Table of Contents · 5 sections
Vitamins are essential organic compounds required in trace amounts for normal metabolism. Knowing the functions and deficiency manifestations of each vitamin is a must-have minimum for any physician. This article provides a comprehensive reference table with clinical correlations.
Fat-soluble vitamins (A, D, E, K)
| Vitamin | Active form | Function | Deficiency | Excess |
|---|---|---|---|---|
| A (retinol) | Retinal, retinoic acid | Vision (rhodopsin), epithelial differentiation, immunity | Night blindness (hemeralopia), xerophthalmia, keratomalacia, squamous metaplasia | Teratogenicity!, pseudotumor cerebri, hepatotoxicity |
| D (cholecalciferol) | 1,25-(OH)₂-D₃ (calcitriol) | ↑ Intestinal absorption of Ca²⁺ and PO₄³⁻, bone mineralization | Rickets (children), osteomalacia (adults) | Hypercalcemia → nephrocalcinosis |
| E (tocopherol) | α-Tocopherol | Antioxidant (membrane protection against lipid peroxidation) | Hemolytic anemia in newborns, neuropathy, ataxia | Rare (↑ bleeding risk when taken with anticoagulants) |
| K (phylloquinone) | Menaquinone | Carboxylation of clotting factors (II, VII, IX, X) and proteins C and S | Bleeding tendency (↑ PT/INR). In newborns — hemorrhagic disease of the newborn | — |
ADEK mnemonic: fat-soluble → absorbed with fats → impaired in fat malabsorption (cystic fibrosis, cholestasis, celiac disease).
Water-soluble B-complex vitamins
| Vitamin | Coenzyme | Function | Deficiency |
|---|---|---|---|
| B₁ (thiamine) | TPP (thiamine pyrophosphate) | Cofactor for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, transketolase | Beriberi (dry — neuropathy; wet — heart failure), Wernicke encephalopathy (ataxia, ophthalmoplegia, confusion), Korsakoff syndrome |
| B₂ (riboflavin) | FMN, FAD | Redox reactions (ETC, β-oxidation) | Cheilosis (lip fissures), glossitis, seborrheic dermatitis, corneal vascularization |
| B₃ (niacin, PP) | NAD⁺, NADP⁺ | Redox reactions (>200 enzymes) | Pellagra: 3 Ds — dermatitis (Casal's necklace distribution), diarrhea, dementia (+ 4th D — death) |
| B₅ (pantothenic acid) | CoA (coenzyme A) | Acyl group transfer (TCA cycle, β-oxidation, fatty acid synthesis) | Extremely rare: burning feet syndrome |
| B₆ (pyridoxine) | PLP (pyridoxal phosphate) | Transamination, amino acid decarboxylation, heme synthesis (ALA synthase), GABA, serotonin | Peripheral neuropathy, sideroblastic anemia, neonatal seizures |
| B₇ (biotin) | Biotin (covalently bound) | Carboxylation (pyruvate→OAA, acetyl-CoA→malonyl-CoA) | Dermatitis, alopecia (raw eggs — avidin binds biotin) |
| B₉ (folate) | Tetrahydrofolate (THF) | One-carbon unit transfer (purine synthesis, dTMP → DNA) | Megaloblastic anemia, neural tube defects (spina bifida) in the fetus |
| B₁₂ (cobalamin) | Methylcobalamin, adenosylcobalamin | Homocysteine → methionine (with folate), methylmalonyl-CoA → succinyl-CoA | Megaloblastic anemia + subacute combined degeneration of the spinal cord (↑ methylmalonic acid — distinguishes it from folate deficiency!) |
Vitamin C (ascorbic acid)
- Function: hydroxylation of proline and lysine in collagen, antioxidant, ↑ Fe²⁺ absorption, cofactor for dopamine β-hydroxylase
- Deficiency: scurvy — bleeding gums, petechiae, impaired wound healing, loose teeth, anemia
- Sources: citrus fruits, bell peppers, rose hips, kiwi
Clinical Pearls
- In alcoholism: administer thiamine BEFORE glucose (glucose consumes thiamine → can precipitate Wernicke encephalopathy)
- B₁₂ deficiency: neurology + anemia. Folate deficiency: anemia only. Administering folate in B₁₂ deficiency masks the anemia, but neurological symptoms progress!
- Isoniazid (antituberculous) → B₆ deficiency → neuropathy. Always prescribe B₆ together with isoniazid
- Warfarin — vitamin K antagonist. Antidote: vitamin K (phytomenadione)
Frequently asked questions
How to distinguish B₁₂ deficiency from folate deficiency?
Both cause megaloblastic anemia (macrocytosis, hypersegmented neutrophils). Differences: B₁₂ deficiency → ↑ methylmalonic acid + ↑ homocysteine + neurological symptoms (subacute combined degeneration: impaired vibration/proprioceptive sensation, spastic paraparesis). Folate deficiency → normal methylmalonic acid + ↑ homocysteine, no neurology.
Why can fat-soluble vitamins be toxic?
Fat-soluble vitamins (A, D, E, K) accumulate in adipose tissue and the liver (they are not excreted in the urine like water-soluble ones). Excessive intake → cumulative buildup → toxicity. Hypervitaminosis A (teratogenicity — contraindicated in high doses during pregnancy) and D (hypercalcemia) are especially dangerous.
Study biochemistry via interactive lessons. Related topics: Krebs cycle, glycolysis, formed elements of blood, connective tissue.