Vitamina B12; diagnosi, sintomi, terapia
Table of Contents
D
Definizione
La vitamina B12 (cobalamina) è una molecola complessa il cui nucleo centrale è costituito da un anello cirillico, con un atomo centrale di cobalto. L’anello corrinico, come le porfirine, è composto da 4 unità pirroliche. La cobalamina in natura è sintetizzata e utilizzata da alcuni microrganismi (batteri, miceti). Gli animali erbivori se la procurano con l’ingestione di vegetali contaminati dai suddetti microrganismi e la vitamina viene poi utilizzata a livello dei tessuti muscolari e parenchimali, i quali costituiscono la principale forma di approvvigionamento per i carnivori. Per l’organismo umano, che non è in grado di sintetizzare la vitamina, la principale sorgente dietetica di cobalamina è rappresentata dalle proteine animali (carne, pesce, molluschi, latte e latticini, tuorlo d’uovo), anche se modeste quantità di B12 possono essere ingerite da vegetali contaminati da microrganismi.
Fabbisogno minimo giornaliero
La vitamina B12 è presente negli alimenti principalmente sotto forma di 5′-deossiadenosilcobalamina e di metilcobalamina. Il fabbisogno bisogno minimo giornaliero di vitamina B12 da parte dell’organismo umano ammonta circa 2,5 µg normalmente forniti da una dieta adeguata. L’uomo è capace di immagazzinare una notevole quantità della vitamina (2-5 mg di cui circa la metà nel fegato), per cui, anche in carenza di introduzione o assorbimento di B12 occorrono alcuni anni prima di arrivare a una deplezione dei depositi.
La vitamina B12 è metabolicamente attiva rispettivamente sotto forma di metilcobalamina e di adenosilcobalamina. La meticolbalamina catalizza la conversione dell’ omocisteina in metionina. Se la vitamina è carente e, di conseguenza, la reazione è bloccata, si accumula N5-metiltetraidrofolato che non puo’ essere demetilato a tetraidrofolato. Quest’ultima reazione è fondamentale perché i folati vengano trattenuti all’interno delle cellule:se l’acido N5-metiltetraidrofolico non viene demetilato, non può essere trasformato in poliglutammato forma di deposito intracellulare della vitamina ed esce dalle cellule, con conseguente carenza tessutale della vitamina. La carenza di vitamina B12 porta dunque ad un alterazione secondaria del metabolismo dei folati, con conseguente difetto di sintesi di purine e dTMP, quindi di DNA.
Anemia megaloblastica da carenza di vitamina B12
Fra le cause di carenza di vitamina B12 merita particolare menzione quella della soppressione immunomediata del fattore intrinseco (anemia perniciosa). L’anemia perniciosa è una malattia con una documentata predisposizione genetica che colpisce prevalentemente l’adulto anziano (l’età media di insorgenza è di circa 60 anni, anche se esiste una rara forma giovanile). Questa condizione si associa spesso ad altre malattie autoimmuni:
- Malattia di Graves
- Tiroide di Hashimoto
- Malattia di Addison
- Ipoparatiroidismo
- Vitiligo
Nel 90% dei pazienti si ritrovano autoanticorpi anti-cellule parietali e nel 60% autoanticorpi anti-fattore intrinseco: solo questi ultimi sono specifici dell’ anemia perniciosa. A livello istologico è presente un’ infiltrazione linfoplasmacellulare della mucosa gastrica, con atrofia della medesima e atipie cellulari. L’anemia perniciosa rende ragione però solo del 15-20% dei casi di carenza di cobalamina, mentre nell’anziano la causa più frequente 60-70% è costituita da una incapacità di utilizzare la vitamina legata alle proteine alimentari. Questa condizione si associa ad atrofia gastrica e acloridria, la cui patogenesi non è chiara, anche se è stato ipotizzato un ruolo di alcuni microorganismi (Helicobacter pylori, anaerobi.)
Sintomi
Il paziente con anemia da carenza di vitamina B12 lamenta i sintomi dell’anemia cronica e sul piano obiettivo presenta un colorito bianco-giallastro insieme. Le condizioni di nutrizione sono soddisfacenti; anzi talora una succulenza di tessuti conferisce un aspetto pseudoflorido. A livello del tratto gastrointestinale tipica è la glossite di Hunter: bruciore e parestesie linguali associati a ipotrofia, con scomparsa delle papille e aftosi recidivante. Si possono riscontrare diarrea e malassorbimento, causati dall’ alterazione delle cellule epiteliali intestinali. Possono essere presenti una moderata epatosplenomegalia e una febbricola.
Le lesioni neurologiche, che possono anche precedere la comparsa dell’anemia e che non sempre regrediscono completamente anche a seguito della terapia sostitutiva, interessano le fibre nervose periferiche, i cordoni laterali e posteriori del midollo spinale. Si verifica una demielinizzazione, seguita da degenerazione assonale e nei casi più gravi da morte dei neuroni.
Diagnosi
La diagnosi di carenza di vitamina B12 si pone sulla base del quadro clinico ed ematologico e viene confermata dalla riduzione della concentrazione sierica di vitamina B12. A questo punto è fondamentale individuare la causa che ha portato il deficit della vitamina, mediante un accurato esame clinico e le opportune indagini strumentali. Il test di Schilling che viene eseguita mediante somministrazione di vitamina B12, marcata con cobalto radioattivo e legato o meno a fattore intrinseco, permette di appurare se vi è un difettoso assorbimento della vitamina e se tale difetto viene corretto dalla contemporanea somministrazione di fattore intrinseco. In caso di anemia perniciosa, documentata dalla presenza di autoanticorpi anticellule parietali e antifattore intrinseco, è utile eseguire una gastroscopia, la quale documenta una gastrite atrofica e non secerne acidi cloridrico e con il tipico quadro istopatologico di infiltrazione della mucosa da parte di linfociti e plasmacellule .
Terapia
La terapia della carenza di B12 è fondamentalmente sostitutiva, associata a specifici provvedimenti, a seconda della causa che l’ha provocata. La vitamina B12 deve essere somministrata per via parentale, sotto forma di cianocobalamina. Esistono diversi sistemi di somministrazione. Di solito la posologia iniziale è elevata: almeno 100 µg/die per i primi 7 giorni, e comunque almeno 2000 µg nelle prime 6 settimane. Già dopo 4-7 giorni si osserva un marcato incremento del reticolociti e dopo la prima settimana di trattamento l’emoglobina inizia a salire, raggiungendo valori normali entro 1-2 mesi. Anche la sintomatologia neurologica regredisce, a meno che non si siano verificati danni irreversibili.
Gli alimenti ricchi di vitamina B12 sono soprattutto di origine animale. Di seguito indicate alcune fonti di vitamina B12.
- frutti di mare
- fegato e frattaglie
- cereali fortificati con vitamina B12
- merluzzo
- tonno
- sardine
- sgombro
- triglia
- trota
- maiale
- coniglio
- bovino
- uova
- formaggi stagionati come parmigiano, provolone. groviera
- yogurt
- latte
- mozzarella
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