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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2018  |  Volume : 29  |  Issue : 6  |  Page : 1480-1483
Vitamin B1 for type B metabolic acidosis: An underrecognized approach

1 Katz Family Division of Nephrology and Hypertension, University of Miami Miller School of Medicine, Miami, FL, USA
2 Department of Internal Medicine, Universidad Ricardo Palma, Santiago de Surco, Peru

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Date of Submission14-Dec-2017
Date of Acceptance17-Jan-2018
Date of Web Publication27-Dec-2018


Lactic acidosis is a life-threatening and rather common complication and reason for consultation to the nephrologist. The cause for this condition is usually thought to be secondary to hypoperfusion and ischemia collectively. However, many other rare causes have been described, yet there is little awareness of these, consequently delaying optimal care. We present a multifactorial case of lactic acidosis due to thiamine deficiency, liver disease, and lymphoma; all underrecognized causes of Type B lactic acidosis.

How to cite this article:
Dejman A, Riveros J. Vitamin B1 for type B metabolic acidosis: An underrecognized approach. Saudi J Kidney Dis Transpl 2018;29:1480-3

How to cite this URL:
Dejman A, Riveros J. Vitamin B1 for type B metabolic acidosis: An underrecognized approach. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2022 Dec 4];29:1480-3. Available from: https://www.sjkdt.org/text.asp?2018/29/6/1480/248314

   Introduction Top

Lactic acidosis is an alarming finding in any patient given its correlation with mortality and poor outcomes.[1] It is regularly recognized in critically ill patients as it is commonly used in the setting of shock; however, there are numerous causes that remain unfamiliar and may delay optimal management.

We present a case of a chronically ill patient with mantle cell lymphoma and bladder cancer, who presented complaining of nausea and vomiting and was found to have profound anion gap metabolic lactic acidosis with no hemodynamic compromise or hypoperfusion state.

   Case Report Top

A 66-year-old man with a history of Stage IV mantle cell lymphoma diagnosed two years before presentation was treated with bendamustine and only two doses of rituximab (as was limited by an anaphylactic reaction). He had a poor response with persistent gigantic splenomegaly and hypersplenism who developed macroscopic hematuria, and workup revealed transitional cell bladder cancer. He underwent splenectomy three months preceding current presentation, to receive chemotherapy with gemcitabine two months before. Subsequently, weeks after first cycle, he presented to an outside hospital with nausea and vomiting, and workup revealed severe anion gap metabolic acidosis and was referred to our tertiary care center for further management.

At all times, the patient had been hemo-dynamically stable and no clinical or radiological signs of shock or hypoperfusion. His initial arterial blood gas showed a pH of 7.14, bicarbonate of 9 mmol/L, carbon dioxide of 27, oxygen of 57, base excess of negative 20, oxygen saturation of 88%, lactic acid level of 22.4 mmol/L, and anion gap of 29 [Table 1]. He was started on an isotonic solution of 150 mEq bicarbonate mixed in dextrose 5% water at 250 mL/h. With no improvement in the next 48 hours proven by a pH of 7.12, bicarbonate of 13, carbon dioxide of 45, base excess of negative 15, lactic acid of 23.4, and anion gap of 27 [Table 1], it was decided to start the patient on continuous venovenous hemofiltration in attempt to provide more mEq of bicarbonate per hour, prevent a decrease in ionized calcium, prevent volume overload and hyper-osmolality, and remove an unidentified toxin, if any. Despite this intervention, laboratory markers remained intact. While the repeat bone marrow biopsy results were available, it was decided to start empiric intravenous (IV) thiamine supplementation at a dose of 100 mg IV daily x3 doses. After the first infusion, the lactic acid level dropped from >24 to 19.1, and after the second dose, it dropped to 11 [Figure 1]. Of note, chemotherapy was given after the second infusion of thiamine. The patient received a second dose of chemotherapy and third IV thiamine infusion, but he succumbed to rapid presumptive septic shock that same day. Thiamine level came back days after at 8 μg/dL, low-normal level.
Table 1: Laboratory values in relation to disease status and effects of thiamine infusion and chemotherapy.

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Figure 1: Trend of lactic acid during patient’s hospital stay with represented interventions.

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   Discussion Top

Lactic acidosis was first described as a surrogate for illness severity and poor outcome in 1964.[2] Since then, we know that hyper-lactatemia may arise from tissue hypoxia or hypoperfusion (Type A) or from other causes not related to tissue hypoxia (Type B).[3]

The scope of this report emphasizes on the Type B lactic acidosis as our patient presented with severe hyperlactatemia to the expense of three presumptive underlying causes known to cause Type B lactic acidosis: liver disease in the setting of metastatic cancer, thiamine deficiency, and mantle cell lymphoma.

The liver accounts for up to 70% of whole-body lactate clearance.[4] In aerobic conditions, pyruvate is produced through glycolysis and then enters the Krebs cycle, mostly dodging lactate production. Under anaerobic conditions, lactate is an end product of glycolysis and feeds into the Cori cycle as a substrate for gluconeogenesis.[5] However, in liver disease, hyperlactatemia results from both reduced clearance and increased production and is an important prognostic factor.[4]

In hemodynamically stable patients with sepsis, lactate clearance by the liver can be decreased, possibly through pyruvate dehy-drogenase inhibition. In sepsis and low-flow states, chronic liver disease further compromises lactate clearance. Nonetheless, chronic liver disease alone causes only minimal hyperlactatemia.[4]

Thiamine serves as a cofactor for multiple cellular enzymes. Particularly, for the span of our case, it is essential for the catalyzation of pyruvate into acetyl-coA to enter the Krebs cycle and produce adenosine-triphosphate in an aerobic environment.[5] In the absence of thiamine, anaerobic metabolism predominates and lactate production increases.[6] The development of elevated lactate in both serum and cerebrospinal fluid secondary to thiamine deficiency has been well described in the literature.[7]

Risk factors for thiamine deficiency include states of nutritional deficiency such as alcoholism, chronic liver disease, chronic wasting diseases, hyperemesis gravidarum, anorexia nervosa, and gastric bypass surgery.[8],[9] It is an often-overlooked etiology but easily treated condition that can reverse within 24 h with IV supplementation.[4],[10]

The most common types of malignancies associated with Type B lactic acidosis are rapidly progressive leukemia or lymphoma, often with liver involvement.[5] It was first described in 1963,[11] and since then, case series and case reports conclude that it has an ominous prognosis. Its pathophysiology is poorly understood; however, it has been stipulated that because cancer cells have a high rate of glycolysis and produce a large quantity of lactate, this condition may result from an imbalance between lactate production and hepatic lactate utilization and also others suggest that thiamine or riboflavin deficiency in these patients may play a more fundamental role in the development of Type B lactic acidosis associated with malignancy.[12],[13],[14],[15]

Kumar and Raina reported a case of non-Hodgkin’s lymphoma that debuted with lactic acidosis and was started on sodium bicarbonate and chemotherapy conjunctively, and by day 7 of starting therapy, the lactate levels had a significant decrease.[12] A slightly different case reported by Masood et al narrated a patient with B-cell lymphoma and concomitant thiamine deficiency that had severe lactic acidosis, and within 24 h of infusing IV thiamine, the acidosis corrected entirely. Of note, chemotherapy was given after this correction.[15]

Based on these cases and the aforementioned ones where thiamine-related lactic acidosis resolved within 24 h of infusion, we propose that our patient’s lactic acidosis was likely steered by thiamine deficiency as the levels dropped from >24 to 11 after two infusions. We acknowledge that the patient did receive chemotherapy after the second thiamine infusion, though, based on other reviews discussed in Kumar et al[12] and Sillos et al[13] publications, chemotherapy-driven correction of lactic acidosis is slower. It could, however, be postulated that there exists a possible synergistic effect between thiamine supplementation and chemotherapy in these ill, malnourished, cancer patients.

While its clinical significance has been known for decades, thiamine deficiency remains an unfamiliar condition. Physicians should have an increased awareness of this problem and a low threshold to infuse high-dose thiamine. In summary, acute lactic acidosis carries a threatening prognosis. Rapid diagnosis and initiation of therapy is essential to reducing mortality.

Conflict of interest: None declared.

   References Top

Kraut JA, Madias NE. Lactic acidosis. N Engl J Med 2014;371:2309-19.  Back to cited text no. 1
Broder G, Weil MH. Excess lactate: An index of reversibility of shock in human patients. Science 1964;143:1457-9.  Back to cited text no. 2
Woods HF, Robert C. Clinical and Bio-chemical Aspects of Lactic Acidosis. Oxford: Blackwell Scientific; 1976.  Back to cited text no. 3
Jeppesen JB, Mortensen C, Bendtsen F, Møller S. Lactate metabolism in chronic liver disease. Scand J Clin Lab Invest 2013;73:293-9.  Back to cited text no. 4
Andersen LW, Mackenhauer J, Roberts JC, Berg KM, Cocchi MN, Donnino MW. Etiology and therapeutic approach to elevated lactate levels. Mayo Clin Proc 2013;88:1127-40.  Back to cited text no. 5
Butterworth RF. Thiamine deficiency-related brain dysfunction in chronic liver failure. Metab Brain Dis 2009;24:189-96.  Back to cited text no. 6
Klein M, Weksler N, Gurman GM. Fatal metabolic acidosis caused by thiamine deficiency. J Emerg Med 2004;26:301-3.  Back to cited text no. 7
Donnino MW, Vega J, Miller J, Walsh M. Myths and misconceptions of Wernicke’s encephalopathy: What every emergency physician should know. Ann Emerg Med 2007;50:715-21.  Back to cited text no. 8
Saad L, Silva LF, Banzato CE, Dantas CR, Garcia C Jr. Anorexia nervosa and Wernicke-Korsakoff syndrome: A case report. J Med Case Rep 2010;4:217.  Back to cited text no. 9
Amrein K, Ribitsch W, Otto R, Worm HC, Stauber RE. Severe lactic acidosis reversed by thiamine within 24 hours. Crit Care 2011;15: 457.  Back to cited text no. 10
Field M, Block JB, Rall DP. Lactic acidosis in acute leukemia. Clin Res 1963;11:193-7.  Back to cited text no. 11
Kumar A, Raina V. Non-Hodgkins lymphoma with lactic acidosis at presentation: A case report of a rare oncologic emergency. Indian J Med Paediatr Oncol 2014;35:83-5.  Back to cited text no. 12
[PUBMED]  [Full text]  
Sillos EM, Shenep JL, Burghen GA, Pui CH, Behm FG, Sandlund JT. Lactic acidosis: A metabolic complication of hematologic malignancies: Case report and review of the literature. Cancer 2001;92:2237-46.  Back to cited text no. 13
Friedenberg AS, Brandoff DE, Schiffman FJ. Type B lactic acidosis as a severe metabolic complication in lymphoma and leukemia: A case series from a single institution and literature review. Medicine (Baltimore) 2007;86: 225-32.  Back to cited text no. 14
Masood U, Sharma A, Nijjar S, Sitaraman K. B-cell lymphoma, thiamine deficiency, and lactic acidosis. Proc (Bayl Univ Med Cent) 2017;30:69-70.  Back to cited text no. 15

Correspondence Address:
Dr. Adriana Dejman
Katz Family Division of Nephrology and Hypertension, University of Miami Miller School of Medicine, Miami, FL, 33136
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.248314

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