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Thiamine deficiency is a medical condition of low levels of thiamine (vitamin B 1). [1] A severe and chronic form is known as beriberi. [1] [7] The name beriberi was possibly borrowed in the 18th century from the Sinhalese phrase බැරි බැරි (bæri bæri, “I cannot, I cannot”), owing to the weakness caused by the condition.
Thiamine deficiency and errors of thiamine metabolism are believed to be the primary cause of Wernicke encephalopathy. Thiamine, also called B 1, helps to break down glucose. Specifically, it acts as an essential coenzyme to the TCA cycle and the pentose phosphate shunt. Thiamine is first metabolised to its more active form, thiamine ...
Leigh syndrome (also called Leigh disease and subacute necrotizing encephalomyelopathy) is an inherited neurometabolic disorder that affects the central nervous system. It is named after Archibald Denis Leigh, a British neuropsychiatrist who first described the condition in 1951. [ 2 ]
Thiamine deficiency (vitamin B₁ deficiency), with focus on subclinical forms and nonsevere clinical forms as well as the severe form called beriberi [12] [13]. This topic overlaps substantially with the topic of excessive alcohol use, which impairs B₁ metabolism and leads to hepatic encephalopathy.
In Transketolase Deficiency, also known as SDDHD (Short Stature, Developmental Delay, and congenital Heart Defects), the disease is caused by an inherited autosomal recessive mutation in the TKT gene. A rare disorder of pentose phosphate metabolism with symptoms apparent in infancy including developmental delay and intellectual disability ...
Subacute combined degeneration of spinal cord, also known as myelosis funiculus, or funicular myelosis, [1] also Lichtheim's disease, [2] [3] and Putnam-Dana syndrome, [4] refers to degeneration of the posterior and lateral columns of the spinal cord as a result of vitamin B 12 deficiency (most common).
The enzymes that are dependent on thiamine pyrophosphate are associated with the citric acid cycle (also known as the Krebs cycle), and catalyze the oxidation of pyruvate, α-ketoglutarate and branched chain amino acids. Thus, anything that encourages glucose metabolism will exacerbate an existing clinical or sub-clinical thiamine deficiency. [15]
Niacin deficiency is a consequence of a diet low in both niacin and the amino acid tryptophan, a precursor for the vitamin. Low plasma tryptophan is a non-specific indicator, meaning it can have other causes. The signs and symptoms of niacin deficiency start to revert within days of oral supplementation with large amounts of the vitamin. [23] [24]