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A Case of Bilateral Chronic Central Serous Chorioretinopathy

Thomas Walent, O.D.

Optometric Resident, VHMC Wilkes-Barre, PA

ABSTRACT

Central serous chorioretinopathy (CSCR) is a chorioretinopathy characterized by an exudative neurosenosory retinal detachment with or without an associated detachment of the retinal pigment epithelium. CSCR has several recognized risk factors, and can manifest in several different categories of disease. Pateints’ symptoms vary greatly from mild disturbance to severe visual significance. CSCR usually is self limiting and resolves spontaneously in 4 to 8 weeks. If the patient’s symptoms continue for more than 3 months without resolution, introduction of other therapies should be considered. Much is still no known regarding the pathophysiology of the disease, however with the advent of new imaging technology and techniques designed to further understand the structure and function of the retina, a better understanding has been established regarding the pathophysiology of CSCR. A wide variety of treatment strategies have been postulated targeted towards pathophysiological defects within the retina causing CSCR.

CASE REPORT

In March 2005, a 41 year old white male reported to the Wilkes-Barre VHMC Eye Clinic with complaints of having a visual distortion in his right eye. Patient describes this distortion to be more evident at near. Patient had no ocular history, and a systemic medical history positive for allergic rhinitis and joint pain. Visual acuity testing revealed distance and near VA of 20/20 OU, with complaints of visual distortion in the central vision OD. Amsler grid testing revealed positive metamorphopsia OD, without scotoma. Entrance testing, slit lamp examination and IOP were unremarkable. Dilated fundus exam revealed healthy optic nerves OU, with pigmentary changes within the central macula OD, without retinal fluid or thickening. All other aspects of retinal vasculature, posterior pole, and peripheral retina were unremarkable. The patient was referred to a retinal specialist for retinal evaluation with FA and OCT. The retinal specialist confirmed the diagnosis of a previous episode of Central Serous Chorioretinopathy OD, based on the macular pigmentation.

In March 2007, the patient returned to clinic with a new onset distortion in his right eye at distance and near following a heated argument that he engaged in over the weekend. All aspects of examination were unremarkable with the exception of having a large area of metamorphopsia OD with Amsler grid testing. OCT revealed a serous retinal detachment beneath the fovea. The patient was referred to a retinal specialist who confirmed an old CSCR which is now active in nature. The specialist chose observation as the best course of action for this case.

In March 2009, the patient again returns to the clinic with new onset changes in his vision, complaining of having difficulty with his near vision. The patient reports that he has recently returned to school, and has been under a tremendous amount of stress and anxiety. The examination revealed mild presbyopia OU, with no signs of active CSCR OU. Dilated fundus exam did reveal new pigmentation OS, which may have indicated a small previous episode of CSCR that was asymptomatic to the patient. OCT confirmed this diagnosis, showing no active CSCR, but mild thickening of both maculae.

In April 2011, patient reports new onset distortion OS at near, with a central blind spot. This is particularly bothersome to the patient because his school work had intensified, and must read several hours per day. He admits that he was having great difficulty balancing the stress of school and his personal life, and has great levels of anxiety. Amsler grid testing revealed stable central metamorphopsia OD, and new onset central metamorphopsia with a temp wedge shaped scotoma OS. OCT revealed thickening of the central macula OD with a serous retinal detachment OS. Patient was referred to a retinal specialist who confirmed the new onset serous retinal detachment OS and again advised observation and management of stress levels. The retinal specialist inquired about use of steroids for his systemic conditions, which the patient denied. The following month the patient returned with similar symptoms, which he believed were worsening. OCT revealed serous retinal detachments OU, and dilated fundus exam confirmed these findings, with macular pigmentation OD>OS. The patient’s systemic medical history was again questioned, in which the patient revealed that not only does he use a steroid inhaler for his asthma, but also receives multiple cortisone injection is his shoulders for several years. The patient did not understand that these medications were steroid based.

Observation was again suggested, and he was encouraged to speak to his primary care doctor and orthopedist regarding the use of these medications, which were clearly exacerbating his CSCR.

Over the following months and up to this current point the patient’s symptoms continue, however the serous detachment in his left eye has subsided, and he continues to have a chronic serous RD in his right eye that is not improving. The patient has become increasingly frustrated with his condition and stated, “This needs to stop happening, isn’t there something else you can do?”

INTRODUCTION

Central serous chorioretinopathy (CSCR) is a chorioretinopathy characterized by an exudative neurosenosory retinal detachment with or without an associated detachment of the retinal pigment epithelium. The disease was first described by Albrect von Graffe in 1866, who described it as “relapsing central leutic reintitis”.[i] In 1965, Maumenee was the first to describe a leak at the level of the RPE with utilization of fluorescein angiography in several patients.[ii] Subsequently, Gass drafted very detailed descriptions of the fluorescein angiographic patterns and characteristics of CSCR. Gass coined the term “central serous chorioretinopathy” in 1967.[iii]

Although the condition is often referred to as “Central Serous Retinopathy”, it has been found that it is not in fact a “retinopathy” rather a “choriorentinopathy”. Despite this misnomer, CSCR is the fourth most common “retinopathy” after age related macular degeneration (ARMD), diabetic retinopathy, and branch retinal vein occlusion.[iv]

EPIDEMIOLOGY

Men are more likely to develop CSCR at a ratio of about 6:1. The mean age of onset of disease has been found to be 41 years old. Although CSCR affects mainly middle aged males, several reports have documented cases of disease in young and elderly patients of both sexes.[v] CSCR occurs most commonly in white and Asian populations, and appears to occur less frequently in African Americans.[vi] CSCR has the tendency to be more aggressive in African American patients. It has been postulated that African-Americans have greater sympathetic reactivity to stressors which in turn causes disruption to subfoveal choroidal blood flow, thus exacerbating the disease process.[vii]

RISK FACTORS

Several risk factors have been identified that significantly increase risk of developing CSCR, however many are very poorly understood. Over the past several years, infections, toxins, immunological reactions, neuronal, circulatory, and hormonal regulatory factors have all been implicated in the initiation of the damaging process that leads to CSCR.

One of the first and most recognized risk factors for developing CSCR is having a Type A personality. Type A personality is defined as having quickness to anger, high levels of competitiveness, and having the compulsion to always be in control. CSCR is associated with high levels of stress and anxiety hormones, particularly cortisol and epinerpherine. Those with Type A personalities under stress have higher levels of endogenous stress hormones, often up to 40x the normal level of cortisol and 4x that of epinerpherine.[viii]

On a similar note, a few specific systemic diseases related to having elevated endogenous corticosteroids have been found to be predisposed to developing CSCR. Cushing’s syndrome can result from either high levels of endogenous or exogenous administration of corticosteroids, resulting in elevated levels of systemic cortisol.[ix] Women who are pregnant also may have elevated endogenous cortisol. Several studies have linked this elevation of cortisol levels to CSCR.[x] Along the same lines, elevated levels of endogenous epinephrine, such as in patients with obstructive sleep apnea and systemic hypertension, has been linked with higher risk of CSCR.[xi]

There is also extensive literature that suggests that exposure to exogenous corticosteroids significantly increases incidence of CSCR. Multiple systemic conditions are treated with corticosteroids (ex. asthma, autoimmune disorders, joint inflammation, dermatological conditions, allergic rhinitis, degenerative disc disease requiring epidural, organ transplantation, etc), with varying administration routes, all of which have resulted in secondary CSCR.[xii]Ocular conditions treated with systemic steroids and periorbital/ intraocular injections of Kenelog (optic neuritis, ischemic optic neuropathy, diabetic retinopathy, solar retinopathy, scleritis, anterior uveitis, chorioretiniits, etc) have also been shown in literature to develop subsequent CSCR.[xiii]

CLASSIFICATION

CSCR can broadly be divided into acute, recurrent, and chronic groups. The importance of distinguishing between these specific categories refers to the long term visual prognosis of the patient, and whether or not treatment should be necessitated. The term acute CSCR refers to a self limiting condition which resolves within a few months of initial symptoms, without treatment and with minimal residual changes to the retina. On the other hand, chronic CSCR is defined as “a serous macular elevation, visible biomicroscopically or detected by OCT, that is associated with RPE atrophic areas and subtle leaks or ill defined staining by FA.”[xiv] Chronic cases of disease can further be categorized by chronic CSCR following a single attack, recurrent resolving CSCR and recurrent non-resolving CSCR. Recent studies have shown that 51% of untreated patients suffer a single acute resolving attack, while the remaining 49% have a more complicated version of the disease.[xv] Polak et al noted that the major distinction between chronic and acute disease is the fact that chronic disease has widespread pigment epithelial changes without overt detachment in most cases, whereas in acute diseases there is focal pigment epithelial abnormality and marked detachment.[xvi]

CLINICAL PRESENTATION

Patients will report with a multitude of symptoms upon developing CSCR, many of which can be verified with classic ophthalmic examination techniques. Visual acuity may vary, affecting some patients profoundly and others will not demonstrate a measureable decrease in vision. When shown an Amsler Grid, patients often report an acute onset of central scotoma, metamorphopsia, and micropsia. Contrast sensitivity and color saturation are often diminished. Patients will demonstrate an increase in macular photostress test time. [xvii]

Upon examination of the fundus with contact lens biomicroscopy, a serous macular neurosensory detachment will be present without subretinal bleeding. There are often subretinal lipofuscin deposits present in the area of detachment, referred to as “dots”. Other varying characteristics often found when evaluating CSCR are RPE detachments, areas of retinal epithelial mottling and atrophy (often in a gutter configuration) and subretinal fibrin (especially when the episode happens after pregnancy).

The actual cause of visual loss in CSCR results from the after effects of the neurosensory detachment of the retina, including foveal attenuation, cystoid macular degeneration, and damage of the foveal photoreceptor layer. [xviii] Unlike the profound visual loss that is associated with a rhegmatogenous retinal detachment, the photoreceptors have an unexplained ability to function in the area above serous retinal detachments seen in CSCR. [xix]

In most untreated cases of CSCR, visual acuity will recover quite well, however the quality of vision may suffer. Wong et al concluded that optometrists’ too often “trivialize the situation as patients sometimes suffer the consequences following presumed resolution of the disease”. Patients often remain with symptoms, and may complain of metamorphopsia, decrease in brightness, and alterations in color vision of the affected eye for up to several months following resolution of CSCR.[xx]

PATHOPYSIOLOGY

One of the most least understood aspects about CSCR is whether the pathophysiology of this condition is related to a disorder of primarily the choroid, the retinal pigment epithelium, or both; and whether this disorder is a focal phenomenon or widespread. With the advent of new imaging technology and techniques designed to further understand the structure and function of the retina, a better understanding has been established regarding the pathophysiology of CSCR. Data currently supports both theories; however a definitive conclusion has still yet to be determined.

Choroid Dysfunction Theory

Gass suggested that a focal increase in the permeability of the choriocapillaris was the primary cause of damage to the overlying RPE in patients with CSCR. He suggested that this could create detachment of the RPE, serous retinal detachment and, in 10–15% of patients, serofibrinous subretinal exudation.[xxi]

Following the work of Gass, a groundbreaking study suggested a potential model for the pathogenesis of CSCR based on ICG-videoangiography (ICG-V). Patient with CSCR showed a common finding of diffuse hyperpermeability around active leakage sites seen with ICG-V but not with FA.[xxii] This finding suggested that hyperpermeability was at the level of the choroid rather than the RPE. They proposed that choroidal hyperpermeability causes serous detachments of the RPE, which can induce a small rip or decompensation of the RPE, forming an area of leakage. This in turn leads to diffusion of water, electrolytes, and proteins that causes a neurosensory retinal detachment.

More support of the choroidal dysfunction theory of CSCR involves the postulation that focal areas of choroidal ischemia may be the cause of alterations within choroidal circulation. On study utilizing Fluorescein angiography (FA) and indocyanine green angiography (ICG-A) with a scanning laser ophthalmoscope and a digital imaging system were performed to evaluate choroidal circulation changes in CSCR.[xxiii] They found that dilated capillaries and dilated draining venules in one or more choroidal lobules, following a localized delay in arterial filling. They suggested that this might explain the choroidal hyperpermeability in the area of the damaged RPE. These observations are suggestive of a localized lobular inflammatory disease or ischemic choroiditis.

However, the cause of the choroidal abnormality is still unknown. It has been suggested that the answer may lie in changes of the autoregulation in the choroidal blood flow.[xxiv]

RPE dysfunction theory

An alternative theory suggests that CSCR results from dysfunction of the RPE. This occurs following an undefined insult to the RPE, resulting in either a few impaired RPE cells or even a single RPE cell which causes a reverse in fluid movement in a chorioretinal direction. This subsequently leads to leakage of fluid in the subretinal space and finally to the development of a neurosensory retinal detachment. Spitznas suggested that focal damage to the RPE can reverse the direction of ion secretion and thus lead to greater fluid movement towards the retina than to the choroid.[xxv]

IMAGING

Fluorescein angiography

Fluorescein angiography (FA) is one of the most widely used imaging techniques used to diagnose disorders of retina, particularly those involving areas of subretinal leaking. The most important angiographic feature is an expanding point of fluorescein leakage under a serous detachment of the neurosensory retina without the presence of subretinal neovascularization. The leakage site is hypopigmented due to movement of choroidal fluorescence. The hallmark of CSCR is the presence of a “smokestack” leak, with a reported prevalence ranging from 7%[xxvi] to 25%[xxvii] . Other less common patterns include “inkblot” and “mushroom” leaks.[xxviii]

Fluorescein angiography reveals leaks in the RPE which is present in about 95% of all cases of CSCR. Most of the leaks are located 0.5 – 1.5 mm away from the center of the fovea, and only 10% are found closer to the fovea. The most common sites of leakage are the superior nasal quadrant of the posterior pole. In cases of chronic CSCR multiple RPE leaks are often visualized.[xxix]

Optical coherence tomography (OCT)

Optical coherence tomography (OCT) is a very valuable tool in diagnosing CSCR. OCT holds many advantages to FA, as it is a noninvasive test that is very easily performed, and provides a high resolution three-dimensional image of anatomy of the retina. In patients with active and inactive CSCR, a serous neurosensory retinal detachment is often imaged, many times with an associated pigment epithelial detachment within or outside the area of retinal detachment. Studies also revealed areas of multiple small PED’s within the area of the macula and along the vascular arcades.[xxx] When focusing your attention to the RPE layer of the retina, the image often shows a single or multiple small defects. One particular study performed OCT on 21 eyes with CSCR and found RPE abnormalities in 95% of the eyes with a tiny defect of the RPE within the pigment epithelial detachment. These defects corresponded to leakage points found on fluorescence angiography, thus supporting the RPE dysfunction theory.[xxxi]

Another important finding seen with OCT involves choroidal thickness. Using SD-OCT, the mean thickness of the choroid in patient with CSCR was found to be thickened two-fold when compared to the average population, with mean thickness was found to be 505 µm compared with 272 µm in normal individuals.[xxxii] Researchers suggest the thickening of the choroid relates to increased hydrostatic pressure, and this finding is supportive of the choroid dysfunction theory.

Indocyanine Green Angiography

Indocyanine green angiography (ICGA) is useful when studying and diagnosing CSCR because it is used primarily to image abnormalities within the choroidal structure. This is particularly useful because choroidal dysfunction is one theory of the pathology of CSCR. One study revealed that 63-100% of cases of CSCR demonstrate significant choroidal filling delays, which supports the theory this phenomenon would cause retinal ischemia, which in turn increase choroidal hyperpermeability and lead to serous detachment of the retina. [xxxiii] Along the same lines, areas of choroidal hyperfluorescence indicate choroiocapillary nonperfusion, which is commonly seen in patients with CSCR.[xxxiv] Again, these choroidal circulatory disturbances may be responsible for the subsequent vascular hyperpermeability.

Fundus Autofluorescence

Fundus autofluorescence (FAF) uses stimulated emission of light from certain fluorophores, mainly lipofuscin in order to provide an image of the retina. Lipofuscin content is an indirect measurement of metabolic activity of RPE cells and at the level of the RPE lipofuscin build-up is related to phagocytosis of photoreceptor outer segments. As mentioned earlier, appearance of the fundus in patients with CSCR often have small, subretinal “dots” in the area of detachment. Many have hypothesized that these “dots” are accumulations of lipofuscin.[xxxv] One study indicated that 65% of patients with CSCR had lipofuscin deposits that were imaged with both FAF and confirmed with OCT scans.[xxxvi]

FAF is very useful in diagnosing and classifying between acute and chronic cases of CSCR. In cases of acute CSCR, areas of hyperautofluorescence indicate areas of serous retinal detachment. On the other hand, chronic CSCR demonstrates both areas of hyper and hypoautofluorscence. The relevance to hypoautofluorescence in cases of chronic CSCR relates to treatment strategies. Some suggest that areas of hypoflurorescence near the central macula would not respond well to laser therapy. It has also been noted that hypoflurorescence near the central macula in patients with increased age is a good predictor of decreased visual acuity upon resolution of CSCR.[xxxvii]

TREATMENT

There are few randomized controlled trials with respect to the treatment of CSCR. In approximately 90% of patients, CSCR is self limiting and spontaneously resolves.

The first line of treatment for CSCR should involve a thorough systemic medical history, and discontinuation of all steroid medications, if possible. Studies indicate that 90% of serous detachments will resolve upon discontinuation of steroid.[xxxviii] Lifestyle counseling and other psychological therapies may be suggested as an attempt to reduce stress and anxiety levels. If the patient’s symptoms continue for more than 3 months without resolution, introduction of other therapies should be considered.

Laser focal photocoagulation

Laser photocoagulation works by applying energy to the retina and changing the RPE’s ability to act as a barrier to diffusion. The fluid within a serous retinal detachment in CSCR has a very high concentration of protein and facilitates diffusion of fluid from the choroid underneath the retina. Photocoagulation allows the both the fluid and protein to return in the correct direction back into the choroid due to the permeability of the RPE.[xxxix] Current studies indicate that treatment with laser photocoagulation reduces the length of detachment by up to one month, and decrease the rate of recurrence over an 18 month span from 34% in the untreated group to 0% in the treated group.[xl] The benefit of quicker resolution of CSCR however does not appear to be correlated with improved visual acuity.

Unfortunately laser is only an option for areas of extrafoveal leakage. In all cases, laser treatment results in focal collateral retinal damage. Potential complications include thermal rupture of Bruch’s membrane with or without hemorrhage, secondary choroidal neovascular membrane (CNVM), and misplaced laser spots.[xli]

Photodynamic Therapy

Photodynamic therapy (PDT) with vertiporfin (Visudyne) offers a more precisely directed alternative to photocoagulation. PDT is directed towards the pathological hyperpermeable choroidal microcirculation responsible for CSCR. Vascular remodeling results in decreased permeability and termination of focal RPE leakage.[xlii]

PDT has been shown to cause a resolution of serous detachment and improvement in VA and symptoms through interventional and retrospective studies. These studies were performed under “Treatment of ARMD with PDT” (TAP) protocols, with undesirable reports of complications including changes of the RPE, choriocapillary hypoperfusion, and development of CNVM.[xliii]

A series of studies with modifications of TAP protocols were performed in order to reduce potential complications. One study introduced “safety enhanced PDT” with the use of half-dose vertiporfin (3mg/m2). Findings demonstrated significant improvement of retinal function only in cases of CSCR without PED, and showed no undesirable side effects. These findings have been shown effective at loses as low as 30% of vertiporfin.[xliv] One other protocol using decreased flux has also shown promise. Low-fluence PDT (25 J/cm2 @ 300mW) resulted in reduction of serous retinal detachment and increase in visual acuity without damage to the choriocapillaris in 79-91% of patients.[xlv]

Intravitreal Bevacuzumab

Bevacuzumab (Avastin) is an anti-vascular endothelial growth factor that is primarily used for the treatment of exudative age-related macular degeneration (ARMD) and has been highly studied for the use of retinal conditions. In CSCR, VEGF has a role in vascular permeability by changing tight junctions and inducing vascular fenestration. It has been suggested that use of bevacuzumab may not affect the underlying cause of CSCR directly, but rather act on tight junctions only. Studies report resolution of neurosensory detachment, with improvements in visual acuity and RPE leaks after anti-VEGF therapy, with mixed results.[xlvi] In cases of chronic CSCR with accumulations of subretinal granular deposits from the phagocytosis of photoreceptor segments (“dots”), it has been postulated that these “dots” could prevent the anti-VEGF treatment in chronic CSCR.[xlvii]

Acetazolamide

Acetazolamide (Diamox) is a carbonic anhydrase inhibitor which has many ophthalmic uses, including reduce subretinal fluid in various disorders. It has been suggested that oral administration of acetazolamide may accelerate resolution of acute cases of CSCR. Clinical trials have found that acetazolamide has been found successful in shortening the length of time serous detachment. However, the treatment has shown no effect on recurrence rate or any increase in final visual acuity.[xlviii] Clinicians suggest that this treatment option has potential to be used for patients in need of accelerated resolution of an episode of acute CSCR, such as those that are monocular. In view of potential side effects of acetazolamide such as aplastic anemia, parathesias, nervousness and gastric upset, along with its contraindication for patients with sulfa allergy, its use is limited in the face of other more effective interventions.

Ketoconazole

Ketoconazole (Nizoral) is oral antifungal medication that is an adrenocorticoid antagonist. Those with CSCR have been found to have elevated endogenous levels of cortisol. In a small study of 15 patients, 200mg of ketoconazole was administered for four weeks. The patients demonstrated significantly reduced levels of urinary cortisol, there were no improvements found in resolution of disease or visual acuity when compared to the control group.[xlix] Although reducing endogenous corticosteroids seems to offer a rational approach in resolution of disease, clinical studies offered no benefit.

Mifepristone

Mifepristone (RU-486) is a high affinity progesterone and glucocorticoid antagonist. Mifepristone is used clinically in voluntary early pregnancy termination. A recent small prospective study displayed great promise, where patients were orally given a 200mg dose of mifepristone for 90 days, showed dramatic improvement in symptoms and disease resolution. [l] Due to the moral debate of this medication, and its high cost of treatment ($200 for a 200mg dose), ophthalmic use of mifepristone may be severely delayed in the United States, however further investigation is warranted.

Sleep apnea

A recent series of observational case reports has demonstrated a relationship with CSCR and obstructive sleep apnea syndrome. One study revealed that 22% of 56 consectutive patients with acute CSCR suffered from obstructive sleep apnea syndrome, whereas only 2% of the general population suffers from obstructive sleep apnea.[li] Observational case reports have demonstrated resolution of CSCR and treatment of obstructive sleep apnea syndrome, with rapid resolution of bilateral CSCR with treatment of newly diagnosed obstructive sleep apnea.[lii] Clinicians should consider this diagnosis with CSCR and refer for a sleep study when deemed appropriate.

DISCUSSION

Central serous chorioretinopathy (CSCR) is a chorioretinopathy characterized by an exudative neurosenosory retinal detachment with or without an associated detachment of the retinal pigment epithelium. CSCR has several recognized risk factors, and can manifest in several different categories of disease. Patients’’ symptoms vary greatly from mild disturbance to severe visual significance. CSCR usually is self limiting and resolves spontaneously in 4 to 8 weeks. If the patient’s symptoms continue for more than 3 months without resolution, introduction of other therapies should be considered. Much is still no known regarding the pathophysiology of the disease, however with the advent of new imaging technology and techniques designed to further understand the structure and function of the retina, a better understanding has been established regarding the pathophysiology of CSCR. A wide variety of treatment strategies have been postulated targeted towards pathophysiological defects within the retina causing CSCR.

In the previously described case, the patient was diagnosed with chronic nonresolving CSCR OD, and chronic resolving CSCR OS. The patient had several risk factors, including being a middle aged white male with an admitted Type A personality who was under great deals of stress due to going back to school, and received multiple steroid treatments with cortisone injections in his shoulders and knees for an arthritic condition and use of a steroid based inhaler for asthma. The patient has been visually symptomatic for several years, with noticeable Amsler Grid defects and mild changes in visual acuity. With use of OCT and FA, along with regular fundus examinations, the patient has had multiple accounts of serous retinal detachments without PED’s OU, permanent macular thickening, and macular RPE mottling. Subretinal “dots” were not present upon examination.

Previous treatment strategies included observation, discontinuation of steroids, and implementing coping strategies to relieve physiological stress and anxiety levels. The patient is currently still symptomatic, and exhibits signs of chronic CSCR. If additional treatment strategy were to be introduced, “safety enhanced” and low-fluence PDT would be a very logical choice. This treatment is rather safe, results in minimal side effects, and has been shown in literature to reduce serous detachments and improve visual acuity in even chronic cases of CSCR without PED.[liii] Upon further investigation of efficacy in use of CSCR, use of intravitreal injection of Bevacuzumab and/or oral use of mifepristone may be useful in the future if this patient fails with PDT treatment.

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