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Clinical Characteristics of Posterior Staphylomas in Myopic Eyes With Axial Length Shorter Than 26.5 Millimeters
proliferative vitreoretinopathy (PVR) detachment following scleral buckling procedure alone vs PPV alone would be of interest in regard to bevacizumab treatment effect, this cannot be completed with our study cohort. Vascular endothelial growth factor (VEGF) and plateletderived growth factor (PDGF) remain molecular targets of interest for the prevention of PVR.2–4 We noted several potential reasons for the lack of observed effect of intrasilicone oil bevacizumab injections in our study, including altered half-life of bevacizumab in silicone oil and inclusion of only patients with advanced stages of PVR (grade C). To the point of Drs Takkar and Azad, we agree that anti-VEGF agents may result in different outcomes in eyes without prior vitrectomy or without silicone oil, or if utilized in eyes with milder forms of PVR or with a different treatment schedule. As we stated in the manuscript, perhaps evaluating anti-VEGF agents in ‘‘high-risk primary RD patients who have earlier stages of PVR (grades A or B) or other risk factors for PVR development (eg, associated vitreous hemorrhage or uveitis, extensive retinal detachments, large retinal breaks, etc) may be a better strategy.’’ Such a study would be of considerable interest yet would require a considerably larger enrollment, given the low rate of PVR development following primary RD repair surgery. We also agree that epiretinal membrane (ERM) formation may be influenced by many factors following RD repair surgery, including the anatomy of the posterior hyaloid, and is an imperfect measure of PVR activity; as such, ERM formation was included only as a secondary outcome. Crosstalk between VEGF and PDGF remains a topic of great interest in regard to the treatment and prevention of PVR. Efforts to evaluate anti-VEGF and anti-PDGF agents as well as to identify novel molecular targets in patients with or at risk for PVR are certainly deserving and worthy of future study. JASON HSU M. ALI KHAN WEN-SHI SHIEH ALLEN CHIANG JOSEPH I. MAGUIRE CARL H. PARK SUNIR J. GARG ALLEN C. HO RICHARD S. KAISER
Philadelphia, Pennsylvania SEE THE ORIGINAL ARTICLE FOR ANY DISCLOSURES OF THE authors.
REFERENCES
1. Hsu J, Khan MA, Shieh WS, et al. Effect of serial intrasilicone oil bevacizumab injections in eyes with recurrent proliferative
VOL. 165
vitreoretinopathy retinal detachment. Am J Ophthalmol 2016; 161:65–70.e2. 2. Lei H, Rheaume MA, Kazlauskas A. Recent developments in our understanding of how platelet-derived growth factor (PDGF) and its receptors contribute to proliferative vitreoretinopathy. Exp Eye Res 2010;90(3):376–381. 3. Pennock S, Kazlauskas A. Vascular endothelial growth factor A competitively inhibits platelet-derived growth factor (PDGF)-dependent activation of PDGF receptor and subsequent signaling events and cellular responses. Mol Cell Biol 2012;32(10):1955–1966. 4. Pennock S, Haddock LJ, Mukai S, Kazlauskas A. Vascular endothelial growth factor acts primarily via platelet-derived growth factor receptor a to promote proliferative vitreoretinopathy. Am J Pathol 2014;184(11):3052–3068.
Clinical Characteristics of Posterior Staphylomas in Myopic Eyes With Axial Length Shorter Than 26.5 Millimeters EDITOR: WE READ WITH INTEREST THE ARTICLE ‘‘CLINICAL CHARAC-
teristics of Posterior Staphylomas in Myopic Eyes With Axial Length Shorter than 26.5 Millimeters’’ by Wang and associates.1 In their study, the authors discuss clinical and imaging features of 16 eyes with posterior staphyloma, which do not fit the criteria for pathologic myopia. The study is indeed interesting and provides newer insights into pathogenesis of posterior staphyloma in general. The authors propose their findings to be a part of ‘‘atypical form of pathologic myopia, which share a similar pathogenesis derived from decreased choroidal thickness.’’1 However, it may be difficult to relate posterior staphyloma as the cause or the effect of decreased choroidal thickness, as even the mean axial length of these patients was around 25 mm, only marginally above the normative distribution.2 This minor difference can be explained even by shallow posterior staphylomas themselves rather than a generalized elongation of the eyeball. The posterior pole changes like ‘‘chorioretinal atrophy, Fuchs spots, and macular retinoschisis’’1 noted by the authors can also be due to the focally elongated eyeball in the region of the staphyloma. Previous studies have noted ‘‘posterior staphyloma as the cause of the development of myopic maculopathy and not the reverse.’’3 Hence these cases may be an independent entity in themselves, an idea also pondered by the authors, because the major mechanical support preventing ectasia is sclera, and perhaps its weakening with concurrent aging might be the cause of the disease. Previous literature, too, hypothesizes changes in scleral collagen to be associated with the pathogenetic factors, including inheritance in myopia development.4 Therefore, genetic evaluation of such patients might reveal susceptibility of these individuals to
CORRESPONDENCE
199
scleral thinning and exaggerated loss of scleral support owing to aging. A retrospective or a cross-sectional design might lead to difficulty in deciding between the cause–effect relationship of posterior staphyloma. However, if the authors have noted presence of peripheral retinal degenerations or severe peripheral diffuse choroidal thinning away from the staphylomatous area, it would strengthen their conclusions of the staphyloma being an atypical presentation of pathologic myopia. It would really be valuable if an optical coherence tomography–based analysis of the choroid at the junction of the staphyloma with ‘‘normal’’ eyeball could be done to support such a theory. The authors have presented a unique group of cases of posterior staphyloma and we hope our observations add value to their discussion. SHORYA AZAD BRIJESH TAKKAR
New Delhi, India FUNDING/SUPPORT: NO FUNDING OR GRANT SUPPORT. Financial disclosures: The following authors have no financial disclosures: Shorya Azad and Brijesh Takkar. Both authors attest that they meet the current ICMJE criteria for authorship.
REFERENCES
1. Wang NK, Wu YM, Wang JP, et al. Clinical characteristics of posterior staphylomas in myopic eyes with axial length shorter than 26.5 millimeters. Am J Ophthalmol 2016;162(2):180–190. 2. Hashemi H, Khabazkhoob M, Miraftab M, et al. The distribution of axial length, anterior chamber depth, lens thickness, and vitreous chamber depth in an adult population of Shahroud, Iran. BMC Ophthalmol 2012;12:50. 3. Silva R. Myopic maculopathy: a review. Ophthalmologica 2012; 228(4):197–213. 4. Yin Y, Xiaohong L, Naihong Y, Suping C, Xuyang L. Myopia: a collagen disease? Med Hypotheses 2009;73(4):485–487.
REPLY
ror.3 Drs Azad and Takkar cited the statement ‘‘posterior staphyloma as the cause of the development of myopic maculopathy and not the reverse’’ from a review article by Silva,4 which cited a study by Hayashi and associates.5 In fact, the latter study found that posterior staphyloma was observed more frequently in eyes that showed progression than in those without it. In that study, a posterior staphyloma was identified in 65.8% of eyes with myopic maculopathy; therefore, not all the eyes with myopic maculopathy had a posterior staphyloma.5 Next, Drs Azad and Takkar stated that posterior pole changes such as ‘‘chorioretinal atrophy, Fuchs spots, and macular retinoschisis’’ can also be caused by a focally elongated eyeball in the region of the staphyloma. In our study, patients presented with a low degree of myopia and some patients did not have it before their 40s. Lateral protrusion and angulation could be detected in 3-dimensional magnetic resonance imaging (3D-MRI) of some eyes among our cases, which have not been reported in eyes with a high degree of myopia. Patients in our study usually presented for decreased vision resulting from maculopathy, and peripheral eyeball changes—which do not cause visual disturbances—can only be identified by 3D-MRI. We assumed that some genes might be involved in changes in scleral susceptibility during aging, which result in similar macular pathology at older ages as seen in pathologic myopia. However, these genes are not necessarily the same as those involved in the development of myopia because there is no obvious axial elongation, and the eyes show different clinical features. In this study, we showed decreased choroidal thickness and reflectivity in the ellipsoid zone using spectral-domain optical coherence tomography (SDOCT) scans through the areas and junctions of staphylomas (Figures 1–3).1 The SDOCT technique can show decreased choroidal thickness in very myopic eyes; however, decreased reflectivity in the ellipsoid zone is not common in such eyes without a staphyloma. Although our study was the first to demonstrate this unique group of cases, it could not arrive at a firm conclusion on the pathophysiology involved, because it was a retrospective cross-sectional study. NAN-KAI WANG
WE THANK DRS AZAD AND TAKKAR FOR THEIR INTEREST IN
LAURA LIU
our article.1 We believe that posterior staphyloma in eyes with axial length shorter than 26.5 mm can be considered either as an ‘‘atypical form of pathologic myopia’’ or as ‘‘another disease entity’’ resulting from age-related scleral changes. We examined a large series of patients with extreme myopia and found that posterior pole changes usually developed in eyes with decreased choroidal thickness. We have shown previously that choroidal thickness is a better indicator of the severity of myopic maculopathy than axial length or refractive error.2 Further study showed that choroidal thickness has the strongest association with lacquer crack formation vs axial length and refractive er-
Taoyuan, Taiwan
200
JUNG-PAN WANG
Taipei, Taiwan SEE THE ORIGINAL ARTICLE FOR ANY DISCLOSURES OF THE authors.
REFERENCES
1. Wang NK, Wu YM, Wang JP, et al. Clinical characteristics of posterior staphylomas in myopic eyes with axial length shorter than 26.5 millimeters. Am J Ophthalmol 2016;162:180–190.
AMERICAN JOURNAL OF OPHTHALMOLOGY
MAY 2016
Philadelphia, Pennsylvania SEE THE ORIGINAL ARTICLE FOR ANY DISCLOSURES OF THE authors.
REFERENCES
1. Hsu J, Khan MA, Shieh WS, et al. Effect of serial intrasilicone oil bevacizumab injections in eyes with recurrent proliferative
VOL. 165
vitreoretinopathy retinal detachment. Am J Ophthalmol 2016; 161:65–70.e2. 2. Lei H, Rheaume MA, Kazlauskas A. Recent developments in our understanding of how platelet-derived growth factor (PDGF) and its receptors contribute to proliferative vitreoretinopathy. Exp Eye Res 2010;90(3):376–381. 3. Pennock S, Kazlauskas A. Vascular endothelial growth factor A competitively inhibits platelet-derived growth factor (PDGF)-dependent activation of PDGF receptor and subsequent signaling events and cellular responses. Mol Cell Biol 2012;32(10):1955–1966. 4. Pennock S, Haddock LJ, Mukai S, Kazlauskas A. Vascular endothelial growth factor acts primarily via platelet-derived growth factor receptor a to promote proliferative vitreoretinopathy. Am J Pathol 2014;184(11):3052–3068.
Clinical Characteristics of Posterior Staphylomas in Myopic Eyes With Axial Length Shorter Than 26.5 Millimeters EDITOR: WE READ WITH INTEREST THE ARTICLE ‘‘CLINICAL CHARAC-
teristics of Posterior Staphylomas in Myopic Eyes With Axial Length Shorter than 26.5 Millimeters’’ by Wang and associates.1 In their study, the authors discuss clinical and imaging features of 16 eyes with posterior staphyloma, which do not fit the criteria for pathologic myopia. The study is indeed interesting and provides newer insights into pathogenesis of posterior staphyloma in general. The authors propose their findings to be a part of ‘‘atypical form of pathologic myopia, which share a similar pathogenesis derived from decreased choroidal thickness.’’1 However, it may be difficult to relate posterior staphyloma as the cause or the effect of decreased choroidal thickness, as even the mean axial length of these patients was around 25 mm, only marginally above the normative distribution.2 This minor difference can be explained even by shallow posterior staphylomas themselves rather than a generalized elongation of the eyeball. The posterior pole changes like ‘‘chorioretinal atrophy, Fuchs spots, and macular retinoschisis’’1 noted by the authors can also be due to the focally elongated eyeball in the region of the staphyloma. Previous studies have noted ‘‘posterior staphyloma as the cause of the development of myopic maculopathy and not the reverse.’’3 Hence these cases may be an independent entity in themselves, an idea also pondered by the authors, because the major mechanical support preventing ectasia is sclera, and perhaps its weakening with concurrent aging might be the cause of the disease. Previous literature, too, hypothesizes changes in scleral collagen to be associated with the pathogenetic factors, including inheritance in myopia development.4 Therefore, genetic evaluation of such patients might reveal susceptibility of these individuals to
CORRESPONDENCE
199
scleral thinning and exaggerated loss of scleral support owing to aging. A retrospective or a cross-sectional design might lead to difficulty in deciding between the cause–effect relationship of posterior staphyloma. However, if the authors have noted presence of peripheral retinal degenerations or severe peripheral diffuse choroidal thinning away from the staphylomatous area, it would strengthen their conclusions of the staphyloma being an atypical presentation of pathologic myopia. It would really be valuable if an optical coherence tomography–based analysis of the choroid at the junction of the staphyloma with ‘‘normal’’ eyeball could be done to support such a theory. The authors have presented a unique group of cases of posterior staphyloma and we hope our observations add value to their discussion. SHORYA AZAD BRIJESH TAKKAR
New Delhi, India FUNDING/SUPPORT: NO FUNDING OR GRANT SUPPORT. Financial disclosures: The following authors have no financial disclosures: Shorya Azad and Brijesh Takkar. Both authors attest that they meet the current ICMJE criteria for authorship.
REFERENCES
1. Wang NK, Wu YM, Wang JP, et al. Clinical characteristics of posterior staphylomas in myopic eyes with axial length shorter than 26.5 millimeters. Am J Ophthalmol 2016;162(2):180–190. 2. Hashemi H, Khabazkhoob M, Miraftab M, et al. The distribution of axial length, anterior chamber depth, lens thickness, and vitreous chamber depth in an adult population of Shahroud, Iran. BMC Ophthalmol 2012;12:50. 3. Silva R. Myopic maculopathy: a review. Ophthalmologica 2012; 228(4):197–213. 4. Yin Y, Xiaohong L, Naihong Y, Suping C, Xuyang L. Myopia: a collagen disease? Med Hypotheses 2009;73(4):485–487.
REPLY
ror.3 Drs Azad and Takkar cited the statement ‘‘posterior staphyloma as the cause of the development of myopic maculopathy and not the reverse’’ from a review article by Silva,4 which cited a study by Hayashi and associates.5 In fact, the latter study found that posterior staphyloma was observed more frequently in eyes that showed progression than in those without it. In that study, a posterior staphyloma was identified in 65.8% of eyes with myopic maculopathy; therefore, not all the eyes with myopic maculopathy had a posterior staphyloma.5 Next, Drs Azad and Takkar stated that posterior pole changes such as ‘‘chorioretinal atrophy, Fuchs spots, and macular retinoschisis’’ can also be caused by a focally elongated eyeball in the region of the staphyloma. In our study, patients presented with a low degree of myopia and some patients did not have it before their 40s. Lateral protrusion and angulation could be detected in 3-dimensional magnetic resonance imaging (3D-MRI) of some eyes among our cases, which have not been reported in eyes with a high degree of myopia. Patients in our study usually presented for decreased vision resulting from maculopathy, and peripheral eyeball changes—which do not cause visual disturbances—can only be identified by 3D-MRI. We assumed that some genes might be involved in changes in scleral susceptibility during aging, which result in similar macular pathology at older ages as seen in pathologic myopia. However, these genes are not necessarily the same as those involved in the development of myopia because there is no obvious axial elongation, and the eyes show different clinical features. In this study, we showed decreased choroidal thickness and reflectivity in the ellipsoid zone using spectral-domain optical coherence tomography (SDOCT) scans through the areas and junctions of staphylomas (Figures 1–3).1 The SDOCT technique can show decreased choroidal thickness in very myopic eyes; however, decreased reflectivity in the ellipsoid zone is not common in such eyes without a staphyloma. Although our study was the first to demonstrate this unique group of cases, it could not arrive at a firm conclusion on the pathophysiology involved, because it was a retrospective cross-sectional study. NAN-KAI WANG
WE THANK DRS AZAD AND TAKKAR FOR THEIR INTEREST IN
LAURA LIU
our article.1 We believe that posterior staphyloma in eyes with axial length shorter than 26.5 mm can be considered either as an ‘‘atypical form of pathologic myopia’’ or as ‘‘another disease entity’’ resulting from age-related scleral changes. We examined a large series of patients with extreme myopia and found that posterior pole changes usually developed in eyes with decreased choroidal thickness. We have shown previously that choroidal thickness is a better indicator of the severity of myopic maculopathy than axial length or refractive error.2 Further study showed that choroidal thickness has the strongest association with lacquer crack formation vs axial length and refractive er-
Taoyuan, Taiwan
200
JUNG-PAN WANG
Taipei, Taiwan SEE THE ORIGINAL ARTICLE FOR ANY DISCLOSURES OF THE authors.
REFERENCES
1. Wang NK, Wu YM, Wang JP, et al. Clinical characteristics of posterior staphylomas in myopic eyes with axial length shorter than 26.5 millimeters. Am J Ophthalmol 2016;162:180–190.
AMERICAN JOURNAL OF OPHTHALMOLOGY
MAY 2016