Embedded Files
B12 present only in foods of animal origin; total body stores sufficient for 2–3 y
Binds to intrinsic factor (IF) secreted by gastric parietal cells; absorbed in terminal ileum
Etiologies: malnutrition (alcoholics,vegans), pernicious anemia (PA, autoimmune disease against gastric parietal cells, a/w polyglandular endocrine insufficiency and ↑risk of gastric carcinoma), other causes of ↓ absorption (gastrectomy, sprue, Crohn’s disease),
↑competition (intestinal bacterial overgrowth, fish tapeworm)
Clinical manifestations: neurologic changes (subacute combined degeneration) affecting peripheral nerves, posterior and lateral columns of the spinal cord, and cortex
→ numbness, paresthesias, ↓ vibratory and positional sense, ataxia, dementia
Dx: ↓B12; ↑ homocysteine and methylmalonic acid; anti-IF Ab; Schilling test; ↑ gastrin in PA
Изменения в анализе крови:
анемия (Hb <130/120 г/л),
макроцитарная (MCV >100) или нормоцитарная (MCV 80–100),
нормо-, гиперхромная (MCH >35)
анизоцитоз с преобладанием макроцитоза, гиперхромии (RDW >14,5%),
в эритроцитах телец Жолли, колец Кебота;
гипорегенераторная; ± тромбоцитопения, лейкопения с нейтропенией, макроцитоз и
гиперсегментация нейтрофилов.
Treatment: 1mg B12 IM qd x 7d → q wk x 4–8wk → q month for life
neurologic abnormalities are reversible if treated w/in 6 mo
folate can reverse hematologic abnormalities of B12 deficiency but not neurologic
changes (and can lead to “steal” of B12 stores → worsening of neuro complications)
oral supplementation (2 mg qd) appears feasible as well even w/o IF
Page updated
Google Sites
Report abuse