1. The Sample Scientific Poster - Using Microsoft Office Power Point Template T. Farra 1, M. Jacisin 2 1 Brigham and Womens Hospital, 2 New England College of Optometry, Boston, MA Results - con’t ReferencesReferences Conclusions Conclusions DiscussionDiscussion SampleSample PurposePurpose MethodsMethods ResultsResults IntroductionIntroduction Results - con’t Retinal ganglion cells (RGC) die by apoptosis in both high tension 1 and low tension 2 glaucoma. Ischemia and neuronal compression may deprive the RGCs of essential trophic factors necessary for their survival 3. When apoptosis occurs, the RGC cytoplasmic volume decreases and the cell membrane ruptures, while the nucleus condenses 4. RGC membrane lysis is mediated by phospholipases and oxidative enzymes. Leaky RGC may release other toxic substances such as excitatory amino acids, which further damages neighboring cells 3. Glutamate, an excitatory amino acid, has been found in elevated concentrations in the vitreous body of glaucomatous eyes 5. Steroids are known to be nonspecific blockers of cell membrane lipases 6 which may inhibit apoptosis in this setting. Furthermore, certain glucocorticoids are thought to intercalate into the cell membrane and decrease neuronal and vascular membrane fluidity by inhibiting oxygen free radical-induced lipid peroxidation 7. Studies have shown that RGC survival in vitro is dependent on the addition of steroids to the culture 8. Finally there is data suggesting an immune deviation in patients with NTG 2 where serum antibodies directed to retinal elements have been found. Exogenous steroids could prevent NTG by nonspecifically blunting this aberrant response. To study the association of steroid use and prevalence of NTG in a clinic-based population. The sample consisted of 154 patients: 72 NTG (mean age 69.0  10; 44-85; 25M, 47F) 82 controls (mean age 64.8  11; 44-86; 31M, 51F) Definition of NTG Cases Patients with ONH or NFL appearance consistent with glaucoma. Maximum IOP less then 21mmHg. At least two reliable visual field examinations with reproducible defects consistent with the nerve fiber layer pathology. No evidence of exfoliation or trauma on slit lamp examination and no evidence of an occludable angle or angle recession on gonioscopy. Patients with pre-existing iridotomies were excluded form the study. Definition of Controls No evidence of glaucomatous optic neuropathy: 3 cup/disc ratios < 0.6 OU 3 cup/disc asymmetry < 0.2 3 unremarkable red-free ophthalmoscopic examinations. No family history of glaucoma. Maximum IOP less then 21mmHg. Controls did not undergo visual field testing. The sample was selected from patients aged 40 and older who presented to the Division of Ophthalmology at Brigham and Women’s Hospital from July 1998 to January 1999. Patients were required to have electronic medical records dating back to at least 1996. All patients were examined by a single observer. Each patient was questioned about their past ocular, medical and surgical history, as well as current use of medications. An extensive history of past and present steroid use was obtained which included name of the steroid, dose, frequency of administration, duration, and time period of use. Subsequently, all patients underwent a complete eye examination. Any patient suspected of having glaucomatous optic neuropathy based on the appearance of the optic nerve and nerve fiber layer underwent visual field testing with either the Humphrey or Goldmann perimeters. Patients with unreliable visual fields or no reproducible visual field loss were excluded. Ophthalmic information regarding ocular conditions, surgeries and maximum IOP was corroborated from the patient’s eye records. Non-ophthalmic information was confirmed by a review of the patient’s electronic medical record. These records contained information regarding the patient’s medical conditions, as well as the date of first and filled prescription for all medications. Steroid exposure was defined as a dichotomous variable in three ways relative to July 1, 1997 (1 year prior to the onset of the study). 3 Steroid use for a period of 1 month at any given time in the past. 3 Steroid use prior to July 1, 1997 for at least 1 month. 3 Steroid use after July 1, 1997 for at least 1 month. The Odds ratio for steroid use was calculated using logistic regression analysis for each definition of steroid use. The results were adjusted for age, race, gender, hypertension, diabetes and diseases that were indications for steroid use. The demographic and clinical characteristics of NTG and Control groups is described in Table 1. Table 1: Demographic and Clinical Characteristics of NTG and Control groups.  indicates p>0.05 The NTG group used significantly less steroids then the control group for all definitions of steroid exposure. Fig. 1 and 2 show the proportion of people taking steroids in the NTG and Control group for total steroid use and steroid use excluding anterior segment surgery respectively. * indicates a statistically significant difference between the NTG and Control groups using  2. Fig 1: Steroid Use in NTG and Control groups * * * Fig 2: Steroid Use excluding ocular surgery in NTG and Control groups * ** Logistic regression predicted the Odd’s ratio to be 0.517 Model A (p=0.07), 0.408 Model B (p=0.02), and 0.81 Model C (p>0.05) for the development of NTG. The Odd’s ratios are plotted in Fig. 3 for the 3 Models. Models A, B, and C are described in Table 2. Cataract extraction was significantly higher in the Control group compared to the NTG group. No difference was found in any systemic conditions between cases and controls. Fig. 4 and 5 show the breakdown of conditions requiring steroids in the NTG and Control group for systemic and ant. seg. ocular surgery respectively. Table 2 shows the conditions/procedures included in the Allergic, Inflammatory and Total Ant. Seg. surgery categories. * indicates a statistically significant difference between the NTG and control groups using  2. Fig 5: Breakdown of Ant. Seg. surgeries requiring steroids for NTG and Control groups. * Fig 4: Breakdown of systemic conditions requiring steroids for NTG and Control groups. Table 2: Conditions/Procedures Included in the Allergic, Inflammatory and Ant Seg surg Categories. Fig 6: Type of Steroids Used for systemic conditions in NTG and Control groups. NTG Control Fig. 6 shows the proportion of different types of steroids used for systemic conditions by patients in the NTG and Control groups respectively. Table 3 indicates the specific steroids included in the Inhaler, Topical and Oral categories. Table 3: Specific steroids included in the Inhaler, Topical and Oral categories. The speculation that steroids may prevent apoptosis is plausible based on their ability to inhibit cell membrane lysis mediated by phospholipases and oxidative enzymes. In our study, univariate analysis suggests that steroid use was associated with a reduced odds of having NTG. Problems regarding confounding by indication make the univariate result of this study controversial. Larger scale prevalence studies confirming our univariate finding are necessary. In these studies, very careful estimate of steroid exposure would be indicated. Univariate logistic regression analysis demonstrates a reduced odds of NTG in steroid users. Controlling for age strengthens this association. Controlling by indication for steroid use produces a result that is not statistically significant. Larger numbers of cases and controls will be necessary to demonstrate the true relation between steroid use and NTG. 1Quigley HA, Nickells RW, Kerrigan LA, Pease ME, Thibault DJ, Zack DJ. Retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis. Invest Ophthalmol Vis Sci 1995;36:774- 86. 2Wax MB, Tezel G, Edward PD. Clinical and ocular histopathological findings in a patient with normal- pressure glaucoma. Arch Ophthalmol 1998; 116:993-1001. 3Chew SJ, Ritch R. Neuroprotection: the next breakthrough in glaucoma? Proceedings of the Third Annual Optic Nerve Rescue and Restoration Think Tank. J Glaucoma 1997; 6:263-6. 4Spaeth GL. Glaucoma, apoptosis, death, and life. Acta Ophthalmol Scand Suppl 1998; 227:9-15. 5Dreyer EB, Zurakowski D, Schumer RA, Podos SM, Lipton SA. Elevated glutamate levels in the vitreous body of humans and monkeys with glaucoma. Arch Ophthalmol 1996; 114:299-305. 6Lee HM, Weinstein JN, Meller ST, Hayashi N, Spratt KF, Gebhart GF. The role of steroids and their effects on phospholipase A2 in an animal model of radiculopathy. Spine 1998; 23(11):1191-6. 7Hall ED. Neuroprotective actions of glucocorticoid and nonglucocorticoid steroids in acute neuronal injury. Cell Mol Neurobiol 1993; 13:415-32. 8Lindsey JD, Weinreb RN. Survival and differentiation of purified retinal ganglion cells in a chemically defined microenvironment. Invest Ophthalmol Vis Sci 1994; 35:3640-8.45 Fig 6: Type of Steroids Used for systemic conditions in NTG and Control groups.