Approach Considerations

For practical reasons, replacing thiamine as an initial test may be most feasible. If the patient responds to treatment, it is safe to assume that a measure of thiamine deficiency was responsible for the condition. Thiamine is not toxic in high levels, which means that this route carries little risk. In addition, time is saved in treating the patient and money is saved in testing. (However, although observation of a patient's clinical response to thiamine administration remains the easiest, least expensive form of testing, clinicians usually miss the subclinical forms of beriberi.)

If laboratory confirmation is needed,^[44]measure blood thiamine, pyruvate, alpha-ketoglutarate, lactate, and glyoxylate levels. Also, measure urinary excretion of thiamine and its metabolites. A scarcity of any of these chemicals strongly suggests thiamine deficiency.^[16]

In conjunction with whole blood or erythrocyte transketolase activity preloading and postloading, a thiamine loading test is the best indicator of thiamine deficiency. An increase of more than 15% in enzyme activity is a definitive marker of deficiency. However, this test is expensive and time consuming; it is performed only for criterion-standard proof of deficiency.

Measure urinary methylglyoxal; also measure serum thyroid-stimulating hormone (TSH), to rule out thyrotoxicosis-induced high-output heart failure, if applicable.

An increase in troponin I has been found in heart failure due to thiamine deficiency.^[45]Thiamine is an important enzymatic cofactor in several energy pathways. Its deficiency disrupts cellular processes and leads to myocardial death. Thiamine is also an important factor in the cellular production of glutathione, an antioxidant that myocardial cells need to counteract free radicals. In the absence of glutathione, these cells would die prematurely.

Metabolic acidosis can be seen in thiamine deficiency. This is due to increased lactic acid production from thiamine deficiency. Thiamine pyrophosphate (thiamine derivative) is the coenzyme for the conversion of pyruvate to acetyl coenzyme A. Without it, pyruvate is under used and converts to lactate. It is important to consider thiamine deficiency in the presence of unexplained metabolic acidosis, specifically, lactic acidosis.^{[46, 27]}

Gastrointestinal beriberi is a condition in which patients report abdominal pain due to lactic acidosis.^[47]

A retrospective study by Wani et al indicated that cranial ultrasonography can be used in the diagnosis of infantile encephalitic beriberi, with a finding of hyperechogenicity of the basal ganglia having a sensitivity and specificity of 71% and 92%, respectively, for the disease.^[48]

Treatment & Management

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Beriberi in an adult patient.

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Author

Dieu-Thu Nguyen-Khoa, MD, FACP Associate Clinical Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Physician Specialist, Department of Primary Care and Community Medicine, ValleyCare Olive View-UCLA Medical Center

Dieu-Thu Nguyen-Khoa, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Ginette V Busschots, MD Assistant Professor, Department of Emergency Medicine, Foote Hospital, University of Michigan Medical School

Disclosure: Nothing to disclose.

Phyllis A Vallee, MD Associate Program Director, Department of Emergency Medicine, Henry Ford Hospital

Phyllis A Vallee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Michigan State Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP (Retired) Professor, Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

Dennis W Cope, MD, FACP Emeritus Professor of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Department of Internal Medicine, Olive View-UCLA Medical Center

Dennis W Cope, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Society of General Internal Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Don S Schalch, MD Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Stanley Wallach, MD Executive Director, American College of Nutrition; Clinical Professor, Department of Medicine, New York University School of Medicine

Stanley Wallach, MD is a member of the following medical societies: American College of Nutrition, American Society for Bone and Mineral Research, American Society for Clinical Investigation, American Society for Clinical Nutrition, American Society for Nutritional Sciences, Association of American Physicians, and Endocrine Society

Disclosure: Nothing to disclose.

Population	Age	Allowance, mg/day
Recommended Dietary Allowances (RDAs)
Boys	9-13 years	0.9
Men	>14 years	1.2
Girls	9-13 years	0.9
Women	14-18 years	1.0
Women	>19 years	1.1
Pregnant/lactating women	. . .	1.4
Children	1-3 years	0.5
Children	4-8 years	0.6
Adequate Intakes (AIs)
Infant	0-6 months	0.2
Infant	7-12 months	0.3

Beriberi (Thiamine Deficiency) Workup

Approach Considerations

References

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