Vitamin B1 (Thiamine) is an essential vitamin required for carbohydrate metabolism. It is converted in the intestine to Thiamine pyrophosphate (TPP) which is the active form of Vitamin B1. The high risk factors for thiamine deficiency include old age, long term parenteral nutrition, hemodialysis, malabsorption or alcohol abuse. Severe deficiency causes congestive heart failure (wet beriberi), peripheral neuropathy (dry beriberi), Wernicke encephalopathy (a medical emergency that can progress to coma and death), and Korsakoff syndrome (often irreversible memory loss and dementia that can follow).
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Vitamin B2 is a component of water-soluble Vitamin B complex and is crucial for metabolism and energy production through oxidative phosphorylation. People at higher risk of developing Vitamin B2 deficiency include 1) Vegetarians who consume no/ little milk 2) Pregnant and lactating women and their infants 3) Person with chronic diarrhoea or malabsorption 4) Chronic alcoholics and 5) Infants with rare inborn error of Riboflavin transporter disorder.
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Niacin (also known as vitamin B3) is one of the water-soluble B vitamins. Niacin is the generic name for nicotinic acid (pyridine-3-carboxylic acid), nicotinamide (niacinamide or pyridine-3-carboxamide), and related derivatives, such as nicotinamide riboside [1-3].
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Neurotropic B group vitamins play crucial roles as coenzymes in the nervous system. Particularly Vitamin B1 (Thiamine), Vitamin B6 (Pyridoxine) & Vitamin B12 (Cobalamin) contribute essentially to the maintenance of a healthy nervous system. Vitamin B1 acts as a site-directed antioxidant; Vitamin B6 balances nerve metabolism; Vitamin B12 maintains myelin sheaths.Their importance is highlighted by many neurological diseases related to deficiencies in one or more of these vitamins. Deficiencies of these vitamins can occur mainly in elderly individuals, diabetics, alcoholics, dialysis patients, patients with gastrointestinal diseases etc. and may lead to neurological disturbances e.g. Peripheral neuropathy. On the other hand neurological adverse effects like ataxia, sensory neuropathy etc. have been demonstrated with long-term or high dose use of these vitamins specially Vitamin B6.
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Vitamins are essential constituents of human diet since they are synthesized inadequately or not at all in human body. Vitamin deficiencies affect all ages, the groups most susceptible to deficiencies are pregnant and lactating women, young children because of relatively high need, chronically ill patients and alcoholics. After gastric bypass surgery patients are at high risk of multiple vitamin deficiencies. Conversely, because of widespread use of nutrient supplements, nutrient toxicities are also gaining pathophysiological and clinical importance. Laboratory investigations play an important role in detecting subclinical deficiencies as well as probable toxicities in asymptomatic patients.
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Serum folate concentrations are affected by diet whereas RBC folate is a more reliable indicator of folate status. This assay is useful for identification of folate deficiency when serum folate is normal but there is a high clinical suspicion of nutritional deficiency. It is used in the evaluation of individuals with low serum levels of both folate and iron.
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25-Hydroxy vitamin D represents the main body reservoir and transport form. Mild to moderate deficiency is associated with Osteoporosis / Secondary Hyperparathyroidism while severe deficiency causes Rickets in children and Osteomalacia in adults. Prevalence of Vitamin D deficiency is approximately >50% specially in the elderly. This assay is useful for diagnosis of vitamin D deficiency and Hypervitaminosis D. It is also used for differential diagnosis of causes of Rickets & Osteomalacia and for monitoring Vitamin D replacement therapy.
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1,25-Dihydroxy vitamin D plays a primary role in the maintenance of calcium homeostasis. A part of circulating 25-hydroxy vitamin D is converted to 1, 25-dihydroxy form in the kidneys. Patients who present with hypercalcemia, hyperphosphatemia and low PTH may suffer from unregulated conversion of vitamin D from mono-hydroxy to dihydroxy form as is seen in granulomatous diseases like Sarcoidosis and nutritionally induced Hypervitaminosis D.
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