PE12.1-8,PE13.1-4 | Micronutrients — Glossary

The biologically active form of vitamin D, synthesised from 25-OH-D by renal 1α-hydroxylase (stimulated by PTH); upregulates intestinal TRPV6 channels and calbindin to increase calcium and phosphate absorption.

The active chromophore derived from retinol in rod photoreceptors; isomerised from all-trans retinal by isomerase; combines with opsin to form rhodopsin.

A rare autosomal recessive disorder of apolipoprotein B synthesis; affected individuals cannot assemble chylomicrons or VLDL, causing severe malabsorption of fat-soluble vitamins (especially A and E), leading to acanthocytosis, retinopathy, and spinocerebellar degeneration.

Red blood cells with irregular spiky projections (as opposed to the smooth crenations of echinocytes); seen in abetalipoproteinaemia (due to abnormal membrane lipid composition) and in severe Vitamin E deficiency-related haemolysis.

An enzyme produced by osteoblasts actively synthesising bone matrix; markedly elevated in active rickets reflecting intense unmineralised osteoid production at the growth plate; used to diagnose and monitor treatment.

The most biologically active and tissue-dominant form of Vitamin E; a fat-soluble antioxidant embedded in cell membrane phospholipid bilayers, where it neutralises lipid peroxyl radicals to prevent oxidative membrane damage.

A hepatic protein that preferentially selects alpha-tocopherol from all dietary tocopherol forms for incorporation into VLDL and distribution to peripheral tissues; explains why alpha-tocopherol is the dominant circulating and tissue form of Vitamin E.

Emblica officinalis; the richest known natural source of vitamin C (~600–700 mg/100 g); widely available in India; its vitamin C is relatively heat-stable compared to other sources due to the presence of tannins that protect against oxidation.

A comprehensive national strategy launched in 2018 under POSHAN Abhiyaan to reduce anaemia prevalence by 3% annually; encompasses IFA supplementation, deworming, food fortification, dietary diversification, and behaviour change communication.

Painful fissuring at the corners of the mouth; a mucocutaneous feature seen in riboflavin (B2) deficiency and, less specifically, in other nutritional deficiencies including iron deficiency.

The clinical syndrome of riboflavin (B2) deficiency, characterised by angular stomatitis, magenta-coloured glossitis, seborrhoeic dermatitis, and corneal vascularisation; rarely fatal but often accompanies multiple deficiencies.

The reduced, biologically active form of vitamin C; a water-soluble antioxidant and essential cofactor for hydroxylation reactions including collagen synthesis and iron absorption; cannot be synthesised by humans.

A glycoprotein in raw egg white that binds biotin (B7) with very high affinity, preventing its intestinal absorption; prolonged consumption of raw eggs can cause biotin deficiency.

Infantile scurvy; typically presents at 6–18 months in infants fed exclusively on boiled cow's milk; characterised by pseudoparalysis, subperiosteal haemorrhage, and frog-leg posture.

A clinical syndrome caused by thiamine (B1) deficiency; wet beriberi presents with high-output cardiac failure and oedema; dry beriberi presents with peripheral neuropathy; infantile wet beriberi affects breastfed infants of thiamine-deficient mothers.

Foamy, triangular, white-grey plaques on the bulbar conjunctiva (WHO stage X1A), composed of keratinised epithelial cells and Corynebacterium xerosis; pathognomonic of Vitamin A deficiency in children under 6 years.

The chemically bound, biologically unavailable form of niacin in maize; not absorbed unless the grain is treated with alkali (nixtamalisation); explains why maize-dependent populations develop pellagra unless their diet is supplemented or diversified.

The hepatically hydroxylated storage and transport form of Vitamin D; the correct marker of Vitamin D status in clinical practice; deficiency defined as <20 ng/mL.

A peptide hormone secreted by thyroid parafollicular (C) cells in response to hypercalcaemia; lowers serum calcium by inhibiting osteoclast activity and increasing renal calcium excretion.

The biologically active hormone form of Vitamin D, produced in the renal proximal tubule by 1-alpha-hydroxylase; stimulates intestinal calcium and phosphate absorption and bone mineralisation.

The standard intravenous calcium preparation for treating hypocalcaemic tetany or seizures; contains approximately 9.3 mg (0.23 mmol) elemental calcium per mL; dosed at 1–2 mL/kg (maximum 20 mL) given slowly over 5–10 minutes with continuous cardiac monitoring to avoid bradycardia.

A form of rickets occurring in children with adequate Vitamin D but very low dietary calcium intake; causes secondary hyperparathyroidism and skeletal undermineralisation; endemic in parts of South India and sub-Saharan Africa.

A G-protein-coupled receptor on parathyroid chief cells (and other tissues) that detects minute changes in ionised serum calcium and regulates PTH secretion accordingly; mutations cause familial hypocalciuric hypercalcaemia or neonatal severe primary hyperparathyroidism.

Plant pigments (especially β-carotene) that act as provitamin A; converted to retinol in the intestinal mucosa with an efficiency of approximately 12:1 by dietary weight.

A pathognomonic sign of pellagra: a band of hyperpigmented, desquamating, photosensitive dermatitis distributed around the neck in the collar area, reflecting solar exposure pattern.

Vitamin D synthesised in the skin from 7-dehydrocholesterol under UV-B radiation, and available in animal-source foods; the principal form used for supplementation.

Ipsilateral contraction of facial muscles induced by tapping the facial nerve just anterior to the ear; a screening sign for hypocalcaemia that has limited specificity (positive in up to 25% of normocalcaemic individuals).

A large lipoprotein assembled in intestinal enterocytes to transport dietary fats (including fat-soluble vitamins) via lymphatics to the systemic circulation; absent in abetalipoproteinaemia, causing severe fat-soluble vitamin malabsorption.

VKDB presenting on days 2–7 of life in exclusively breastfed infants who did not receive Vitamin K prophylaxis at birth; manifests as umbilical oozing, gastrointestinal bleeding, ecchymoses; prevented by routine IM Vitamin K at birth.

Coiled, spiral-shaped hairs due to structural defects in the keratin of the hair follicle; a characteristic skin sign of vitamin C deficiency in older children and adults.

Softening of the skull bones (occipital, parietal) in rickets causing a 'ping-pong ball' sensation on palpation; an early sign of rickets in infants under 6 months but also seen in normal premature infants.

Severe and irreversible physical and intellectual disability resulting from extreme iodine deficiency during fetal development; two types: neurological (deaf-mutism, spastic diplegia from first-trimester maternal deficiency) and myxoedematous (hypothyroid features from perinatal deficiency).

The characteristic radiological sign of active rickets on wrist X-ray: the normally sharp, flat metaphyseal border becomes concave (cupped), irregular, and frayed due to failure of provisional calcification.

The oxidised form of vitamin C; transported into cells via glucose transporters (GLUT1/3) and rapidly reduced back to ascorbic acid intracellularly; maintains the active vitamin C pool.

A thyroglobulin tyrosine residue with two iodine atoms added by thyroperoxidase; DIT+DIT coupling produces T4 (thyroxine), the principal secretory product of the thyroid gland.

The apical membrane transporter on duodenal enterocytes that imports Fe²⁺ into the cell; the final common pathway for non-haem iron absorption in the small intestine.

VKDB presenting within 24 hours of birth, caused by maternal drugs that cross the placenta and interfere with Vitamin K (anticonvulsants, rifampicin, warfarin); prevented by antenatal maternal Vitamin K supplementation and neonatal prophylaxis.

Hypocalcaemia occurring within the first 72 hours of life, associated with prematurity, infant of diabetic mother, or perinatal asphyxia; due to immature or suppressed parathyroid response and/or co-existent hypomagnesaemia.

Enlargement of the thyroid gland affecting more than 10% of school-age children in a defined population; caused by chronic iodine deficiency with compensatory TSH-driven thyroid hyperplasia; a public health marker of population-level iodine insufficiency.

The mechanism by which warfarin produces anticoagulation: blocking VKOR traps Vitamin K in the epoxide form, preventing recycling to active Vitamin K, thereby impairing gamma-carboxylation of coagulation factors II, VII, IX, X; directly analogous to the pathophysiology of Vitamin K deficiency.

A chemical reaction in which ferrous iron (Fe²⁺) reacts with hydrogen peroxide to generate highly reactive hydroxyl radicals; relevant to haemolytic anaemia of prematurity, where iron supplementation in Vitamin E-deficient premature infants generates oxidative damage to red cell membranes.

The basolateral iron exporter on enterocytes and macrophages that releases iron into the portal circulation; regulated by hepcidin — hepcidin binds and degrades ferroportin, reducing iron export.

A blood product containing all coagulation factors including the Vitamin K-dependent ones; used in active VKDB bleeding to provide immediate factor replacement while waiting for Vitamin K to take effect (4-6 hours); dose 10-15 mL/kg.

A characteristic position adopted by infants with scurvy: hips flexed, abducted, and externally rotated to minimise tension on the painful subperiosteal haemorrhages; resembles the resting posture of a frog.

A reversible state of PTH deficiency or resistance induced by hypomagnesaemia; magnesium is required for both PTH exocytosis from parathyroid chief cells and for Gs-protein signalling at PTH receptors, so its depletion mimics surgical hypoparathyroidism.

The Vitamin K-dependent enzymatic conversion of glutamic acid residues in coagulation protein precursors to gamma-carboxyglutamic acid (Gla), which enables calcium binding and membrane anchoring essential for coagulation factor function.

Bowing of the legs (bow-legs) due to softening and bending of the tibiae and femora from weight-bearing in active rickets; the most visible deformity in walking-age children.

A substance that interferes with thyroid hormone synthesis or iodine utilisation, thereby promoting goitre development; found in cruciferous vegetables (cabbage, cassava, millet); clinically relevant only when iodine intake is already marginal.

Dietary iron derived from animal-source foods (meat, poultry, fish) in which iron is bound within a porphyrin ring; absorbed intact via haem carrier protein 1 with ~20–25% bioavailability, not inhibited by dietary factors.

Vitamin E deficiency–related haemolytic anaemia in premature infants (<34 weeks gestation), presenting at 4–6 weeks of life with falling haemoglobin, thrombocytosis, and oedema; exacerbated by iron supplementation; Coombs-negative.

A horizontal groove at the line of diaphragmatic attachment on the chest wall in rickets, caused by inward pulling of the softened costal cartilage by the diaphragm during inspiration.

A liver-derived antimicrobial peptide that is the master regulator of systemic iron homeostasis; it reduces iron absorption and macrophage iron release by binding and internalising ferroportin; elevated in inflammation (explaining anaemia of chronic disease).

An intermediate amino acid that accumulates when methionine synthesis is impaired by B12 or folate deficiency; elevated plasma homocysteine is associated with cardiovascular risk and can serve as a biomarker of deficiency.

The principal mineral constituent of bone and teeth — a crystalline calcium phosphate compound [Ca10(PO4)6(OH)2] that provides structural hardness and serves as a metabolic calcium and phosphate reservoir.

A neutrophil with 5 or more nuclear lobes seen on peripheral blood smear; >5% of neutrophils with ≥5 lobes is diagnostic of megaloblastic erythropoiesis from B12 or folate deficiency.

Toxicity due to excessive Vitamin A intake; acute form causes raised intracranial pressure (bulging fontanelle in infants); chronic form causes bone pain, hepatotoxicity, and alopecia; teratogenic in the first trimester.

Vitamin D toxicity from supplemental excess; defined biochemically as serum 25(OH)D >150 ng/mL with hypercalcaemia; causes polyuria, vomiting, nephrocalcinosis, metastatic calcification.

A syndrome of neuromuscular hyperexcitability caused by a fall in serum ionised calcium below ~1.1 mmol/L; clinically manifest as carpopedal spasm, Trousseau sign, Chvostek sign, laryngospasm, and generalised seizures.

The average daily dietary intake level sufficient to meet the nutrient requirement of nearly all (97–98%) healthy individuals in a defined life-stage and gender group; published by the Indian Council of Medical Research–National Institute of Nutrition (2020 edition).

The iron-folic acid formulation for children 6–59 months under NIPI/AMB: each 1 mL contains 20 mg elemental iron and 100 mcg folic acid; prescribed at 1 mL biweekly (twice per week) for prevention.

Bleeding within the cranial vault (subdural, subarachnoid, or intracerebral); the most devastating complication of late VKDB, presenting with tense fontanelle, vomiting, lethargy, seizures; mortality 20%, neurological sequelae 30-50%.

A glycoprotein secreted by gastric parietal cells, essential for binding vitamin B12 in the stomach and enabling its absorption in the terminal ileum; absent in pernicious anaemia (autoimmune destruction of parietal cells).

The full spectrum of adverse health outcomes resulting from inadequate iodine intake, including subclinical cognitive impairment, endemic goitre, hypothyroidism, and cretinism; the single most common cause of preventable intellectual disability worldwide.

The free, unbound fraction of serum calcium (~50% of total); the biologically active fraction that determines neuromuscular excitability and triggers PTH secretion; not affected by albumin concentration changes.

Anaemia resulting from depletion of body iron stores, leading to insufficient iron for haemoglobin synthesis; the most common nutritional anaemia worldwide; characterised by microcytic, hypochromic red cells on peripheral smear.

Colliquative necrosis (melting) of the cornea due to severe Vitamin A deficiency (WHO stage X3B); irreversible, leading to perforation, phthisis bulbi, and permanent blindness.

Spoon-shaped nails with upward curvature of the nail plate; a chronic sign of severe iron deficiency caused by impaired keratinisation; takes months to develop and months to resolve with treatment.

The principle (if not always the named test) of confirming Vitamin K deficiency by observing correction of a prolonged PT within 4-6 hours of Vitamin K administration; response confirms the diagnosis.

VKDB presenting at 2 weeks to 6 months of age in exclusively breastfed infants or those with fat malabsorption; the most dangerous form — intracranial haemorrhage in 30-50% of cases; mortality 20%; prevented by birth prophylaxis.

Hypocalcaemia developing after day 4–7 of life in a term neonate, most commonly caused by feeding with unmodified cow's milk (high phosphate load depresses ionised calcium via the Ca-phosphate solubility product mechanism).

A chain-reaction process in which reactive oxygen species attack polyunsaturated fatty acids in cell membranes, generating lipid peroxyl radicals that propagate further membrane damage; the primary mechanism of Vitamin E-deficiency disease.

The standard intravenous preparation for treating symptomatic hypomagnesaemia in children; dosed at 25–50 mg/kg (maximum 2 g per dose) infused over 30–60 minutes with continuous cardiac monitoring; also used in eclampsia and acute severe asthma.

Anaemia caused by impaired DNA synthesis (due to B12 or folate deficiency) leading to large, immature red-cell precursors in the bone marrow; peripheral smear shows macrocytes (MCV >100 fL) and hypersegmented neutrophils.

Vitamin K produced by intestinal bacteria and present in fermented foods (natto, cheese); contributes to the body's Vitamin K economy but is insufficient alone to prevent VKDB in neonates with sterile guts.

A metabolic intermediate that accumulates in B12 deficiency when adenosylcobalamin-dependent methylmalonyl-CoA mutase activity fails; elevated urine/plasma MMA helps distinguish B12 from folate deficiency.

The biologically active chelated complex of magnesium and adenosine triphosphate required for all phosphotransferase (kinase) reactions; ATP without Mg2+ cannot serve as a substrate for most ATPases and kinases.

Anaemia characterised by small red cells (MCV <80 fL) with reduced haemoglobin content (MCH <27 pg) and pale appearance; the peripheral-smear hallmark of iron deficiency anaemia in Stage 3.

A thyroglobulin tyrosine residue with one iodine atom added by thyroperoxidase; an intermediate in thyroid hormone synthesis that is coupled with diiodotyrosine (DIT) to produce T3.

The lipid-rich insulating layer around peripheral nerve axons; highly vulnerable to lipid peroxidation due to its high PUFA content; progressive demyelination in chronic Vitamin E deficiency produces peripheral neuropathy.

Congenital IDD caused by iodine deficiency at or after birth leading to thyroid atrophy; characterised by profound hypothyroid features (puffy facies, growth failure, dry skin, constipation) with intellectual disability; notably DOES NOT include deaf-mutism or spastic diplegia.

India's programme delivering oral megadose Vitamin A supplementation through the immunisation platform: 1 lakh IU at 9 months, then 2 lakh IU every 6 months from 18 months up to 5 years.

A population-level screening test performed on filter-paper blood spots collected on day 3–5 of life; neonatal TSH >5 mIU/L in more than 3% of neonates in a population indicates iodine deficiency at the community level; also used to detect congenital hypothyroidism early.

Deposition of calcium salts within the renal tubules, a complication of chronic hypercalcaemia (including hypervitaminosis D); may lead to nephrolithiasis and renal impairment.

The most severe form of congenital IDD caused by severe maternal iodine deficiency in the first trimester of pregnancy, resulting in deaf-mutism, spastic diplegia, intellectual disability, and squint; not reversible with postnatal iodine; thyroid function may appear normal at birth.

A unit expressing the total niacin available from a food, including both preformed niacin and the amount synthesised from dietary tryptophan (60 mg tryptophan = 1 mg niacin equivalent).

The preferred form of niacin used therapeutically to treat pellagra, as it corrects NAD+ deficiency without causing the flushing (prostaglandin-mediated vasodilation) that occurs with nicotinic acid.

India's national programme for the elimination of IDD, launched in 1962 and restructured in 1992; implements USI, urinary iodine surveys, neonatal TSH screening, goitre surveys, and community education through state health departments.

The earliest clinical manifestation of Vitamin A deficiency, resulting from impaired rhodopsin regeneration; manifests as difficulty seeing in dim light or at dusk.

India's programme for universal iron and folic acid supplementation launched in 2013, targeting children 6 months to 5 years, school-age children, and adolescents with age-specific IFA formulations and schedules.

Dietary iron from plant foods and fortified products existing as Fe³⁺; requires reduction to Fe²⁺ by gastric acid and vitamin C before absorption via DMT1; bioavailability 1–10%, inhibited by phytates, tannins, and calcium.

The absorption of dietary iron from plant sources and fortified foods; requires reduction of Fe³⁺ to Fe²⁺ by acidic pH and vitamin C in the duodenum before transport into enterocytes by DMT1.

A metabolic bone disease in children caused by deficiency of calcium, vitamin D, or both, resulting in failure of osteoid mineralisation; characterised by rachitic rosary, frontal bossing, cupped/frayed metaphyses on X-ray, elevated ALP, and elevated PTH.

A Vitamin K-dependent protein produced by osteoblasts that binds hydroxyapatite and regulates bone mineralisation; illustrates the role of Vitamin K beyond coagulation, in bone and vascular health.

An 84-amino-acid polypeptide secreted by the chief cells of the parathyroid glands in response to a fall in ionised serum calcium; raises serum calcium by promoting bone resorption, renal calcium reabsorption, and activation of vitamin D.

Bony spurs seen at the corners of the metaphysis on X-ray in scurvy; formed by calcification of the margins of the Trümmerfeld zone; paired with the Trümmerfeld zone as a diagnostic radiological sign.

A disease caused by niacin (B3) deficiency, characterised by the '3 Ds': Dermatitis (photosensitive, symmetric), Diarrhoea, and Dementia; associated with maize-dependent diets low in niacin and tryptophan.

Small petechial haemorrhages around hair follicles on the skin, caused by capillary fragility from defective collagen in vessel walls; a characteristic skin sign of vitamin C deficiency.

Dysfunction of peripheral nerves, manifesting as loss of deep tendon reflexes, vibration and proprioception; caused by lipid peroxidation of myelin sheaths in chronic Vitamin E deficiency.

Follicular hyperkeratosis ('toad skin') occurring in Vitamin A deficiency; dry, rough, horny papules on the lateral upper arms, thighs, and shoulders.

The principal dietary form of Vitamin K, found in green leafy vegetables; the form most commonly used for prophylaxis and treatment of Vitamin K deficiency bleeding.

Organic phosphorus compounds found in the bran and germ of cereals, legumes, and nuts; they chelate non-haem iron in the gut lumen and inhibit its absorption via DMT1; represent the primary barrier to iron absorption in vegetarian diets.

A compulsive craving for non-food substances (clay, paper, ice, chalk, soil); a symptom associated with iron deficiency; the mechanism is uncertain but resolves with iron repletion.

Accumulation of lipofuscin and disruption of photoreceptor outer segments due to lipid peroxidation; causes night blindness and visual field loss; a feature of chronic Vitamin E deficiency in malabsorption syndromes.

Biologically inactive precursors of Vitamin K-dependent coagulation factors (principally PIVKA-II, des-gamma-carboxyprothrombin); elevated in Vitamin K deficiency before PT is prolonged; used as a sensitive early marker.

The chemical form of iodine used for salt fortification in India; preferred over potassium iodide (KI) because iodate is more stable in tropical heat and humidity, resisting degradation during transport and storage.

An enzyme that hydroxylates proline residues in procollagen chains to form hydroxyproline; requires vitamin C as a cofactor; its inactivity in scurvy prevents stable collagen triple-helix formation.

A coagulation test measuring the extrinsic pathway (Factor VII) and common pathway (Factors X, V, II, fibrinogen); markedly prolonged in VKDB because Factors VII, X, and II are all Vitamin K-dependent; the most sensitive test for VKDB.

An apparent inability to move a limb due to severe pain rather than true neurological paralysis; occurs in infantile scurvy from subperiosteal haemorrhage and periosteal irritation.

Raised intracranial pressure without a space-occupying lesion; a feature of both acute Vitamin A toxicity and chronic hypervitaminosis A; presents as bulging fontanelle in infants, headache and vomiting in older children.

The active coenzyme form of vitamin B6 (pyridoxine); required for aminotransferases, decarboxylases (neurotransmitter synthesis including GABA, serotonin, dopamine), and glycogen phosphorylase.

A rare inherited metabolic disorder (antiquitin/ALDH7A1 deficiency) presenting with refractory neonatal seizures that respond dramatically to IV pyridoxine 100 mg; requires lifelong pyridoxine supplementation.

Palpable beading at the costochondral junctions due to metaphyseal widening in rickets; a classic chest sign in active disease.

Eleusine coracana; a cereal grain commonly consumed in South India containing approximately 350 mg calcium per 100 g — the most calcium-dense Indian grain and an important complementary food for toddlers on vegetarian or dairy-free diets.

The average daily dietary intake level sufficient to meet the nutrient requirements of nearly all (97–98%) healthy individuals in a particular age and sex group; the standard reference for nutritional adequacy.

Persistently low serum calcium that does not normalise despite adequate calcium and vitamin D supplementation; classically due to co-existing hypomagnesaemia that must be corrected before calcium homeostasis can be restored.

Nuclear receptors activated by retinoic acid that regulate transcription of genes controlling epithelial cell differentiation; their action explains why Vitamin A deficiency leads to keratinising metaplasia of mucosal epithelia.

The alcohol form of Vitamin A (preformed), found in animal-source foods; the principal circulating and storage form of Vitamin A in mammals.

The unit used to express Vitamin A dietary requirements, accounting for the lower bioavailability of carotenoids versus preformed retinol; 1 RAE = 1 µg retinol = 12 µg β-carotene.

A transport protein synthesised by the liver that carries retinol in the circulation, complexed with transthyretin (TTR); its synthesis is reduced in protein-energy malnutrition, compounding functional Vitamin A deficiency.

The photosensitive pigment in rod photoreceptors, formed by combining 11-cis retinal with the protein opsin; essential for dark adaptation and night vision.

Failure of mineralisation of the growing growth plate and osteoid in children, caused by Vitamin D deficiency, dietary calcium deficiency, or metabolic disorders; characterised by skeletal deformity, growth impairment, and hypocalcaemic manifestations.

The clinical syndrome of severe vitamin C deficiency; caused by failure of collagen synthesis leading to haemorrhage, bone disease, and impaired wound healing; called Barlow's disease when it occurs in infants.

Elevated PTH secretion in response to hypocalcaemia (from any cause including Vitamin D deficiency); PTH drives skeletal calcium resorption, phosphaturia, and renal calcitriol synthesis.

A serum marker of total body iron stores; values <12 mcg/L indicate depleted iron stores (Stage 1 iron deficiency); the earliest laboratory abnormality in developing iron deficiency.

A membrane transport protein on thyroid follicular cells that actively concentrates iodide from plasma into the thyroid against a concentration gradient of 20–40 fold; the primary mechanism of iodide uptake by the thyroid.

Progressive incoordination and gait disturbance caused by degeneration of spinocerebellar tracts and the posterior column, a consequence of chronic Vitamin E deficiency in fat malabsorption disorders.

A single large oral dose of Vitamin D3 (600,000 IU in children >3 months) used to treat nutritional rickets; preferred in India due to reliable one-time delivery overcoming adherence barriers.

A neurological complication of B12 deficiency causing demyelination of the posterior and lateral columns of the spinal cord; manifests as loss of proprioception and vibration sense, ataxia, and upper motor neuron signs; not caused by folate deficiency.

Bleeding between the periosteum and the underlying bone cortex, occurring in scurvy due to defective collagen in vessel walls; causes extreme tenderness and swelling along long bones, most commonly the femur and tibia.

The active coenzyme form of folate (B9); accepts and donates one-carbon units in purine and thymidylate synthesis; essential for DNA replication in rapidly dividing cells including erythroid precursors.

The dose of elemental iron prescribed to treat established iron deficiency anaemia: 3–6 mg/kg/day divided into 2–3 doses; much higher than the preventive IFA programme doses.

The active coenzyme form of vitamin B1 (thiamine); acts as a cofactor for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, both essential for aerobic glucose metabolism.

Elevated platelet count (>500 × 10⁹/L); occurs in the haemolytic anaemia of prematurity syndrome associated with Vitamin E deficiency; the mechanism is reactive, related to the anaemia-driven elevation of thrombopoietin.

A thyroid enzyme that oxidises iodide and catalyses iodination of thyroglobulin tyrosine residues to form monoiodotyrosine and diiodotyrosine, and their coupling to produce T3 and T4; the key enzyme in thyroid hormone synthesis requiring iodine as substrate.

A water-soluble formulation of Vitamin E that is absorbed by bile-independent mechanisms; the appropriate supplement for patients with chronic cholestasis or fat malabsorption who cannot absorb oil-based Vitamin E.

The relatively stable radical formed when alpha-tocopherol donates a hydrogen atom to a lipid peroxyl radical; can be regenerated to active Vitamin E by ascorbic acid (Vitamin C), illustrating the antioxidant synergism between these two vitamins.

A measure of transferrin's capacity to bind iron; TIBC rises in iron deficiency as the liver produces more transferrin to capture scarce iron; a raised TIBC combined with low serum iron indicates iron-deficient erythropoiesis.

The percentage of transferrin binding sites occupied by iron (serum iron ÷ TIBC × 100); normal 20–45%; falls below 15% in iron-deficient erythropoiesis (Stage 2), indicating insufficient iron supply to bone marrow.

Carpal spasm (obstetrician's hand posture — wrist flexion, MCP flexion, IP extension, thumb adduction) induced by inflating a blood-pressure cuff above systolic for 3 minutes; the most sensitive clinical test for latent hypocalcaemia.

Transient receptor potential melastatin channel 6; a magnesium-permeable ion channel in the intestinal epithelium and renal distal convoluted tubule responsible for active magnesium reabsorption; loss-of-function mutations cause familial hypomagnesaemia with secondary hypocalcaemia.

A transverse lucent band seen at the metaphysis on X-ray in scurvy, reflecting failure of osteoid mineralisation and trabecular destruction; one of the pathognomonic radiological signs of scurvy.

The WHO/UNICEF/ICCIDD-recommended strategy of fortifying all salt for human and livestock consumption with iodine; in India mandated as ≥30 ppm potassium iodate at production and ≥15 ppm at household level; the most cost-effective strategy for IDD elimination.

The concentration of iodine in urine, used as the primary population-level indicator of iodine nutritional status; median UIC 100–199 mcg/L in school-age children indicates adequate iodine intake; <50 mcg/L indicates severe deficiency.

The enzyme that recycles Vitamin K epoxide (the inactive oxidised form) back to active Vitamin K after each carboxylation reaction; the target of warfarin, which blocks this recycling, depleting active Vitamin K and impairing coagulation.

Bleeding disorder in neonates and infants caused by deficiency of Vitamin K-dependent coagulation factors; classified into early (<24h), classic (day 2-7), and late (2 weeks-6 months) forms; entirely preventable with IM prophylaxis at birth.

An acute neurological emergency from severe thiamine deficiency, characterised by the triad of ophthalmoplegia, ataxia, and confusion; precipitated by administering glucose without thiamine in depleted patients.

A dense ring of calcification seen around the epiphysis on X-ray in scurvy; represents the relatively preserved zone of provisional calcification; appears on healing.

The most common hereditary form of rickets, caused by loss-of-function mutations in the PHEX gene, leading to elevated FGF23, renal phosphate wasting, and hypophosphataemia; serum calcium and 25-OH-D are normal, distinguishing it from nutritional rickets.

The ocular manifestations of Vitamin A deficiency, classified by WHO into stages XN (night blindness) through XF (fundal changes), with keratomalacia (X3B) representing irreversible corneal melting.