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Journal Français d'Ophtalmologie
Volume 38, n° 8
pages 709-716 (octobre 2015)
Doi : 10.1016/j.jfo.2015.02.007
Received : 30 October 2014 ;  accepted : 11 February 2015
Long-term results of low-fluence photodynamic therapy for chronic central serous chorioretinopathy
Résultats à long terme de la photothérapie dynamique en fluence réduite pour les choriorétinites séreuses centrales chroniques
 

E. Leys a, b, , S. Tuttle a, F. Rasquin c, F. Neu c, L. Postelmans a
a Brugmann university hospital, ophthalmology department, place Arthur Van Gehuchten 4, 1020 Brussel, Belgium 
b Saint-Pierre university hospital, ophthalmology department, rue Haute, 322, 1000 Brussels, Belgium 
c Erasme university hospital, ophthalmology department, 808, route de Lennik, 1070 Brussels, Belgium 

Corresponding author at: Brugmann university hospital, ophthalmology department, place Arthur Van Gehuchten 4, 1020 Brussel, Belgium.
Summary
Purpose

To evaluate long-term results of low-fluence photodynamic therapy (PDT) with verteporfin in the treatment of chronic central serous chorioretinopathy (CCSC).

Methods

Retrospective medical record review of 38eyes (34patients) who received low-fluence PDT for the treatment of CCSC. Visual acuity (VA), fundus biomicroscopy, fluorescein angiography (FA), indocyanine green angiography (ICG) and optical coherence tomography (OCT) were analyzed.

Results

Thirty-eight eyes (34patients) with CCSC received low-fluence PDT. Mean follow-up after PDT was 43.97months. Mean logMar best corrected VA (BCVA) improved significantly from 0.33 to 0.11 at the last follow-up which corresponds to a gain of 2.2lines. At 3months, complete resolution of central subretinal fluid was achieved on OCT after 1PDT in 37eyes and after 2PDTs in 1eye (retreated at 3months after first PDT). One patient developed choroidal neovascularization (CNV) 4years after his low-fluence PDT and received anti-vascular endothelial growth factor (VEGF) injections.

Conclusion

Low-fluence PDT with verteporfin for CCSC seems efficacious and safe in the long-term.

The full text of this article is available in PDF format.
Résumé
Objectifs

Évaluer les résultats à long terme de la photothérapie dynamique (PDT) par vertéporfine en fluence réduite dans le traitement des choriorétinites séreuses centrales chroniques (CRSCC).

Méthode

Étude rétrospective incluant 38yeux (34patients) ayant reçu un traitement par PDT en fluence réduite pour une CRSCC. L’acuité visuelle (AV), le fond d’œil, l’angiographie à la fluorescéine (FA), l’angiographie au vert d’indocyanine (ICG) et la tomographie par cohérence optique (OCT) ont été analysés.

Résultats

Un traitement par PDT en fluence réduite a été réalisé dans 38yeux (34patients). Le suivi moyen après la PDT était de 43,97mois. Une amélioration significative de l’acuité visuelle moyenne en LogMar a été notée en passant de 0,33 avant traitement à 0,11 à la dernière visite et représente un gain de ligne de 2,2. Une disparition complète du décollement séreux rétinien fut démontrée sur l’OCT 3mois après traitement après 1séance dans 37yeux et après 2séances dans 1œil (la seconde PDT ayant été réalisée 3mois après la première chez ce patient). Un patient a développé des néovaisseaux choroïdiens 4ans après son traitement par PDT et a bénéficié d’injections intravitréennes d’anti-VEGF.

Conclusion

La PDT en fluence réduite pour les CRSCC est un traitement sûr et efficace à long terme.

The full text of this article is available in PDF format.

Keywords : Chronic central serous chorioretinopathy, Low-fluence, Photodynamic therapy, Choroidal vascular hyperpermeability, Macular neurosensory detachment, Serous retinal detachment, Verteporfin

Mots clés : Choriorétinite séreuse centrale chronique, Fluence réduite, Photothérapie dynamique, Hyperperméabilité choroïdienne, Décollement séreux rétinien, Vertéporfine


Introduction

Central serous chorioretinopathy (CSC) is an idiopathic disease characterized by a macular detachment of the neurosensory retina. The etiology of this disease remains unclear and many theories have emerged since the 1960s. Early studies based on fluorescein angiography showed that the macular detachment resulted from a leakage in the retinal pigment epithelium (RPE) due to a breakdown of the external blood retinal barrier. Recently, Indocyanine green angiography (ICGA) has improved the understanding of this disease by describing the choroidal circulation. ICGA shows a delay in choroidal arteries and choriocapillaris circulation causing an ischemic stress which can lead to venous congestion and choroidal hyperpermeability [1]. A disruption in the continuity of the detached RPE would then permit a leakage of the choroidal exudate [2, 3, 4]. Although the precise physiopathology of this condition remains unknown, corticosteroids either endo- or exogenous have demonstrated their importance in this condition [5, 6]. The latest studies suggest that an elevation of catecholamins or an overaction of the mineralocorticoid pathway could result in a vasodilatation and hyperpermeability of the choroidal vessels [7]. Since a few years, enhanced depth imaging optical coherence tomography (EDI-OCT) has also demonstrated its role in completing the analysis of this choroidal disease by showing an increase in choroidal thickness and lumen area of abnormal choroidal vessels [8].

CSC is also known to be associated with male gender, pregnancy, stress, Cushing's syndrome, steroid-producing tumors and type A personality [9, 10].

Acute CSC usually resolves spontaneously in 3 to 4months and patients have a good visual prognosis [11]. However, 15 to 50% tend to develop recurrent or persistent detachment [11, 12, 13].

The long lasting detachment of the neurosensory retina combined with the decompensation of the RPE may lead to cystoid macular degeneration, foveal atrophy and damage of the photoreceptor layer with an irreversible significant vision loss of 3lines or more in 15% to 50% of cases [14, 15, 16].

Presently, photodynamic therapy (PDT) with verteporfin and thermal laser photocoagulation (TLP) remain the best treatment options. Many studies suggest that TLP is mainly effective in acute CSC demonstrating a clear extra foveal focal leakage on FA as it offers a more rapid absorption of subretinal fluid. However, TLP can cause inadvertent coagulation of the fovea, iatrogenic RPE damage, permanent scotoma, scar formation and CNV [17, 18]. On the other hand, PDT shows good anatomic and functional results in CCSC. Spaide et al. gave a well accepted definition of “chronic” CSC characterized by a serous macular elevation, visible microscopically or detected by OCT, that is associated with subtle leaks of ill-defined staining of retinal pigment epithelium on FA [4]. ICGA then shows a characteristic pattern of multifocal patchy hyperfluorescence best seen in the midphase of the ICG with dispersion of the dye and silhouetting of the larger choroidal vessels against a brighter background later in the angiographic sequence [19].

A PDT treatment has the advantage of reducing choroidal vascular hyperpermeability on an extended area while TLP treats the leaking point from the RPE into the subretinal space visible on fluoroangiography [20]. Nevertheless, complications with standard fluence PDT have also been described such as foveal atrophy, RPE changes, choriocapillaris ischemia and secondary choroidal neovascularization (CNV) [21, 22, 23, 24, 25].

Therefore, the use of modified PDT parameters such as low-fluence PDT have been evaluated by some authors [26, 27] and shows encouraging results with a significant reduction of side effects.

In addition of supporting the effectiveness of low-fluence PDT in the treatment of CCSC, and since long-term studies are few, our study aims to demonstrate the maintenance of good results over time.

Materials and methods

Retrospective review of medical records of 38eyes of 34consecutive patients with CCSC.

Patients included in our study showed serous macular elevation on fundus examination, confirmed by OCT in association with RPE atrophic areas and subtle leaks of ill-defined staining by FA according to Spaide's definition. Patients received low-fluence PDT between January 2003 and September 2013 at Brugmann and Erasme Brussels University Hospitals, Belgium. Most patients were referred to our center, some with a long duration of symptoms. When this was the case, treatment was performed promptly. Diagnosis of CCSC was based on fundoscopic examination, fluorescein angiography (FA), ICGA (Heidelberg Retina Angiography; Heidelberg Engineering, Heidelberg, Germany) and time-domain (TD) OCT (Stratus OCT, Carl Zeiss) or high resolution spectral-domain (SD) OCT (Spectralis, Heidelberg Engineering). Exclusion criteria were:

choroidal neovascularization at the time of the treatment;
treatment with focal laser or any previous treatment with standard PDT, anti-VEGF and steroid intra-ocular injections and;
associated age-related macular disease, polypoidal choroidal vasculopathy or any other macular diseases that could confound with the CCSC.

During follow-up, all patients were asked to visit us at least once during the first 6months. Afterwards, the visits were organized every year. Snellen best corrected visual acuity and OCT examinations were performed at every visit. FA was performed in all patients at baseline, at approximately 3months and at the last follow-up visit. ICGA was performed whenever a recurrence was suspected.

Vertepofin (visudyne®) dose was 6mg/m2body surface area, diluted in 30mL infusion solution, given by a 10-minute intravenous infusion. Light was applied 15minutes after the start of infusion. All patients received a single-spot PDT treatment. The spot size was measured using the greatest linear dimension (GLD) of the area of choroidal hyperpermeability observed on ICGA. The spot size could be extended, if necessary, to areas of leakage and edema based on FA and OCT analysis. The treatment spot size was 1000microns larger than the GLD of the lesion on the retina to allow a 500micron border, ensuring full coverage of the lesion. The maximum spot size was 6400μm. In this low-fluence PDT protocol, a total light energy of 25J/cm2, a light dose rate of 300mW/cm2, and a time of photosensitization of 83seconds were used.

Analysis of retinal thickness in this study was performed using the central retinal thickness measurement whether it was on time-domain (TD) OCT (Stratus OCT, Carl Zeiss) or high resolution spectral-domain (SD) OCT (Spectralis, Heidelberg Engineering).

For statistical analysis, SPSS software version 17.0 was used. Data were analyzed using the Wilcoxon signed-rank test. Snellen BCVA was converted to logarithm of the minimal angle of resolution (logMAR) BCVA and its corresponding line number for analysis. A P value of 0.05 was considered statistically significant and tests were 2 tailed.

Results

Thirty-eight eyes from 34patients received half-fluence PDT for CCSC. Demographic details, clinical findings and treatment results are summarized in Table 1.

The mean age of the 34patients at the moment of treatment was 52.2years (range, 31–68). Thirty-one patients (92%) were men and three (8%) were women. The mean follow-up period was longer than 3years (mean: 43.97months, range: 12–98months; median: 42months). The mean duration of CSC, defined by the period between first time the patient described symptoms of CSC and treatment was 3.75years (range: 1–16years).

All the patients showed a choroidal hyperpermeability on ICGA. Mean PDT spot size was 4410.52μm (range, 2200–6400μm). The spot size was extended to maximal size of 6400μm in 10eyes to include areas of leakage and/or edema based on FA and OCT analysis.

First follow-up examination was carried out at 1month to 6weeks in 33 out of 38eyes. At that time of visit, complete resolution of central SRF was observed on OCT in 29eyes. Central SRF resolved completely in 3 more eyes at 3months. One patient showed persistent central serous detachment 1 and 2months after treatment. A second low-fluence PDT was given to the patient 2months after the first treatment. Two months after his second PDT treatment, we observed a resolution of central SRF. First follow-up examination was conducted at 3months in 5 of the 38eyes with disappearance of central SRF on OCT in all of them.

Central retinal thickness (CRT) measured on time-domain (TD) OCT (Stratus OCT, Carl Zeiss) or high resolution spectral-domain (SD) OCT (Spectralis, Heidelberg Engineering) was collected before treatment and at last follow-up in 32eyes in which measurements were conducted on the same OCT during the hole follow-up period. Mean CRT before low-fluence PDT was 348.94μm (median: 350.5μm, interquartile range: 266.25–395.75μm) and at last follow-up it was 211.09μm (median: 202.5μm, interquartile range: 183–235.5μm) (Figure 1). Mean duration between those two measurements was 32.25months (median: 24months, range: 12–84months). Reduction of fluid during that period was statistically significant (P <0.0001). The measurements of the six other eyes (six patients) could not be used because of the long follow-up of those patients. Indeed, their initial central retinal thickness had been measured on TD OCT (Stratus OCT, Carl Zeiss) while later in the follow-up, retinal thickness was evaluated on SD high resolution OCT (Spectralis, Heidelberg Engineering).



Figure 1


Figure 1. 

Central retinal thickness before and after low-fluence PDT (after a mean follow-up of 32.25months) in 32 of the 38eye (in whom OCT was available on same OCT before and after treatment).

Zoom

Central retinal thickness measurements was available 1 to 3months after treatment and at last follow-up in 21eyes with a minimal follow-up of 2years. Mean CRT in this group was 202.1μm at the first follow-up visit (median: 182μm; interquartile range: 168–227μm) and at last follow-up visit it was 206.7μm (median: 208μm; interquartile range: 181–237μm). The mean follow-up period was 41months (median: 36months; range 24–84months). There was no significant statistical difference in mean CRT between first and last follow-up (P <0.005).

Mean BCVA in LogMar scale at baseline was 0.33 or 0.47 in Snellen visual acuity (median 0.3, interquartile range: 0.4–0.15). At the first follow-up visit after PDT, mean logMar BCVA was 0.21 or 0.62 in Snellen visual acuity (median 0.13; interquartile range: 0.3–0.05), at six months it was 0.13 or 0.75 in Snellen visual acuity (median: 0.08 interquartile range: 0.3–0) and at last follow-up it was 0.11 or 0.78 in Snellen visual acuity (median: 0.08 interquartile range: 0.22–0). Between initial examination and last follow-up, mean visual acuity improved by 2.2lines in logMar scale. Throughout the follow-up period, a statistically significant improvement was observed between baseline BCVA and respectively first follow-up and 6months mean BCVA (P <0.0001). The mean BCVA (logMar) at baseline, first follow-up, 6months and last follow-up are shown in Figure 2.



Figure 2


Figure 2. 

Change in mean logarithm of the minimal angle of resolution (logMar) best-corrected visual acuity (BCVA) of the 38eyes with CCSC before and after treatment by low-fluence PDT.

Zoom

Twenty-five eyes had a follow-up of at least 3years (Mean period 53.28; range, 36–96months; median, 48months). In this group, mean BCVA (logMar) before PDT was 0.32 or 0.48 in Snellen visual acuity (median: 0.3; interquartile range of 0.4–0.15). At 1 year it was 0.09 or 0.82 in Snellen VA (median: 0; interquartile range: 0.22–0), at 2years it was 0.11 or 0.78 in Snellen VA (median: 0.025; interquartile range: 0.22–0) and at last visit it was 0.09 or 0.82 in Snellen VA (median: 0; interquartile range: 0.22–0). The improvement of visual acuity after a mean period of more than 4 years was statistically significant (P <0.0001). Mean BCVA (logMar) before PDT at 1, 2years and at last visit are shown in Figure 3.



Figure 3


Figure 3. 

Change in mean logarithm of the minimal angle of resolution (logMar) best-corrected visual acuity (BCVA) before PDT, at 1 and 2years after PDT and at last visit in the 25patients with follow-up of at least 3years.

Zoom

Visual acuity improved 3 or more lines in 16eyes (42.11%) in logMar scale with an initial mean BCVA of 0.51 in logMar or 0.31 in Snellen VA (median: 0.4; interquartile range: 0.7–0.3) and a final mean BCVA of 0.11 in logMar or 0.82 in Snellen VA (median: 0.025; interquartile range: 0.24–−0.08). In this group, mean follow-up was equal to 4 years (47.38months; median 48months; range 12–96). Visual improvement was statistically significant (P <0. 0001).

Visual acuity improved by 1 or more lines in 13eyes (34.21%) in logMar scale with an initial mean BCVA of 0.25 in logMar or 0.56 in Snellen VA (median: 0.22; interquartile range: 0.3–0.15) and a final mean BCVA of 0.1 or 0.8 in Snellen VA (median: 0.05; interquartile range: 0.1–0). In this group, the mean follow-up was more than 3years (47.53months; median 48months; range 12–72).

A gain of less than 1 line was observed in 2eyes (5.26%) with an initial mean BCVA of 0.15 in logMar scale (0.7 in Snellen VA) and a final BCVA of 0.07 in logMar scale (0.85 in Snellen VA) after a mean follow-up of 16months.

Visual acuity remained stable in 5 eyes (13.16%) over a mean period of 53months (median: 36; range: 24–108).

A loss of 0.5lines in logMar scale was observed in 2eyes respectively (5.26%). Their initial BCVA was 0 (1.0 in Snellen VA) for the first eye and 0.05 (0.88 Snellen VA) for the second, and their final BCVA was 0.05 (0.88 in Snellen scale) and 0.1 (0.8 in Snellen VA) respectively. Those two last patients each had a follow-up of 24months.

The mean gain of lines between BCVA in LogMar scale before low-fluence PDT and at last follow-up visit for the total group of 38eyes after treatment is represented in Table 2.

One patient developed juxtafoveal CNV approximately 4years (47months) after his low-fluence PDT treatment. His initial BCVA was 0.3 in LogMar scale (0.5 in Snellen VA) and his BCVA 3months after low-fluence PDT was 0 in LogMar scale (1.0 in Snellen VA). His follow-up visits at respectively 1, 2 and 3years after treatment showed no recurrence of SRF and a stabilized BCVA. When he presented 47months after treatment, the patient described metamorphopsia without any change in VA (BCVA of 0 in LogMar scale, 1.0 in Snellen VA). Investigations showed the presence of CNV.

The patient received 5monthly injections of ranibizumab. At his control visits 1, 2, 3, and 6months after the last dose of Ranibizumab, there were no signs of persisting CNV on FA, OCT and fundus examination, his symptoms had disappeared and his VA was stable. A control visit is scheduled in 1month (1year after last ranibizumab) or earlier if the patient has any complains. No systemic adverse events were noticed in our study.

Discussion

A precise distinction between the acute and chronic form of central serous chorioretinopathy is lacking in current literature. However, there is a general belief that the “acute” form of CSC refers to a self limiting CSC that resolves spontaneously in several months without any treatment. On the other hand, Spaide et al. gave a well accepted definition of “chronic” CSC characterized by a serous macular elevation associated with subtle leaks of ill-defined staining of retinal pigment epithelium on FA [4] and a multifocal patchy hyperfluorescence best seen in the midphase of the ICG indicating choroidal hyperpermeability.

The acute form of CSC can therefore be considered as a benign condition without any treatment necessity. Unfortunately, a minority of cases progress to chronic CSC where a prolonged detachment of the macula can cause a severe and irreversible loss of vision [15, 16].

Currently, there is no standard treatment for chronic CSC established by clinical trials and best treatment options remain TLP and PDT with verteporfin. Before the advent of PDT, TLP represented the only available treatment for chronic CSC. Nevertheless, if TLP can be directed at focal leaks and has been proven to accelerate the reabsorption of SRF, outcomes are variable and complications such as inadvertent coagulation of the fovea, induction of choroidal neovascularization and progressive enlargement of the chorioretinal atrophy are well-known [17, 18]. Maruko et al. studied the resolution of subretinal fluid after TLP and PDT in 12 and 8eyes respectively. The subretinal fluid resolved in both disease groups; however, the choroidal thickness and hyperpermeability seen during ICGA was reduced after PDT suggesting that PDT reduces choroidal hyperpermeability seen in CSC and may work by a different mechanism than TLP [28].

Experimental studies have suggested that the main mechanism of action of verteporfin therapy is intravascular damage leading to thrombus formation and selective vascular occlusion. Direct endothelial cell damage probably results from the production of singlet oxygen and other free radicals with alteration of cell membranes [29]. However, other experimental studies have also described a choroidal atrophy following standard PDT secondary to choroidal hypoperfusion [30]. For this reason and to prevent other ocular complications such as induction of CNV, choroidal ischemia and RPE atrophy, modified parameters have been evaluated.

Along with the low-fluence PDT, other modified parameters have been studied in the treatment of CCSC such as the use of half the dose of verteporfin. The latter was evaluated by Chan et al. in 48eyes. They found an improvement of BCVA and complete resolution of fluid after half dose verteprofin [31]. Unfortunately, in the study of Shinojima et al., a recurrent pigment epithelial detachment with or without retinal detachment was identified during the one-year follow-up of 5 out of their 17patients after half-dose verteporfin for the treatment of CCSC [32].

Recently Reibaldi and al. demonstrated a complete resolution of subretinal fluid after low-fluence PDT for CCSC in 21eyes (91%). In a second study, they described a significant improvement in macular sensitivity after PDT for CCSC with greater efficacy of low-fluence PDT in comparison to standard parameters [26, 27].

However, even if many studies show very encouraging results with low-fluence PDT, long-term follow-up studies are lacking in literature.

In our study, the mean follow-up period was longer than 3.5years (43.9months). We found an improvement in visual acuity in 31 out of 38eyes (81.58%).

Those results are very similar to those found in the recent study of Silva et al. In that study, 46eyes had been treated with standard PDT for CCSC with a minimal follow-up period of 48months (mean follow-up 56.8months). They found an improvement in VA in 74% of eyes with a main gain of line of 2 in logMar scale [33]. The gain of line in our series is equal to 2.2lines in the total group of 38eyes. When we observed the group of patients with a minimal follow-up of three years (mean follow-up of 53.28months) we found an improvement of VA of 2.3lines (initial mean BCVA of 0.32 and final mean BCVA of 0.09) in 26eyes.

Our initial mean VA was much higher than the one in Silva et al.’s study. This observation could suggest a more advanced disease and/or longer duration of disease in their population of patients than ours.

Resolution of subretinal fluid was achieved in 93.4% of cases in Silva et al. study at 48months while we found a resolution of 94.7% of cases at last follow-up visit. No recurrences were noted in any of the patients during the study.

Five eyes had a stabilization of their vision. Two patients showed a small decrease in vision.

Those patients had a high VA before treatment and a dry OCT after low-fluence PDT. Their symptoms disappeared and both patients claimed to have recovered an excellent subjective visual outcome.

Those 2cases reveal one of the bias of the study. Indeed, the patients treated with a high VA before treatment cannot experience any more increase of their VA after treatment. However, those patients seem to feel a subjective benefit of the treatment that we cannot measure in terms of VA.

Two out of the five patients mentioned above in whom no improvement of VA was noted had a longer CCSC duration (3years and 16years before PDT treatment for the patients with stable visual acuity). Although these eyes showed resolution of subretinal fluid on OCT images, the visual acuity did not improve as predicted. This observation could suggest that an earlier treatment would result in a better final visual acuity. Indeed, studies that have been analyzing high resolution OCT images have reported the correlation between IS/OS line and visual acuity [34, 35]. Long lasting retinal detachment causing damages to the photoreceptor outer segments may thus explain the poor visual outcome after a delayed treatment.

Since our study is the longest evaluating effects of low-fluence PDT in CCSC, an interesting finding was to follow central retinal thickness in time after treatment. We were able to collect those data in 21eyes with a minimal follow-up of 24months. Those results can show there is no statistical significant change between CRT performed just after low-fluence PDT and at the last visit in the group of patient with a minimal follow-up of 24months. This indicates the absence of significant thinning of the retinal thickness in time in our patients. However, this study was not designed to evaluate CRT and further studies analyzing OCT findings more precisely should be needed.

One patient developed juxtafoveal CNV several years after his treatment. Low-fluence PDT had shown good results in this patient on OCT findings (performed at 3months, 1year and every year after the treatment) as well as FA (performed every year) and ICGA (performed before treatment, 1year and 3years after treatment). There are a few possibilities which could explain the presence of CNV in this case. A small neovascular activity could have been present before treatment and gone unnoticed on initial examinations. This neovascular complication might also have occurred during the natural course of disease [35]. Finally, it could have developed as a consequence of the PDT treatment.

Although PDT treatment was performed 4years before the development of CNV, this complication can occur after a PDT treatment [24]. Therefore, the use of modified parameters such as low-fluence PDT has been presented as a possible safer option in the treatment of CCSC. For safety reasons, further studies evaluating the long-term effects of low-fluence PDT should been carried out.

This study has its shortcomings as it was not a prospective, randomized and controlled clinical study. Secondly, it was not designed to evaluate retinal sensitivity and choroidal response after treatment. More precise functional studies as electro-retinography, micoperimetry, EDI-OCT and contrast sensitivity should complete the evaluation of long-term effects of low-fluence PDT in the treatment of CCSC. However, these long-term results are very encouraging as good visual acuity and complete resolution of subretinal fluid seems to be maintained over time. Our results confirm indirect evidence suggesting that lower fluence PDT might be as beneficial as standard PDT in the treatment of CCSC, which already has diseased RPE and choriocapillaris [25, 26].

In conclusion, this study is the first evaluating long-term effects of low-fluence PDT. Our results were comparable to the similar recent long-term study of Silva et al. evaluating standard PDT in the treatment of CCSC. In a condition where RPE is already damaged by the disease, it should be preferable to chose low-fluence parameters as they give the same results with a possible lower risk of complications.

Disclosure of interest

The authors declare that they have no conflict of interest concerning this article.

References

Komatsu H., Young-Devall J., Peyman G., Yoneya S. Choriocapillary blood propagation in normal volunteers and in patients with central serous chorioretinopathy Br J Ophthalmol 2010 ;  94 : 289-291 [cross-ref]
Prunte C., Flammer J. Choroidal capillary and venous congestion in central serous chorioretinopathy Am J Ophthalmol 1996 ;  121 : 26-34 [cross-ref]
Kitaya N., Nagaoka T., Hikichi T., Sugawara R., Fukui K., Ishiko S., and al. Features of abnormal choroidal circulation in central serous chorioretinopathy Br J Ophthalmol 2003 ;  87 : 709-712 [cross-ref]
Spaide R.F., Campeas L., Haas A., Yannuzzi L.A., Fisher Y.L., Guyer D.R., and al. Central serous chorioretinopathy in younger and older adults Ophthalmology 1996 ;  103 : 2070-2079discussion 9-80.
Zakir S.M., Shukla M., Simi Z.U., Ahmad J., Sajid M. Serum cortisol and testosterone levels in idiopathic central serous chorioretinopathy Indian J Ophthalmol 2009 ;  57 : 419-422 [cross-ref]
Yoshioka H., Katsume Y., Akune Experimental central serous chorioretinopathy in monkey eyes: fluorescein angiographic findings Ophthalmologica 1982 ;  185 : 168-178 [cross-ref]
Bousquet E., Beydoun T., Zhao M., Hassan L., Offret O., Behar-Cohen F. Mineralocorticoid receptor antagonism in the treatment of chronic central serous chorioretinopathy: a pilot study Retina 2013 ;  33 : 2096-2102 [cross-ref]
Hua R., Liu L., Li C., Chen. Evaluation of the effects of photodynamic therapy on chronic central serous chorioretinopathy based on the mean choroidal thickness and the lumen area of abnormal choroidal vessels Photodiagnosis Photodyn Ther 2014 ;  11 : 519-525 [cross-ref]
Haimovici R., Koh S., Gagnon D., Lehrfeld T., Wellik S. Risk factors for central serous chorioretinopathy: a case-control study Ophthalmology 2004 ;  111 : 244-249 [cross-ref]
Yannuzzi L.A. Type-A behavior and central serous chorioretinopathy Retina 1987 ;  7 : 111-131 [cross-ref]
Klein M.L., Van Buskirk E.M., Friedman E., Gragoudas E., Chandra S. Experience with non treatment of central serous choroidopathy Arch Ophthalmol 1974 ;  91 : 247-250
Castro-Correia J., Coutinho M.F., Rosas V., Maia J. Long-term follow-up of central serous retinopathy in 150 patients Doc Ophthalmol 1992 ;  81 : 379-386
Torron C., Melcon B., Ferrer E., Ruiz O., Olivan J.M., Honrubia F.M. Central serous choroidopathy. Long term study Arch Soc Esp Oftalmol 2000 ;  75 : 103-108
Piccolino F.C., de la Longrais R.R., Ravera G., Eandi C.M., Ventre L., Abdollahi A., and al. The foveal photoreceptor layer and visual acuity loss in central serous chorioretinopathy Am J Ophthalmol 2005 ;  139 : 87-99 [inter-ref]
Bandello F., Virgili G., Lanzetta P., Pirracchio A., Menchini U. ICG angiography and retinal pigment epithelial decompensation (CRSC and epitheliopathy) J Fr Ophtalmol 2001 ;  24 : 448-451 [inter-ref]
Levecq L., Hoebeke M., Guagnini A.P., Snyers B. Diffuse retinal epitheliopathy: study of 30 eyes Bull Soc Belge Ophtalmol 2003 ; 55-62
Ficker L., Vafadis G., While A. Long-term follow-up of a prospective trial of argon laser photocoagulation in the treatment of central serous retinopathy Br J Ophthalmol 1998 ;  72 : 829-834
Yannuzzi L.A., Slakter J.S., Kaufman S.R. Laser treatment of diffuse retinal pigment epitheliopathy Eur J Ophthalmol 1992 ;  2 : 103-114
Yannuzi L.A., Slakter J.S., Sorenson J.A., Guyer D.R., Orlock D.A. Digital indocyanine green videoangiography and choroidal neovascularization Retina 1992 ;  12 : 191-223
Yannuzzi L.A., Slakter J.S., Gross N.E., Spaide R.F., Costa D., Huang S.J., and al. Indocyanine green angiography-guided photodynamic therapy for treatment of chronic central serous chorioretinopathy Retina 2003 ;  23 : 288-298 [cross-ref]
Postelmans L., Pasteels B., Coquelet P., El Ouardighi H., Verougstraete C., Schmidt-Erfurth U. Severe pigment epithelial alterations in the treatment area following photodynamic therapy for classic choroidal neovascularization in young females Am J Ophthalmol 2004 ;  138 : 803-808 [inter-ref]
Cardillo Piccolino F., Eandi C.M., Ventre L., Rigault de la Longrais R.C., Grignolo F.M. Photodynamic therapy for chronic central serous chorioretinopathy Retina 2003 ;  23 : 752-763
Lee P., Kim K., Lee W.S. Severe choroidal ischemia following photodynamic therapy for pigment epithelial detachment and chronic central serous chorioretinopathy Jpn J Ophthalmol 2009 ;  53 : 52-56 [cross-ref]
Colucciello M. Choroidal neovascularization complicating photodynamic therapy for central serous retinopathy Retina 2006 ;  26 : 239-242 [cross-ref]
Chan W.M., Lam D.S., Lai T.Y., Tam B.S., Liu D.T., Chan C.K. Choroidal vascular remodelling in central serous chorioretinopathy after indocyanine green guided photodynamic therapy with verteporfin: a novel treatment at the primary disease level Br J Ophthalmol 2003 ;  87 : 1453-1458 [cross-ref]
Reibaldi M., Cardascia N., Longo A., Furino C., Avitabile T., Faro S., and al. Standard-fluence versus low-fluence photodynamic therapy in chronic central serous chorioretinopathy: a nonrandomized clinical trial Am J Ophthalmol 2009 ;  149 : 307-315
Reibaldi M., Boscia F., Avitabile T., Uva M.G., Russo A., Zagari M., and al. Functional retinal changes measured by microperimetry in standard-fluence vs low-fluence photodynamic therapy in chronic central serous chorioretinopathy Am J Ophthalmol 2011 ;  151 : 953-960 [inter-ref]
Maruko I., Iida T., Sugano Y., Ojima A., Ogasawara M., Spaide R.F. Subfoveal choroidal thickness after treatment of central serous chorioretinopathy Ophthalmology 2010 ;  117 : 1792-1799 [cross-ref]
Schmidt-Erfurth U., Hasan T. Mechanisms of action of photodynamic therapy with verteporfin for the treatment of age-related macular degeneration Surv Ophthalmol 2000 ;  45 : 195-214 [cross-ref]
Zacks D.N., Ezra E., Terada Y., Michaud N., Connolly E., Gragoudas E.S., and al. Verteporfin photodynamic therapy in the rat model of choroidal neovascularization: angiographic and histologic characterization Invest Ophthalmol Vis Sci 2002 ;  43 : 2384-2391
Chan W.M., Lai T.Y., Lai R.Y., Tang B.W., Liu D.T., Lam D.S. Safety enhanced photodynamic therapy for chronic central serous chorioretinopathy: one-year results of a prospective study Retina 2008 ;  28 : 85-93 [cross-ref]
Shinojima A., Kawamura A., Mori R., Fujita K., Yuzawa M. Detection of morphologic alterations by spectral-domain optical coherence tomography before and after half-dose verteporfin photodynamic therapy in chronic central serous chorioretinopathy Retina 2011 ;  31 : 1912-1920 [cross-ref]
Silva R.M., Ruiz-Moreno J.M., Gomez-Ulla F., Montero J.A., Gregorio T., Cachulo M.L., and al. Photodynamic therapy for chronic central serous chorioretinopathy: a 4-year follow-up study Retina 2012 ;  33 : 309-315
Moon J.W., Yu H.G., Kim T.W., Kim H.C., Chung H. Prognostic factors related to photodynamic therapy for central serous chorioretinopathy Graefes Arch Clin Exp Ophthalmol 2009 ;  247 : 1315-1323 [cross-ref]
Matsumoto H., Sato T., Kishi S. Outer nuclear layer thickness at the fovea determines visual outcomes in resolved serous chorioretinopathy Am J Ophthalmol 2009 ;  148 : 105-110



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