The Experts below are selected from a list of 186 Experts worldwide ranked by ideXlab platform
Darren G Gregory - One of the best experts on this subject based on the ideXlab platform.
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treatment of acute stevens johnson syndrome and toxic epidermal necrolysis using amniotic membrane a review of 10 consecutive cases
Ophthalmology, 2011Co-Authors: Darren G GregoryAbstract:Purpose To describe the clinical course, treatments, and outcomes of 10 consecutive patients treated with amniotic membrane transplantation (AMT) applied to the Eyelid margins, palpebral conjunctiva, and ocular surface during the acute phase of Stevens–Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN). Design Prospective case series of 10 consecutive patients treated by 1 surgeon. Participants Ten consecutive patients with severe ocular surface and Eyelid Inflammation treated with AMT during the acute phase of SJS or TEN. Intervention Cryopreserved amniotic membrane was applied to the Eyelids and ocular surface of each patient during the first 10 days of illness. Repeat AMT was performed every 10–14 days as long as severe ocular surface Inflammation and epithelial sloughing persisted. Main Outcome Measures Visual acuity, dry eye severity, and scarring of the ocular surface and Eyelids were assessed after a follow-up of ≥6 months. Results All patients had best-corrected visual acuity of ≥20/30, with 9 of the 10 seeing 20/20. Dry eye severity was moderate or less in all patients. Overall ocular surface and Eyelid scarring was mild to moderate in all patients. Conclusions In acute SJS and TEN, AMT is an effective treatment for severe ocular surface and Eyelid Inflammation, greatly decreasing the risk of significant ocular and visual sequelae. Financial Disclosure(s) The author has no proprietary or commercial interest in any materials discussed in this article.
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Treatment of Acute Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis Using Amniotic Membrane: A Review of 10 Consecutive Cases
Ophthalmology, 2011Co-Authors: Darren G GregoryAbstract:Purpose To describe the clinical course, treatments, and outcomes of 10 consecutive patients treated with amniotic membrane transplantation (AMT) applied to the Eyelid margins, palpebral conjunctiva, and ocular surface during the acute phase of Stevens–Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN). Design Prospective case series of 10 consecutive patients treated by 1 surgeon. Participants Ten consecutive patients with severe ocular surface and Eyelid Inflammation treated with AMT during the acute phase of SJS or TEN. Intervention Cryopreserved amniotic membrane was applied to the Eyelids and ocular surface of each patient during the first 10 days of illness. Repeat AMT was performed every 10–14 days as long as severe ocular surface Inflammation and epithelial sloughing persisted. Main Outcome Measures Visual acuity, dry eye severity, and scarring of the ocular surface and Eyelids were assessed after a follow-up of ≥6 months. Results All patients had best-corrected visual acuity of ≥20/30, with 9 of the 10 seeing 20/20. Dry eye severity was moderate or less in all patients. Overall ocular surface and Eyelid scarring was mild to moderate in all patients. Conclusions In acute SJS and TEN, AMT is an effective treatment for severe ocular surface and Eyelid Inflammation, greatly decreasing the risk of significant ocular and visual sequelae. Financial Disclosure(s) The author has no proprietary or commercial interest in any materials discussed in this article.
Christophe Baudouin - One of the best experts on this subject based on the ideXlab platform.
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emerging strategies for the diagnosis and treatment of meibomian gland dysfunction proceedings of the ocean group meeting
Ocular Surface, 2017Co-Authors: Gerd Geerling, Christophe Baudouin, Pasquale Aragona, Yonca A Akova, Kostas G Boboridis, Maurizio Rolando, J M Benitezdelcastillo, Jesus Merayolloves, M Labetoulle, Martin SteinhoffAbstract:Meibomian gland dysfunction (MGD) is a common and chronic disorder that has a significant adverse impact on patients' quality of life. It is a leading cause of evaporative dry eye disease (DED), as meibomian glands play an important role in providing lipids to the tear film, which helps to retard the evaporation of tears from the ocular surface. MGD is also often present in conjunction with primary aqueous-deficient DED. Obstructive MGD, the most commonly observed type of MGD, is the main focus of this article. MGD is probably caused by a combination of separate conditions: primary obstructive hyperkeratinization of the meibomian gland, abnormal meibomian gland secretion, Eyelid Inflammation, corneal Inflammation and damage, microbiological changes, and DED. Furthermore, skin diseases such as rosacea may play a part in its pathology. Accurate diagnosis is challenging, as it is difficult to differentiate between ocular surface diseases, but is crucial when choosing treatment options. Ocular imaging has advanced in recent years, providing ophthalmologists with a better understanding of ocular diseases. This review presents a literature update on the 2011 MGD workshop and an optimized approach to accurate diagnosis of MGD using currently available methods and tests. It also outlines the emerging technologies of interferometry, non-contact meibography, keratography and in vivo confocal laser microscopy, which offer exciting possibilities for the future. Selected treatment options for MGD are also discussed.
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Revisiting the vicious circle of dry eye disease: a focus on the pathophysiology of meibomian gland dysfunction
British Journal of Ophthalmology, 2016Co-Authors: Christophe Baudouin, Elisabeth Messmer, Pasquale Aragona, Gerd Geerling, Yonca A Akova, José Benítez-del-castillo, Kostas G Boboridis, Jesús Merayo-lloves, Maurizio Rolando, Marc LabetoulleAbstract:Meibomian gland dysfunction (MGD) is the most frequent cause of dry eye disease (DED). Eyelid Inflammation, microbial growth, associated skin disorders as well as potentially severe corneal complications culminate to make MGD a complex multifactorial disorder. It is probable that MGD is a heterogeneous condition arising from any combination of the following five separate pathophysiological mechanisms: Eyelid Inflammation, conjunctival Inflammation, corneal damage, microbiological changes and DED resulting from tear film instability. The pathogenesis of both MGD and DED can be described in terms of a 'vicious circle': the underlying pathophysiological mechanisms of DED and MGD interact, resulting in a double vicious circle. The MGD vicious circle is self-stimulated by microbiological changes, which results in increased melting temperature of meibum and subsequent meibomian gland blockage, reinforcing the vicious circle of MGD. Meibomian gland blockage, dropout and Inflammation directly link the two vicious circles. MGD-associated tear film instability provides an entry point into the vicious circle of DED and leads to hyperosmolarity and Inflammation, which are both a cause and consequence of DED. Here we propose a new pathophysiological scheme for MGD in order to better identify the pathological mechanisms involved and to allow more efficient targeting of therapeutics. Through better understanding of this scheme, MGD may gain true disease status rather than being viewed as a mere dysfunction.
Gerd Geerling - One of the best experts on this subject based on the ideXlab platform.
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emerging strategies for the diagnosis and treatment of meibomian gland dysfunction proceedings of the ocean group meeting
Ocular Surface, 2017Co-Authors: Gerd Geerling, Christophe Baudouin, Pasquale Aragona, Yonca A Akova, Kostas G Boboridis, Maurizio Rolando, J M Benitezdelcastillo, Jesus Merayolloves, M Labetoulle, Martin SteinhoffAbstract:Meibomian gland dysfunction (MGD) is a common and chronic disorder that has a significant adverse impact on patients' quality of life. It is a leading cause of evaporative dry eye disease (DED), as meibomian glands play an important role in providing lipids to the tear film, which helps to retard the evaporation of tears from the ocular surface. MGD is also often present in conjunction with primary aqueous-deficient DED. Obstructive MGD, the most commonly observed type of MGD, is the main focus of this article. MGD is probably caused by a combination of separate conditions: primary obstructive hyperkeratinization of the meibomian gland, abnormal meibomian gland secretion, Eyelid Inflammation, corneal Inflammation and damage, microbiological changes, and DED. Furthermore, skin diseases such as rosacea may play a part in its pathology. Accurate diagnosis is challenging, as it is difficult to differentiate between ocular surface diseases, but is crucial when choosing treatment options. Ocular imaging has advanced in recent years, providing ophthalmologists with a better understanding of ocular diseases. This review presents a literature update on the 2011 MGD workshop and an optimized approach to accurate diagnosis of MGD using currently available methods and tests. It also outlines the emerging technologies of interferometry, non-contact meibography, keratography and in vivo confocal laser microscopy, which offer exciting possibilities for the future. Selected treatment options for MGD are also discussed.
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Revisiting the vicious circle of dry eye disease: a focus on the pathophysiology of meibomian gland dysfunction
British Journal of Ophthalmology, 2016Co-Authors: Christophe Baudouin, Elisabeth Messmer, Pasquale Aragona, Gerd Geerling, Yonca A Akova, José Benítez-del-castillo, Kostas G Boboridis, Jesús Merayo-lloves, Maurizio Rolando, Marc LabetoulleAbstract:Meibomian gland dysfunction (MGD) is the most frequent cause of dry eye disease (DED). Eyelid Inflammation, microbial growth, associated skin disorders as well as potentially severe corneal complications culminate to make MGD a complex multifactorial disorder. It is probable that MGD is a heterogeneous condition arising from any combination of the following five separate pathophysiological mechanisms: Eyelid Inflammation, conjunctival Inflammation, corneal damage, microbiological changes and DED resulting from tear film instability. The pathogenesis of both MGD and DED can be described in terms of a 'vicious circle': the underlying pathophysiological mechanisms of DED and MGD interact, resulting in a double vicious circle. The MGD vicious circle is self-stimulated by microbiological changes, which results in increased melting temperature of meibum and subsequent meibomian gland blockage, reinforcing the vicious circle of MGD. Meibomian gland blockage, dropout and Inflammation directly link the two vicious circles. MGD-associated tear film instability provides an entry point into the vicious circle of DED and leads to hyperosmolarity and Inflammation, which are both a cause and consequence of DED. Here we propose a new pathophysiological scheme for MGD in order to better identify the pathological mechanisms involved and to allow more efficient targeting of therapeutics. Through better understanding of this scheme, MGD may gain true disease status rather than being viewed as a mere dysfunction.
Marc Labetoulle - One of the best experts on this subject based on the ideXlab platform.
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Revisiting the vicious circle of dry eye disease: a focus on the pathophysiology of meibomian gland dysfunction
British Journal of Ophthalmology, 2016Co-Authors: Christophe Baudouin, Elisabeth Messmer, Pasquale Aragona, Gerd Geerling, Yonca A Akova, José Benítez-del-castillo, Kostas G Boboridis, Jesús Merayo-lloves, Maurizio Rolando, Marc LabetoulleAbstract:Meibomian gland dysfunction (MGD) is the most frequent cause of dry eye disease (DED). Eyelid Inflammation, microbial growth, associated skin disorders as well as potentially severe corneal complications culminate to make MGD a complex multifactorial disorder. It is probable that MGD is a heterogeneous condition arising from any combination of the following five separate pathophysiological mechanisms: Eyelid Inflammation, conjunctival Inflammation, corneal damage, microbiological changes and DED resulting from tear film instability. The pathogenesis of both MGD and DED can be described in terms of a 'vicious circle': the underlying pathophysiological mechanisms of DED and MGD interact, resulting in a double vicious circle. The MGD vicious circle is self-stimulated by microbiological changes, which results in increased melting temperature of meibum and subsequent meibomian gland blockage, reinforcing the vicious circle of MGD. Meibomian gland blockage, dropout and Inflammation directly link the two vicious circles. MGD-associated tear film instability provides an entry point into the vicious circle of DED and leads to hyperosmolarity and Inflammation, which are both a cause and consequence of DED. Here we propose a new pathophysiological scheme for MGD in order to better identify the pathological mechanisms involved and to allow more efficient targeting of therapeutics. Through better understanding of this scheme, MGD may gain true disease status rather than being viewed as a mere dysfunction.
Colleen M. Cebulla - One of the best experts on this subject based on the ideXlab platform.
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Known and novel ocular toxicities of biologics, targeted agents, and traditional chemotherapeutics
Graefe's Archive for Clinical and Experimental Ophthalmology, 2019Co-Authors: Anne L. Kunkler, Elaine M. Binkley, Dimosthenis Mantopoulos, Andrew J. Hendershot, Matthew P. Ohr, Kari L. Kendra, Frederick H. Davidorf, Colleen M. CebullaAbstract:Purpose Increases in cancer with an aging population and the rapid development of new chemotherapeutics underscore the need for ophthalmologists to identify and manage potential ocular toxicities. This retrospective case series reports the ocular side effects of traditional and novel chemotherapeutic agents from a large center. Methods The medical records of 3537 adult patients 18 years and older who presented to an academic ophthalmology department on high-risk medications identified by ICD-9 search between January 2010 and February 2015 were reviewed. A cancer diagnosis, as well as a temporal association with chemotherapeutic use and ocular side effect, was deemed necessary for inclusion in the study. The main measures were ocular side effects in cancer patients taking chemotherapy, ocular imaging abnormalities, and the outcome of each side effect. Results Of the 161 oncology patients referred to the ophthalmology clinic for chemotherapeutic screening or ocular side effect, 31 (19.3%) were identified as having an ocular adverse reaction due to a novel or traditional chemotherapeutic medication. A novel flattening of the corneal curvature with hyperopic shift and corneal microcysts was identified in a patient taking the antibody–drug conjugate mirvetuximab soravtansine and was reversible with topical steroids. A bilateral medium-vessel choroidal vasculopathy with serous retinal detachment was seen with ipilimumab. The most frequent medication with ocular toxicity was interferon- α (2b) (IFN- α (2b)) (6/31, 19.4%); headache was typical in these patients (83.3%). Ibrutinib ocular toxicity was second most common (5/31, 16.1%), usually causing red or dry eye, while one patient developed branch retinal artery occlusion. Retinal abnormalities documented on OCT imaging occurred with IFN- α (2b), ipilimumab, binimetinib, and docetaxel, while rod-cone ERG abnormality was seen with cisplatin. Inflammatory conditions included anterior scleritis with zoledronic acid, focal Eyelid Inflammation with veliparib, bilateral chemosis with R-CHOP, iritis, and blepharospasm with IFN- α (2b). AION occurred with pemetrexed, and transient vision loss with hyperemic disc OS was seen with FOLFOX. Two patients (2/31, 6.5%) developed permanent vision loss. Six patients were lost to follow-up, and the clinical course was unknown (6/31, 19.4%). Conclusions and relevance Cases of permanent visual loss were observed; yet, in the majority of side effects, they improved with topical therapy and/or holding the medication. Further research is needed to elucidate the incidence and the pathophysiology of these side effects and maximize patient quality of life.
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Known and novel ocular toxicities of biologics, targeted agents, and traditional chemotherapeutics.
Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2019Co-Authors: Anne L. Kunkler, Elaine M. Binkley, Dimosthenis Mantopoulos, Andrew J. Hendershot, Matthew P. Ohr, Kari L. Kendra, Frederick H. Davidorf, Colleen M. CebullaAbstract:Increases in cancer with an aging population and the rapid development of new chemotherapeutics underscore the need for ophthalmologists to identify and manage potential ocular toxicities. This retrospective case series reports the ocular side effects of traditional and novel chemotherapeutic agents from a large center. The medical records of 3537 adult patients 18 years and older who presented to an academic ophthalmology department on high-risk medications identified by ICD-9 search between January 2010 and February 2015 were reviewed. A cancer diagnosis, as well as a temporal association with chemotherapeutic use and ocular side effect, was deemed necessary for inclusion in the study. The main measures were ocular side effects in cancer patients taking chemotherapy, ocular imaging abnormalities, and the outcome of each side effect. Of the 161 oncology patients referred to the ophthalmology clinic for chemotherapeutic screening or ocular side effect, 31 (19.3%) were identified as having an ocular adverse reaction due to a novel or traditional chemotherapeutic medication. A novel flattening of the corneal curvature with hyperopic shift and corneal microcysts was identified in a patient taking the antibody–drug conjugate mirvetuximab soravtansine and was reversible with topical steroids. A bilateral medium-vessel choroidal vasculopathy with serous retinal detachment was seen with ipilimumab. The most frequent medication with ocular toxicity was interferon-α(2b) (IFN-α(2b)) (6/31, 19.4%); headache was typical in these patients (83.3%). Ibrutinib ocular toxicity was second most common (5/31, 16.1%), usually causing red or dry eye, while one patient developed branch retinal artery occlusion. Retinal abnormalities documented on OCT imaging occurred with IFN-α(2b), ipilimumab, binimetinib, and docetaxel, while rod-cone ERG abnormality was seen with cisplatin. Inflammatory conditions included anterior scleritis with zoledronic acid, focal Eyelid Inflammation with veliparib, bilateral chemosis with R-CHOP, iritis, and blepharospasm with IFN-α(2b). AION occurred with pemetrexed, and transient vision loss with hyperemic disc OS was seen with FOLFOX. Two patients (2/31, 6.5%) developed permanent vision loss. Six patients were lost to follow-up, and the clinical course was unknown (6/31, 19.4%). Cases of permanent visual loss were observed; yet, in the majority of side effects, they improved with topical therapy and/or holding the medication. Further research is needed to elucidate the incidence and the pathophysiology of these side effects and maximize patient quality of life.
