0
We're unable to sign you in at this time. Please try again in a few minutes.
Retry
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
Retry
There may be a problem with your account. Please contact the AMA Service Center to resolve this issue.
Contact the AMA Service Center:
Telephone: 1 (800) 262-2350 or 1 (312) 670-7827  *   Email: subscriptions@jamanetwork.com
Error Message ......
Clinical Sciences |

Treatment of Cystoid Macular Edema in Retinitis Pigmentosa With Intravitreal Triamcinolone FREE

Lucia Scorolli, MD; Mariachiara Morara, MD; Alessandro Meduri, MD; Letizia Bacchi Reggiani, MD; Giuseppe Ferreri, MD; Sergio Z. Scalinci, MD; Renato A. Meduri, MD
[+] Author Affiliations

Author Affiliations: Departments of Pathophysiological Optics (Drs Scorolli, Morara, A. Meduri, Scalinci, and R. A. Meduri) and Cardiology (Dr Reggiani), University of Bologna, Bologna, and Department of Ophthalmology, University of Messina, Messina (Dr Ferreri), Italy.


Arch Ophthalmol. 2007;125(6):759-764. doi:10.1001/archopht.125.6.759.
Text Size: A A A
Published online

Objective  To evaluate the results of treatment with intravitreal triamcinolone acetonide injection in patients with cystoid macular edema secondary to retinitis pigmentosa.

Methods  This prospective, nonrandomized comparative trial included 20 eyes of 20 patients with cystoid macular edema secondary to retinitis pigmentosa (group A) and 20 eyes of 20 control individuals (group B) with the same characteristics who declined treatment. All treated eyes received an intravitreal injection of 0.1 mL of triamcinolone acetonide (4 mg). The total follow-up was 12 months. The main outcome measures were best-corrected visual acuity, central macular thickness measured by optical coherence tomography, and intraocular pressure.

Results  No statistically significant changes were observed in best-corrected visual acuity. Central macular thickness showed statistical differences between the 2 groups. Intraocular pressure showed a statistically significant increase after the first day, at 1 month, and at 3 months in both groups but no significant increase afterward.

Conclusions  Intravitreal triamcinolone administration may be useful for select cases of cystoid macular edema in patients with retinitis pigmentosa but its efficacy seems to be limited over time. Therefore, to obtain a good anatomical result and an improvement of best-corrected visual acuity, further treatment would be necessary after 6 months.

Figures in this Article

Retinitis pigmentosa (RP) is a hereditary condition with an incidence in Italy of 1 in 4000. It is very heterogeneous, both phenotypically and genetically. No effective approach for prevention, stabilization, or reversal exists for the majority of RP cases. More than 70 different genetic defects (27 identified genes1) have been identified including autosomal recessive (16%), autosomal dominant (22%), and X-linked (9%), with the remaining cases being simplex (with no known inheritance pattern). Actually, many in the simplex RP group are likely to have hereditary causes as has been shown in a number of genetic studies (fully 20% of simplex males have X-linked RP, according to several studies).24

Retinitis pigmentosa is a degenerative process of the retina primarily affecting the rod photoreceptors and retinal pigment epithelium (RPE). Although the rod photoreceptors appear to be the primary target of the disease, there is histological and functional evidence for cone photoreceptor damage that is likely secondary to the rod degeneration.5,6 In most cases, patients show an early night blindness and loss of peripheral field of vision but central vision is generally preserved until the late stages of the disease.

In spite of this, in RP, different studies have shown a prevalence of cystoid macular edema (CME) of about 10% to 15%, most of these in cases without an inheritance pattern.7 This complication leads to a reduced visual acuity in such patients. Different therapies have been proposed to resolve CME, such as laser photocoagulation; vitreoretinal surgery, including pars plana vitrectomy associated with posterior hyaloid dissection; removal of the posterior inner limiting membrane and gas tamponade; carbonic anhydrase inhibitors; and systemic corticosteroids. According to previous studies, the most effective therapies seem to be acetazolamide and corticosteroids.812

Intravitreal triamcinolone acetonide has already been used in different retinal pathological conditions complicated by CME in their clinical development.13 The purpose of our study was to evaluate the anatomical and visual results of treatment with intravitreal triamcinolone injections in patients with CME secondary to RP.

Our prospective study included 20 eyes of 20 patients with CME secondary to RP (12 men, 8 women) ranging in age from 28 to 54 years (mean ± SD age, 40.2 ± 13 years) (group A). Patients were randomly selected from the Retinitis Pigmentosa Association, which is related to the Low Vision Centre, Department of Pathophysiological Optics, University of Bologna. Institutional review board approval was obtained for the study.

Inclusion criteria, present in all 20 eyes, were presence of ocular findings of RP (perivascular bone spiculelike pigmentation, attenuated retinal arterioles); contracted visual field; nonrecordable or markedly reduced a-wave and b-wave amplitudes in the rod and mixed responses on electroretinography; CME documented by contact lens ophthalmoscopy, fluorescein angiography (FA) (all patients had CME with leakage at FA), and optical coherence tomography (OCT), present for 6 months or more (until 18 months); best-corrected visual acuity (BCVA) of 20/200 or better; and ineffective treatment with 250 mg of oral acetazolamide twice daily for 1 month. All patients showed no CME resolution at OCT evaluation and persistent leakage at FA after 1 month. Exclusion criteria were having systemic syndromes associated with RP-like fundus appearance, diabetes mellitus, ocular inflammatory diseases, primary vascular diseases, glaucoma, or ocular hypertension.

All patients agreed to this procedure and signed an informed consent form obtained by the ethical committee of the hospital. All treated eyes received an intravitreal injection of 0.1 mL of triamcinolone acetonide (Kenacort-A [40 mg/mL]; Bristol-Myers Squibb, New York, NY). The injections were performed by the same surgeon (L.S.) at the Department of Pathophysiological Optics, S. Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy. Surgery was performed with topical anesthesia using 4% oxybuprocaine hydrochloride and lidocaine hydrochloride eyedrops. The injection site was 4 mm posterior to the limbus (all eyes were phakic) in the inferotemporal quadrant. The injection of 0.1 mL of purified triamcinolone acetonide (4 mg) was performed using a 30-gauge needle on a 1-mL syringe, with a contemporary paracentesis performed to decrease the intraocular pressure (IOP). Indirect ophthalmoscopy was chosen to confirm the intravitreal localization of the corticosteroid. After surgery, topical ciprofloxacin eyedrops were used 3 times a day for 1.5 weeks and timolol maleate eyedrops, twice a day for a 3-week period.

A control group (group B) was also selected consisting of 20 eyes of a further 20 patients with CME secondary to RP and a mean ± SD age of 39.5 ± 11.3 years (9 men, 11 women). Group B included patients who had refused surgical treatment (intravitreal injection of triamcinolone).

Evaluation parameters were BCVA of the 2 groups measured using Early Treatment of Diabetic Retinopathy Study and logarithm of the minimum angle of resolution (logMAR) visual acuity charts, central macular thickness measured by Stratus OCT 3 using Retinal Thickness Map Analysis software (Carl Zeiss Meditec, Dublin, Calif) to consider the thickness of the foveal zone, and IOP measured by Goldmann applanation tonometry at slitlamp. Complications related to intravitreal injection of corticosteroids were recorded. Patients were examined on day 1, after 1 month, and then after 3, 6, and 12 months.

Statistical analysis was performed using SPSS 13.0 for Windows (SPSS Inc, Chicago, Ill). Continuous variables are expressed as mean ± SD; categorical variables are expressed as numbers and percentages. Separate repeated-measures analysis of variance models were used to assess differences between group A and group B patients for the within-subjects effect of modifying BCVA, central macular thickness, and IOP. The Mauchly sphericity test was used to examine the form of covariance matrix; in case of violation of assumption, the Huynh-Feldt correction factor was considered to obtain the adjusted P values for each univariate F test involving the interval effect. Bonferroni correction was used for multiple post hoc comparisons. P values <.05 were considered significant.

The BCVA results during follow-up are shown in the Table and Figure 1. There was no difference between mean BCVA values for group A and group B patients over time (P = .78), while in general, the mean BCVA values changed significantly from baseline to 12 months (P<.001).

Place holder to copy figure label and caption
Figure 1.

Mean best-corrected visual acuity (BCVA) values. Bonferroni post hoc test results: 12 months vs baseline, P<.05; 12 months vs 1 month, P<.05; 12 months vs 3 months, P<.05; and 12 months vs 6 months, P<.05. logMAR indicates logarithm of the minimum angle of resolution.

Graphic Jump Location

Group A and group B had statistically significant mean central macular thickness values as measured by OCT (P<.001), as shown in the Table and Figure 2. Mean central macular thickness values changed significantly from baseline to 12 months (P < .001). Figure 3 shows the OCT results of a case from before treatment until 18 months after treatment.

Place holder to copy figure label and caption
Figure 2.

Mean central macular thickness (CMT) values as measured by optical coherence tomography. Bonferroni post hoc test results: baseline vs 1 month, P<.05; baseline vs 3 months, P<.05; baseline vs 6 months, P<.05; 3 months vs 12 months, P<.05; 6 months vs 12 months, P<.05; and 3 months vs 6 months, P<.05.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 3.

Optical coherence tomography results of a case before treatment (A), 6 months after treatment (B), 12 months after treatment (C), and 18 months after treatment (D).

Graphic Jump Location

Ten eyes (50%) developed IOP values of 21 mm Hg or more; of those, 2 eyes (10%) showed an IOP of between 30 and 35 mm Hg. These values were recorded on the first day after treatment with the injection and returned to baseline values 6 months after treatment. The mean IOP values during follow-up are shown in the Table and Figure 4; the 2 groups had statistically different mean values. The pattern of difference between mean IOP values for group A and group B patients changed across intervals. All eyes that showed ocular hypertension (IOP>21 mm Hg) were treated with a topical IOP-lowering medication (0.5% timolol maleate eyedrops twice daily for 1 month) until the IOP returned to its original value.

Place holder to copy figure label and caption
Figure 4.

Mean intraocular pressure (IOP) values. Bonferroni post hoc test results: 1 day vs baseline, P<.05; 1 day vs 1 month, P<.05; 1 day vs 3 months, P<.05; 1 day vs 3 months, P<.05; 1 day vs 6 months, P<.05; and 1 day vs 12 months, P<.05.

Graphic Jump Location

No injection-related complications were encountered, and no cases of endophthalmitis, postoperative cataract, or acute ocular hypertension were recorded.

The mechanism of CME in patients with RP is not clear. The pathogenesis of CME is probably due to an RPE pumping mechanism reduction, which occurs in cases characterized by later spreading of the FA staining at the level of the RPE in the late transit phases of FA.14 A dysfunction of anticarbonic anhydrase and enolase activity by autoantibodies in the RPE may lie at the root of edema formation.

Autoantibodies to enzymes and other important cytoplasmatic and membrane proteins have been found frequently in association with other autoimmune disease, even in first-degree relatives.15,16 For example, antipyruvate dehydrogenase antibodies have been detected in insulin-dependent diabetes mellitus and stiff-man syndrome.17 Another disorder, autoimmune angioedema, is characterized by recurrent episodes of edema and by the presence of autoantibodies that react with C1 inhibitor. It has been shown that the autoantibody binds to C1 inhibitor and facilitates its proteolytic cleavage by specific enzymes.18,19

Autoantibodies to carbonic anhydrase 1 and 2 have been detected in sera of patients with a variety of autoimmune diseases: 30% of patients with systemic lupus erythematosus, polymyositis, and systemic sclerosis; 21% of patients with Sjögren syndrome; and 69% of patients with endometriosis. Only 11.8% of control individuals had antibodies to carbonic anhydrase 2.2022

Some authors have observed an important relationship between CME in RP and the presence of circulating antiretinal antibodies.23 According to these authors,2224 CME in RP is a negative prognostic factor and is associated with an increase of circulating antiretinal antibodies and with anatomical features that could aggravate visual recovery. These authors suggest an autoimmune process. Heckenlively et al23 think that a breakdown of the blood-retinal barrier during the retinal degenerative process could release retinal proteins into the circulation that could be antigenic. This can explain how retinal antigens sensitize the immune system and how antiretinal antibodies can reach the retina when normally the blood-retinal barrier would prevent this option. The presence of antiretinal antibodies is quite common, with 37% of patients showing indirect immunofluorescent activity.22,25 However, it is not known whether antiretinal antibodies in general or specific ones are harmful and if there are cofactors that may contribute to pathogenicity.

The steroids could exert the effect by several mechanisms, which include reducing levels of proinflammatory cytokines, reducing levels of vascular endothelial growth factor, and increasing blood-retinal barrier function with edema resolution. Intravitreal steroids have an effect on diseases with marked inflammatory composite in their immunopathogenesis. For this reason, we feel they are useful for patients with RP.

Corticosteroids reduce inflammation by suppressing inflammatory cell proliferation and migration and decreasing the synthesis and release of other proinflammatory molecules (prostaglandins and leukotrienes, vascular endothelial growth factor, and intercellular adhesion molecule 1).2629 By intravitreal injection, a large dose of medication is delivered directly to its site of action; this does not occur using alternative ways of administration.3035

Soluble cortisone is eliminated from the eye within 24 hours after a single intravitreal injection.31 Machemer suggested using a crystalline form of corticosteroid that provides intraocularly available cortisone for a considerably longer period.26,36 Triamcinolone is a crystalline form of steroid that has been reported to be present intraocularly in measurable concentrations up to 1.5 years after intravitreal injection.37

A recent study by Yeung et al38 reported on a possible cytotoxic effect of triamcinolone. They cultured an RPE cell line (ARPE-19) and added corticosteroids (0.01-1 mg/mL) or vehicle (0.025% benzyl alcohol) diluted in culture medium. Subsequently, the culture medium containing corticosteroid or vehicle was refreshed daily. After 1, 3, and 5 days, the proliferated amount of cells with and without corticosteroid treatment was determined. They found that triamcinolone caused a significant reduction in cell numbers throughout the whole range of concentrations when cells were exposed to it for more than 1 day. Compared with dexamethasone sodium phosphate and hydrocortisone, triamcinolone showed the higher relative toxicity.

Another study from Yeung et al39 compared in vitro the cytotoxic effect of triamcinolone on human glial cells (cell line SVG). The study concluded that triamcinolone had cytotoxic effects on both SVG and the RPE, with higher efficacy on SVG. The results suggest that triamcinolone toxic effects on 1 cell type may not reliably indicate its toxic effects on other cells.

Narayanan at al40 performed experiments on R28 (retinal neurosensory cells) and ARPE-19 cells with 1 mg/mL of triamcinolone acetonide and concluded that triamcinolone has toxic effects on proliferating cells of retinal origin in vitro at doses normally used in clinical practice. In in vivo experiments, Bakri and Beer41 showed that preservative-free triamcinolone had no toxic effects on the retina. They used a formulation that did not contain benzyl alcohol as a preservative. In conclusion, benzyl alcohol at concentrations modestly higher than that present in the commercial drug has toxic effects on the eye. It is suggested that if commercial-preserved triamcinolone is to be used clinically, decanting or another means of removing the benzyl alcohol should be considered.

We selected OCT to study macular edema because previous studies showed a similar capacity between OCT and FA in monitoring CME and all the included eyes had CME with leakage at FA at the beginning of the study.42,43 Optical coherence tomography could detect cystoid macular lesions in patients with RP even in eyes with either little or no dye accumulation on FA or cystic macular lesions visible by ophthalmoscopy.42 Stanga et al43 presented preliminary findings showing that OCT imaging is at least as sensitive as FA for identifying CME and is a useful procedure for evaluating a response to therapy.44 Moreover, we preferred OCT because of the psychological condition of patients with RP: they refused to undergo FA several times.

In our study, all patients showed an anatomical improvement at 3 months after intravitreal injection of triamcinolone; in terms of visual acuity, 12 of 20 eyes showed an improvement, 4 of 20 remained stable, and 4 of 20 showed worsening. Our results show that the median ± SD central macular thickness decreased from 459.89 ± 96.4 μm (range, 310-625 μm) to 306.75 ± 81.8 μm (range, 214-485 μm) at 1 month; 272.78 ± 64.6 μm at 3 months; 302.89 ± 75.7μm at 6 months; and 442 ± 95.5 μm (range, 325-607 μm) at 12 months, which is similar to the baseline thickness. Our BCVA results, as shown in the Table, were not statistically significant, but some eyes experienced a line gain across time. These results were unexpected based on previous reports of CME in RP that showed an improvement of anatomical resolution and BCVA only at the 1-month follow-up.13

Finally, intravitreal triamcinolone administration may be useful for select cases of CME in patients with RP, but its efficacy seems to be limited over time and it is necessary to repeat the treatment after 6 months to maintain good anatomical results and improved BCVA.

From previous studies4244 and our surgical experience in the treatment of CME associated with diabetic retinopathy, retinal vein occlusion, uveitis, and pseudophakic CME, we know that repeat intravitreal triamcinolone injections can lead to several complications such as glaucoma, postinjection infectious endophthalmitis, cataract, rhegmatogenous retinal detachment, and internal limiting membrane thickening.

A new possibility for treating macular edema with corticosteroids has been proposed (phase 3 clinical trials). It consists of a steroid, microsized, biodegradable ocular implant that provides sustained delivery of dexamethasone directly to the target disease site. Ninety days following implantation, patients showed a statistically significant improvement in visual acuity.45

A longer follow-up period with repeated injection treatments would be useful to determine if the related benefits of the treatment are sufficient to overcome the risks from the disease. Moreover, when a decrease in CME and central macular thickness occurs, a subthreshold laser macular grid could be useful because anatomical structures are more preserved by a negative laser effect.4548 It also would be useful to repeat the intravitreal injection after 6 months because the visual acuity improvement permits better psychological and functional behavior in patients with this type of disease.

Correspondence: Lucia Scorolli, MD, Department of Pathophysiological Optics, University of Bologna, Via Zuccardi Merli 1, 40141 Bologna, Italy (luciascorolli@yahoo.it).

Submitted for Publication: February 27, 2006; final revision received September 28, 2006; accepted October 4, 2006.

Financial Disclosure: None reported.

 RetNet Retinal Information Network Web site. www.sph.uth.tmc.edu/retnet. Accessed June 2006 
Wang  DYChan  WMTam  PO  et al.  Gene mutations in retinitis pigmentosa and their clinical implications. Clin Chim Acta 2005;3515- 16
PubMed Link to Article
Wang  DYChan  WMTam  PO  et al.  Genetic markers for retinitis pigmentosa. Hong Kong Med J 2005;11281- 288
PubMed
Kalloniatis  MFletcher  EL Retinitis pigmentosa: understanding the clinical presentation, mechanisms and treatment options. Clin Exp Optom 2004;8765- 80
PubMed Link to Article
John  SKSmith  JEAguirre  GDMilam  AH Loss of cone molecular markers in rhodopsin-mutant human retinas with retinitis pigmentosa. Mol Vis 2000;6204- 215
PubMed
Alexander  KRRajagopalan  ASRaghuram  AFishman  GA Activation phase of cone phototransduction and the flicker electroretinogram in retinitis pigmentosa. Vision Res 2006;462773- 2785
PubMed Link to Article
Fishman  GAMaggiano  JMFishman  M Foveal lesion seen in RP. Arch Ophthalmol 1977;951993- 1996
PubMed Link to Article
Moldow  BSander  BLarsen  M  et al.  The effect of acetazolamide on passive and active transport of fluorescein across the blood-retina barrier in retinitis pigmentosa complicated by macular oedema. Graefes Arch Clin Exp Ophthalmol 1998;236881- 889
PubMed Link to Article
Giusti  CForte  RVingolo  EM Deflazacort treatment of cystoid macular edema in patients affected by retinitis pigmentosa: a pilot study. Eur Rev Med Pharmacol Sci 2002;61- 8
PubMed
García-Arumí  JMartinez  VSararols  LCorcostegui  B Vitreoretinal surgery for cystoid macular edema associated with retinitis pigmentosa. Ophthalmology 2003;1101164- 1169
PubMed Link to Article
Fishman  GAGilbert  LDFiscella  GKimura  AEJampol  LM Acetazolamide for treatment of chronic macular edema in retinitis pigmentosa. Arch Ophthalmol 1989;1071445- 1452
PubMed Link to Article
Newsome  DABlacharski  PA Grid photocoagulation for macular edema in patients with retinitis pigmentosa. Am J Ophthalmol 1987;103161- 166
PubMed
Ozdemir  HKaracorlu  MKaracorlu  S Intravitreal triamcinolone acetonide for treatment of cystoid macular oedema in patients with retinitis pigmentosa. Acta Ophthalmol Scand 2005;83248- 251
PubMed Link to Article
Heckenlively  JRSolish  AMChant  SMMeyers-Elliott  RH Autoimmunity in hereditary retinal degenerations, II: clinical studies: antiretinal antibodies and fluorescein angiogram findings. Br J Ophthalmol 1985;69758- 764
PubMed Link to Article
Rogers  SWAndrews  PIGahring  LC  et al.  Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis. Science 1994;265648- 651
PubMed Link to Article
el Far  OMarqueze  BLeveque  C  et al.  Antigens associated with N- and L-type calcium channels in Lambert-Eaton myasthenic syndrome. J Neurochem 1995;641696- 1702
PubMed Link to Article
Moodie  FDLeaker  BCambridge  GTotty  NFSegal  AW Alpha enolase: a novel cytosolic autoantigen in ANCA positive vasculitis. Kidney Int 1993;43675- 681
PubMed Link to Article
Jackson  JFeighery  C Autoimmune angioedema: a new role for autoantibody in disease pathogenesis. Autoimmunity 1990;7181- 187
PubMed Link to Article
Mandle  RBaron  CRoux  E  et al.  Acquired C1 inhibitor deficiency as a result of an autoantibody to the reactive center region of C1 inhibitor. J Immunol 1994;1524680- 4685
PubMed
Inagaki  YJinno-Yoshida  YHamasaki  YUeki  H A novel autoantibody reactive with carbonic anhydrase in sera from patients with systemic lupus erythematosus and Sjogren syndrome. J Dermatol Sci 1991;2147- 154
PubMed Link to Article
Itoh  YReichlin  M Antibodies to carbonic anhydrase in systemic lupus erythematosus and other rheumatic diseases. Arthritis Rheum 1992;3573- 82
PubMed Link to Article
Kiechle  FLQuattrociocchi-Longe  TMBrinton  DA Carbonic anhydrase antibody in sera from patients with endometriosis. Am J Clin Pathol 1994;101611- 615
PubMed
Heckenlively  JRJordan  BLAptsiauri  N Association of antiretinal antibodies and cystoid macular edema in patients with retinitis pigmentosa. Am J Ophthalmol 1999;127565- 573
PubMed Link to Article
Wolfensberger  TJAptsiauri  NGodley  BDownes  SBird  AC Antiretinal antibodies associated with cystoid macular edema [in German]. Klin Monatsbl Augenheilkd 2000;216283- 285
PubMed Link to Article
Chant  SMHeckenlively  JRMeyers-Elliott  RH Autoimmunity in hereditary retinal degeneration, I: basic studies. Br J Ophthalmol 1985;6919- 24
PubMed Link to Article
Jonas  JBHayler  ASofker  JKPanda-Jonas  S Intravitreal injection of crystalline cortisone as adjunctive treatment of proliferative diabetic retinopathy. Am J Ophthalmol 2001;131468- 471
PubMed Link to Article
Moshfeghi  DMKaiser  PKScott  IU  et al.  Acute endophthalmitis following intravitreal triamcinolone acetonide injection. Am J Ophthalmol 2003;136791- 796
PubMed Link to Article
Roth  DBChieh  JSpirn  MJGreen  SNYarian  DLChaudhry  NA Noninfectious endophthalmitis associated with intravitreal triamcinolone injection. Arch Ophthalmol 2003;1211279- 1282
PubMed Link to Article
Penfold  PLWen  LMadigan  MCGillies  MCKing  NJProvis  JM Triamcinolone acetonide modulates permeability and intercellular adhesion molecule-1 (ICAM-1) expression of the ECV304 cell line implications for macular degeneration. Clin Exp Immunol 2000;121458- 465
PubMed Link to Article
Jonas  JBKreissig  IHugger  PSauder  GPanda-Jonas  SDegenring  R Intravitreal triamcinolone acetonide for age related macular degeneration. Br J Ophthalmol 2003;87462- 468
PubMed Link to Article
Karacorlu  MOzdemir  HKaracorlu  S Intravitreal triamcinolone acetonide for the treatment of chronic pseudophakic macular oedema. Acta Ophthalmol Scand 2003;81648- 652
PubMed Link to Article
McCartney  HJDrysdale  IOGornall  AGBasu  PK An autoradiographic study of the penetration of subconjunctivally injected hydrocortisone into the normal and inflamed rabbit eye. Invest Ophthalmol 1965;4297- 302
PubMed
Tessler  HLam  S Cystoid macular edema. Pepose  JSHolland  GNWilhelmus  KRedsOcular Infection and Immunity. St Louis, Mo CV Mosby1996;553- 589
Wakefield  DMcCluskey  PPenny  R Intravenous pulse methylprednisolone therapy in severe inflammatory eye disease. Arch Ophthalmol 1986;104847- 851
PubMed Link to Article
Tehrani  NNSaeed  TMurray  PI Deep intramuscular methylprednisolone for the treatment of cystoid macular oedema in uveitis. Eye 2000;14 ((pt 5)) 691- 694
PubMed Link to Article
Jonas  JBHayler  JKPanda-Jonas  S Intravitreal injection of crystalline cortisone as adjunctive treatment of proliferative vitreoretinopathy. Br J Ophthalmol 2000;841064- 1067
PubMed Link to Article
Jonas  JB Intraocular availability of triamcinolone acetonide after intravitreal injection. Am J Ophthalmol 2004;137560- 562
PubMed Link to Article
Yeung  CKChan  KPChan  CKPang  CPLam  DS Cytotoxicity of triamcinolone on cultured human retinal pigment epithelial cells: comparison with dexamethasone and hydrocortisone. Jpn J Ophthalmol 2004;48236- 242
PubMed Link to Article
Yeung  CKChan  KPChiang  SWPang  CPLam  DS The toxic and stress responses of cultured human retinal pigment epithelium (ARPE19) and human glial cells (SVG) in the presence of triamcinolone. Invest Ophthalmol Vis Sci 2003;445293- 5300
PubMed Link to Article
Narayanan  RMungcal  JKKenney  MCSeigel  GMKuppermann  BD Toxicity of triamcinolone acetonide on retinal neurosensory and pigment epithelial cells. Invest Ophthalmol Vis Sci 2006;47722- 728
PubMed Link to Article
Bakri  SJBeer  PM Choroidal neovascularization after radial optic neurotomy for central retinal vein occlusion. Retina 2004;24610- 611
PubMed Link to Article
Hirakawa  HIijima  HGohdo  TTsukahara  S Optical coherence tomography of cystoid macular edema associated with retinitis pigmentosa. Am J Ophthalmol 1999;128185- 191
PubMed Link to Article
Stanga  PEDownes  SMAhuja  RM  et al.  Comparison of optical coherence tomography and fluorescein angiography in assessing macular edema in retinal dystrophies: preliminary results. Int Ophthalmol 2001;23321- 325
PubMed Link to Article
Apushkin  MAFishman  GAJanowicz  MJ Monitoring cystoid macular edema by optical coherence tomography in patients with retinitis pigmentosa. Ophthalmology 2004;1111899- 1904
PubMed Link to Article
Tranos  PGWickremasinghe  SSStangos  NTTopouzis  FTsinopoulos  IPavesio  CE Macular edema. Surv Ophthalmol 2004;49470- 490
PubMed Link to Article
Kylstra  JAWierzbicki  TWolbarsht  MLLanders  MB  IIIStefansson  E The relationship between retinal vessel tortuosity, diameter, and transmural pressure. Graefes Arch Clin Exp Ophthalmol 1986;224477- 480
PubMed Link to Article
Molnar  IPoitry  STsacopoulos  MGilodi  NLeuenberger  PM Effect of laser photocoagulation on oxygenation of the retina in miniature pigs. Invest Ophthalmol Vis Sci 1985;261410- 1414
PubMed
Moorman  CMHamilton  AM Clinical applications of the MicroPulse diode laser. Eye 1999;13 ((pt 2)) 145- 150
PubMed Link to Article

Figures

Place holder to copy figure label and caption
Figure 1.

Mean best-corrected visual acuity (BCVA) values. Bonferroni post hoc test results: 12 months vs baseline, P<.05; 12 months vs 1 month, P<.05; 12 months vs 3 months, P<.05; and 12 months vs 6 months, P<.05. logMAR indicates logarithm of the minimum angle of resolution.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

Mean central macular thickness (CMT) values as measured by optical coherence tomography. Bonferroni post hoc test results: baseline vs 1 month, P<.05; baseline vs 3 months, P<.05; baseline vs 6 months, P<.05; 3 months vs 12 months, P<.05; 6 months vs 12 months, P<.05; and 3 months vs 6 months, P<.05.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 3.

Optical coherence tomography results of a case before treatment (A), 6 months after treatment (B), 12 months after treatment (C), and 18 months after treatment (D).

Graphic Jump Location
Place holder to copy figure label and caption
Figure 4.

Mean intraocular pressure (IOP) values. Bonferroni post hoc test results: 1 day vs baseline, P<.05; 1 day vs 1 month, P<.05; 1 day vs 3 months, P<.05; 1 day vs 3 months, P<.05; 1 day vs 6 months, P<.05; and 1 day vs 12 months, P<.05.

Graphic Jump Location

Tables

References

 RetNet Retinal Information Network Web site. www.sph.uth.tmc.edu/retnet. Accessed June 2006 
Wang  DYChan  WMTam  PO  et al.  Gene mutations in retinitis pigmentosa and their clinical implications. Clin Chim Acta 2005;3515- 16
PubMed Link to Article
Wang  DYChan  WMTam  PO  et al.  Genetic markers for retinitis pigmentosa. Hong Kong Med J 2005;11281- 288
PubMed
Kalloniatis  MFletcher  EL Retinitis pigmentosa: understanding the clinical presentation, mechanisms and treatment options. Clin Exp Optom 2004;8765- 80
PubMed Link to Article
John  SKSmith  JEAguirre  GDMilam  AH Loss of cone molecular markers in rhodopsin-mutant human retinas with retinitis pigmentosa. Mol Vis 2000;6204- 215
PubMed
Alexander  KRRajagopalan  ASRaghuram  AFishman  GA Activation phase of cone phototransduction and the flicker electroretinogram in retinitis pigmentosa. Vision Res 2006;462773- 2785
PubMed Link to Article
Fishman  GAMaggiano  JMFishman  M Foveal lesion seen in RP. Arch Ophthalmol 1977;951993- 1996
PubMed Link to Article
Moldow  BSander  BLarsen  M  et al.  The effect of acetazolamide on passive and active transport of fluorescein across the blood-retina barrier in retinitis pigmentosa complicated by macular oedema. Graefes Arch Clin Exp Ophthalmol 1998;236881- 889
PubMed Link to Article
Giusti  CForte  RVingolo  EM Deflazacort treatment of cystoid macular edema in patients affected by retinitis pigmentosa: a pilot study. Eur Rev Med Pharmacol Sci 2002;61- 8
PubMed
García-Arumí  JMartinez  VSararols  LCorcostegui  B Vitreoretinal surgery for cystoid macular edema associated with retinitis pigmentosa. Ophthalmology 2003;1101164- 1169
PubMed Link to Article
Fishman  GAGilbert  LDFiscella  GKimura  AEJampol  LM Acetazolamide for treatment of chronic macular edema in retinitis pigmentosa. Arch Ophthalmol 1989;1071445- 1452
PubMed Link to Article
Newsome  DABlacharski  PA Grid photocoagulation for macular edema in patients with retinitis pigmentosa. Am J Ophthalmol 1987;103161- 166
PubMed
Ozdemir  HKaracorlu  MKaracorlu  S Intravitreal triamcinolone acetonide for treatment of cystoid macular oedema in patients with retinitis pigmentosa. Acta Ophthalmol Scand 2005;83248- 251
PubMed Link to Article
Heckenlively  JRSolish  AMChant  SMMeyers-Elliott  RH Autoimmunity in hereditary retinal degenerations, II: clinical studies: antiretinal antibodies and fluorescein angiogram findings. Br J Ophthalmol 1985;69758- 764
PubMed Link to Article
Rogers  SWAndrews  PIGahring  LC  et al.  Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis. Science 1994;265648- 651
PubMed Link to Article
el Far  OMarqueze  BLeveque  C  et al.  Antigens associated with N- and L-type calcium channels in Lambert-Eaton myasthenic syndrome. J Neurochem 1995;641696- 1702
PubMed Link to Article
Moodie  FDLeaker  BCambridge  GTotty  NFSegal  AW Alpha enolase: a novel cytosolic autoantigen in ANCA positive vasculitis. Kidney Int 1993;43675- 681
PubMed Link to Article
Jackson  JFeighery  C Autoimmune angioedema: a new role for autoantibody in disease pathogenesis. Autoimmunity 1990;7181- 187
PubMed Link to Article
Mandle  RBaron  CRoux  E  et al.  Acquired C1 inhibitor deficiency as a result of an autoantibody to the reactive center region of C1 inhibitor. J Immunol 1994;1524680- 4685
PubMed
Inagaki  YJinno-Yoshida  YHamasaki  YUeki  H A novel autoantibody reactive with carbonic anhydrase in sera from patients with systemic lupus erythematosus and Sjogren syndrome. J Dermatol Sci 1991;2147- 154
PubMed Link to Article
Itoh  YReichlin  M Antibodies to carbonic anhydrase in systemic lupus erythematosus and other rheumatic diseases. Arthritis Rheum 1992;3573- 82
PubMed Link to Article
Kiechle  FLQuattrociocchi-Longe  TMBrinton  DA Carbonic anhydrase antibody in sera from patients with endometriosis. Am J Clin Pathol 1994;101611- 615
PubMed
Heckenlively  JRJordan  BLAptsiauri  N Association of antiretinal antibodies and cystoid macular edema in patients with retinitis pigmentosa. Am J Ophthalmol 1999;127565- 573
PubMed Link to Article
Wolfensberger  TJAptsiauri  NGodley  BDownes  SBird  AC Antiretinal antibodies associated with cystoid macular edema [in German]. Klin Monatsbl Augenheilkd 2000;216283- 285
PubMed Link to Article
Chant  SMHeckenlively  JRMeyers-Elliott  RH Autoimmunity in hereditary retinal degeneration, I: basic studies. Br J Ophthalmol 1985;6919- 24
PubMed Link to Article
Jonas  JBHayler  ASofker  JKPanda-Jonas  S Intravitreal injection of crystalline cortisone as adjunctive treatment of proliferative diabetic retinopathy. Am J Ophthalmol 2001;131468- 471
PubMed Link to Article
Moshfeghi  DMKaiser  PKScott  IU  et al.  Acute endophthalmitis following intravitreal triamcinolone acetonide injection. Am J Ophthalmol 2003;136791- 796
PubMed Link to Article
Roth  DBChieh  JSpirn  MJGreen  SNYarian  DLChaudhry  NA Noninfectious endophthalmitis associated with intravitreal triamcinolone injection. Arch Ophthalmol 2003;1211279- 1282
PubMed Link to Article
Penfold  PLWen  LMadigan  MCGillies  MCKing  NJProvis  JM Triamcinolone acetonide modulates permeability and intercellular adhesion molecule-1 (ICAM-1) expression of the ECV304 cell line implications for macular degeneration. Clin Exp Immunol 2000;121458- 465
PubMed Link to Article
Jonas  JBKreissig  IHugger  PSauder  GPanda-Jonas  SDegenring  R Intravitreal triamcinolone acetonide for age related macular degeneration. Br J Ophthalmol 2003;87462- 468
PubMed Link to Article
Karacorlu  MOzdemir  HKaracorlu  S Intravitreal triamcinolone acetonide for the treatment of chronic pseudophakic macular oedema. Acta Ophthalmol Scand 2003;81648- 652
PubMed Link to Article
McCartney  HJDrysdale  IOGornall  AGBasu  PK An autoradiographic study of the penetration of subconjunctivally injected hydrocortisone into the normal and inflamed rabbit eye. Invest Ophthalmol 1965;4297- 302
PubMed
Tessler  HLam  S Cystoid macular edema. Pepose  JSHolland  GNWilhelmus  KRedsOcular Infection and Immunity. St Louis, Mo CV Mosby1996;553- 589
Wakefield  DMcCluskey  PPenny  R Intravenous pulse methylprednisolone therapy in severe inflammatory eye disease. Arch Ophthalmol 1986;104847- 851
PubMed Link to Article
Tehrani  NNSaeed  TMurray  PI Deep intramuscular methylprednisolone for the treatment of cystoid macular oedema in uveitis. Eye 2000;14 ((pt 5)) 691- 694
PubMed Link to Article
Jonas  JBHayler  JKPanda-Jonas  S Intravitreal injection of crystalline cortisone as adjunctive treatment of proliferative vitreoretinopathy. Br J Ophthalmol 2000;841064- 1067
PubMed Link to Article
Jonas  JB Intraocular availability of triamcinolone acetonide after intravitreal injection. Am J Ophthalmol 2004;137560- 562
PubMed Link to Article
Yeung  CKChan  KPChan  CKPang  CPLam  DS Cytotoxicity of triamcinolone on cultured human retinal pigment epithelial cells: comparison with dexamethasone and hydrocortisone. Jpn J Ophthalmol 2004;48236- 242
PubMed Link to Article
Yeung  CKChan  KPChiang  SWPang  CPLam  DS The toxic and stress responses of cultured human retinal pigment epithelium (ARPE19) and human glial cells (SVG) in the presence of triamcinolone. Invest Ophthalmol Vis Sci 2003;445293- 5300
PubMed Link to Article
Narayanan  RMungcal  JKKenney  MCSeigel  GMKuppermann  BD Toxicity of triamcinolone acetonide on retinal neurosensory and pigment epithelial cells. Invest Ophthalmol Vis Sci 2006;47722- 728
PubMed Link to Article
Bakri  SJBeer  PM Choroidal neovascularization after radial optic neurotomy for central retinal vein occlusion. Retina 2004;24610- 611
PubMed Link to Article
Hirakawa  HIijima  HGohdo  TTsukahara  S Optical coherence tomography of cystoid macular edema associated with retinitis pigmentosa. Am J Ophthalmol 1999;128185- 191
PubMed Link to Article
Stanga  PEDownes  SMAhuja  RM  et al.  Comparison of optical coherence tomography and fluorescein angiography in assessing macular edema in retinal dystrophies: preliminary results. Int Ophthalmol 2001;23321- 325
PubMed Link to Article
Apushkin  MAFishman  GAJanowicz  MJ Monitoring cystoid macular edema by optical coherence tomography in patients with retinitis pigmentosa. Ophthalmology 2004;1111899- 1904
PubMed Link to Article
Tranos  PGWickremasinghe  SSStangos  NTTopouzis  FTsinopoulos  IPavesio  CE Macular edema. Surv Ophthalmol 2004;49470- 490
PubMed Link to Article
Kylstra  JAWierzbicki  TWolbarsht  MLLanders  MB  IIIStefansson  E The relationship between retinal vessel tortuosity, diameter, and transmural pressure. Graefes Arch Clin Exp Ophthalmol 1986;224477- 480
PubMed Link to Article
Molnar  IPoitry  STsacopoulos  MGilodi  NLeuenberger  PM Effect of laser photocoagulation on oxygenation of the retina in miniature pigs. Invest Ophthalmol Vis Sci 1985;261410- 1414
PubMed
Moorman  CMHamilton  AM Clinical applications of the MicroPulse diode laser. Eye 1999;13 ((pt 2)) 145- 150
PubMed Link to Article

Correspondence

CME
Also Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
Please click the checkbox indicating that you have read the full article in order to submit your answers.
Your answers have been saved for later.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
Submit a Comment

Multimedia

Some tools below are only available to our subscribers or users with an online account.

Web of Science® Times Cited: 19

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Collections
PubMed Articles