Discussion
Thiamin functions as a coenzyme in the metabolism of carbohydrates and branched-chain amino acids. It is vital for two types of reactions in human body; decarboxylation of α-ketoacids and transketolation. Thiamin has not been linked to toxicity.1 With limited body storage, Thiamine deficiency can occur in as short as 14 days.2
Thiamin deficiency can present as Beriberi in its two types wet and dry, or the Wernicke-Korsakoff syndrome.   Dry Beriberi present as symmetrical sensory and motor peripheral neuropathy. Wet type mainly has cardiac involvement with cardiomyopathy.1 presentation can be as severe as multiorgan failure.3
Nowadays this disease is uncommon in developed countries. Most cases seen are related to patients who underwent bariatric surgeries or who suffer from alcoholism and severe malnutrition.4–6Thiamin deficiency has been described in patients on total parenteral nutrition (TPN) if adequate vitamin replacement is not provided.7
Cardiac Beriberi can be a challenging diagnosis for patients presenting with dilated cardiomyopathy. The diagnosis can be made based on clinical signs and symptoms associated with dilated cardiomyopathy, peripheral neuropathy, malnutrition and absence of other with response to Thiamin supplementation.8
Thiamin plays an integral role in TCA cycle. Its deficiency leads to Adenosine accumulation and decreased ATP production. This can be seen in Beriberi heart disease. It can be chronic which starts as high output state secondary to peripheral vasodilation and decreased vascular resistance. If this state continues along with decreased myocardial contractility, it can lead to low output state.8–12Acute Beriberi (Shoshin beriberi) can present with low cardiac output and even cardiogenic shock. This deficiency can lead to myonecrosis which was described in two autopsy studies13Aggressive repletion of thiamine results in dramatic improvement in systolic heart function8,11,14, this was also seen in our patient.
In our review in literature, we didn’t find any cases where Thiamin was linked to rhabdomyolysis. Suspected mechanism likely similar to cardiomyopathy. Dramatic improvement in total CK level along with improved energy level and decreased calf tenderness clinically support this theory.
In conclusion, patients presenting with rhabdomyolysis and signs of heart failure who are malnourished might be experiencing Beriberi disease. Thiamin, water soluble vitamin, is not associated with toxicity. Aggressive replacement of Thiamin should be attempted given dramatic improvement if this is the etiology.