Introduction:Vitamin B1, also known as thiamine, and its crucial role in energy metabolism and proper functioning of the nervous and cardiovascular systems. Thiamine is an essential vitamin that must be obtained through diet since the body does not produce it naturally. It is stored in the liver but only lasts for about 18 days. Thiamine is absorbed in the duodenum and transported across the blood-brain barrier. The recommended daily intake varies based on age, health condition, and life stages.Thiamine plays a vital role in various biochemical pathways in the brain, including energy production, lipid metabolism, neurotransmitter synthesis, and synaptic transmission. Thiamine deficiency can have diverse clinical effects, affecting the nervous and cardiovascular systems most severely and potentially leading to death if left untreated.Different thiamine deficiency syndromes are identified, including dry beriberi (peripheral neurologic manifestations), wet beriberi (cardiac effects), gastrointestinal beriberi (digestive symptoms), and Wernickes encephalopathy (neuropsychiatric condition). While alcohol abuse-associated malnutrition is a common cause of Wernickes encephalopathy in developed countries, it can also occur due to other factors such as decreased thiamine absorption, increased body requirements, or thiamine loss in certain medical conditions.Thiamine deficiency is considered a potential public health concern, particularly in communities in South Asia and West Africa, where diets heavily reliant on polished rice or cassava may contribute to the risk. Studies have shown varying prevalence rates of thiamine deficiency in different populations, including healthy adults and pregnant/lactating mothers in South-East Asia and India. While specific population-based studies are lacking in the Kashmiri population, preliminary evidence suggests the presence of thiamine deficiency disorders in infants, peripartum females, and adults with diverse presentations. Objectives: Early detection and treatment of Patients with Encephalopathy related to Thiamine deficiency Study Design/ Methodology:The study was hospital-based and prospective in nature, conducted in the Department of General Medicine, SMHS, GMC - Srinagar from May 2021 to September 2022. The study was done on patients aged more than 18 years of age attending emergency department of Government Medical College, Srinagar with acute onset encephalopathy. Observations And Results:In this study, 96 patients with acute onset encephalopathy were recruited based on CAM score criteria. The patients were divided into two groups: a low thiamine group and a normal thiamine group, based on their whole-blood thiamine levels. Among the patients, 15.6% had normal thiamine levels, while 84.4% had low thiamine levels. The mean thiamine level in the normal thiamine group was 5.46±4.44 ug/dL, and in the low thiamine group, it was 1.35±0.42 ug/dL (p=0.0001). Patients with normal thiamine levels were excluded from further analysis, leaving a group of 84.4% of patients with thiamine deficiency.Within the thiamine deficiency group, patients were further divided into responders and non-responders based on their response to a thiamine challenge. The responders group comprised 17 patients, including 11 males, 6 females (including 3 pregnant females), with a mean age of 36.25±9.44. Non-responders had a mean age of 61.8±15. Among responders, 70.58% had recurrent vomiting compared to 37.5% in non-responders. Confusion was the most common initial presentation in both groups, followed by lethargy. Behavioural changes were seen in a higher percentage of responders compared to non-responders. Ataxia was more prevalent in the responders group.Various laboratory parameters were analyzed between responders and non-responders. There was no significant difference in mean pH, sodium, potassium, total protein, serum albumin, and blood sugar levels between the two groups. However, lactate levels and the drop in lactate following thiamine therapy were higher in responders. Responders had lower levels of serum urea and serum creatinine compared to non-responders.MRI brain findings suggestive of Wernickes encephalopathy were observed in 53% of responders. Polished rice consumption was common among all patients, with 85% of responders and 62% of non-responders consuming polished rice as their main staple diet. Traditional salt tea intake was also prevalent in both groups. Conclusions: Thiamine deficiency can manifest in various clinical scenarios, including recurrent vomiting, hypoxia, electrolyte imbalances (such as hyponatremia and hypernatremia), and systemic diseases like uremia, hepatic encephalopathy, and septic shock. Pregnant women, who experience increased demand and may have thiamine loss due to vomiting, are also at risk of developing thiamine deficiency.The diagnosis of thiamine deficiency is primarily clinical and is confirmed by the response of neurological signs to high-dose intravenous thiamine treatment. MRI is considered the most valuable paraclinical study for diagnosis. Elevated serum lactate levels and the response of lactate to high-dose parenteral thiamine can serve as surrogate markers for thiamine-responsive encephalopathy. It is crucial to administer high doses of parenteral thiamine immediately to patients suspected of having encephalopathy due to thiamine deficiency to prevent complications associated with Wernicke-Korsakoff syndrome.
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