Emocromatosi: cause, sintomi, trattamento
Table of Contents
Che cos’è l’emocromatosi?
Per emocromatosi si intende la presenza di un eccesso di ferro che si localizza prevalentemente nel fegato e che può interessare altri organi (pancreas, miocardio, ipofisi, surrene, linfonodi, cute) fino a divenire sistemico; può evolvere dopo i 50 anni in una pigmentazione cutanea, una cirrosi epatica e talvolta in un diabete. Il ferro, elemento in traccia indispensabile per la vita è presente normalmente nell’organismo umano adulto in quantità comprese tra 2 e 6 mg. Nell’ emocromatosi l’accumulo di ferro può eccedere i 50 mg, di cui più di un terzo si localizza nel fegato; il metallo si accumula prevalentemente all’interno degli epatociti, sotto forma di emosiderina.
Quali sono le cause delle emocromatosi?
Le cause di un accumulo di ferro possono essere diverse:
- Aumentato assorbimento di ferro (emocromatosi ereditaria o genetica)
- Sovraccarico di ferro secondario
- L’emocromatosi di tipo 2, di tipo 3 e di tipo 4.
Nell’ emocromatosi ereditaria la mutazione del gene HFE è responsabile nel 90% dei casi dell’espressione clinica di emocromatosi, almeno nelle popolazioni di origine nord Europea. In altre popolazioni compresa la popolazione italiana e mediterranea, la percentuale di associazione tra malattia e gene HFE si riduce notevolmente. Il gene HFE è legato al gene TFR (gene che codifica per il recettore della transferrina) e il loro prodotto si identifica con il sensore che percepisce la quantità totale di ferro nell’organismo. In altri termini l’attività di HFE e TFR regola l’assorbimento e il trasporto del ferro. Il meccanismo con il quale si realizza l’aumento dell’assorbimento del ferro nei pazienti con mutazione HFE è mediato dalla riduzione o assenza di epcidina.
Emocromatosi di tipo 2 giovanile
L’emocromatosi ereditaria di tipo 2 (emocromatosi giovanile) è una patologia autosomica recessiva rara dovuta a mutazioni nel gene HJV con conseguente alterazione della trascrizione della proteina emoiuvelina o a mutazioni nel gene HAMP, che codifica direttamente per l’epcidina. E’ una forma piuttosto severa che insorge precocemente e, se non trattata, può portare alla morte entro i trenta anni di età. E’ dovuta ad un aumentato assorbimento del ferro a livello intestinale, oppure il sovraccarico di ferro che si osserva nelle popolazioni africane o afro-americane in cui l’accumulo di ferro è il risultato di un’interazione tra un difetto ereditario sconosciuto e abitudini alimentari particolari (abuso di bevande alcooliche fermentate in contenitori in lega di ferro). I sintomi e i segni comprendono epatomegalia progressiva e ipogonadismo ipogonadotropo
Emocromatosi tipo 3
Mutazioni nel gene TFR2 (recettore 2 della transferrina) i sintomi e i segni sono simili all’emocromatosi ereditaria di tipo 1 (HFE).
Emocromatosi tipo 4
Tipo 4 (ferroportinopatia): mutazioni nel gene SLC40A1. Le manifestazioni cliniche sono più lievi che nella forma di tipo 1, con patologia epatica modesta e lieve anemia. Si manifesta nella prima decade di vita.
Sovraccarico di ferro secondario
Questo gruppo comprende il sovraccarico di ferro dovuto o associato a difetti nella produzione dei globuli rossi (anemie diseritropoietiche), epatopatie croniche di varia eziologia, somministrazione eccessiva di ferro per via parenterale (trasfusioni, preparati di ferro per venosa o intramuscolare) od orale. La talassemia major e l’anemia sideroblastica sono i due esempi più studiati di sovraccarico di ferro secondario alla somministrazione ripetuta di trasfusioni di sangue e/o ad un’alterata produzione dei globuli rossi (eritropoiesi inefficace).
Manifestazioni cliniche della emocromatosi
L’esordio clinico dell’ emocromatosi abbraccia un insieme di segni e sintomi tra i quali:
- Astenia
- Malessere
- Perdita di peso
- Iperpigmentazione cutanea
- Dolore addominale
- Riduzione della libido
- Diabete mellito.
Nelle fasi più avanzate della patologia si osserva epatosplenomegalia, aumento ulteriore della:
- Pigmentazione cutanea
- Spider nevi (angioma stellato)
- Artropatia
- Ascite
- Aritmie cardiache
- Atrofia testicolare
- Ginecomastia
- Perdita della normale distribuzione plifera corporea
Epatomegalia è presente nel 95% dei pazienti sintomatici ma più del 50% di loro hanno solo una lieve alterazione della funzionalità epatica, nonostante l’epatomegalia e la fibrosi. Un aumento della pigmentazione cutanea si osserva in più del 90% dei pazienti con emocromatosi
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