpable
mass with mild diffuse tenderness and 2+ edema of the entire
left leg. His bicarbonate level was 18 mmol/L (reference range,
24 mmol/L). Other laboratory findings revealed a lactic acid level
of 6.7 mmol/L (reference range, 0.5–2 mmol/L) and hemoglobin
of 10.2 g/dL (reference range, 13.5–17.5 g/dL). His anion gap
was calculated to be 21 (reference range, 12–14). Liver function
tests, including albumin and total protein levels, were normal
(Table 1). A computed tomographic scan of the abdomen showed
a 9.8 × 8.4 × 12.0 cm retroperitoneal mass that appeared contiguous with the left kidney, with moderate left-sided hydronephrosis
(Figure 1). A left nephrostomy tube was placed. Biopsy of the
retroperitoneal mass confirmed it to be a diffuse large B-cell
lymphoma (Figure 2).
Despite adequate resuscitation and hydration, the patient’s
lactic acid level remained elevated. At that point, his thiamine
level was obtained, and the patient was treated with intravenous
thiamine (500 mg every 8 hours). By the morning, the lactic
acid level was 1.5 mmol/L. His thiamine level was found to be
0.9 μg/dL (reference range, 2.5–7.5 μg/dL). He was then started
Proc (Bayl Univ Med Cent) 2017;30(1):69–70
Table 1. Laboratory findings
Test
Value
Sodium (mEq/L)
136
Potassium (mEq/L)
4.3
Chloride (mEq/L)
97
Bicarbonate (mmol/L)
18
Blood urea nitrogen (mg/dL)
18
Creatinine (mg/dL)
0.9
Glucose (mg/dL)
135
Anion gap
21
Alanine aminotransferase (U/L)
45
Aspartate aminotransferase (U/L)
38
Alkaline phosphatase (U/L)
98
Albumin (g/dL)
3.6
Total protein (g/dL)
6.5
Total bilirubin (mg/dL)
0.5
Lactic acid (mmol/L)
6.7
Hemoglobin (g/dL)
10.2
Hematocrit
30.5%
White blood cell count (cell/mcL)
7400
Platelets (/mcL)
210,000
on chemotherapy for his malignancy. He had a prolonged hospital course with a chemotherapy-related complication of bone
marrow suppression but eventually responded well and was
transferred back to his hometown for physical rehabilitation
and follow-up with oncology.
DISCUSSION
Type A lactic acidosis is commonly found in patients with
marked tissue hypoperfusion that can be caused by sepsis,
From the Department of Internal Medicine, State University of New York Upstate
Medical University, Syracuse, New York.
Corresponding author: Umair Masood, MD, Department of Internal Medicine,
State University of New York Upstate Medical University, 750 East Adams Street,
Syracuse, NY 13204 (e-mail: [email protected]).
69
Figure 1. CT of the abdomen showing a left retroperitoneal mass contiguous
with the left kidney with some associated hydronephrosis.
cardiac failure, or hypovolemia. On the contrary, type B lactic
acidosis is found in the absence of tissue hypoperfusion (1). It
is a rare occurrence in patients with lymphomas, leukemias, and
solid neoplasms. While the mechanism is not entirely understood, there are many proposed theories, which include intrinsic
lactate production by the tumor cells, impaired clearance of
lactate in kidney or liver dysfunction, and riboflavin or thiamine
deficiency (2). Tumor cells have been found to have increased
lactate production, as they primarily utilize aerobic glycolysis,
which is also known as Warburg effect (3).
Thiamine acts as a cofactor for various enzymes involved in
aerobic metabolism, such as pyruvate dehydrogenase. Therefore,
its deficiency promotes anaerobic metabolism, which results
in the production of lactate (3). Only a few reported cases illustrate this phenomenon in patients with lymphomas (4, 5).
The cases have generally been reported in pediatric patients
receiving parenteral nutrition without vitamin supplementation.
Friedenberg et al examined this phenomenon in hematological
malignancies and found type B lactic acidosis due to thiamine
deficiency in patients with leukemia rather than lymphoma
(6). Seligmann et al reported subclinical thiamine deficiency
in 35% of 14 untreated CLL patients (7). Lactate levels were
not reported in either of the studies.
70
Figure 2. Hematoxylin and eosin stain, 20×, showing lymphoid cells with fine
nuclear chromatin, scant pale cytoplasm, and round nuclei consistent with diffuse large B cell lymphoma.
Acknowledgments
The authors thank Dr. Daniel Zaccarini for providing the
histological image.
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Baylor University Medical Center Proceedings
Volume 30, Number 1