DOCSLIB.ORG

Postoperative Intraocular Pressure After Cataract Surgery: Influence of Surgical Technique and Antiglaucoma Medication

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Postoperative Intraocular Pressure After Cataract Surgery: Influence of Surgical Technique and Antiglaucoma Medication Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication Doctoral thesis at the Medical University of Vienna for obtaining the academic degree Doctor of Medicine (Dr. med. univ.) Submitted by Ali Asadi Supervisor Univ. Prof. Dr. med. Georg Rainer Department of Ophthalmology, Medical University of Vienna Vienna, 05.2011 Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication Danksagung Ich bin meinem Betreuer Herrn Univ. Prof. Dr. Georg Rainer zu großem Dank verpflichtet. Er hat mich stetig betreut, unterstützt, professionell angeleitet und mir einen breiten Einblick in die Behandlung dieses Themas und generell in das wissenschaftliche Arbeiten gewährt. 2 Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication Zusammenfassung: Die Standardoperationstechnik in der Kataraktchirurgie ist derzeit die Phakoemulsifikation mit Implantation einer faltbaren Intraokularlinse unter Einsatz von viskochirurgischen Substanzen. Die häufigste Spätkomplikation nach der Kataraktoperation ist der Nachstar, eine Trübung der hinteren Linsenkapsel. Daher werden chirurgische Methoden untersucht, die den Nachstar verhindern können. Es konnte gezeigt werden, dass die Operationstechnik mit Präparation einer kreisrunden Öffnung in der hinteren Linsenkapsel (hintere Kapsulorhexis) den Nachstar wirksam verhindern kann. Diese Operationstechnik könnte jedoch zu einem höheren postoperativen Augeninnendruckanstieg im Vergleich zur Standardoperationstechnik führen. Der postoperative Augeninnendruckanstieg ist die häufigste Frühkomplikation nach der Kataraktoperation und kann zu einem Hornhautödem, zu Schmerzen und zu einer Schädigung des Sehnerven führen, insbesondere bei Glaukompatienten, die bereits einen vorgeschädigten Sehnerven haben. Eine Vermeidung des postoperativen Augeninnendruck- anstieges ist insofern von großer Bedeutung, da die Patienten zunehmend ambulant operiert werden und schon kurz nach der Operation entlassen werden. Deshalb haben wir 2 prospektive, randomisierte Studien durchgeführt, die erste, um den postoperativen Augeninnendruckanstieg nach Kataraktoperation mit hinterer Kapsulorhexis mit jenem nach Standardkataraktoperation zu vergleichen und die zweite, um die Wirkung der Kombination von Azetazolamid und Timolol mit jener der fixen Dorzolamid-Timolol Kombination auf den postoperativen Augeninnendruckanstieg zu vergleichen. In unserer ersten Studie war der Augeninnendruckanstieg 6 Stunden nach Kataraktoperation mit hinterer Kapsulorhexis signifikant höher als nach Standardkataraktoperation (11.1 + 8.7 mm Hg vs. 4.9 ± 5.7 mm Hg). Darüber hinaus zeigten sich signifikant mehr Augeninnen- druckspitzen von 10 mm Hg oder höher nach Kataraktoperation mit hinterer Kapsulorhexis als nach Standardkataraktoperation (13 Augen vs. 6 Augen). 3 Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication In unserer zweiten Studie konnte dieser hohe Augeninnendruckanstieg 6 Stunden nach der Operation sowohl mit der Kombination von Azetazolamid und Timolol als auch mit der fixen Dorzolamid-Timolol Kombination vollständig verhindert werden (-0,9 + 4,8 mm Hg vs. -1,1 + 4,1 mm Hg). Mit unserer ersten Studie konnten wir zeigen, dass die Kataraktoperation mit hinterer Kapsulorhexis zu einem signifikant höher postoperativen Augeninnendruckanstieg und zu signifikant häufigeren Augeninnendruckspitzen führt als die Standardkataraktoperation. Mit unserer zweiten Studie konnten wir jedoch zeigen, dass dieser hohe postoperative Augeninnendruckanstieg sowohl mit der Kombination von Azetazolamid und Timolol als auch mit der fixen Dorzolamid-Timolol Kombination vollständig verhindert werden kann. 4 Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication ABSTRACT: Currently, the standard surgical technique in cataract surgery is phacoemulsification cataract surgery, implantation of a foldable intraocular lens (IOL) and the use of an ophthalmic viscosurgical device (OVD). However, posterior capsular opacification (PCO) is the most frequent long-term complication after cataract surgery. Therefore, surgical methods to prevent after cataract are under investigation. One surgical method is the creation of a primary posterior continuous curvilinear capsulorhexis (PPCCC) during cataract surgery. This method has been shown to be effective in preventing PCO. However, this surgical method might cause a higher postoperative intraocular pressure (IOP) increase than standard cataract surgery. An increase in postoperative IOP is the most frequent short term complication after cataract surgery. This increase may lead to corneal epithelial edema and pain in the early postoperative period, and additionally, this increase may cause damage, especially in glauco- ma patients who already have a compromised optic disc. This complication is a matter of great importance, especially in those patients who get treated at an out-patient clinic and are discharged soon after surgery. Therefore, we performed 2 prospective, randomized studies, first to evaluate postoperative intraocular pressure (IOP) after cataract surgery with PPCCC compared to standard cataract surgery and secondly to evaluate the effect of the combination of acetazolamide and timolol compared to that of the fixed timolol-dorzolamide combination on postoperative IOP after cataract surgery with PPCCC. In our first study mean IOP increase at 6 hours postoperatively was significantly higher after cataract surgery with PPCCC than after standard cataract surgery (11.1 + 8.7 mm Hg vs. 4.9 + 5.7 mm Hg). Furthermore, significant more IOP spikes of 10 mm Hg or higher were found after cataract surgery with PPCCC than after standard cataract surgery (13 eyes vs. 6 eyes). 5 Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication In our second study mean IOP increase at 6 hours postoperatively could be completely prevented with the combination of acetazolamide and timolol as well as with the fixed dorzolamid-timolol combination (mean IOP decrease: -0.9 + 4.8 mm Hg vs. -1.1 + 4.1 mm Hg). Summarizing, we could show that cataract surgery with PPCCC causes a significant higher IOP increase and significant more IOP spikes than standard cataract surgery. However, the combination of a acetazolamide and timolol as well as the fixed dorzolamid-timolol combina- tion is effective in preventing this high IOP increase after cataract surgery with PPCCC. 6 Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication Table of Contents INTRUDCTION…………………………………………….. 12 1. Cataract…………………………………………………... 12 1.1. Epidemiology.……………………………………………………………... 13 1.2. Etiology and Risk Factors.……………………………………………….. 14 1.3. Classification of Cataract.………………………………………………... 16 1.3.1. Morphological Classification.………………………………………. 16 1.3.2. Maturity Classification........................................................................ 16 1.3.3. Classifying by Age of Manifestation.………………………………... 16 1.4. Age-Related Cataract.....………………………………………………….. 17 1.5. Congenital Cataract..…………………………………………………….. 17 1.6. Metabolic Cataract..………………………………………………………. 18 1.6.1. Diabetic Cataract..…………………………………………………... 18 1.6.2. Galactosemic Cataract and Galactose Intake ...…..…………………. 18 1.6.3. Other Types of Metabolic Cataract.......………….……………………19 1.7. Traumatic Cataract..……………………………….……………………… 20 1.8. Toxic Cataract...……………………………………………………………. 20 1.9. Cataracta Complicata...……………………………………………………. 21 7 Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication Table of Contents 1.10. Symptoms of Cataract………………………………………………….. 21 1.10.1. Nuclear Cataract…………………………………………………... 21 1.10.2. Cortical Cataract………………………………………………….. 22 1.10.3. Subcapsular Cataract……………………………………………... 22 2. Cataract Surgery……………………….………………… 23 2.1. History of Cataract Surgery………………………..……………………. 23 2.2. Intraocular Lenses (IOLs)…………………………..……………………. 26 2.3. Ophthalmic Viscosurgical Devices (OVDs)………..……………………. 27 2.3.1. Sodium Hyaluronate……………………………..………………….. 27 2.3.2. Methylcellulose…………………………………..………………….. 28 2.3.3. Chondroitin Sulfate………………………………..……………….... 29 2.4. Anesthesia for Cataract Surgery………………………..……………….. 29 2.4.1. Retrobulbar Anesthesia……………………………..……………….. 29 2.4.2. Peribulbar Anesthesia………………………………..……………… 30 2.4.3. Topical Anesthesia……………………………………..…………….. 30 2.4.4. Sub-Tenon´s Block………………………………………..………….. 31 2.5. Intracapsular Cataract Extraction (ICCE).…………………………….. 31 2.6. Extracapsular Cataract Extraction (ECCE).…………………………… 32 2.6.1 Manual Extracapsular Cataract Extraction (ECCE).………...……..... 32 2.6.2 Phacoemulsification Cataract Surgery….……………………………... 33 8 Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication Table of Contents 2.7. Primary Posterior Continuous Curvilinear capsulorhexis (PPCCC)..... 36 3. Complications of Cataract Surgery……………....…….. 37 3.1. Intraoperative Complications.…………………………………….……… 37 3.1.1. Complications of Incision…………………………….……..………. 37 3.1.1.1. Incision Burn………………...……………….………..……. 37 3.1.1.2. Iris Prolapse…………………….……………………..…... 38 3.1.2. Floppy Iris…………………………………………....………….….. 38 3.1.3. Vitreous Pressure…………………………………….……………...
Load more

Recommended publications
  • Genes in Eyecare Geneseyedoc 3 W.M
    Genes in Eyecare geneseyedoc 3 W.M. Lyle and T.D. Williams 15 Mar 04 This information has been gathered from several sources; however, the principal source is V. A. McKusick’s Mendelian Inheritance in Man on CD-ROM. Baltimore, Johns Hopkins University Press, 1998. Other sources include McKusick’s, Mendelian Inheritance in Man. Catalogs of Human Genes and Genetic Disorders. Baltimore. Johns Hopkins University Press 1998 (12th edition). http://www.ncbi.nlm.nih.gov/Omim See also S.P.Daiger, L.S. Sullivan, and B.J.F. Rossiter Ret Net http://www.sph.uth.tmc.edu/Retnet disease.htm/. Also E.I. Traboulsi’s, Genetic Diseases of the Eye, New York, Oxford University Press, 1998. And Genetics in Primary Eyecare and Clinical Medicine by M.R. Seashore and R.S.Wappner, Appleton and Lange 1996. M. Ridley’s book Genome published in 2000 by Perennial provides additional information. Ridley estimates that we have 60,000 to 80,000 genes. See also R.M. Henig’s book The Monk in the Garden: The Lost and Found Genius of Gregor Mendel, published by Houghton Mifflin in 2001 which tells about the Father of Genetics. The 3rd edition of F. H. Roy’s book Ocular Syndromes and Systemic Diseases published by Lippincott Williams & Wilkins in 2002 facilitates differential diagnosis. Additional information is provided in D. Pavan-Langston’s Manual of Ocular Diagnosis and Therapy (5th edition) published by Lippincott Williams & Wilkins in 2002. M.A. Foote wrote Basic Human Genetics for Medical Writers in the AMWA Journal 2002;17:7-17. A compilation such as this might suggest that one gene = one disease.
    [Show full text]
  • Upregulations of Clcn3 and P-Gp Provoked by Lens Osmotic Expansion in Rat Galactosemic Cataract
    Hindawi Journal of Diabetes Research Volume 2017, Article ID 3472735, 8 pages https://doi.org/10.1155/2017/3472735 Research Article Upregulations of Clcn3 and P-Gp Provoked by Lens Osmotic Expansion in Rat Galactosemic Cataract 1 2 1 Lixia Ji, Lixia Cheng, and Zhihong Yang 1Department of Pharmacology, School of Pharmacy, Qingdao University, Qingdao, China 2Department of Endocrinology, People’s Hospital of Weifang, Weifang, China Correspondence should be addressed to Lixia Ji; [email protected] Received 21 September 2017; Accepted 1 November 2017; Published 21 November 2017 Academic Editor: Hiroshi Okamoto Copyright © 2017 Lixia Ji et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. Lens osmotic expansion, provoked by overactivated aldose reductase (AR), is the most essential event of sugar cataract. Chloride channel 3 (Clcn3) is a volume-sensitive channel, mainly participating in the regulation of cell fundamental volume, and P-glycoprotein (P-gp) acts as its modulator. We aim to study whether P-gp and Clcn3 are involved in lens osmotic expansion of galactosemic cataract. Methods and Results. In vitro, lens epithelial cells (LECs) were primarily cultured in gradient galactose medium (10–60 mM), more and more vacuoles appeared in LEC cytoplasm, and mRNA and protein levels of AR, P-gp, and Clcn3 were synchronously upregulated along with the increase of galactose concentration. In vivo, we focused on the early stage of rat galactosemic cataract, amount of vacuoles arose from equatorial area and scattered to the whole anterior capsule of lenses from the 3rd day to the 9th day, and mRNA and protein levels of P-gp and Clcn3 reached the peak around the 9th or 12th day.
    [Show full text]
  • Sudheendran-Dissertation
    © Copyright by Narendran Sudheendran 2013 All Rights Reserved STUDYING MOUSE EMBRYONIC DEVELOPMENT WITH OCT A Dissertation Presented to the Faculty of the Department of Biomedical Engineering University of Houston In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy in Biomedical Engineering by Narendran Sudheendran December 2013 STUDYING MOUSE EMBRYONIC DEVELOPMENT WITH OCT ___________________________ Narendran Sudheendran Approved: ________________________________ Chair of the Committee Kirill V. Larin, Associate Professor, Department of Biomedical Engineering Committee Members: ________________________________ Irina V. Larina, Assistant Professor, Department of Molecular Physiology and Biophysics, Baylor College of Medicine ________________________________ Rajesh C. Miranda, Associate Professor, Department of Neuroscience and Experimental Therapeutics, TAMHSC College of Medicine _______________________________ Howard Gifford, Associate Professor, Department of Biomedical Engineering _______________________________ Yingchun Zhang, Assistant Professor, Department of Biomedical Engineering ____________________________ _______________________________ Suresh K. Khator, Associate Dean, Metin Akay, Professor and Chairman, Cullen College of Engineering Department of Biomedical Engineering ACKNOWLEDGEMENTS I am extremely thankful to my advisor, Dr. Kirill Larin, for his guidance, support and encouragement throughout this work. I am extremely grateful to Dr. Irina Larina for her time and effort to help me during the entire course of my project. I would especially like to thank Saba, Maleeha, Dr. Shameena Bake and Chen for helping me with the experiments. I thank Esteban, Shang and Manmohan for reviewing my dissertation. I am thankful to Mohamad, Kiran, Venu, Stepan, Jiasong, Peter and the rest of the BOL team for their support and encouragement. I would like to thank Dr. Rajesh C. Miranda and Dr. Howard Gifford and Dr. Yingchun Zhang for their time to serve on my defense committee.
    [Show full text]
  • Dismetabolic Cataracts
    ndrom Sy es tic & e G n e e n G e f T o Journal of Genetic Syndromes Cavallini et al., J Genet Syndr Gene Ther 2013, 4:7 h l e a r n a r p u DOI: 10.4172/2157-7412.1000165 y o J & Gene Therapy ISSN: 2157-7412 Case Report Open Access Dismetabolic Cataracts: Clinicopathologic Overview and Surgical Management with B-MICS Technique Cavallini GM1, Forlini M1, Masini C1, Campi L1, Chiesi C1, Rejdak R2 and Forlini C3* 1Institute of Ophthalmology, University of Modena, Modena, Italy 2Department of Ophthalmology, Medical University of Lublin, Lublin, Poland 3Department of Ophthalmology, “Santa Maria Delle Croci” Hospital, Ravenna, Italy Abstract Background: Dismetabolic cataract is a loss of lens transparency due to an insult to the nuclear or lenticular fibers, caused by a metabolic disorder. The lens opacification may occur early or later in life, and may be isolated or associated to particular syndromes. We describe some of these metabolic conditions associated with cataract formation, and in particular we report our experience with a patient affected by lathosterolosis that presented bilateral cataracts. Methods: Our patient was a 7-years-old little girl diagnosed with lathosterolosis at age 2 years, through gas cromatography/mass spectrometry method for plasma sterol profile that revealed a peak corresponding to cholest- 7-en-3β-ol (lathosterol). Results: The lens samples obtained during surgical removal with B-MICS technique were sent to the Department of Pathology and routinely processed and stained with haematoxylin-eosin and PAS; then, they were examined under a light microscope. Histological examination revealed lens fragments with the presence of fibers disposed in a honeycomb way, samples characterized by the presence of homogeneous eosinophilic lens fibers, and other fragments characterized by bulgy elements referable to cortical fibers with degenerative characteristics.
    [Show full text]
  • Textbook of Ophthalmology, 5Th Edition
    Textbook of Ophthalmology Textbook of Ophthalmology 5th Edition HV Nema Former Professor and Head Department of Ophthalmology Institute of Medical Sciences Banaras Hindu University Varanasi India Nitin Nema MS Dip NB Assistant Professor Department of Ophthalmology Sri Aurobindo Institute of Medical Sciences Indore India ® JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD. New Delhi • Ahmedabad • Bengaluru • Chennai Hyderabad • Kochi • Kolkata • Lucknow • Mumbai • Nagpur Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd B-3 EMCA House, 23/23B Ansari Road, Daryaganj, New Delhi 110 002 I ndia Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672 Rel: +91-11-32558559 Fax: +91-11-23276490 +91-11-23245683 e-mail: [email protected], Visit our website: www.jaypeebrothers.com Branches 2/B, Akruti Society, Jodhpur Gam Road Satellite Ahmedabad 380 015, Phones: +91-79-26926233, Rel: +91-79-32988717 Fax: +91-79-26927094, e-mail: [email protected] 202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East Bengaluru 560 001, Phones: +91-80-22285971, +91-80-22382956, 91-80-22372664 Rel: +91-80-32714073, Fax: +91-80-22281761 e-mail: [email protected] 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road Chennai 600 008, Phones: +91-44-28193265, +91-44-28194897 Rel: +91-44-32972089, Fax: +91-44-28193231, e-mail: [email protected] 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road Hyderabad 500 095, Phones: +91-40-66610020, +91-40-24758498 Rel:+91-40-32940929 Fax:+91-40-24758499, e-mail: [email protected] No. 41/3098, B & B1, Kuruvi Building, St.
    [Show full text]
  • In Vitro Anticataract Activity of Tamarindus Indica Linn. Againest Glucose-Induced Cataractogenisis
    Results IN VITRO ANTICATARACT ACTIVITY OF TAMARINDUS INDICA LINN. AGAINEST GLUCOSE-INDUCED CATARACTOGENISIS Dissertation submitted to The Tamil Nadu Dr. M. G. R. Medical University, Chennai in partial fulfillment of the award of degree of MASTER OF PHARMACY (PHARMACOLOGY) Submitted by SRIKANTH MERUGU Under the guidance of Mrs. M. UMA MAHESWARI, M. Pharm., (Ph.D.,) Assistant Professor, Department of Pharmacology MARCH – 2009 COLLEGE OF PHARMACY SRI RAMAKRISHNA INSTITUTE OF PARAMEDICAL SCIENCES COIMBATORE – 641 044. 1 Results IN VITRO ANTICATARACT ACTIVITY OF TAMARINDUS INDICA LINN. AGAINEST GLUCOSE-INDUCED CATARACTOGENISIS Dissertation submitted to The Tamil Nadu Dr. M. G. R. Medical University, Chennai in partial fulfillment of the award of degree of MASTER OF PHARMACY (PHARMACOLOGY) MARCH – 2009 COLLEGE OF PHARMACY SRI RAMAKRISHNA INSTITUTE OF PARAMEDICAL SCIENCES COIMBATORE – 641 044. 2 Results CERTIFICATE This is to certify that the dissertation entitled “IN VITRO ANTICATARACT ACTIVITY OF TAMARINDUS INDICA L. AGAINEST GLUCOSE-INDUCED CATARACTOGENISIS” being submitted to The Tamil Nadu Dr. M.G.R. Medical University, Chennai in partial fulfillment of the Master of Pharmacy programme in Pharmacology, carried out by Mr. SRIKANTH MERUGU in the Department of Pharmacology, College of Pharmacy, SRIPMS, Coimbatore, under my direct guidance and supervision to my fullest satisfaction. Mrs. M. UMA MAHESWARI, M.Pharm., (Ph.D.,) Assistant Professor, Dept. In-charge Department of Pharmacology, College of Pharmacy, SRIPMS, Place: Coimbatore Coimbatore –44. Date: 3 Results CERTIFICATE This is to certify that the dissertation entitled “IN VITRO ANTICATARACT ACTIVITY OF TAMARINDUS INDICA L. AGAINEST GLUCOSE-INDUCED CATARACTOGENISIS.” was carried out by Mr. SRIKANTH MERUGU, in the Department of Pharmacology, College of Pharmacy, Sri Ramakrishna Institute of Paramedical Sciences, Coimbatore, which is affiliated to The Tamil Nadu Dr.
    [Show full text]
  • Old Theories and New Ideas on Ocular Function
    Old Theories and New Ideas on Ocular Function Can the Choroid Affect ination in cadavers, to demonstrate that associated with its hyperproliferative Primate Eye Size? only the global layer of each rectus ex- property. ■ traocular muscle inserts on and rotates Earlier studies with chicks have shown the eye. The orbital layer instead inserts that choroid thickness is actively regu- on that muscle’s connective tissue pul- lated in response to retinal defocus and ley, translating it along the muscle axis. Is Glaucoma Only a may be involved in the regulation of eye This finding implies that pulleys, which Disease of the Eye? growth. In two articles in this issue, act as functional origins of the extraoc- Glaucoma is a disease of the optic nerve Troilo et al. (p. 1249) and Hung et al. (p. ular muscles, are under powerful active that also results in the degeneration of 1259) independently show that the pri- control. ■ mate choroid also undergoes changes ganglion cells within the retina. While in thickness associated with visual ex- glaucomatous changes within the retina perience and experimentally induced Is ‘Visual Acuity’ the Best and optic nerve are well-described, little changes in eye size and refraction. Measure of Visual is known about the degeneration that There is some evidence that these occurs postsynaptically within the LGN, changes, although much smaller than Function? a primary site of visual integration. This those seen in chick, might also partially Is visual acuity the most appropriate vi- study by Weber et al. (p. 1370) shows compensate for imposed retinal de- sual function to measure in determining that glaucoma has a significant effect on focus.
    [Show full text]
  • Review Article Does Phacoemulsification Speed the Progression of Diabetic Retinopathy? a Meta-Analysis
    Int J Clin Exp Med 2016;9(6):8874-8882 www.ijcem.com /ISSN:1940-5901/IJCEM0019867 Review Article Does phacoemulsification speed the progression of diabetic retinopathy? A meta-analysis Shengxia Wang1,2, Qian Xu2, Yunhong Du2, Xinyi Wu1 1Department of Ophthalmology, Qilu Hospital of Shandong University, 107 Wenhua Xi Road, Jinan 250012, Shandong, People’s Republic of China; 2Department of Ophthalmology, The Central Hospital of Tai’an, 29 Longtan Road, Taishan, Tai’an 271000, Shandong, People’s Republic of China Received November 16, 2015; Accepted April 14, 2016; Epub June 15, 2016; Published June 30, 2016 Abstract: The objective of the present study is to evaluate the influence of phacoemulsification on postoperative progression of diabetic retinopathy and incidence of diabetic macular edema in patients with diabetes and cataract. To perform a meta-analysis for this study, the computerized databases including Medline, Embase and Cochrane library were searched to identify eligible studies, in which patients with diabetes and cataract received phacoemul- sification in one eye and the non-operated contralateral eye was considered as the control group. The progression rate of diabetic retinopathy and incidence of diabetic macular edema in two study groups were extracted from the enrolled articles. Statistical analyses were performed using CMA-2 software, where dichotomous variables were ex- pressed as odds ratio (OR) and 95% confidence intervals. As a result, a total of 7 articles were eventually included in this meta-analysis. Both the progression rate of diabetic retinopathy and incidence of diabetic macular edema in the operated eye after phacoemulsification (OR=1.53, 95% CI: 1.04-2.26, P=0.03) was higher than the non-operated contralateral control (OR=1.86, 95% CI: 1.03-3.37, P=0.04).
    [Show full text]
  • Possibility of Clinical Application of Vitamin E to Cataract Prevention
    Serial Review J. Clin. Biochem. Nutr., 35, 35–45, 2004 Vitamin E Guest Editor: Etsuo Niki Possibility of Clinical Application of Vitamin E to Cataract Prevention Yoshiji Ohta* Department of Chemistry, School of Medicine, Fujita Health University, Toyoake 470–1192, Japan Received 30 October, 2003; Accepted 10 November, 2003 Summary It has been implicated that oxidative stress is involved in the development of aged-related and diabetic cataracts in humans and also in cataract development in a variety of in vivo experimental cataract models. Therefore, this article will review the possibility of the clinical application of vitamin E to cataract prevention, based on data concerning the level of vitamin E in normal and cataractous lenses of humans and experimental animals, the relationship between dietary vitamin E intake and the risk of cataracts, the effect of vita- min E supplementation on cataract development in humans, and the effect of oral or parenteral vitamin E treatment or topical vitamin E instillation on cataract development in a variety of in vivo experimental cataract models. These data reported so far may allow us to think of a possibility that vitamin E is clinically applied to cataract development. Key Words: cataract (humans and experimental animals), oxidative stress, vitamin E, cataract prevention Cataract treatment in humans is now conducted Introduction by surgical operation, i.e., cataract surgery, and then intraocular lenses are inserted into the cataract sur- Cataract is the major cause of blindness world- gery-operated eyes to recover visual acuity. However, wide. About 40% of the estimated 42 million blind an ideal treatment of cataracts is carried out without people worldwide are blind from cataract [1].
    [Show full text]
  • Radical Scavenger and Active Oxygen Eliminating Agent
    (19) TZZ__T (11) EP 1 897 549 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: A61K 31/198 (2006.01) 24.08.2011 Bulletin 2011/34 (86) International application number: (21) Application number: 06757009.3 PCT/JP2006/311269 (22) Date of filing: 06.06.2006 (87) International publication number: WO 2006/132205 (14.12.2006 Gazette 2006/50) (54) RADICAL SCAVENGER AND ACTIVE OXYGEN ELIMINATING AGENT RADIKALFÄNGER UND AKTIVEN-SAUERSTOFF-ELIMINIERENDES MITTEL PIÈGE À RADICAUX ET AGENT D’ÉLIMINATION DE L’OXYGÈNE ACTIF (84) Designated Contracting States: • SPENCER J P E ET AL: "Conjugates of AT BE BG CH CY CZ DE DK EE ES FI FR GB GR catecholamines with cysteine and GSH in HU IE IS IT LI LT LU LV MC NL PL PT RO SE SI Parkinson’s disease: Possible mechanisms of SK TR formation involving reactive oxygen species" JOURNAL OF NEUROCHEMISTRY 199811 US, (30) Priority: 07.06.2005 JP 2005166842 vol. 71, no. 5, November 1998 (1998-11), pages 2112-2122, XP002538225 ISSN: 0022-3042 (43) Date of publication of application: • AKIYAMA N ET AL: "Involvement of H2O2 and 12.03.2008 Bulletin 2008/11 O2<-> in the cytotoxicity of N-[beta]-alanyl-5-S- glutathionyl-3,4-dihyd roxyphenylalanine (5-S- (73) Proprietor: InBiotex Inc. GAD), a novel insect-derived anti-tumor Bunkyo-ku, Tokyo 1130033 (JP) compound" CANCER SCIENCE 20030401 JP, vol. 94,no.4,1April2003(2003-04-01),pages400-404, (72) Inventors: XP002538226 ISSN: 1347-9032 • NATORI, Shunji • JAE YOON LEEM ET AL: "Purification and Ibaraki characterization of N-[beta]-alanyl-5-S- 3001622 (JP) glutathionyl 3,4- dihydroxyphenylalanine, a • OOTSU, Kunimiki novel antibacterial substance of Sarcophaga 1950071 (JP) peregrina (flesh fly)" JOURNAL OF BIOLOGICAL • OKUYAMA, Hajime CHEMISTRY 1996 US, vol.
    [Show full text]
  • TYPES of Cfltfirflct TYPES of CATARACT
    TYPES OF CflTfiRflCT TYPES OF CATARACT 1. Senile Cataract 2. Diabetic Cataract 3. Galactosemic Cataract 4. Xylose Cataract 5. Toxic Cataract 6. Radiation Cataract 7. Nutritional Cataract 8. Traumatic Cataract 9. Cold Cataract 10. Genetic Cataract. 11. Development Cataract Senile Cataract The great majority of human cataracts are senile cataracts. The human lens normally undergoes changes with age : it slowly increases in size as new lens fibers develop throughout life; older lens fibers in the depths of the lens become dehydrated, compacted and "sclerosed", a yellow brown pigment accumulates. The increase in the optical density of the nucleus tends to increase the refractive power of the lens so that less hyperoptic spectacle correction may be needed in old age. The yellow brown pigment may become so dense as to constitute nuclear sclerosis and later brunescent cataract. Cortical cataract, however, is the development of vacuoles and water clefts in the lens cortex that tend to increase in extent and in the advanced state give the lens a pear like appearance. Approximately 60% of human beings have some alterations in lens transparency after 60 years of age. Progression of lens changes differ among individuals and lens opacities can cause visual deficits in a shorter or longer period of time. 22 Diabetic Cataracts Increased levels of glucose in the aqueous and lens are found in patients with diabetes mellitus. In general, the glucose concentration in the aqueous parallels the concentrations in the plasma. From the aqueous, glucose diffuses rapidly into the lens. The lens metabolizes glucose through four main pathways. 1. Anaerobic glycolysis 2.
    [Show full text]
  • Nonenzymatic Glycosylation, Sulfhydryl Oxidation, and Aggregation of Lens Proteins in Experimental Sugar Cataracts*
    NONENZYMATIC GLYCOSYLATION, SULFHYDRYL OXIDATION, AND AGGREGATION OF LENS PROTEINS IN EXPERIMENTAL SUGAR CATARACTS* BY V. M. MONNIER, V. J. STEVENS,~ AND A. CERAMI From the Laboratory of Medical Biochemistry, The Rockefeller University, New York 10021 In studies of human cataracts, Dische and Zil (I) first noted that the proteins of the human cataractous lens were associated with a marked increase in sulflaydryl oxidation to form disulfide bonds. The correlation of disulfide bonds and cataract formation has been combined subsequently by a number of other workers studying animal and human cataracts (2-6). These disulfide bonds can act as intermolecular crosslinks and have been proposed to be partly responsible for the polymerization of the lens proteins in the formation of high molecular weight aggregates. Protein aggregates > 150 × 106 dahons have been detected in aged normal lenses as well as in human cataracts (7, 8) and recently a disulfide-linked high molecular weight protein associated with the fiber cell membrane has been isolated from human cataracts and characterized (9). One of the physical characteristics of protein aggregates of this size is their ability to scatter light. Based on theoretical consideration, Benedek (10) has hypothesized that the formation of protein aggregates of tool wt > 50 × 106 dahons could scatter light sufficiently to account for cataract formation in the lens. This is substantiated by the work of Spector and colleagues (11) who found that light backscattering of the lens parallels the increase in high molecular weight protein in the aging lens. In contrast to studies of human senile cataractogenesis, little is known of the physical state of the lens proteins of the sugar cataracts formed in diabetes and galactosemia.
    [Show full text]