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Show "j 1986 Raven Pre__, N~w York Exophthalmos Induced by Exogenous Steroids Barrett Katz, M.D., and Raymond Carmody, M.D. Two (as~'s of bilat~'ral exophthalmos se(ondarv to d'nmk steroid ther,'pv Me pr~·sented. Exophthalmos has been reported in Cushing's dise,ls~', in which endogenous st~'roid produ(tion is elevated. Exophthalmos asslKiated with (hronic exogenous steroid ,1dministratilm is an unusual although benign form of o(ular pro-ptosis. . Key Words: Cushing's disease-Exophthalmos-Orbit disease- Proptosis-Steroid therapy. From the D~'partm~'ntsof Ophlhalmologv ,md Nl'UWs(il'nn's (B.K.), Uniwrsily of C.llilornid, Sdn Dil'gO, LI jOll,l, C,lih'rni,l; and Dl'partment of Radiology (R. c.), Uni\'l'rsitv of Ariwna, Tucson, Arizona. Address (orrt'spondl'nn' dnd rtoprinl re'Jul'sts to Dr. B. Katz, UCSD EYl' Cenll'f, M-lIIX, UniVl'fSily of Californi,l, S,m Dil'gO, La Jolla, CA 'I2()YJ, USA 250 Exophthalmos induced by the endogenous overproduction of steroids has been recognized in patients with Cushing's syndrome (1). It is reported to occur in perhaps 6-89i: of such patients, and may even be the initial manifestation of Cushing's disease (2). Exophthalmos developing in patients receiving exogenous steroid therapy is a phenomenon rarely observed, given the many patients treated with chronic steroid therapy (3,4). It is the purpose of this report to present two such cases. CASE REPORTS Case 1 A 66-vear-old native-born man was followed in our out'patient clinic for chronic obstructive pulmonary disease (CaPO), hypertension, and atherosclerotic coronary vascular disease. His capo was steroid-dependent, and he had been on chronic prednisone therapy for almost a decade. He had been followed ophthalmologically for posterior subcapsular cataract, and was surgically aphakic on the right side. He was evaluated again for ocular prominence and foreign body sensation in each eve. On examination his vision was 20/25 in the right eye (0. D.), and counting fingers in the left eye (0.5.). Applanation tonometry was in the low teens both in primary positio~ and in upgaze. Color vision was intact in each eye, and pupillary responses were normal. Ocular motility was unremarkable without signs of restrictio~ or slowed saccades, There was bilateral orbital fullness, with increased resistance to retropulsion on each side. Exophthalmometry measured 22 mm 0.0. and 24 mm 0.5. There was scleral show inferiorly on each side, although no lid lag was present superiorly. The anterior segments showed mild bogginess and chemosis of both conjunctival surfaces. No injection of the conjunctival tissue was present over the insertion of the recti muscles. The left EXOPHTHALMOS [NOLleU) BY EXOGENOUS STEROIDS 251 lens showed dense central posh:'rior subcapsular change, and both posterior poles were normal. Formal visual field tt'sting was norm,ll from the right eye, with central scotonhl ,1I1d constridion to all isopters from the left l')'L'. There was no historv of thyroid disL'ase or symptomatolog)!, ,1I1d till' p,ltiL'nt W,lS euthyroid on testing to include T3 radioimmuno,lss,ly, frl'L' T·t free thyroxine index, T3 uptake, ,1I1d thvroidstimulating hormonl' (TSH) levels. Blood gases showed a pH of 7.52, pO~ of bb mm, pCO~ of 3-l mm, and HCO~ Llf 2~ mm. Cl)mputl'd tomography (CT) Llf the orbits revl'aled nwderate bilateral proptosis with nll evidence fllr enlargenll'nt of the muscle bellies. Tlll'rt' was increased prominence of the orbital fat lln t'ach side, withllut evidence for retrobulbar mass (Fig. 1). The patient remains well on his usual dosages of prednisllne without signs of increasing proptosis, anterior segment compromise, or optic nerve compression. Case 2 A 63-vear-old native-born man was followed in our outpatient clinic for COPO for 7 years. For the previous 5 years he had been steroid-dependent, and on changing doses of prednisone. For the previous year he had been noted to have bilateral proptosis, and was referred for evaluation. On examination his vision was 20/25 in each fiG. 1. Case 1. Enhanced CT scan of the orbits shows bilateral proptosis. worse on the left. The broken white line connecting the lateral walls of the orbits is used to determine the presence of proptosis. Normally the posterior one-third of the globe falls behind this line. l'ye. His color vision was intact bilaterally. Applanation tonometry revealed intraocular pressures in the mid-teens without change on upgaze. His pupillilrY responses were normal, and ocular motility l'xamination was unremarkable, without signs of restriction or slowed saccades. Both orbits showl'd fullness of soft tissue structures, and increased rt'sistance to retropulsion. There was scleral show inferiorly and superiorly on each side, with mild lid lag. Anterior segments revealed a bogginess to the conjunctival tissue, though without injection. Both lenses showed early posterior subcapsular changes. Examination of his posterior poles was normal. Exophthalmometry revealed 25 mm 0.0., and 28 mm 0.5. Formal visual field testing bilaterally revealed full and normal isopters both centrally and peripherally. There was no history of thyroid disease and the patient was chemically euthyroid, with normal T3 radioimmunoassay, T3 uptake, free T4, free thyroxine index, TSH levels, and thyrotropin-releasing hormone (TRH) stimulation testing. Blood gases revealed a pH of 7.53, pOz of 53 mm, pCOz of 32 mm, and HC03 of 26 mm. CT examination of the orbits revealed bilateral proptosis with increased retrobulbar fat. The muscle bellies themselves were not enlarged, and no masses were present (Fig. 2). The patient has been followed without reduction of his steroid dosage, yet without progression of his exophthalmos, comprise of his anterior segments, or compression of his optic nerves. DISCUSSION Both of these patients had evidence of orbital fiG. 2. Case 2. Enhanced CT scan shows bilateral proptosis due to increased orbital fat. 252 H. /\II"I"Z liND R. CARMODY pwptosis coincith'nt with long-Il'rlll chmnic L'XOgl'llllUS steroid tl1l'r,lpv. Tlll'v Wl'rl' l'uthymid, <lnd their CT findings indudl'd llnlv incrl',lSl'd orbitJI f<lt with norlll,ll f,11 ,1ltl'nU,1Iion v<llul'.s. Thl're W,lS 11ll incre,lse in ,1ttenu,ltion ,1fter contr,lst enh<lncenwnt. TI1l'ir l'xtr,lllcul,lr lllusciL's Wl'rL' norrn,ll, ,lS \\'l're their optic lll'rVl'S. Nothing 10 suggest inn, lllllll<ltlll'\', \',lscul,lr, or infillr,ltive disease of orbit, ll structures could be dl'lllonstr,llL'd on CT. We SUSpl't-t thl' l'tiologv of our p,ltil'nls' exophthalnllls W<lS L'xogenous stemid ther<lpy, The inCrt',lsed prolllinence of f,11 tissue in Cushing's dist'ase is well known clinically. Certainly the orbit wntains f<lt, and that fat Illight be expected to participate in changes fWIll chronic exogL'nous stemid therapy. Such changes would be mJnifest as pmptl'sis. Experimental work in rats, guinea pigs, and rabbits has shown that exogenously administered steroids can reproducibly induce exophthalmos (5-8). The pathophysiology of this experimental exophthalmos has not been elucidated. Both of our patients had underlying chronic obstructive pulmonary disease, with chronic hvpoxia. One might consider that it was chronic hypoxia which led to orbital congestion and exophthalmos. Perhaps the decreased p02 produced orbital vasodilation with increased blood tlmv and I Clill Nl'lIr(l'(ll'hlllllllll(lI, V(li. h, No. ~, 19Hh orbital edema. Yet experimental data seem to suggest a more verifiable link with exogenous steroid (5-1'). Neither of our patients had exophthalmos prior to the initiation of steroid therapy, though (;'Jch did have hypoxia. Why clinically apparent steroid-induced exophthalmos is not more commonly recognized is not clear. Regardless, it appears to be a benign exophthalmos whose diagnosis remains one of exclusion of the more common etiologies of orbital dist'ase. REFERENCES I. Pilltz C~, Knowlton A). Ragan C. Natural history of Cushing', wndrome. Alii I ;'vled 1952;13:597-614. 2. Morg~n DC', M~'on AS. Exophthalmos in Cushing's syndrllme {ir I'ded I 1958;2:-+81--+. 3. Slan,kv HH, Kolberl G. Garlner S bophthalmos induced by steroid,. Arcl1 01'11/1It1111/<l1 1967;77:579-81. -+ Cllhen BA, Som PM, HaHner PH, Friedman AH. Steroid e,ophlh~lmll'. I C.'I11I'"1 :1:<:'/:'1 T'l/lIo..:r 1981;5:907-8. 5. Aterman K, Greenberg S7\1. Experimental exophthalmos in r,lls produced bl' ,'urti"'ne. [lId"CYlII"!.'XII 1953;52:510-7. h. Aterman K, Greenbl'rg S~1. E'perimental exophthalmos prc>duc'L'd bl' cllrtisllne in rab. Ar<'!, 01'htllall1lol 195-+; 51:822-31. 7. Williams AW. bophthalmos in cortisone treated experimental animab Br I Exl' Patlh'/ 1953;3-1:621--1. 8. Williams A\\' Patho!'enesis L,i wrtis'1De induced exophthalmos in guinea pi!,s. Br I Ex!, Path,'1 1955;36:2-+5-7. |
