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Rivista di Medicina Nucleare e Imaging Molecolare

A Journal on Nuclear Medicine and Molecular Imaging
Affiliated to the Society of Radiopharmaceutical Sciences and to the International Research Group of Immunoscintigraphy
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The Quarterly Journal of Nuclear Medicine 1999 December;43(4):307-12

lingua: Inglese

Graves’ oph­thal­mop­athy and 131I ­therapy

Marcocci C., Bartalena L., Tanda M. L., Manetti L., Dell'Unto E., Mazzi B., Rocchi R., Barbesino G., Pinchera A.

From the Department of Endocrinology and Metabolism University ­of Pisa, ­Pisa, ­Italy


Graves’ oph­thal­mop­athy is an auto­im­mune pro­cess ­initiated and main­tained by ­antigen(s) ­shared by the thy­roid and the ­orbit. A ­matter of argu­ment con­cerns the ­choice of the ­method of treat­ment for ­Graves’ hyper­thyr­oi­dism ­when clin­i­cally evi­dent oph­thal­mop­athy is ­present. Res­to­ra­tion of euthyr­oi­dism ­appears to be ben­e­fi­cial for oph­thal­mop­athy. On the ­other ­hand the con­tin­uing dis­ease ­activity asso­ciated ­with the recur­rence of hyper­thyr­oi­dism ­appears to ­adversely ­affect the ­course of oph­thal­mop­athy. For ­these rea­sons it is our ­opinion ­that in ­patients ­with ­Graves’ hyper­thyr­oi­dism and oph­thal­mop­athy the per­ma­nent con­trol of thy­roid hyper­func­tion by abla­tion of thy­roid ­tissue ­should be ­obtained by radio­io­dine ­therapy or thy­roi­dec­tomy. The ratio­nale for an abla­tive ­strategy is the fol­lowing: i) per­ma­nent con­trol of hyper­thyr­oi­dism ­avoids exac­er­ba­tions of eye dis­ease asso­ciated ­with recur­rence of hyper­thyr­oi­dism; ii) hypo­thy­roidism, ­which fol­lows thy­roid ­tissue abla­tion, ­should be ­regarded as a ther­a­peutic end ­point ­rather ­than as an unde­sir­able ­result; iii) abla­tion of thy­roid ­tissue may ­result in the ­removal of ­both the thy­roid-­orbit ­cross-­reacting ­antigen(s) and the ­major ­source of thy­roid-auto­reac­tive lym­pho­cytes. The rela­tion­ship ­between radio­io­dine ­therapy and the ­course of GO is a ­matter of con­tro­versy, and ­some ­authors ­have sug­gested ­that radio­io­dine admin­is­tra­tion may be asso­ciated ­with a wors­ening of pre­ex­isting oph­thal­mop­athy. ­This was not ­observed ­when radio­io­dine treat­ment was asso­ciated ­with a 3-­month ­oral ­course of prednisone. The devel­op­ment or pro­gres­sion of GO ­after radio­io­dine ­therapy ­might be due to the ­release of thy­roid anti­gens fol­lowing radi­a­tion ­injury and to sub­se­quent exac­er­ba­tions of auto­im­mune reac­tions ­directed ­towards anti­gens ­shared by the thy­roid and the ­orbit. The ­view ­that radio­io­dine ­therapy may be asso­ciated ­with a pro­gres­sion of oph­thal­mop­athy is not ­shared by ­some ­authors who ­claim ­that the ­apparent ­link ­between pro­gres­sion of oph­thal­mop­athy and radio­io­dine ­therapy ­might ­simply be coin­ci­dental, ­reflecting the nat­ural his­tory of the disease. The radio­io­dine-asso­ciated exac­er­ba­tion of eye dis­ease ­might be ­used as an argu­ment ­against the use of radio­io­dine ­therapy in ­patients ­with oph­thal­mop­athy. We do not ­share ­this ­view, ­since the out­word ­effects of radio­io­dine on eye dis­ease can ­easily be pre­vented by con­com­i­tant admin­is­tra­tion of glu­co­cor­ti­coids. Glu­co­cor­ti­coid treat­ment ­should be lim­ited, in our ­opinion, to ­patients ­with clin­i­cally evi­dent eye dis­ease and to ­those ­without oph­thal­mop­athy but ­with ­other ­known ­risk fac­tors, ­such as ­smoking.

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