A 31-year-old previously healthy female presented to the Emergency Department with two days of severe epigastric pain, nausea, rectal bleeding, and non-bloody emesis. She endorsed 50 pounds of unintentional weight loss over the past year that she attributed to decreased appetite and “picky eating.” The patient reported social drinking and denied any drug use or smoking.

The initial evaluation of this patient should focus on narrowing a relatively broad differential diagnosis. Her symptoms could be explained by gastrointestinal causes such as peptic ulcer disease, gastritis, and malignancy, given the epigastric pain, rectal bleeding, and weight loss. Pancreatic and hepatobiliary causes, including pancreatitis, cholecystitis, and hepatitis, should also be considered especially, given her reported social drinking. Infectious etiologies including gastroenteritis and viral hepatitis are also possible diagnoses. Less likely diagnostic considerations may include metabolic and endocrine abnormalities such as hyperthyroidism, primary adrenal insufficiency, and uncontrolled diabetes, all of which could potentially explain her weight loss and decreased appetite. Occasionally, hematological conditions, such as anemia, or malignancies including leukemia or lymphoma, can also present with similar symptoms.

On arrival at the hospital, the patient was noted to be tachycardic but afebrile and otherwise hemodynamically stable. Her BMI was 26.1kg/mg2. The physical exam was notable for epigastric abdominal tenderness without rebound or guarding. There was no organomegaly. Initial laboratory workup was significant for profound acidemia with a pH of 7.29, anion gap of 31 mmol/L, a lactic acid level of 13.7 mmol/L, and a bicarbonate level of 9 mmol/L. AST and total bilirubin were elevated to 55U/L and 3.0 mg/dL, respectively. The remainder of the CMP was normal. CBC showed macrocytic anemia (Hemoglobin 9.8 g/dL, MCV 119.2 fL), leukocytosis (WBC of 12.39 x 103 µL) and an elevated platelet count (402,000 µL).

Normal lactate levels are under 2 mmol/L, levels between 2 mmol/L and 4 mmol/L are considered hyperlactatemia and levels at or above 4 mmol/L are regarded as severe. Lactic acidosis is also characterized by a pH of 7.35 or lower. Elevated lactate levels correlate with a higher mortality risk, even without organ failure or shock, can significantly impact patients with sepsis, and are associated with higher in-hospital 30-day mortality rates.1 Lactic acidosis may impair cardiac function and reduce vascular responsiveness to vasopressors. However, lactic acidosis is considered an aggravating factor rather than a direct cause of mortality. It tends to act as a precipitator and exacerbate existing comorbidities, which impacts their progression and associated mortality risks without an established direct causal relationship with mortality.1

The initial workup for her symptoms and the concurrent lactic acidosis was focused on evaluating for infectious sources or possible malignancy. On ultrasound, her gallbladder was distended with sludge without specific findings of acute cholecystitis. The surgical team recommended magnetic resonance cholangiopancreatography (MRCP) and intravenous (IV) antibiotics. The patient was admitted to the inpatient medical unit for further evaluation and treatment. Blood and urine cultures were without evidence of infection. An MRCP showed no cholecystitis or choledocholithiasis but was suggestive of hepatic steatosis. Esophagogastroduodenoscopy (EGD) and colonoscopy did not reveal any concerning source of bleeding, infection, or malignancy. Antibiotics were discontinued.

The differential diagnosis for lactic acidosis includes Type-A, Type-B, and Type-D etiologies.2 Type-A lactic acidosis commonly results from tissue hypoperfusion and hypoxia and typically occurs in the setting of oxygen consumption-delivery mismatch; examples include septic shock and tissue hypoxia. Type-D lactic acidosis arises from the overproduction of D-lactic acid due to the proliferation of intestinal bacteria, typically observed in individuals with short bowel syndrome or other conditions leading to gastrointestinal malabsorption. Type-B lactic acidosis is less common and is related to the inability of mitochondria to process pyruvate and alternative metabolic pathways, resulting in lactic acid accumulation. Type-B processes may include thiamine deficiency, mitochondrial myopathies, diabetes, liver disease, malignancy, and certain medications.1, 2

Type-D lactic acidosis was excluded based on a lack of relevant history. Workup for conditions associated with hypoperfusion and hypoxia, including infection and malignancy, was also unrevealing. On admission to the hospital, the patient was noted to have significant macrocytic anemia, normal vitamin B12 levels, and undetectable folate levels. Subsequently, other vitamin and mineral levels were checked revealing that her copper, vitamin A, ceruloplasmin, and thiamine levels were low.

Supply of thiamine is entirely dependent on dietary intake as it is not made endogenously. Therefore, in poor oral consumption or excess excretion, thiamine stores can be depleted in as little as 18-20 days.3 Thiamine deficiency is known to be more common among patients with chronic alcohol use and is often associated with other nutritional deficiencies.4 The uptake of thiamine and other aspects of its utilization are influenced by alcohol, potentially in the development of thiamine deficiency in alcohol use disorders.5

Further discussion with the patient and her family revealed that the patient had minimized her alcohol use to the medical teams. The patient eventually admitted drinking an unspecified amount of beer daily, coupled with a poor diet that primarily consisted of fried foods, if any food was consumed. The patient’s significant alcohol use and minimal food intake corresponded to her laboratory evidence of nutritional deficiencies, including deficient levels of folate and thiamine.

Thiamine deficiency disorders can present with a broad range of clinical symptoms, often leading to delayed diagnosis. Thiamine deficiencies are classically associated with signs of neurologic toxicity, including encephalopathy, peripheral neuropathy, ataxia, and hearing loss. Thiamine-deficient patients can also present with musculoskeletal weakness, atrophy, and heart failure. Other manifestations may include transaminitis, acute abdominal pain, vomiting, and acidosis, as was seen in our patient. The administration of thiamine has been shown to improve the various symptoms quickly. Up to 20% of critically ill patients have evidence of thiamine deficiency; however, the disorder remains underdiagnosed.2 Thiamine deficiency should be considered an etiology of lactic acidosis, even in patients without neurologic deficits or an overt history of alcohol use disorder.

The patient was placed on vitamin supplementation, including folate and thiamine. Her lactate levels began normalizing within one day of fluid replenishment and thiamine supplementation. The patient’s abdominal pain and nausea improved with appropriate pain medication, nutritional supplementation, and fluid resuscitation. Her infectious workup remained negative throughout her hospitalization. The patient quickly improved with vitamin administration and was discharged in stable condition with close primary care follow-up and referral to a substance use specialist.

This case illustrates the intricate relationship between nutritional deficiencies and chronic alcohol use, emphasizing the importance of a thorough history and clinical assessment in identifying underlying causes of common presentations, including abdominal pain and nausea. Our patient’s minimized disclosure of alcohol use and poor dietary intake highlighted the challenges that SGIM clinicians may face in obtaining accurate clinical information and the necessity for SGIM providers to maintain a high index of suspicion for nutritional deficiencies in patients both with and without a history of chronic alcohol use. Successful management and resolution of the patient’s symptoms after nutritional supplementation emphasize the importance of early identification and intervention in cases of nutritional deficiencies.


  1. Foucher CD, Tubben RE. 2023. Lactic acidosis. https://www.ncbi.nlm.nih.gov/books/NBK470202/. In StatPearls. Treasure Island, FL: StatPearls Publishing. Updated March 26, 2023. Accessed February 15, 2024.
  2. Attaluri P, Castillo A, Edriss H, et al. 2018. Thiamine deficiency: An important consideration in critically ill patients. Am J Med Sci. 2018 Oct;356(4):382-390. doi:10.1016/j.amjms.2018.06.015. Epub 2018 Jun 21.
  3. O’Donnell K. 2017. Lactic acidosis: A lesser known side effect of thiamine deficiency. Practical Gastroenterology. 41(3):24–31.
  4. Grochowski C, Blicharska E, Baj J, et al. 2019. Serum iron, magnesium, copper, and manganese levels in alcoholism: A systematic review. Molecules. 2019 Apr 7;24(7):1361. doi:10.3390/molecules24071361.
  5. Singleton CK, Martin PR. 2001. Molecular mechanisms of thiamine utilization. Curr Mol Med. 2001 May;1(2):197-207. doi:10.2174/1566524013363870



Clinical Practice, SGIM, Social Determinants of Health

Author Descriptions

Ms. Holod (Monique_E_Holod@rush.edu) is a fourth-year medical student at Rush Medical College. Dr. Solka (Kathryn_A_Solka@rush.edu) is an assistant professor in the Department of Surgery at Rush University Medical Center and the Course Director of “Food to Fuel” (the gastrointestinal system, nutrition, and metabolism course) at Rush Medical College. Dr. Abrams (Richard_Abrams@rush.edu) is an associate professor of internal medicine at Rush University Medical Center and the Associate Dean of the Learning Environment for Rush Medical College. Dr. Sweet (Michelle_Sweet@rush.edu) is an associate professor of internal medicine at Rush University Medical Center and the Assistant Dean for the Rush Medical College M4 Curriculum.