June 2014 Brief Communications
tests, and proper treatment are important in cases of unusual ocular infection.
References 1. Forbes BA, Weissfeld AS. Bailey and Scott’s diagnostic microbiology. St. Louis: Mosby; 1998. p. 476‑85. 2. Chang YH, Pao SI, Chen YJ, Chen JT. A narrow silicone sponge to close a wider retinal tear: The open‑book technique of scleral buckling. Ophthalmic Surg Lasers Imaging 2011;42:263‑4. 3. Roldán‑Pallarés M, del CastilloSanz JL, Awad‑El Susi S, Refojo MF. Long‑term complications of silicone and hydrogel explants in retinal reattachment surgery. Arch Ophthalmol 1999;117:197‑201. 4. Kiernan, DF, Chin EK, Sclafani LA, Saidel MA. Multiple drug‑resistant Alcaligenesxylosoxidans keratitis in a sanitation worker. Eye Contact Lens 2009;35:212‑4. 5. Huang ZL, Chen YF, Chang SW, Lin KK, Hsiao CH. Recurrent Alcaligenesxylosoxidans keratitis. Cornea 2005;24:489‑90. 6. Lucatelli JF, Cantarelli VV, Picoli SU. Conjunctivitis due
Delleman (Oculocerebrocutaneous) Syndrome: Case report Tomás Ortiz‑Basso, Rodolfo Vigo, Sebastián Iacouzzi1, Jorge Prémoli Delleman syndrome is an unusual entity, characterized by ocular cysts or microphthalmia, focal dermal anomalies and cerebral malformations. In the following article, we carry out a review of the disease and we present the case of a patient with microphthalmos and palpebral coloboma. As we could not put orbital expanders at an early stage, we performed reconstructive surgery. Key words: Oculocerebrocutaneous syndrome, orbit, plastic surgery
The oculocerebrocutaneous syndrome is an unusual entity, given by a spontaneous mutation which affects the eye, brain and skin.
toachromobacterxylosoxidans: Case report. Arq Bras Oftalmol 2009;72:261‑3. 7. Pan TH, Heidemann DG, Dunn SP, Chow CY, Gossage D. Delayed onset and recurrent Alcaligenesxylosoxidans keratitis. Cornea 2000;19:243‑5. 8. Bosshard PP, Zbinden R, Abels S, Böddinghaus B, Altwegg M, Böttger EC. 16S rRNA gene sequencing versus the API 20 NE system and the VITEK 2 ID‑GNB card for identification of nonfermentingGram‑negative bacteria in the clinical laboratory. JClinMicrobiol 2006;44:1359‑66. 9. Weissgold DJ, Kirkpatrick B, Iverson M. Acute postoperative Alcaligenesxylosoxidansendophthalmitis. Retina 2003;23:578‑80. 10. S h i e S S , H u a n g C T , L e u H S . C h a r a c t e r i s t i c s o f Achromobacterxylosoxidans bacteremia in northern Taiwan. J MicrobiolImmunol Infect 2005;38:277‑82. Cite this article as: Hsu C, Chang Y, Chen J. Scleral buckle infection with Alcaligenes xylosoxidans. Indian J Ophthalmol 2014;62:739-41. Source of Support: Nil. Conflict of Interest: None declared.
It was described by Delleman in the year 1981 and since then, nearly 40 cases have been reported. In the following article we present a case, reviewing the main features of the disease.
Case Report A male newborn patient was evaluated for genetic syndrome. He presented microphthalmos in the right eye and coloboma in the lower lid [Fig. 1]. The left eye had no anomalies. He had a lesion in the scalp compatible with bilateral aplasia cutis, and, in the periocular region there were multiple mobile cutaneous appendages, as well as pits on the cheek and appendages on nostrils. In the lumbar region, he had a small lesion of aplasia cutis surrounded by hair growth. MRI showed an encephalic trunk of dysmorphic aspect, with slight hypoplasia of the central vermis [Fig. 2]. We performed an echocardiogram, which showed no
Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.136277 PMID: ***
Department of Ophthalmology, 1Division of Pediatric Plastic Surgery, Ophthalmology Service, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina Correspondence to: Dr. Tomás Ortiz-Basso, Bolivia 630, CP (L6300GDD), Santa Rosa, La Pampa, Argentina. E-mail: [email protected] Manuscript received: 24.06.13; Revision accepted: 15.10.13
741
Figure 1: Newborn with Delleman Syndrome
742
Indian Journal of Ophthalmology
structural cardiopathy and an abdominal renal ultrasound, with no anomalies. Genitalia, hands and feet were normal. He did not have convulsions. He was the second child of a non‑consanguineous couple. Both parents were 32, Argentinean, teachers, and healthy. The sister was 1 year and 9 months old, and she had unilateral microtia. There were no miscarriages, or any other data of importance in the genealogy. The pregnancy was controlled, with no complications and teratogenic exposure. Newborn in term (39 weeks), vaginal delivery with adequate weight for the gestational age (3200 g). Karyotype 46 normal XY. Given the poor palpebral support, we could not put orbital expanders. We waited for 4 months, when the hemoglobin had improved and he acquired the necessary conditions to undergo surgery, and we performed reconstructive surgery of the eyelid. We used a cutaneous appendage as a flap, to give shape to the lower lid [Figs. 3 and 4]. In this way, we created an adequate cavity to put orbital expanders [Fig. 5].
Vol. 62 No. 6
presence of an orbital cyst or microphthalmia, associated with palpebral colobomas, focal dermal malformations and cerebral anomalies.[1‑3] Some more severe forms present hydrocephaly, anophthalmos, palatine fissure or cleft palate. In the skin, you can find areas of focal aplasia or hypoplasia, even alopecia. The formation of cutaneous appendages in the periocular region is a characteristic.[4,5] Neurological anomalies can be manifested by convulsions and psychomotor development disorders. These include polymicrogyria, ventricular system malformations, cerebral or cerebellum cysts and agenesia of the corpus callosum. Malformations of the midline and mesencephalon are pathognomonic.[4‑6]
As Delleman described, the syndrome is characterized by the
There is no determined etiology yet, but there is a hypothesis that suggests a sporadic mutation in the fifth or sixth week of development. It states that it is associated with a somatic mosaicism, which compromises the development of the ectodermal structures.[7] Other authors suggested that there would be a relation with the chromosome X, given the higher prevalence of this syndrome in men. Also, based on the appearance of malformations in structures of the midline and mesencephalon, it could be due to an early anomaly in the
Figure 2: MRI showed an encephalic trunk of dysmorphic aspect
Figure 3: Eyelid reconstruction
Figure 4: Forming the flap
Figure 5: Postoperative
Discussion
June 2014 Brief Communications
development, when the organizing center is establishing the limits between the mesencephalon and the brain.[6] Delleman syndrome usually shares some characteristics with certain syndromes such as Goldenhar or Goltz. The first one, also known as oculo‑auriculo‑vertebral syndrome, is characterized by the presence of a dermoid cyst and auditory and vertebral anomalies. The second one is associated to microphthalmia, dermic hypoplasia, polysyndactyly and bad dentition.[5,8,9] These kind of syndromes can be differentiated by the pattern of cerebral malformations. The ones in the midline and mesencephalon are characteristic of Delleman syndrome.[6] Our case presented a coloboma of the lower lid, which hindered the early placement of orbital expanders. The importance of putting expanders in an early stage is known for the correct orbito‑facial growth. The normal size of an eye at birth is 70% of the adult, and by the time it is 3 months, it is 40%. However, the size of the face evolves quickly; by the time it is 3 months, which presents 40% of the adult size, by the age of 2 it is 70%, and at 5.5 years of age it is 90%. This development in an anophthalmic or microphthalmic cavity is torpid, which is why the early placement of expanders is important, as well as its timely replacement as the orbital cavity develops.[10,11]
Acknowledgment Patricia Adduci for English translation and manuscript preparation.
References 1. Delleman JW, Oorthuys JW. Orbital cyst in addition to congenital cerebral and focal dermal malformations: A new entity? Clin Genet 1981;19:191‑8. 2. Delleman JW, Oorthuys JW, Bleeker‑Wagemakers EM, ter Haar BG,
743
Ferguson JW. Orbital cyst in addition to congenital cerebral and focal dermal malformations: A new entity. Clin Genet 1984;25:470‑2. 3. Saatci AO, Arikan G, Saatci P, Saatci Y, Kavukcu S. Oculocerebrocutaneous syndrome. J Pediatr Ophthalmol Strabismus2008:45:181‑3. Arora V, Kim UR, Khazei HM. Delleman Oorthuys syndrome: ‘Oculocerebrocutaneous syndrome’. Indian J Ophthalmol 2009;57:387‑9. 4. Patil SJ, Phadke SR. Delleman syndrome. Indian Pediatr 2006;43:173‑4. 5. Moog U, Jones MC, Bird LM, Dobyns WB. Oculocerebrocutaneous syndrome: The brain malformation defines a core phenotype. J Med Genet 2005;42:913‑21. 6. Hoo JJ, Kapp‑Simon K, Rollnick B, Chao M. Oculocerebrocutaneous (Delleman) syndrome: A pleiotropic disorder affecting ectodermal tissues with unilateral predominance. Am J Med Genet 1991;40:290‑3. 7. Sujit Kumar GS, Haran RP, Rajshekhar V. Delleman syndrome with Goldenhar overlap. J Pediatr Neurosci 2009;4:53‑5. 8. Roszkowski M, Dabrowski D. Encephalo‑cranio‑cutaneous lipomatosis (ECCL) :Haberland syndrome. A case report with review of the literature. Neurol Neurochir Pol 1997;31:607‑13. 9. Chen D, Heher K. Management of the anophthalmic socket in pediatric patients. Curr Opin Ophthalmol 2004;15:449‑53. 10. Ragge NK, Subak‑Sharpe ID, Collin JR. A practical guide to the management of anophthalmia and microphthalmia. Eye (Lond) 2007;21:290‑300. 11. Farkas LG, Posnick JC, Hreczko TM, Pron GE. Growth patterns in the orbital region: A morphometric study. Cleft Palate Craniofac J 1992;29:315‑8. Cite this article as: Ortiz-Basso T, Vigo R, Iacouzzi S, Prémoli J. Delleman (Oculocerebrocutaneous) Syndrome: Case report. Indian J Ophthalmol 2014;62:741-3. Source of Support: Nil. Conflict of Interest: None declared.
Mucoepidermoid carcinoma ex pleomorphic adenoma of the lacrimal gland: A rare presentation
tumor for two years after complete excision of the tumor but computed tomography at the end of two and a half years showed a recurrent lesion in the region of the lacrimal gland. This makes long term follow up of patients with these rare lacrimal tumors imperative with a minimum period of at least five years.
Lily Daniel, Shalinee Rao1, Radhakrishnan Muthusamy, Deepika Yerramsetti
Key words: Carcinoma ex pleomorphic adenoma, lacrimal gland tumors, mucoepidermoid carcinoma
Carcinoma ex pleomorphic adenoma in lacrimal gland is a rare entity unlike its salivary gland counterpart. This rare tumor poses a diagnostic challenge to clinicians as pre‑operative diagnosis is difficult and diagnosis is only by careful pathological assessment. We report this uncommon lesion in a 62‑year‑old lady, wherein the malignant component was mucoepidermoid carcinoma. The elderly patient remained clinically and radiologically free of the Department of Ophthalmology, Orbit and Oculoplastic Surgeon, 1 Department of Pathology, Sri Ramachandra University Teaching Hospital, Chennai, Tamil Nadu, India Correspondence to: Dr. Lily Daniel, Asst Professor and Senior Consultant in Ophthalmology, Orbit and Oculoplastic Surgeon, Sri Ramachandra University Teaching Hospital, Chennai ‑ 600 116, Tamil Nadu, India. E‑mail: [email protected] Manuscript received: 22.06.13; Revision accepted: 21.02.14
Pleomorphic adenoma (PA) or benign mixed tumor, the most common epithelial neoplasm of lacrimal gland arises from its epithelial and myoepithelial components. Carcinoma ex pleomorphic adenoma (CEPA) also called carcinoma in PA or malignant mixed tumor is defined as a carcinoma arising from a primary (de novo) or recurrent benign PA.[1] Both benign and malignant components of the lesion are to be identified for a diagnosis of CEPA, the malignant components most Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.136281 PMID: ***
Copyright of Indian Journal of Ophthalmology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
tests, and proper treatment are important in cases of unusual ocular infection.
References 1. Forbes BA, Weissfeld AS. Bailey and Scott’s diagnostic microbiology. St. Louis: Mosby; 1998. p. 476‑85. 2. Chang YH, Pao SI, Chen YJ, Chen JT. A narrow silicone sponge to close a wider retinal tear: The open‑book technique of scleral buckling. Ophthalmic Surg Lasers Imaging 2011;42:263‑4. 3. Roldán‑Pallarés M, del CastilloSanz JL, Awad‑El Susi S, Refojo MF. Long‑term complications of silicone and hydrogel explants in retinal reattachment surgery. Arch Ophthalmol 1999;117:197‑201. 4. Kiernan, DF, Chin EK, Sclafani LA, Saidel MA. Multiple drug‑resistant Alcaligenesxylosoxidans keratitis in a sanitation worker. Eye Contact Lens 2009;35:212‑4. 5. Huang ZL, Chen YF, Chang SW, Lin KK, Hsiao CH. Recurrent Alcaligenesxylosoxidans keratitis. Cornea 2005;24:489‑90. 6. Lucatelli JF, Cantarelli VV, Picoli SU. Conjunctivitis due
Delleman (Oculocerebrocutaneous) Syndrome: Case report Tomás Ortiz‑Basso, Rodolfo Vigo, Sebastián Iacouzzi1, Jorge Prémoli Delleman syndrome is an unusual entity, characterized by ocular cysts or microphthalmia, focal dermal anomalies and cerebral malformations. In the following article, we carry out a review of the disease and we present the case of a patient with microphthalmos and palpebral coloboma. As we could not put orbital expanders at an early stage, we performed reconstructive surgery. Key words: Oculocerebrocutaneous syndrome, orbit, plastic surgery
The oculocerebrocutaneous syndrome is an unusual entity, given by a spontaneous mutation which affects the eye, brain and skin.
toachromobacterxylosoxidans: Case report. Arq Bras Oftalmol 2009;72:261‑3. 7. Pan TH, Heidemann DG, Dunn SP, Chow CY, Gossage D. Delayed onset and recurrent Alcaligenesxylosoxidans keratitis. Cornea 2000;19:243‑5. 8. Bosshard PP, Zbinden R, Abels S, Böddinghaus B, Altwegg M, Böttger EC. 16S rRNA gene sequencing versus the API 20 NE system and the VITEK 2 ID‑GNB card for identification of nonfermentingGram‑negative bacteria in the clinical laboratory. JClinMicrobiol 2006;44:1359‑66. 9. Weissgold DJ, Kirkpatrick B, Iverson M. Acute postoperative Alcaligenesxylosoxidansendophthalmitis. Retina 2003;23:578‑80. 10. S h i e S S , H u a n g C T , L e u H S . C h a r a c t e r i s t i c s o f Achromobacterxylosoxidans bacteremia in northern Taiwan. J MicrobiolImmunol Infect 2005;38:277‑82. Cite this article as: Hsu C, Chang Y, Chen J. Scleral buckle infection with Alcaligenes xylosoxidans. Indian J Ophthalmol 2014;62:739-41. Source of Support: Nil. Conflict of Interest: None declared.
It was described by Delleman in the year 1981 and since then, nearly 40 cases have been reported. In the following article we present a case, reviewing the main features of the disease.
Case Report A male newborn patient was evaluated for genetic syndrome. He presented microphthalmos in the right eye and coloboma in the lower lid [Fig. 1]. The left eye had no anomalies. He had a lesion in the scalp compatible with bilateral aplasia cutis, and, in the periocular region there were multiple mobile cutaneous appendages, as well as pits on the cheek and appendages on nostrils. In the lumbar region, he had a small lesion of aplasia cutis surrounded by hair growth. MRI showed an encephalic trunk of dysmorphic aspect, with slight hypoplasia of the central vermis [Fig. 2]. We performed an echocardiogram, which showed no
Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.136277 PMID: ***
Department of Ophthalmology, 1Division of Pediatric Plastic Surgery, Ophthalmology Service, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina Correspondence to: Dr. Tomás Ortiz-Basso, Bolivia 630, CP (L6300GDD), Santa Rosa, La Pampa, Argentina. E-mail: [email protected] Manuscript received: 24.06.13; Revision accepted: 15.10.13
741
Figure 1: Newborn with Delleman Syndrome
742
Indian Journal of Ophthalmology
structural cardiopathy and an abdominal renal ultrasound, with no anomalies. Genitalia, hands and feet were normal. He did not have convulsions. He was the second child of a non‑consanguineous couple. Both parents were 32, Argentinean, teachers, and healthy. The sister was 1 year and 9 months old, and she had unilateral microtia. There were no miscarriages, or any other data of importance in the genealogy. The pregnancy was controlled, with no complications and teratogenic exposure. Newborn in term (39 weeks), vaginal delivery with adequate weight for the gestational age (3200 g). Karyotype 46 normal XY. Given the poor palpebral support, we could not put orbital expanders. We waited for 4 months, when the hemoglobin had improved and he acquired the necessary conditions to undergo surgery, and we performed reconstructive surgery of the eyelid. We used a cutaneous appendage as a flap, to give shape to the lower lid [Figs. 3 and 4]. In this way, we created an adequate cavity to put orbital expanders [Fig. 5].
Vol. 62 No. 6
presence of an orbital cyst or microphthalmia, associated with palpebral colobomas, focal dermal malformations and cerebral anomalies.[1‑3] Some more severe forms present hydrocephaly, anophthalmos, palatine fissure or cleft palate. In the skin, you can find areas of focal aplasia or hypoplasia, even alopecia. The formation of cutaneous appendages in the periocular region is a characteristic.[4,5] Neurological anomalies can be manifested by convulsions and psychomotor development disorders. These include polymicrogyria, ventricular system malformations, cerebral or cerebellum cysts and agenesia of the corpus callosum. Malformations of the midline and mesencephalon are pathognomonic.[4‑6]
As Delleman described, the syndrome is characterized by the
There is no determined etiology yet, but there is a hypothesis that suggests a sporadic mutation in the fifth or sixth week of development. It states that it is associated with a somatic mosaicism, which compromises the development of the ectodermal structures.[7] Other authors suggested that there would be a relation with the chromosome X, given the higher prevalence of this syndrome in men. Also, based on the appearance of malformations in structures of the midline and mesencephalon, it could be due to an early anomaly in the
Figure 2: MRI showed an encephalic trunk of dysmorphic aspect
Figure 3: Eyelid reconstruction
Figure 4: Forming the flap
Figure 5: Postoperative
Discussion
June 2014 Brief Communications
development, when the organizing center is establishing the limits between the mesencephalon and the brain.[6] Delleman syndrome usually shares some characteristics with certain syndromes such as Goldenhar or Goltz. The first one, also known as oculo‑auriculo‑vertebral syndrome, is characterized by the presence of a dermoid cyst and auditory and vertebral anomalies. The second one is associated to microphthalmia, dermic hypoplasia, polysyndactyly and bad dentition.[5,8,9] These kind of syndromes can be differentiated by the pattern of cerebral malformations. The ones in the midline and mesencephalon are characteristic of Delleman syndrome.[6] Our case presented a coloboma of the lower lid, which hindered the early placement of orbital expanders. The importance of putting expanders in an early stage is known for the correct orbito‑facial growth. The normal size of an eye at birth is 70% of the adult, and by the time it is 3 months, it is 40%. However, the size of the face evolves quickly; by the time it is 3 months, which presents 40% of the adult size, by the age of 2 it is 70%, and at 5.5 years of age it is 90%. This development in an anophthalmic or microphthalmic cavity is torpid, which is why the early placement of expanders is important, as well as its timely replacement as the orbital cavity develops.[10,11]
Acknowledgment Patricia Adduci for English translation and manuscript preparation.
References 1. Delleman JW, Oorthuys JW. Orbital cyst in addition to congenital cerebral and focal dermal malformations: A new entity? Clin Genet 1981;19:191‑8. 2. Delleman JW, Oorthuys JW, Bleeker‑Wagemakers EM, ter Haar BG,
743
Ferguson JW. Orbital cyst in addition to congenital cerebral and focal dermal malformations: A new entity. Clin Genet 1984;25:470‑2. 3. Saatci AO, Arikan G, Saatci P, Saatci Y, Kavukcu S. Oculocerebrocutaneous syndrome. J Pediatr Ophthalmol Strabismus2008:45:181‑3. Arora V, Kim UR, Khazei HM. Delleman Oorthuys syndrome: ‘Oculocerebrocutaneous syndrome’. Indian J Ophthalmol 2009;57:387‑9. 4. Patil SJ, Phadke SR. Delleman syndrome. Indian Pediatr 2006;43:173‑4. 5. Moog U, Jones MC, Bird LM, Dobyns WB. Oculocerebrocutaneous syndrome: The brain malformation defines a core phenotype. J Med Genet 2005;42:913‑21. 6. Hoo JJ, Kapp‑Simon K, Rollnick B, Chao M. Oculocerebrocutaneous (Delleman) syndrome: A pleiotropic disorder affecting ectodermal tissues with unilateral predominance. Am J Med Genet 1991;40:290‑3. 7. Sujit Kumar GS, Haran RP, Rajshekhar V. Delleman syndrome with Goldenhar overlap. J Pediatr Neurosci 2009;4:53‑5. 8. Roszkowski M, Dabrowski D. Encephalo‑cranio‑cutaneous lipomatosis (ECCL) :Haberland syndrome. A case report with review of the literature. Neurol Neurochir Pol 1997;31:607‑13. 9. Chen D, Heher K. Management of the anophthalmic socket in pediatric patients. Curr Opin Ophthalmol 2004;15:449‑53. 10. Ragge NK, Subak‑Sharpe ID, Collin JR. A practical guide to the management of anophthalmia and microphthalmia. Eye (Lond) 2007;21:290‑300. 11. Farkas LG, Posnick JC, Hreczko TM, Pron GE. Growth patterns in the orbital region: A morphometric study. Cleft Palate Craniofac J 1992;29:315‑8. Cite this article as: Ortiz-Basso T, Vigo R, Iacouzzi S, Prémoli J. Delleman (Oculocerebrocutaneous) Syndrome: Case report. Indian J Ophthalmol 2014;62:741-3. Source of Support: Nil. Conflict of Interest: None declared.
Mucoepidermoid carcinoma ex pleomorphic adenoma of the lacrimal gland: A rare presentation
tumor for two years after complete excision of the tumor but computed tomography at the end of two and a half years showed a recurrent lesion in the region of the lacrimal gland. This makes long term follow up of patients with these rare lacrimal tumors imperative with a minimum period of at least five years.
Lily Daniel, Shalinee Rao1, Radhakrishnan Muthusamy, Deepika Yerramsetti
Key words: Carcinoma ex pleomorphic adenoma, lacrimal gland tumors, mucoepidermoid carcinoma
Carcinoma ex pleomorphic adenoma in lacrimal gland is a rare entity unlike its salivary gland counterpart. This rare tumor poses a diagnostic challenge to clinicians as pre‑operative diagnosis is difficult and diagnosis is only by careful pathological assessment. We report this uncommon lesion in a 62‑year‑old lady, wherein the malignant component was mucoepidermoid carcinoma. The elderly patient remained clinically and radiologically free of the Department of Ophthalmology, Orbit and Oculoplastic Surgeon, 1 Department of Pathology, Sri Ramachandra University Teaching Hospital, Chennai, Tamil Nadu, India Correspondence to: Dr. Lily Daniel, Asst Professor and Senior Consultant in Ophthalmology, Orbit and Oculoplastic Surgeon, Sri Ramachandra University Teaching Hospital, Chennai ‑ 600 116, Tamil Nadu, India. E‑mail: [email protected] Manuscript received: 22.06.13; Revision accepted: 21.02.14
Pleomorphic adenoma (PA) or benign mixed tumor, the most common epithelial neoplasm of lacrimal gland arises from its epithelial and myoepithelial components. Carcinoma ex pleomorphic adenoma (CEPA) also called carcinoma in PA or malignant mixed tumor is defined as a carcinoma arising from a primary (de novo) or recurrent benign PA.[1] Both benign and malignant components of the lesion are to be identified for a diagnosis of CEPA, the malignant components most Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.136281 PMID: ***
Copyright of Indian Journal of Ophthalmology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
