ISSN: 2320-5407 Int. J. Adv. Res.

11(05), 723-732

Journal Homepage: -www.journalijar.com

Article DOI:10.21474/IJAR01/16925
DOI URL: http://dx.doi.org/10.21474/IJAR01/16925

RESEARCH ARTICLE
A STUDY OF THIAMINE DEFICIENCY IN PATIENTS WITH ACUTE ONSETENCEPHALOPATHY

Dr. Maleeha Wani, Dr. Adil Bashir, Dr. Masood Tanvir, Dr. Sobia Nisar, Dr. Umair Altaf, Dr. Junaid and
Dr. Zubair
Department of Medicine, GMC Srinagar.
……………………………………………………………………………………………………....
Manuscript Info Abstract
……………………. ………………………………………………………………
Manuscript History Introduction:Vitamin B1, also known as thiamine, and its crucial role
Received: 20 March 2023 in energy metabolism and proper functioning of the nervous and
Final Accepted: 22 April 2023 cardiovascular systems. Thiamine is an essential vitamin that must be
Published: May 2023 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
Key words:-
Thiamine, Encephalopathy,Confusion absorbed in the duodenum and transported across the blood-brain
Assessment Method (CAM) 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 Wernicke's encephalopathy
(neuropsychiatric condition). While alcohol abuse-associated
malnutrition is a common cause of Wernicke's 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

Corresponding Author:- Dr. Irtifa Nazir Kanth

Address:- Department of Medicine, GMC Srinagar. 723
ISSN: 2320-5407 Int. J. Adv. Res. 11(05), 723-732

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 Wernicke's 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.

Copy Right, IJAR, 2023,. All rights reserved.

……………………………………………………………………………………………………....
Introduction:-
Vitamin B1, also known as thiamine, is one of the eight essential B vitamins that help the body convert food
(carbohydrates, fat, and protein) into energy. These vitamins are vital for the proper functioning of the central and
peripheral nervous systems. The human body does not produce endogenous thiamine; therefore, it must be ingested.
1 Thiamine is a water-soluble vitamin stored primarily in the liver; however, storage only lasts up to 18 days. 2-4

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Thiamine is absorbed in the duodenum by an active, carrier mediated, rate-limited process, and at the blood–brain
barrier, its transport occurs through both passive and active mechanisms. 5,6 The recommended dose of thiamine for
an average, healthy adult is 1·4 mg per day or 0·5 mg of thiamine per 1000 kcal consumed. This dose is higher in
children, in critically ill conditions, and during pregnancy and lactation.7 The American Society for Parenteral and
Enteral Nutrition recommends a thiamine intake of 1.2 mg to a maximum of 10 mg per day.8 In cells, thiamine is
converted to thiamine pyrophosphate which is the main metabolic form of thiamine9 and is necessary for several
biochemical pathways in the brain, such as intermediate carbohydrate metabolism (for energy production by ATP
synthesis), lipid metabolism (for production and maintenance of myelin sheath), and production of amino acids and
glucose-derived neurotransmitters (e.g., glutamic acid; GABA) 10. Thiamine also seems to have a role in
acetylcholinergic and serotoninergic synaptic transmission and axonal conduction.11

Specifically, thiamine pyrophosphate (TPP) also known as thiamine diphosphate (TDP) is a cofactor for two
enzymes in oxidative pathways after glycolysis. These include the pyruvate dehydrogenase complex, which converts
pyruvate to acetyl-CoA, and the α-ketoglutarate dehydrogenase complex which converts α-ketoglutarate to succinyl-
CoA.12 TPP is also a cofactor for the branched-chain α-ketoacid dehydrogenase complex which converts leucine,
isoleucine, and valine into acetyl-CoA and succinyl-CoA, which are then similarly fed into the ATP-generating
Krebs cycle (Figure 1).12 In addition to serving as a cofactor for these three important enzymes, TPP is a cofactor
for the biochemical reactions that are driven by transketolase in the anabolic pentose phosphate pathway. NAD(P)H,
one of the products of the pentose phosphate pathway, is required for the synthesis of fatty acids and steroid
hormones. It is also required in the reduction of glutathione (an endogenous antioxidant). Ribose 5-phosphate, a
substrate for nucleotide and nucleic acid synthesis, is also generated by this thiamine-dependent pathway.12

Because of its critical role in oxidative ATP synthesis, thiamine is essential for the proper function of most tissues
and organs. Therefore, thiamine deficiency can have myriad clinical effects. Major organs, including the brain and
heart, account for almost 60% of basal energy expenditure; as such, thiamine deficiency affects nervous and
cardiovascular systems most dramatically, it can even lead to death rapidly, if not corrected. The main thiamine
deficiency syndromes defined in humans include the following.12

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Dry beriberi: primarily characterized by peripheral neurologic manifestations, such as paresthesia, weakness, or
paralysis.

Wet beriberi: exemplified by cardiac effects, including decompensated systolic heart failure with associated
pulmonary and peripheral edema, tachycardia, a widened pulse pressure and/ or hypotension, and/or cardiogenic
shock (also known as Shoshin beriberi).

Gastrointestinal beriberi –14 that includes nausea and vomiting, abdominal pain, and lactic acidosis. Wernicke's
encephalopathy (WE): a neuropsychiatric condition with a myriad of symptoms ranging from hearing loss,
dysthermia, seizures, Behavioural disturbances, dystonias to coma.

In developed countries, over 80% of WE cases occur in the context of malnutrition associated with alcohol abuse.25
However, WE have also been described in other disorders associated with decreased intestinal absorption of
thiamine (low intake or malabsorption), an increase of the body requirements (as in systemic diseases) or loss of
soluble thiamine (dialysis). Not all individuals with a similar degree of malnutrition and alcoholism develop WE, so
it is believed that there are genetic and environmental factors contributing to the expression of this disease.24

Based on existing biomarker studies and case reports of thiamine-responsive conditions, along with information on
the use of polished rice or cassava as primary staples in the diets of many poor households in LMIC, the risk of
thiamine deficiency is thought to be of potential public health importance in many communities in South Asia and
West Africa. 27, 28. The prevalence of thiamine deficiency in healthy Indian adults was found to be around 11% in
a study.29 Studies from South-East Asia have reported a prevalence of 27-78% in pregnant and lactating mothers.30
Although widespread population-based studies in the Kashmiri population have not yet been done, however,
preliminary works that are done, reveal a significant presence of thiamine deficiency disorders in infants (31,32),
peripartum females,33 and adults 34,35 having diverse presentations.

Aims And Objectives:-

Early detection and treatment of Patients with Encephalopathy related to Thiamine deficiency.

Materials And Methods:-

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 conducted according to Declaration of Helsinki
1976. The ethical clearance for the study was granted by the Institutional Ethical Committee.

Study Subjects:
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.

Inclusion Criteria:
Patients presenting with altered mental status and acute confusion/ delirium fulfilling the criteria by CONFUSION
ASSESSMENT METHOD (CAM) score.

Exclusion Criteria:
• Patients with NCCT Head or MRI Brain documented stroke
• Patients with a history or apparent signs of alcohol intoxication, drug intoxication, or any kind of poisoning.
• Those patients whose caregivers denied consent for the study.

Methodology:-
We registered 96 patients, with acute onset encephalopathy fulfilling the inclusion criteria. A detailed history as well
as general physical and systemic examination of all patients was done. 24 hr dietary recall was obtained from each
patient. Diet analysis was done using Diet cal software. Standardized questionnaires were used wherever applicable.

Baseline investigations and whole blood thiamine levels were conducted in all patients. Added biochemical/
radiological investigations were done on need bases. The whole-Blood thiamine levels were measured by using
High-Performance Liquid Chromatography (HPLC). A cut-off of 2.5 ug/dL was defined as BELOW NORMAL, the

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concentration below which patients were considered to be thiamine deficient. The Confusion Assessment Method
(CAM), a standardized evidence-based tool for quick and accurate identification and recognition of delirium, was
used for assessing the patients. The criteria proposed by Caine et al. for the diagnosis of wernickes encephalopathy,
approved by the European Federation of Neurological Societies, was used for assessing the patients. It states that a
diagnosis of Wernicke’s encephalopathy should be considered in any patient with two of the following:
• Nutritional deficiency
• Altered mental state or memory
• Oculomotor abnormalities
•Cerebellar dysfunction

Patients with acute onset encephalopathy

(N =96)

RECRUITMENT

Baseline biochemical investigations and whole blood

thiamine levels.

Thiamine Challenge
(600 mg i.v)

Normal thiamine Levels(>2.5mg/dl)

ANALYSIS (N=15)

Responders Non-responders
(N=17) (N=64)

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Thiamine hydrochloride of 600 mg was given intravenously to all these patients, and assessed for any other
contributory factor for encephalopathy. Patients were reassessed after 6 hours. Based on the response to the thiamine
challenge alone, we divided the patients with low thiamine levels further into two groups – responders and non-
responders. Responders were those patients who responded to the parenteral thiamine challenge and did not have
any contributory factor for encephalopathy. Responders did not receive any other therapy. Following response, these
patients further received thiamine hydrochloride 300 mg given intravenously thrice daily. The other group of
patients were those who received standard medical therapy specific for their illness along with intravenous thiamine
and did not respond to the thiamine challenge alone. This group was classified as ‘non-responders’.

Observations And Results: -

A total of 96 patients were recruited in the study who fulfilled the CAM score criteria for acute onset
encephalopathy. Based on the whole-blood thiamine levels patients were divided into two groups viz., low thiamine
group and normal thiamine group. Out of 96 patients, 15 patients (15.6%) had normal thiamine levels while 81
patients (84.4%) had low thiamine levels. In the normal thiamine group, the mean thiamine level was 5.46±4.44
(ug/dL) while in the low thiamine group, the mean thiamine level was 1.35±0.42 ug/dl (p=0.0001). The baseline
demographic and clinical characteristics of the two groups are presented in table1.

Table 1:- Baseline demographic characteristics of patients with low and normal thiamine levels.
Low thiamine (n=81) Normal thiamine (n=15) P-value

Age (Years) 50.08±17.91 62.50±11.90 0.196

Systolic BP 122.31±18.47 122.0±21.67 0.974

Diastolic BP 76.54±11.29 78±13.03 0.797

SpO2 90.41±5.79 86.33±14.57 0.433

Pulse beats/min 94.88±20.65 93.40±13.22 0.880

Recurrent Vomiting 36(44.44%) 5(33.33%) 0.212

Confusion 65(80.2%) 4(26.66%) 0.0002

Lethargy 37(45.67%) 9(60%) 0.47

Ataxia 26(32.1%) 4(26.66%) 0.015

Nystagmus 17(20.9%) 5(33.33%) 0.016

Agitation 7(8.64%) 3(20%) 0.039

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Urinary incontinence 9(11.11%) 5(33.33%) 0.16

Seizures 15(18.51%) 3(20%) 0.44

Stupor 10(12.34%) 8(53.33%) 0.01

Patients with normal thiamine levels were then excluded. 84.4% patients had thiamine deficiency. This group was
further divided into responders and non-responders based on response to thiamine challenge, responders were 17 in
number with 11 males and 6 females, including 3 pregnant females. Mean age of this group was 36.25±9.44 in
contrast to non-responders whose mean age was 61.8±15.1 [p value-0.001]: among responders 70.58% had recurrent
vomiting which was seen in 37.5% of patients in non-responders’ group-patients were assessed as per CAM score
and Caine criteria. Confusion was the most common initial presentation among responders, present in 88% of
patients followed by lethargy which was present in 59%. In non-responders’ confusion was present in 68.7%
patients and lethargy was present in 42.18% of patients. Behavioural change presenting as agitation was seen in 17%
patients in responders group and 6.2% patients in non-responders group. As compared to responders, stupor as a
clinical presentation was more commonly present in non-responders, 14.06%. Ataxia was present in 58.8% of
patients in responders group compared to 25% in non-responders.Patients in non-responders group were assessed for
the concomitant conditions contributing to encephalopathy. Hypoxia was the most frequently found condition
associated with thiamine deficiency present in 25% of patients followed by uremic encephalopathy (17.18%),
hepatic encephalopathy (14.06%) and septic shock (12.5%) the comorbidities which were seen in non-responders
were hypertension (65.62%), diabetes mellitus (51.5%), COPD (26.56%), chronic kidney disease (17.18%), chronic
liver disease (14.06%), chronic heart failure (14.06%). Mean thiamine levels were lower in responders than in non-
responders. However, the difference did not reach statistical significance (p-0.176). Responders had a higher Spo2
with mean of 95.7 2.63 as compared to 86±4.5 in partial responders [p value -0.005]. Mean Svo2 of70.80 ±14.18 in
responders and 55.94434.10 in partial responders [p value -0.3]. The mean pH was comparable between the two
groups with a p value of0.6. Mean lactate was higher in responders (1.92±1.59) than in partial responders
(1.61±1.06) although it did not reach statistical significance [p value=0.6] but the mean lactate drop following
thiamine therapy was more in responders than in partial responders. Other laboratory parametersseen included mean
serum urea of (27. 4±11.99) in responders and (39.45±29.76) in non-responders. Mean serum creatinine was higher
in non-responders (1.38 ±0.71) as compared to responders (1.04±0.33) [p value -0.2]. Mean serum total protein and
serum albumin were comparable in the two groups with p value of0.9 and 0.8 respectively. Mean sodium and
potassium levels in responders were (140±4. 5) and (3. 88±0, 44) innon-responders 144. 38±7 .8) and (3. 88±0.44)
[p value- 0.4 for sodium and 0.039 for potassium mean blood sugar levels were higher in non-responders
(153.8±81.16) than responders (125±14.47) but it did not reach statistical significance p value 0.4. Mean total
leukocytes count in responders was (8.41±2.7) and in non-responders was (12.65±6.7) [p-value =0.4]. 9 patients
(53%) in responders’ group had MRI brain findings suggestive of Wernicke’s encephalopathy.4 (23.5%) patients
had findings of bilateral mammillary body hyper intensity and 5(29.4%) patients had T2 flair in medial thalami,
periaqueductal gray, along 3rd ventricle 1 patient had MRI brain suggestive of cerebral amyloid angiopathy.
3(17.6%) patients had normal MRI brain all the patients had a history of consuming polished rice as their main
staple diet, washed once to three times before cooking. 85% patients in responders group consumed polished rice as
compared to 62% in non-responders’ group. The total thiamine consumption per day for responders and non-
responders was same 0. 5010. 15 mg traditional salt tea intake was seen in 91% patients of responders as compared
to 86% of patients in non-responders’ group. 15:58

Discussion:-
Thiamine deficiency causes beriberi, which is classically categorized as wet or dry. Wet beriberi presents primarily
with cardiovascular symptoms. Patients with dry beriberi present with symmetric peripheral neuropathy, Wernicke’s
encephalopathy and gastric beriberi. Our study suggests presence of non-alcoholic Wernicke’s encephalopathy
associated with low thiamine levels as a cause of acute onset confusional state in our population. In addition, the low

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levels of thiamine in patients with encephalopathies of other aetiologies, suggests presence of background thiamine
deficiency, precipitated by acute illness.

Rice is the staple food of the Kashmiri population and all the patients recruited in our study consumed rice. But
interestingly, consumption of polished rice was observed in 80% of the patients in the low thiamine group as
compared to 65% patients in the normal thiamine group, reaching statistical significance (p=0.030). Polished rice is
a poor source of thiamine as milling of rice removes the thiamine-rich layer of the rice grain. It is high in
carbohydrate content resulting in thiamine calorie imbalance. Also, faulty cooking practices like washing the rice
two to three times before cooking and discarding the fluid after boiling of rice has been documented in our study to
be significantly associated with low thiamine levels. There have also been studies documenting the effects of
chlorine in tap water on thiamine. We also found consumption of traditional salt tea to be significantly associated
with thiamine deficiency (p=0.059). It has been postulated that tea contains anti-thiamine factors therefore
predisposing people to thiamine deficiency disorders.

We enrolled 96 patients who fulfilled the CAM score criteria, out of which, 84.37% of patients had thiamine
deficiency. On further evaluation and application of criteria proposed by Caine et al, 20.9% of patients were found
to have Wernicke’s encephalopathy and 79% of patients had thiamine deficiency with acute illnesses of other
aetiologies. Patients in the isolated thiamine deficiency group were relatively younger than those with other
concomitant illnesses, with a mean age of presentation of 36.35 9.44 years. Increased metabolic rate and therefore
high demand for thiamine explains younger patients in this group. Patients with isolated thiamine deficiency
presented with a history of acute onset of behavioural abnormalities, the most common being confusion (88%),
followed by lethargy (59%). Agitation was present in 17% of cases, and seizures, predominantly generalized tonic
clonic variants, in 17.6%. Antepartum isolated thiamine deficiency was documented in 3 pregnant females, all
presenting with confusion.

In our study population, 79% of patients with thiamine deficiency had concomitant clinical conditions that were
attributed as a cause of encephalopathy and correction of these conditions reversed the encephalopathy. They were
labelled as non-responders because the response to parenteral thiamine alone could not be documented as they
received the standard medical therapy for the concomitant illness. A possible operative mechanism could be an
altered thiamine metabolism along with an increased requirement of the vitamin often associated with deficient oral
intake or increased loss. The most common acute illness documented was type 1 respiratory failure. Hypoxia was
present in 25% of cases. The mean SpO2 in our patients was 86±4.4%. As our study was conducted during the
COVID-19 pandemic with a greater number of hospital admissions being pneumonia or its subsequent
complications, this might be a possible bias. Hypoxia with hypercarbia was seen in 10.9% of patients. Septic shock
was present in 12.5% of patients with thiamine deficiency. CKD with uremic encephalopathy as a concomitant
illness was seen in 17.18% of patients, with decreased concentration of thiamine transporters, increased
concentration of guanidosuccinic acid and wash out during dialyses as possible associated mechanisms. Hepatic
encephalopathy associated with thiamine deficiency was present in 14.06% of our patients. Alterations in hepatic
storage and metabolism of thiamine as well as interference from increased concentrations/ altered metabolisms of
various hepatic substrates are the likely operatives.

Our study is the first of its kind to assess the various laboratory parameters which can be associated with thiamine
deficiency. The mean whole-blood thiamine level in our patients with isolated thiamine deficiency was 1.26±0.34
mcg/dL. The whole blood sample has been considered to be a superior sample type for analysis of thiamine
concentration as it takes into account both plasma thiamine and TMP, and, erythrocyte TDP which accounts for
~90% thiamine in blood. A low potassium level with mean potassium of 3.34±0.4 mol/L was also observed in
patients with isolated thiamine deficiency. This can be explained by the presence of inadequate dietary intake along
with recurrent vomiting seen majority of patients of this group. Another significant laboratory abnormality that was
observed in our study was a higher percentage SVo2 with a mean of 70.8±14.18 % in these patients. This finding
can be explained by the fact that there is decreased oxygen consumption because of decreased availability of
thiamine required in multiple biochemical pathways. This also explains the high lactate seen in these patients. In our
study, we documented a mean lactate of 1.92±1.59 mmol/dL which responded to high doses of intravenous thiamine
and these patients were referred to as responders. In the non-responders group mean lactate level was also raised,
however, the drop in lactate following high-dose parenteral thiamine could not be classified as a response to
thiamine as they also received the standard medical therapy for the concomitant condition.

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MRI has a sensitivity of only 53%, but a high specificity of 93%. Findings typically reported include an increased
T2 signal, bilaterally symmetrical, in the paraventricular regions of the thalamus, the hypothalamus, mamillary
bodies, the periaqueductal region, the floor of the fourth ventricle and midline cerebellum. Unusual sites of lesio ns
include cortical regions and the splenium of the corpus callosum. 53% our patients with isolated thiamine deficiency
showed MRI changes in these typical areas, including bilateral mammillary body hyperintensities in 23.5% and T2
FLAIR in medial thalami in 29.4%. About 17.6% of our patients had normal brain MRI.

Conclusions:-
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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