About all

Poag medical abbreviation. POAG: Understanding Primary Open-Angle Glaucoma – Causes, Symptoms, and Treatments

by alexxlab

What is Primary Open-Angle Glaucoma (POAG). How is POAG diagnosed and treated. What are the risk factors for developing POAG. Can POAG be prevented or slowed down. How does POAG affect vision and quality of life. What are the latest research developments in POAG treatment. Who is most at risk for POAG.

Содержание

What is Primary Open-Angle Glaucoma (POAG)?

Primary open-angle glaucoma (POAG) is a chronic, progressive eye condition characterized by increased intraocular pressure (IOP) that can lead to optic nerve damage and vision loss. It is the most common form of glaucoma, affecting millions of people worldwide.

POAG develops slowly over time, often without noticeable symptoms in its early stages. This makes regular eye exams crucial for early detection and treatment.

Key characteristics of POAG:

  • Open anterior chamber angle
  • Elevated intraocular pressure
  • Progressive optic nerve damage
  • Visual field defects
  • Asymptomatic in early stages

What Causes Primary Open-Angle Glaucoma?

The exact cause of POAG is not fully understood, but several factors contribute to its development:

Genetic factors:

Research has identified several genes associated with POAG. For example, a study by Monemi et al. (2005) discovered a novel adult-onset POAG gene on chromosome 5q22.1. Additionally, Park et al. (2007) found an interaction between two glaucoma genes, optineurin and myocilin, which may play a role in the disease’s pathogenesis.

Impaired aqueous humor drainage:

In POAG, the drainage system of the eye (trabecular meshwork) becomes less efficient over time, leading to increased intraocular pressure. This elevated pressure can damage the optic nerve fibers, resulting in vision loss.

Age-related changes:

The risk of developing POAG increases with age, particularly after 40. Age-related changes in the eye’s structure and function may contribute to the disease’s progression.

How is Primary Open-Angle Glaucoma Diagnosed?

Diagnosing POAG involves a comprehensive eye examination and several specialized tests:

  1. Tonometry: Measures intraocular pressure
  2. Ophthalmoscopy: Examines the optic nerve for signs of damage
  3. Visual field testing: Assesses peripheral vision
  4. Gonioscopy: Evaluates the angle where the iris meets the cornea
  5. Optical Coherence Tomography (OCT): Provides detailed images of the optic nerve and retinal nerve fiber layer

Early diagnosis is crucial for preventing vision loss. The Ocular Hypertension Treatment Study (Kass et al., 2002) demonstrated that topical ocular hypotensive medication can delay or prevent the onset of POAG in individuals with elevated intraocular pressure.

What are the Risk Factors for Developing POAG?

Several factors increase the likelihood of developing primary open-angle glaucoma:

  • Age (over 40)
  • Family history of glaucoma
  • African or Hispanic ancestry
  • High intraocular pressure
  • Thin corneas
  • Myopia (nearsightedness)
  • Diabetes
  • Hypertension
  • Prolonged use of corticosteroids

Interestingly, studies have found associations between POAG and other neurodegenerative diseases. Bayer et al. (2002) reported a high occurrence rate of glaucoma among patients with Alzheimer’s disease. Similarly, Tamura et al. (2006) observed a high frequency of open-angle glaucoma in Japanese patients with Alzheimer’s disease.

What are the Current Treatment Options for POAG?

The primary goal of POAG treatment is to lower intraocular pressure and prevent further optic nerve damage. Treatment options include:

1. Medications:

Topical eye drops are often the first-line treatment for POAG. These medications work by either reducing aqueous humor production or improving its outflow.

  • Prostaglandin analogs (e.g., latanoprost, travoprost)
  • Beta-blockers (e.g., timolol)
  • Alpha-agonists (e.g., brimonidine)
  • Carbonic anhydrase inhibitors (e.g., dorzolamide)
  • Rho kinase inhibitors (e.g., netarsudil)

A study by Narayanaswamy et al. (2007) compared the efficacy and safety of branded latanoprost (Xalatan) with generic latanoprost in POAG patients, finding comparable results.

2. Laser Therapy:

Laser treatments can be used to improve aqueous humor drainage:

  • Selective Laser Trabeculoplasty (SLT)
  • Argon Laser Trabeculoplasty (ALT)

3. Surgery:

When medications and laser therapy are insufficient, surgical interventions may be necessary:

  • Trabeculectomy
  • Drainage implant surgery
  • Minimally invasive glaucoma surgery (MIGS)

The Collaborative Initial Glaucoma Treatment Study (Lichter et al., 2001) compared initial treatment with medications versus surgery, providing valuable insights into treatment efficacy.

How Effective are Current POAG Treatments?

The effectiveness of POAG treatments varies among individuals. However, several studies have demonstrated positive outcomes:

The Early Manifest Glaucoma Trial (Heijl et al., 2002) showed that reducing intraocular pressure slowed glaucoma progression. Patients with lower IOP experienced less visual field loss and optic disc changes.

Musch et al. (2008) analyzed factors associated with intraocular pressure before and during 9 years of treatment in the Collaborative Initial Glaucoma Treatment Study. They found that both medical and surgical treatments effectively lowered IOP, with surgery achieving slightly lower pressures.

A study by Franks et al. (2006) compared the efficacy of travoprost 0.004% with latanoprost 0.005%/timolol 0.5% in POAG patients, demonstrating comparable IOP-lowering effects.

What are the Future Directions in POAG Research and Treatment?

Ongoing research aims to improve POAG diagnosis, treatment, and prevention:

1. Genetic research:

Identifying genetic markers for POAG could lead to earlier detection and personalized treatment approaches. The discovery of new glaucoma-associated genes, such as the one reported by Monemi et al. (2005), opens up possibilities for gene therapy and targeted treatments.

2. Neuroprotection:

Developing therapies that directly protect retinal ganglion cells and the optic nerve from damage, independent of IOP reduction.

3. Stem cell therapy:

Exploring the potential of stem cells to regenerate damaged trabecular meshwork tissue or replace lost retinal ganglion cells.

4. Novel drug delivery systems:

Developing sustained-release formulations or implants to improve medication adherence and efficacy.

5. Artificial intelligence:

Utilizing AI and machine learning algorithms to improve early detection and predict disease progression.

How Can POAG be Prevented or Its Progression Slowed?

While POAG cannot be completely prevented, several strategies can help reduce the risk of developing the disease or slow its progression:

  • Regular eye exams: Early detection is crucial for preventing vision loss.
  • Maintaining a healthy lifestyle: Regular exercise, a balanced diet, and avoiding smoking can contribute to overall eye health.
  • Managing other health conditions: Controlling diabetes and hypertension may help reduce the risk of POAG.
  • Protecting eyes from injury: Wearing protective eyewear during sports or hazardous activities can prevent eye injuries that may increase glaucoma risk.
  • Medication adherence: For those diagnosed with POAG, strictly following prescribed treatment regimens is essential for managing the disease.

The Ocular Hypertension Treatment Study (Kass et al., 2002) demonstrated that early treatment of elevated intraocular pressure could delay or prevent the onset of POAG in high-risk individuals.

How Does POAG Affect Quality of Life?

Primary open-angle glaucoma can significantly impact an individual’s quality of life, especially as the disease progresses:

Vision-related impacts:

  • Difficulty with daily activities such as reading, driving, and recognizing faces
  • Increased risk of falls and accidents due to impaired peripheral vision
  • Challenges in low-light conditions

Emotional and psychological effects:

  • Anxiety and depression related to vision loss and fear of blindness
  • Reduced independence and social isolation
  • Decreased self-esteem and confidence

Economic burden:

  • Costs associated with ongoing medical treatment and potential surgical interventions
  • Potential loss of income due to vision impairment
  • Expenses related to vision aids and assistive devices

A study by Gogate et al. (2011) highlighted the impact of socioeconomic factors on glaucoma blindness in India, emphasizing the need for improved awareness and access to care.

What is the Global Impact of POAG?

Primary open-angle glaucoma is a significant global health concern:

  • Prevalence: POAG affects millions of people worldwide, with numbers expected to increase as populations age.
  • Demographic variations: The Baltimore Eye Survey (Sommer et al., 1991) found differences in POAG prevalence among racial groups, with higher rates in African Americans compared to white Americans.
  • Economic impact: The cost of glaucoma treatment and management places a substantial burden on healthcare systems globally.
  • Research focus: Organizations like the National Eye Institute (NEI) have dedicated significant resources to glaucoma research and treatment development.

The American Academy of Ophthalmology (AAO) provides comprehensive guidelines for POAG management, emphasizing the importance of individualized treatment approaches and regular follow-ups.

How Can Patients Manage Living with POAG?

Living with primary open-angle glaucoma requires active participation in one’s care and adaptation to potential vision changes:

1. Medication adherence:

Consistently using prescribed eye drops is crucial for maintaining lower intraocular pressure and slowing disease progression.

2. Regular follow-ups:

Attending scheduled eye exams allows for timely adjustments to treatment plans and monitoring of disease progression.

3. Lifestyle modifications:

  • Maintaining a healthy diet rich in antioxidants
  • Engaging in regular, moderate exercise
  • Avoiding smoking and limiting alcohol consumption
  • Managing stress through relaxation techniques

4. Home adaptations:

Making changes to the living environment to accommodate vision changes, such as improving lighting and removing tripping hazards.

5. Support groups:

Joining glaucoma support groups can provide emotional support and practical tips for managing the condition.

6. Assistive devices:

Utilizing low vision aids and adaptive technologies to maintain independence and quality of life.

The Glaucoma Research Foundation offers valuable resources and information for patients living with POAG, emphasizing the importance of education and self-management in successful disease management.

What are the Challenges in POAG Research and Treatment?

Despite significant advancements in POAG management, several challenges remain:

1. Early detection:

Developing more sensitive and specific screening methods to identify POAG in its earliest stages remains a priority.

2. Treatment adherence:

Improving patient compliance with medication regimens is crucial for effective disease management. Studies have shown that poor adherence can significantly impact treatment outcomes.

3. Personalized medicine:

Tailoring treatments to individual patients based on genetic, environmental, and lifestyle factors is an ongoing area of research.

4. Neuroprotection:

Developing therapies that directly protect the optic nerve from damage, independent of IOP reduction, remains a significant challenge.

5. Long-term efficacy:

Ensuring the sustained effectiveness of treatments over extended periods is essential for preventing vision loss.

6. Access to care:

Addressing disparities in access to glaucoma screening, diagnosis, and treatment, particularly in underserved populations and developing countries.

Ongoing research, such as the studies cited throughout this article, continues to address these challenges and improve outcomes for POAG patients.

In conclusion, primary open-angle glaucoma remains a significant challenge in ophthalmology. However, with ongoing research, improved diagnostic techniques, and advances in treatment options, the outlook for POAG patients continues to improve. Early detection, proper management, and patient education are key to preserving vision and maintaining quality of life for those affected by this condition.

Current primary open-angle glaucoma treatments and future directions

1. Monemi S, Spaeth G, DaSilva A, et al. Identification of a novel adult-onset primary open-angle glaucoma (POAG) gene on 5q22.1. Hum Mol Genet. 2005;14(6):725–733. [PubMed] [Google Scholar]

2. Tamura H, Kawakami H, Kanamoto T, et al. High frequency of open-angle glaucoma in Japanese patients with Alzheimer’s disease. J Neurol Sci. 2006;246(1–2):79–83. [PubMed] [Google Scholar]

3. Vyas P, Naik U, Gangaiah JB. Efficacy of bimatoprost 0.03% in reducing intraocular pressure in patients with 360 degrees synechial angle-closure glaucoma: a preliminary study. Indian J Ophthalmol. 2011;59(1):13–16. [PMC free article] [PubMed] [Google Scholar]

4. NEI Glaucoma and Optic Neuropathies Program [Web page] Bethesda, MD: National Eye Institute; 2009. [Accessed March 3, 2011]. [updated 2009]. Available from: http://www.nei.nih.gov/strategicplanning/nationalplan1.pdf. [Google Scholar]

5. Dipiro J, Talbert RL, Yee GC, Wells BG, Posey LM, editors. Pharmacotherapy: A Pathophysiologic Approach. 7th ed. New York, NY: McGraw Hill; 2009. [Google Scholar]

6. Heiting G, Haddrill M. Glaucoma: Types, Symptoms, Diagnosis and Treatment [updated Dec, 2011] [Accessed June 6, 2012]. Available from: http://www.allaboutvision.com/conditions/glaucoma.htm#typesofglaucoma.

7. Park BC, Tibudan M, Samaraweera M, Shen X, Yue BY. Interaction between two glaucoma genes, optineurin and myocilin. Genes Cells. 2007;12(8):969–979. [PubMed] [Google Scholar]

8. Musch DC, Gillespie BW, Niziol LM, Cashwell LF, Lichter PR. Factors associated with intraocular pressure before and during 9 years of treatment in the Collaborative Initial Glaucoma Treatment Study. Ophthalmology. 2008;115(6):927–933. [PMC free article] [PubMed] [Google Scholar]

9. Heijl A, Leske MC, Bengtsson B, Hyman L, Hussein M. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch Ophthalmol. 2002;120(10):1268–1279. [PubMed] [Google Scholar]

10. AAO. American Academy of Ophthalmology Glaucoma Panel, Primary Open Angle Glaucoma. [Web page] San Francisco, CA: AAO PPP Glaucoma Panel, Hoskins Center for Quality Eye Care; 2010. [Accessed March 3, 2011]. Available from: http://www.aao.org/ppp. [Google Scholar]

11. Lichter PR, Musch DC, Gillespie BW, Guire KE, Janz NK, Wren PA, et al. Interim clinical outcomes in the Collaborative Initial Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery. Ophthalmology. 2001;108(11):1943–1953. [PubMed] [Google Scholar]

12. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6):701–713. [PubMed] [Google Scholar]

13. Sommer A, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans. The Baltimore Eye Survey. Arch Ophthalmol. 1991;109(8):1090–1095. [PubMed] [Google Scholar]

14. Gogate P, Deshpande R, Chelerkar V, Deshpande S, Deshpande M. Is glaucoma blindness a disease of deprivation and ignorance? A case-control study for late presentation of glaucoma in India. Indian J Ophthalmol. 2011;59(1):29–35. [PMC free article] [PubMed] [Google Scholar]

15. Bayer AU, Keller ON, Ferrari F, Maag KP. Association of glaucoma with neurodegenerative diseases with apoptotic cell death: Alzheimer’s disease and Parkinson’s disease. Am J Ophthalmol. 2002;133(1):135–137. [PubMed] [Google Scholar]

16. Bayer AU, Ferrari F, Erb C. High occurrence rate of glaucoma among patients with Alzheimer’s disease. Eur Neurol. 2002;47(3):165–168. [PubMed] [Google Scholar]

17. GRF. Glaucoma Research Foundation. [Website] San Francisco: Glaucoma Research Foundation; [Accessed February 25, 2011]. [updated May 1, 2009]; Available from: http://www.glaucoma.org/learn/diagnostic_test. php. [Google Scholar]

18. Narayanaswamy A, Neog A, Baskaran M, et al. A randomized, crossover, open label pilot study to evaluate the efficacy and safety of Xalatan in comparison with generic Latanoprost (Latoprost) in subjects with primary open angle glaucoma or ocular hypertension. Indian J Ophthalmol. 2007;55(2):127–131. [PubMed] [Google Scholar]

19. Katzung BG. Basic and Clinical Pharmacology. 7th ed. Norwalk, CT: Appleton and Lange; 1997. [Google Scholar]

20. Franks WA, Renard JP, Cunliffe IA, Rojanapongpun P. A 6-week, double-masked, parallel-group study of the efficacy and safety of travoprost 0.004% compared with latanoprost 0:005%/timolol 0.5% in patients with primary open-angle glaucoma or ocular hypertension. Clin Ther. 2006;28(3):332–339. [PubMed] [Google Scholar]

21. Blondeau P, Rousseau JA. Allergic reactions to brimonidine in patients treated for glaucoma. Can J Ophthalmol. 2002;37(1):21–26. [PubMed] [Google Scholar]

22. Kerr CR, Hass I, Drance SM, Walters MB, Schulzer M. Cardiovascular effects of epinephrine and dipivalyl epinephrine applied topically to the eye in patients with glaucoma. Br J Ophthalmol. 1982;66(2):109–114. [PMC free article] [PubMed] [Google Scholar]

23. Diggory P, Cassels-Brown A, Vail A, Hillman JS. Randomised, controlled trial of spirometric changes in elderly people receiving timolol or betaxolol as initial treatment for glaucoma. Br J Ophthalmol. 1998;82(2):146–149. [PMC free article] [PubMed] [Google Scholar]

24. Schuman JS. Effects of systemic beta-blocker therapy on the efficacy and safety of topical brimonidine and timolol. Brimonidine Study Groups 1 and 2. Ophthalmology. 2000;107(6):1171–1177. [PubMed] [Google Scholar]

25. ClinicalPharmacology. Drug Monographs. [Web database]: Clinical Pharmacology; [updated 2009–2010] [Accessed March 3, 2011]. Available from: http://www.clinicalpharmacology-ip.com/default.aspx.

26. Micromedex. Drug Monograph. [Web database]: Micromedex; [updated 2011] [Accessed March 3, 2011]. Available from: http://www.thomsonhc.com.

27. Kammer JA, Katzman B, Ackerman SL, Hollander DA. Efficacy and tolerability of bimatoprost versus travoprost in patients previously on latanoprost: a 3-month, randomised, masked-evaluator, multicentre study. Br J Ophthalmol. 2010;94(1):74–79. [PMC free article] [PubMed] [Google Scholar]

28. Denis P, Baudouin C, Bron A, et al. First-line latanoprost therapy in ocular hypertension or open-angle glaucoma patients: a 3-month efficacy analysis stratified by initial intraocular pressure. BMC Ophthalmol. 2010;10:4. [PMC free article] [PubMed] [Google Scholar]

29. Ang A, Reddy MA, Shepstone L, Broadway DC. Long term effect of latanoprost on intraocular pressure in normal tension glaucoma. Br J Ophthalmol. 2004;88(5):630–634. [PMC free article] [PubMed] [Google Scholar]

30. Stankiewicz A, Wierzbowska J, Siemiatkowska A, et al. The additive effect of dorzolamide hydrochloride (Trusopt) and a morning dose of bimatoprost (Lumigan) on intraocular pressure and retrobulbar blood flow in patients with primary open-angle glaucoma. Br J Ophthalmol. 2010;94(10):1307–1311. [PMC free article] [PubMed] [Google Scholar]

31. Mansberger SL, Hughes BA, Gordon MO, et al. comparison of initial intraocular pressure response with topical β-adrenergic antagonists and prostaglandin analogues in African American and White individuals in the Ocular Hypertension Treatment Study. Arch Ophthalmol. 2007;125(4):454–459. [PubMed] [Google Scholar]

32. Watson PG, Barnett MF, Parker V, Haybittle J. A 7 year prospective comparative study of three topical beta blockers in the management of primary open angle glaucoma. Br J Ophthalmol. 2001;85(8):962–968. [PMC free article] [PubMed] [Google Scholar]

33. Robin AL. Ocular hypotensive efficacy and safety of a combined formulation of betaxolol and pilocarpine. Trans Am Ophthalmol Soc. 1996;94:89–101. discussion 101–103. [PMC free article] [PubMed] [Google Scholar]

34. Suzuki Y, Iwase A, Araie M, et al. Risk factors for open-angle glaucoma in a Japanese population: the Tajimi Study. Ophthalmology. 2006;113(9):1613–1617. [PubMed] [Google Scholar]

35. Mitchell P, Hourihan F, Sandbach J, Wang JJ. The relationship between glaucoma and myopia: the Blue Mountains Eye Study. Ophthalmology. 1999;106(10):2010–2015. [PubMed] [Google Scholar]

36. Higginbotham EJ, Olander KW, Kim EE, Grunden JW, Kwok KK, Tressler CS. Fixed combination of latanoprost and timolol vs individual components for primary open-angle glaucoma or ocular hypertension: a randomized, double-masked study. Arch Ophthalmol. 2010;128(2):165–172. [PubMed] [Google Scholar]

37. Sellem E, Rouland JF, Baudouin C, et al. Predictors of additional intraocular pressure reduction in patients changed to latanoprost/timolol fixed combination. BMC Ophthalmol. 2010;10:10. [PMC free article] [PubMed] [Google Scholar]

38. Martinez A, Sanchez-Salorio M. A comparison of the long-term effects of dorzolamide 2% and brinzolamide 1%, each added to timolol 0.5%, on retrobulbar hemodynamics and intraocular pressure in open-angle glaucoma patients. J Ocul Pharmacol Ther. 2009;25(3):239–248. [PMC free article] [PubMed] [Google Scholar]

39. Nakamoto K, Yasuda N. Effect of concomitant use of latanoprost and brinzolamide on 24-hour variation of IOP in normal-tension glaucoma. J Glaucoma. 2007;16(4):352–357. [PubMed] [Google Scholar]

40. Kimal Arici M, Topalkara A, Guler C. Additive effect of latanoprost and dorzolamide in patients with elevated intraocular pressure. Int Ophthalmol. 1998;22(1):37–42. [PubMed] [Google Scholar]

41. Maruyama K, Shirato S. Additive effect of dorzolamide or carteolol to latanoprost in primary open-angle glaucoma: a prospective randomized crossover trial. J Glaucoma. 2006;15(4):341–345. [PubMed] [Google Scholar]

42. Higginbotham EJ, Schuman JS, Goldberg I, et al. One-year, randomized study comparing bimatoprost and timolol in glaucoma and ocular hypertension. Arch Ophthalmol. 2002;120(10):1286–1293. [PubMed] [Google Scholar]

43. Rhee DJ, Peace JH, Mallick S, Landry TA, Bergamini MV. A study of the safety and efficacy of travoprost 0.004%/timolol 0.5% ophthalmic solution compared to latanoprost 0.005% and timolol 0.5% dosed concomitantly in patients with open-angle glaucoma or ocular hypertension. Clin Ophthalmol. 2008;2(2):313–319. [PMC free article] [PubMed] [Google Scholar]

44. Doi LM, Melo LA, Jr, Prata JA., Jr Effects of the combination of bimatoprost and latanoprost on intraocular pressure in primary open angle glaucoma: a randomised clinical trial. Br J Ophthalmol. 2005;89(5):547–549. [PMC free article] [PubMed] [Google Scholar]

45. Dapling RB, Cunliffe IA, Longstaff S. Influence of apraclonidine and pilocarpine alone and in combination on post laser trabeculoplasty pressure rise. Br J Ophthalmol. 1994;78(1):30–32. [PMC free article] [PubMed] [Google Scholar]

46. Parrish RK, Feuer WJ, Schiffman JC, Lichter PR, Musch DC. Five-year follow-up optic disc findings of the Collaborative Initial Glaucoma Treatment Study. Am J Ophthalmol. 2009;147(4):717–724. e711. [PMC free article] [PubMed] [Google Scholar]

47. Cheung W, Guo L, Cordeiro MF. Neuroprotection in glaucoma: drug-based approaches. Optom Vis Sci. 2008;85(6):406–416. [PMC free article] [PubMed] [Google Scholar]

48. Steigerwalt RD, Gianni B, Paolo M, Bombardelli E, Burki C, Schonlau F. Effects of Mirtogenol on ocular blood flow and intraocular hypertension in asymptomatic subjects. Mol Vis. 2008;14:1288–1292. [PMC free article] [PubMed] [Google Scholar]

49. He Y, Leung KW, Zhang YH, et al. Mitochondrial complex I defect induces ROS release and degeneration in trabecular meshwork cells of POAG patients: protection by antioxidants. Invest Ophthalmol Vis Sci. 2008;49(4):1447–1458. [PubMed] [Google Scholar]

50. University of Roma La Sapienza. ClinicalTrialsgov [website on the Internet] Bethesda, MD: US National Library of Medicine; 2010. [Accessed March 3, 2011]. Retinal nerve fibres layers thickness study in glaucomatous patients. [updated December 3, 2010]. Available from: http://clinicaltrials. gov/ct2/show/{“type”:”clinical-trial”,”attrs”:{“text”:”NCT01254006″,”term_id”:”NCT01254006″}}NCT01254006?term={“type”:”clinical-trial”,”attrs”:{“text”:”NCT01254006″,”term_id”:”NCT01254006″}}NCT01254006&rank=1. NLM identifier: NCT01254006. [Google Scholar]

51. Future Products Management. ClinicalTrialsgov [website on the Internet] Bethesda, MD: US National Library of Medicine; 2005. [Accessed March 3, 2011]. Treatment of glaucomatous neuropathy with food additives. [updated March 10, 2009]. Available from: http://clinicaltrials.gov/ct2/show/{“type”:”clinical-trial”,”attrs”:{“text”:”NCT00196677″,”term_id”:”NCT00196677″}}NCT00196677?term={“type”:”clinical-trial”,”attrs”:{“text”:”NCT00196677″,”term_id”:”NCT00196677″}}NCT00196677&rank=1. NLM identifier: NCT00196677. [Google Scholar]

52. Sooft Italia. ClinicalTrialsgov [website on the Internet] Bethesda, MD: US National Library of Medicine; 2009. [Accessed March 30, 2011]. Effects of the oral administration of an association of forskolin with rutin and vitamins B on intraocular pressure in patients affected by primary open angle glaucoma and treated with either beta-blockers or prostaglandin eye drops. [updated June 5, 2012]. Available from: http://clinicaltrials.gov/ct2/show/{“type”:”clinical-trial”,”attrs”:{“text”:”NCT00863811″,”term_id”:”NCT00863811″}}NCT00863811?term={“type”:”clinical-trial”,”attrs”:{“text”:”NCT00863811″,”term_id”:”NCT00863811″}}NCT00863811.&rank=1. NLM identifier: NCT00863811. [Google Scholar]

53. Zhong L, Bradley J, Schubert W, et al. Erythropoietin promotes survival of retinal ganglion cells in DBA/2 J glaucoma mice. Invest Ophthalmol Vis Sci. 2007;48(3):1212–1218. [PubMed] [Google Scholar]

54. Zhan GL, Camras CB, Palmberg PF, Toris CB. Effects of marijuana on aqueous humor dynamics in a glaucoma patient. J Glaucoma. 2005;14(2):175–177. [PubMed] [Google Scholar]

55. Tomida I, Azuara-Blanco A, House H, Flint M, Pertwee RG, Robson PJ. Effect of sublingual application of cannabinoids on intraocular pressure: a pilot study. J Glaucoma. 2006;15(5):349–353. [PubMed] [Google Scholar]

56. Fang JH, Wang XH, Xu ZR, Jiang FG. Neuroprotective effects of bis(7)-tacrine against glutamate-induced retinal ganglion cells damage. BMC Neurosci. 2010;11:31. [PMC free article] [PubMed] [Google Scholar]

57. Vorwerk CK, Lipton SA, Zurakowski D, Hyman BT, Sabel BA, Dreyer EB. Chronic low-dose glutamate is toxic to retinal ganglion cells. Toxicity blocked by memantine. Invest Ophthalmol Vis Sci. 1996;37(8):1618–1624. [PubMed] [Google Scholar]

58. Dreyer 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(3):299–305. [PubMed] [Google Scholar]

59. Yucel YH, Gupta N, Zhang Q, Mizisin AP, Kalichman MW, Weinreb RN. Memantine protects neurons from shrinkage in the lateral geniculate nucleus in experimental glaucoma. Arch Ophthalmol. 2006;124(2):217–225. [PubMed] [Google Scholar]

60. Osborne NN. Recent clinical findings with memantine should not mean that the idea of neuroprotection in glaucoma is abandoned. Acta Ophthalmol. 2009;87(4):450–454. [PubMed] [Google Scholar]

61. Ko ML, Peng PH, Hsu SY, Chen CF. Dietary deficiency of vitamin E aggravates retinal ganglion cell death in experimental glaucoma of rats. C Eye R. 2010;35(9):842–849. [PubMed] [Google Scholar]

62. Roh YJ, Moon C, Kim SY, Park MH, Bae YC, Chun MH, et al. Glutathione depletion induces differential apoptosis in cells of mouse retina, in vivo. Neurosci Lett. 2007;417(3):266–270. [PubMed] [Google Scholar]

63. The Catholic University of Korea. ClinicalTrials gov [website on the Internet] Bethesda, MD: US National Library of Medicine; 2007. [Accessed March 3, 2011]. Evaluation of systemic glutathione level in patients with normal tension glaucoma. [updated June 14, 2010]. Available from: http://clinicaltrials.gov/ct2/show/{“type”:”clinical-trial”,”attrs”:{“text”:”NCT00570362″,”term_id”:”NCT00570362″}}NCT00570362?term={“type”:”clinical-trial”,”attrs”:{“text”:”NCT00570362″,”term_id”:”NCT00570362″}}NCT00570362&rank=1. NLM identifier: NCT00570362. [Google Scholar]

64. Luksch A, Rainer G, Koyuncu D, et al. Effect of nimodipine on ocular blood flow and colour contrast sensitivity in patients with normal tension glaucoma. Br J Ophthalmol. 2005;89(1):21–25. [PMC free article] [PubMed] [Google Scholar]

65. Piltz JR, Bose S, Lanchoney D. The effect of nimodipine, a centrally active calcium antagonist, on visual function and mascular blood flow in patients with normal-tension glaucoma and control subjects. J Glaucoma. 1998;7(5):336–342. [PubMed] [Google Scholar]

66. Harris A, Evans DW, Cantor LB, Martin B. Hemodynamic and visual function effects of oral nifedipine in patients with normal-tension glaucoma. Am J Ophthalmol. 1997;124(3):296–302. [PubMed] [Google Scholar]

67. Cellini M, Possati GL, Caramazza N, Profazio V, Caramazza R. The use of flunarizine in the management of low-tension glaucoma: a color Doppler study. Acta Ophthalmol Scand Suppl. 1997;224:57–58. [PubMed] [Google Scholar]

Your Quick Quide to Common Eye Care Abbreviations

In healthcare, abbreviations are frequently used to save time and make notes or charts shorter and easier to read. Eye care abbreviations are no different, which are used to make everything flow smoother. When reading or listening to health information, it is important to make sure that you understand the meaning of any abbreviations that are used. These are a few of the most common and most important abbreviations that are used in eye care.

 

The Most Common Eye Care Abbreviations: OD, OS, and OU

Some of the most abundant abbreviations that are used in eye care are OD, OS, and OU. These abbreviations stand for the right eye (OD), left eye (OS), and both eyes (OU).

These abbreviations may be used to indicate which eye has a disease or condition, may note which eye was tested or evaluated, or can be used to direct which eye needs a particular medication or treatment.

These three abbreviations are derived from the Latin words oculus dexter (OD), oculus sinister (OS), and oculus uterque (OU) which translates roughly to the right eye, left eye, and both eyes.

 

IOP and POAG

For a glaucoma treatment, the abbreviations IOP and POAG are often used. IOP stands for intraocular pressure while POAG is short for primary open-angle glaucoma.

In glaucoma, eye pressure is a key indicator of risk and progression. This is the intraocular pressure of the eye.

The term primary open-angle glaucoma (POAG) is used frequently as the most common type of glaucoma. This means that there is no other disease causing glaucoma and that the type of glaucoma is not angle closure.

 

Gtts, BID, QID, and QHS

When prescribing eye drops, the abbreviations gtts, BID, QID, and QHS are often used. These abbreviations are for drops (gtts), twice a day (BID), four times a day (QID), and once a day at nighttime (QHS).

The abbreviation for drops comes from the Lain word gutta which means drop. This abbreviation is often seen written in prescription instructions.

Each of the abbreviations BID, QID, and QHS are used to indicate how often medication or treatment should be used daily.

These abbreviations come from the Latin phrases bis in die, quarter in die, and quaque hora somni which are translated as twice a day, four times a day, and every night at bedtime.

What to Do If You Are Unsure What an Abbreviation Means

If you see an abbreviation or hear a term that you are unsure what it means, there are a few options to learn what the term is.

The quickest option is to ask your doctor or healthcare provider who gave you the information what the meaning of the abbreviation is. Most doctors are more than happy to give a thorough explanation.

Another option is to use an internet search to find a reliable source of information for the meaning of a particular term or abbreviation.

While the internet provides a wide array of resources, it is important to make sure that you only consult reliable sources.

 

Our eye doctor at Brooklyn Eye Care excels in the prescription of glasses, contact lenses, the diagnosis of a variety of eye diseases, and learning about eye care abbreviations. Call our optometrist at (763) 999-6116 to schedule your appointment today. Our eye doctor, Dr. Vivian Ekemezie provides the highest quality optometry services and eye exams in the Brooklyn Park, MN area.