Author/Editor		Henč-Petrinović, Ljerka; Kuzmanović, Biljana; Dominis, Mara; Petrinović-Dorešić, Jelena
Title		Orbital amyloidosis
Translated title		Amiloidoza orbite
Type		članek
Source		Zdrav Vestn
Vol. and No.		Letnik 71, št. Suppl 2
Publication year		2002
Volume		str. II-75-8
Language		eng
Abstract		Background. Authors want to present echographic characteristics of two stages of development of bilateral orbital involvement in primary systemic amyloidosis in 10-year follow-up of a case. Methods. A 65 year old white female with 10-year-long history of orbital involvement in primary systemic amyloidosis presented to us with large nasal left upper palpebro-bulbar mass that produced lateral displacement of the globe, marked reduction of ocular motility in all directions and ptosis covering the pupil. Direct and transbulbar echography, pathohistological analysis, and immunohistochemistry were used to confirm the diagnosis of amyloid. The mass was partially removed and the lid reconstructed. Results. The echographic examination of the orbits performed in 1990 showed an epibulbar and parabulbar low-reflectivity orbital mass in the upper temporal part of the right orbit. A widened right lateral rectus muscle of low reflectivity was also documented. Ten years later direct echography of the medial part of the left upper lid discloses palpebral extension of the orbital mass. It has irregular, inhomogeneous, medium to high reflectivity with rough granular structure and calcifications. Transbulbar echography revealed changes in both orbits. There is widening of the orbital fat echo with the higher reflectivity. All extraocular muscles are enlarged, including insertions. The widest is the right lateral rectus muscle. The muscle sheaths are thickened, widened with easily detected higher inner reftectivity than in the muscle itself. There is irregular, inhomogeneous, medium to high reflectivity of the muscles with scarce calcification. Conclusions. The initial stage of orbital amyloidosis is characterized with low reflectivity. Ten years later, the mass reflectivity inhomogeneously increased and calcifications developed.
Summary		Izhodišča. Avtorji predstavljajo ehografske značilnosti dveh faz razvoja obojestranske prizadetosti očesne votline pri primarni sistemski amiloidozi po 10-letnem spremljanju bolnice. Metode. Prikazan je primer 65-letne bolnice z 10-letno anamnezo prizadetosti očesne votline zaradi primarne sistemske amiloidoze z velikim nabreklim tvorom pri nosu na levi strani zgornje očesne veke, ki je povzročil stranski zamik zrkla, opazno zmanjšanje očesne gibljivosti v vseh smereh s povešenjem očesne veke, ki je zakrivala zenico. Za potrditev diagnoze amiloida smo uporabili neposredno ehografijo in ehografijo skozi nabreklino, patohistološko analizo in imunohistokemijo. Tvor je bil delno odstranjen in veka je bila rekonstruirana. Rezultati. Ehografski pregled očesnih votlin, narejen leta1990, je kazal na epibulbaren in parabulbaren tvor očesne votline z nizko reflektivnostjo v zgornjem senčnem delu desne očesne votline. Ugotovljena je bila tudi razširjena desna stranska mišica rectus z nizko reflektivnostjo. Deset let pozneje je ehografija medialnega dela leve zgornje veke pokazala palpebralno ekstenzijo tvora očesne votline. Vidno je bilo nepravilno, nehomogeno tkivo s srednje do visoko reflektivnostjo z grobo zrnato strukturo in kalcifikacijami. Ehografija skozi nabreklino je odkrila spremembe v obeh očesnih votlinah. Šlo je za širjenje maščobe v očesni votlini, ki je imela višjo odbojnost. Vse zunajočesne mišice vključno z vezmi so bile povečane. Najširša je bila desna stranska mišica rectus. Mišične ovojnice so bile zadebeljene, razširjene s preprosto zaznavno notranjo odbojnostjo, ki je bila višja kot v sami mišici. Šlo je za nepravilno, nehomogeno, srednjo do visoko odbojnost mišic s posamičnimi kalcifikacijami. Zaključki. Značilnost začetne faze amiloidoze očesne votline je v nizki odbojnosti. Deset let kasneje je odbojnost tvora nehomogeno narasla in razvila se je kalcifikacija.
Descriptors		ORBITAL DISEASES AMYLOIDOSIS AGED