This section describes the pathophysiology of glaucoma, its prevalence, associated risk factors, and its impact on quality of life. This slide illustrates.

This section describes the pathophysiology of glaucoma, its prevalence, associated risk factors, and its impact on quality of life. This slide illustrates the impaired vision from a glaucomatous eye (top right) compared with a healthy eye (top left).

Glaucoma Glaucoma encompasses a group of chronic ocular diseases characterized by progressive damage to the optic nerve, which can lead to visual field loss and eventual blindness.1 Glaucoma is a major cause of blindness worldwide.1 Elevated IOP is a primary risk factor for glaucoma. However, the etiology is multifactorial, and other risk factors include age and race (glaucoma is more common in black populations).1

Glaucoma Prevalence

Prevalence of POAG and CACG
The total prevalence of POAG and CACG is approximately equal worldwide, although it varies among countries.1 Most CACG cases are in Asia, while cases of POAG are more equally distributed worldwide.1

Prevalence of POAG in European, African, and Asian People by Age
Detailed analysis among European and African populations revealed that the prevalence of POAG increases with age.1 The prevalence of POAG in Asia is also age-related, but this effect is not as pronounced as in the European and African populations.1 Throughout the world, the age of onset of glaucoma varies by population. In African populations, the age of onset is much younger, and the proportion of young people is higher than in other populations; therefore screening for glaucoma is recommended to begin at age 30. The age of onset is later in European populations; therefore screening for glaucoma begins at age 50.1

Risk Factors for Glaucoma
Elevated IOP is the primary treatable risk factor for the development of glaucoma.1 In addition, a family history of glaucoma is associated with an increased risk.1 Patients of African ancestry are at greater risk of developing glaucoma, as are patients with severe myopia or previous eye trauma.1 Other risk factors include long-term use of corticosteroids.1

Aims of Treatment Glaucoma often has an insidious onset and is asymptomatic in the early stages. Early diagnosis and prompt initiation of treatment are essential to try to minimize glaucomatous damage and vision loss. Medical treatment is the mainstay of management, with the goal of therapy being to reduce the IOP to slow further optic nerve damage. Laser treatment and surgery provide alternatives if IOP is not adequately controlled with medical treatment.

Quality of Life (QOL) World Health Organization (WHO) Definition
QOL is an important aspect of glaucoma, and due consideration should be given to this. WHO defines QOL as: “An individual’s perception of their position in life in the context of the culture and value systems in which they live and in relation to their goals, expectations, standards and concerns.”1 Health-related QOL issues include physical health (functional state), psychologic state (including health perceptions), level of independence, and social relationships.1 To help maintain a healthy status, patient management should focus not only on the treatment of the disease but also the effect of both diagnosis and treatment on the individual.

A better understanding of the impact of glaucoma diagnosis can be established through sensitive discussion with patients about their concerns, symptoms, and feelings. This in turn may help guide treatment choice and allow the likelihood of compliance to treatment to be assessed. A survey of 341 patients showed that 15% felt more depressed since the diagnosis of glaucoma and 59% of patients felt minimally disturbed by their treatment.1

Summary: Glaucoma

Introduction: IOP Lowering1
This section reviews the importance of lowering IOP and discusses how evidence from studies translates into everyday clinical practice.1

Importance of IOP Lowering
A cumulative body of evidence confirms that elevated IOP is an important risk factor for primary open-angle glaucoma (POAG). Evidence comes from the following 2 important sources: Epidemiologic studies (both cross-sectional and longitudinal population studies) Randomized controlled trials in patients with high-pressure glaucoma, normal-tension glaucoma (NTG), and ocular hypertension

This slide presents data from the Baltimore Eye Survey, one of the largest epidemiologic studies ever undertaken. This study was a cross-sectional survey of 4,674 eyes in black patients and ,770 eyes in white patients.1 The results showed that IOP is a significant risk factor for the development of glaucomatous optic nerve damage, with the prevalence of glaucoma increasing with IOP in both black and white individuals. While other risk factors such as age, race, and family history also have been identified, the role of IOP as a risk factor has been a universal finding in population studies conducted in other communities and countries.

It is important to note that glaucomatous optic nerve damage can occur even when IOP is within the normal range. The prevalence of newly identified glaucoma in people who have an IOP within the normal range (21 mm Hg) varies between different populations, as shown in the slide.1-5 In Japanese populations, approximately two thirds of OAG patients have an IOP within the normal range.2 IOP is the major risk factor that is treatable and for which data from long-term studies suggest that effective control can slow the likelihood of glaucomatous progression. However, it is reasonable to assume that the role of IOP-dependent and IOP-independent factors leading to progression differs between patients with NTG and those with elevated IOP.

Association Between Postsurgical IOP and Visual Field Defect: AGIS
Some of the most compelling evidence supporting an association between IOP and glaucomatous progression comes from a subanalysis of the prospective Advanced Glaucoma Intervention Study (AGIS) in patients after surgical intervention with moderate-to-severe glaucoma damage.1 In the predictive analysis, 738 eyes were categorized into 3 groups based on IOP determinations over the first three 6-month follow-up visits and were followed up to 7 years (n=430 at 84 months). This analysis showed that patients with an average IOP <14 mm Hg over the first 18 months of treatment had a significantly lower mean change in visual defect score at 96 months (8 years) than patients with an average IOP of >17.5 mm Hg (P=.002).

The associated analysis of the AGIS1 data assessed the relationship between postsurgical IOP and change in visual field defect score in patients with open-angle glaucoma not adequately controlled by medication. A total of 586 eyes received either argon laser trabeculoplasty or trabeculectomy and were followed for 6 or more years (n=422 at 7 years). IOP was measured with a Goldmann applanation tonometer every 6 months, and the eyes were grouped based on the percentage of visits at which IOP was <18 mm Hg.1 Patients who consistently achieved an IOP <18 mm Hg at all visits over 6 years (mean IOP = 12.3 mm Hg) had mean changes from baseline in visual field defect score close to zero during follow-up.1 In contrast, patients who achieved an IOP <18 mm Hg at fewer than half of visits (mean IOP = 20.2 mm Hg) over 6 years had an estimated worsening in visual field defect score over follow-up of 0.63 units (P=.083).1 These data support an association between low IOP and reduced progression of visual field defect.

IOP Fluctuations and Risk of Glaucoma Progression
Recent data suggested that large fluctuations in IOP are a significant risk factor for glaucoma progression.1 This study suggested that patients without markedly elevated IOP, but with large fluctuations in 24-hour IOP, were more than 5 times as likely to have glaucomatous progression than patients with smaller fluctuations.1 By year 8 of follow-up, the cumulative risk of progression for patients in the upper quartile of the range of home IOP measured over 5 days was 88%, compared with 57% for patients in the lower quartile.1 To correlate diurnal IOP fluctuations with glaucoma progression, 64 patients (105 eyes) performed self-tonometry at home 5 times a day for 5 days. All patients had open-angle glaucoma and documented IOP <25 mm Hg throughout the follow-up period (a mean of 5 years). Measurements of progression were made by the clinician at the time of the follow-up examination and were based on the examination of multiple visual fields at and before the visit, including dilation, patient performance during perimetry, lens opacities, and operator reliability.

Studies suggested that reducing IOP slows the likelihood of disease progression in patients with NTG. The results of the Collaborative Normal-Tension Glaucoma Study of 140 patients showed that in treated patients whose IOP was reduced by more than 30% from baseline, there was significantly less deterioration in visual field end points (P<.0001) than in untreated patients.1 In conclusion, the Collaborative Normal-Tension Glaucoma Study Group adds support to the hypothesis that lowering IOP slows the likelihood of disease progression.

Tailoring Target IOP to the Individual Patient
The goal of current treatment strategies in glaucoma is to lower IOP.1 However, few specific criteria exist to guide the physician as to the appropriate target pressure for each individual. When translating the evidence from clinical trials to the individual patient, consideration needs to be given not only to the IOP at presentation but also the rate of progressive damage and the possibility of central vision loss within the expected lifetime of the patient. Factors that need to be considered in establishing appropriate IOP targets include: The extent of the damage to the optic nerve and the consequent vision loss The IOP level at which damage occurred The patient’s life expectancy In NTG, at least a 30% reduction in IOP is required to lower the risk of developing further visual field changes.2 The AGIS results suggested that maintaining IOP <18 mm Hg does not ensure the preservation of the visual field.3 The risk-benefit ratio of interventions must always be individually assessed.

IOP Lowering and Glaucoma Progression
There is good evidence to suggest that lowering IOP can slow the progression of glaucoma. In addition, evidence suggested that large fluctuations in diurnal IOP were a significant risk factor for the progression of glaucoma independent of the IOP measures obtained in the office.1,2 It has been suggested that round-the-clock measurement of IOP (with assessment of average IOP and peak IOP) provides a more meaningful gauge of the relationship between IOP and glaucomatous progression.

The Importance of IOP Lowering: Summary
In summary, population studies support an association between the risk of progressive visual loss and increasing IOP. Even eyes with IOP in the normal range are susceptible to glaucomatous changes. In a subanalysis of the AGIS,1 an association between low postsurgical IOP and reduced progression of visual field deficit was shown. The mainstay of glaucoma treatment is therefore a sustained and substantial IOP reduction. When translating the evidence from clinical trials to individuals, realistic IOP targets should be tailored for the treatment of the individual patient. The targets should be based on pretreatment IOP levels, the age of the patient, the duration, number, and type of risk factors present, and the extent of optic nerve damage.

24-Hour Variation of IOP

Overview I would like to begin with an overview of this presentation. First, I will review the scientific data supporting the circadian rhythm of aqueous humor flow and intraocular pressure. The effect of first-line treatment approaches on aqueous humor outflow will be presented. This presentation will examine a number of studies where IOP was evaluated over a 24-hour period in both treated and untreated patients with ocular hypertension and glaucoma compared with healthy controls. A study published in 2003 by Liu and colleagues (Invest Ophthalmol Vis Sci. 2003; 44: ) examined 24-hour IOP in patients with newly diagnosed early glaucomatous changes and controls with healthy eyes. The study showed that both healthy eyes and eyes with early glaucomatous changes showed higher nocturnal supine IOP than diurnal sitting IOP. Three additional studies by Orzalesi et al. (Invest Ophthalmol Vis Sci. 2000;41: ), Larsson (Ophthalmology. 2001;108: ), and Liu, Kripke, and Weinreb (Am J Ophthalmol. 2004;138: ) evaluated 24-hour IOP among subjects with OHT or glaucoma who were randomized to receive either latanoprost or timolol. The 2004 study by Liu, Kripke, Weinreb will be presented in greater detail. The data from these trials support the activity of latanoprost during both the diurnal and nocturnal periods. In these studies, timolol showed activity only during the diurnal period.

Both intraocular pressure (IOP) and the rate of aqueous flow follow a circadian rhythm
In most patients, there is a circadian rhythm of aqueous humor flow, with the highest rates measured during morning hours, slightly lower rates during afternoon hours, and rates during sleep that are approximately one half of those during the morning. The various studies of IOP in normal eyes have found that a rhythmic pattern of diurnal variation does occur. References: Brubaker RF. Flow of aqueous humor in humans. Invest Ophthalmol Vis Sci. 1991; 32: Wilensky JT. Diurnal variations in intraocular pressure. Tr Am Ophth Soc. 1991;89:

Circadian Rhythm of Aqueous Humor Formation and Flow
Brubaker described a study of aqueous humor flow performed in the human eye at different times of the day. In 1958, investigators found the rate of aqueous humor flow to be much lower during sleep than during waking hours. This was confirmed by light scattering measurements in the anterior chamber of the eye. Investigators found the light scattering to be a result of varying protein concentrations in the aqueous humor, which were found to be related to a circadian rhythm of aqueous humor formation. Sleeping subjects were found to have the lowest rates of aqueous flow and sleeping under a bright light during nighttime hours, to simulate daytime, does not alter the nocturnal suppression of flow. References: Brubaker RF. Flow of aqueous humor in humans. Invest Ophthalmol Vis Sci. 1991;32: Koskela T, Brubaker RF. The nocturnal suppression of aqueous humor flow in humans is not blocked by bright light. Invest Ophthalmol Vis Sci. 1991;32:

Effect of Treatments on Aqueous Humor Outflow
Many drugs have been tested for their effects on aqueous humor flow and formation in the human eye. Several classes of drugs have been shown to inhibit aqueous humor formation. Carbonic anhydrase inhibitors, such as acetazolamide, inhibit aqueous humor production and suppress flow. However, the systemic administration of these drugs has been associated with systemic side effects, leading to many interests in topically applicable drugs with similar effects. “The precise mechanism of the ocular hypotensive action of timolol is not clearly established at this time. Tonography and fluorophotometry studies in man suggest that its predominant action may be related to reduced aqueous formation. However, in some studies a slight increase in outflow facility was also observed.” Prostaglandins were found to lower intraocular pressure by improving outflow. References: Brubaker RF. Flow of aqueous humor in humans. Invest Ophthalmol Vis Sci. 1991;32: Timoptic [package insert]. Whitehouse Station, NJ: Merck & Co Inc; 2001.

Data From a Sleep Lab Study Shows That IOP Is Higher At Night
A total of 24 untreated patients with newly diagnosed early glaucoma and 24 age-matched controls with healthy eyes were enrolled in this study. Measurements of IOP, blood pressure, and heart rate were taken every 2 hours during a 24-hour period from the 48 subjects. In the 16-hour diurnal awake period, IOP was measured sitting and supine using a pneumatonometer, and blood pressure and heart rate were measured supine. In the 8-hour nocturnal sleep period, all measurements were taken in the supine position. Mean diurnal and nocturnal IOP in the glaucoma group were compared with data obtained from the control group with healthy eyes. In order to decrease any potential biases in collecting IOP measurements during the 24-hour period, the investigators conducted the study in a sleep laboratory, collected additional data on sleep periods prior to the study start, monitored exposure to light and physical activity, and restricted alcohol and caffeine use. The subjects were asked to maintain a daily 8-hour sleep period for 7 days before the experiment. In addition, light intensity in the laboratory was kept at a specified level and the 8-hour period of darkness in the subject’s room was adjusted to correspond to each individual’s sleep time. For subjects in both groups, nocturnal supine IOP was higher than diurnal sitting IOP. Mean diurnal IOP, either sitting or supine, was significantly higher in the glaucoma group than in the control group. Reference: Liu JHK, Zhang X, Kripke DF, Weinreb RN. Twenty-four-hour intraocular pressure pattern associated with early glaucomatous changes. Invest Ophthalmol Vis Sci. 2003; 44:

Controlling for Factors That Can Influence IOP Measurements During a 24-h Period

Systemic Disorders Coexisting With Glaucoma
Many patients with glaucoma have coexisting systemic disorders that may complicate their management. A retrospective review of records of 100 patients with OAG was conducted at the Bryan Glaucoma Clinic, Duke University Eye Center. This slide shows the 8 most common comorbidities to glaucoma identified in this study’s population. Cardiovascular conditions were the most commonly found coexisting disorders. Nearly half the patients (48%) had systemic hypertension and more than a third (35%) suffered from coronary artery disease and arteriosclerosis. -blockers can exacerbate cardiac effects, such as arrhythmias and heart failure, and respiratory effects such as bronchospasm. In 8% of the patients, depression or anxiety was present. Such CNS side effects have been associated with the use of -blockers. Please see full prescribing information for XALATAN. References: Gottfredsdottir MS, Allingham RR, Shields MB. Physicians’ guide to interactions between glaucoma and systemic medications. J Glaucoma. 1997;6: Timoptic [package insert]. Whitehouse Station, NJ: Merck & Co Inc; 2001.

A survey of 148 ophthalmologists in December 2002 showed that prostaglandins (PGs) have become the first-line treatment of choice for most patients. The next most widely prescribed choice remains the b-blockers. Reference: Wave 6 awareness and usage tracking study. Isis Research. January 2003, Pharmacia & Upjohn Company, Kalamazoo, Mich.

Three Factors Affect IOP
Three variables determine a steady-state IOP: the rate of aqueous humor formation and flow, outflow resistance, and episcleral venous pressure References: American Academy of Ophthalmology, Basic and Clinical Science Glaucoma Section 10, 2001 page 14 . Liu JHK, Kripke DF, Weinreb RN. Comparison of the nocturnal effects of once-daily timolol and latanoprost on intraocular pressure. Am J Ophthalmol. 2004;138:

References

References (cont’d)

EBM may be described as “the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients.” In short, it seeks to provide optimal, up-to-date care for our patients.

The process of EBM is not an ivory tower concept useful only for academicians but can be easily learned and practiced by clinicians to deliver the most efficacious interventions for maximizing the quality of life for individual patients.

When new clinical data are published, EBM suggests some basic questions:
What exactly are the results? Are the results valid? How can I apply these results to my patients?

Evidence-based medicine is not cookbook medicine; it incorporates your clinical expertise and intuition in treating glaucoma.1 Clinical experience and clinical instinct are crucial to the practice of clinical medicine. Evidence-based medicine incorporates your training in pathophysiology, history taking, diagnostic workup, and physical examination with new available data to make the best decisions for your patients.2

When making clinical decisions, use the strongest evidence available
When making clinical decisions, use the strongest evidence available. There are many sources of evidence, but the strongest conclusions can be drawn from prospective, randomized, controlled clinical trials, considered to be the gold standard of EBM.1 At the lower end of the hierarchy are clinical observation and experience. Therapeutic approaches often start here and are confirmed by cross-sectional and cohort studies and eventually validated by randomized controlled trials (RCTs).2,3 Each has a role in decision making and should be weighted appropriately to its strength.

The randomized, controlled clinical trial is considered to be the gold standard because an adequate sample size and a low potential for bias occurs when the trial is well designed and performed. Down the hierarchy, the potential for bias becomes increasingly greater. As the potential bias increases, the validity decreases.1,2

The hierarchy of clinical evidence is not absolute; not all randomized, controlled clinical trials are created equal.1 The clinician must evaluate study characteristics individually to determine the validity of the conclusions and their applicability to patients.2 A checklist of questions is helpful to assess the validity of the study characteristics.2-4 The more “yes” answers, the greater the validity.

Since patients with chronic diseases are responsible for carrying out most of the treatment plan,1 successful management depends on patients’ active collaboration with their health care providers.2 Hence patient behavior is particularly relevant to the long-term management of ocular hypertension and glaucoma.

In glaucoma, avoidance of progressive visual impairment is more likely if the patient follows medical instructions.1 Following medical instructions involves being both compliant and persistent in following treatment recommendations.2 To be compliant, a patient must use the medication as directed and make the recommended glaucoma follow-up visits.1,2 Patients who do not comply with their glaucoma physician visits are also more likely to be noncompliant with their medication.1 Once a patient is taking medication properly, persistency refers to their continuing therapy over time. Because the most common reasons that patients discontinue therapy involve adverse effects, persistency is considered a surrogate marker for efficacy (physician decision) and tolerability (patient decision).3

It is critical that patients with glaucoma maintain a high level of compliance1 to ensure successful treatment.2 Patients should understand that daily fluctuations in intraocular pressure (IOP) can be large even in compliant patients whose IOP is relatively controlled.3 If patients fail to take their medication consistently and as prescribed, even larger fluctuations in IOP are likely and may adversely affect disease outcome.3,4

The results of a prospective study by Asrani and colleagues, assessing diurnal fluctuations in IOP in 64 patients with glaucoma, suggest that the risk of progression may be more strongly associated with fluctuations in IOP than with elevated IOP. Disease remained stable after 8 years in 43% of patients in the lowest quartile of home IOP range but in only 12% of the patients in the highest quartile. The authors considered this finding striking, since the prognosis was based on only a single 5-day monitoring period. IOP ranges, both diurnal range and day-to-day variation in IOP, were associated with a significant risk of progression.

A different prospective study of the association between regulation of IOP and visual field (VF) outcome was conducted by Bergeå et al in 76 patients with pseudoexfoliation or primary open-angle glaucoma (POAG) who had completed a study of primary treatment with argon laser trabeculoplasty or pilocarpine. VF decay was more highly correlated with IOP fluctuation (range and peak) and mean IOP than with IOP at start or degree of IOP reduction. This finding suggests that an IOP curve may be preferable to single, random IOP measurements in both scientific studies and clinical practice.

Generally speaking, glaucoma patients are not good about visit compliance.1,2
In a retrospective study of 5352 people screened at multiple community sites, 59% of 1331 people scheduled for a definitive follow-up examination did not appear for the visit.1 In a case-control study of 1100 patients with definitive or suspected glaucoma, more than 40% were noncompliant with prescribed visits.2 When interviewed, 59 of 100 patients taking eyedrops for the treatment of glaucoma reported that they had not taken their medication as prescribed, despite the fact that every patient reported that they understood the doctor’s instructions and 98% believed that the physician was helpful and concerned.3

Patients may be noncompliant with visits because of forgetfulness, failure to receive an appointment, lack of transportation or escort, denial of the seriousness of the disease, and cost or lack of insurance.1,2 In one study, over 74% of glaucoma suspects contacted by telephone following a definitive examination for glaucoma listed the cost of examination or the lack of insurance coverage as a reason for not having more frequent eye examinations prior to participating in a community-based vision screening program.1 Reasons for drug noncompliance include forgetfulness, absence from home or leaving medication home, inconvenient dosing regimen, and adverse effects or intolerance.3

As mentioned earlier, it is important that patients with glaucoma remain on therapy over time.1
Otherwise, the disease will not be effectively managed over the long term—a serious issue given the observation that the protective effect of IOP control appears to become more pronounced over time.1,2

The impact of long-term control of IOP on disease progression is illustrated by data collected during the Advanced Glaucoma Intervention Study (AGIS)—a randomized study measuring the relationship between postsurgical IOP and VF defect score. During the study, 586 eyes received either argon laser trabeculoplasty or trabeculectomy and were followed for 6 or more years. Surgical interventions were supplemented by medical treatment to reduce IOP to less than 18 mm Hg. IOP was measured with a Goldmann applanation tonometer every 6 months, and the eyes were retrospectively grouped into 4 groups based on the percentage of visits at which IOP was <18 mm Hg: Group A reached at 100% of visits Group B reached at 75% to <100% of visits Group C reached at 50% to <75% of visits Group D reached at 0% to <50% of visits Results of this study in advanced glaucoma patients managed by surgery and medical treatment support the protective role of low IOP. When IOP was <18 mm Hg at all visits (group A), the mean change in VF defect score stayed close to zero for the duration of the study. In the other groups, the mean change in score progressively increased over time. Starting at 54 months, the mean changes for the 4 groups diverged, remaining consistently ranked according to group. Group D showed the most progression—an increase of 0.63 units in VF defect score.

Data from a retrospective, observational study based on managed care claims over 18 months for 1006 monotherapy-prescribed patients with glaucoma suggest that poor persistence is common. Following an initial prescription, patients were considered to be discontinued if they failed to refill their prescription within 120 days (2.5-, 5-, or 10-mL bottle) or 180 days (15-mL bottle or multiple bottles). It is important to keep in mind that the generous time periods allowed before patients were considered to have discontinued the medication may have overestimated the duration of therapy before discontinuation. Over the course of the study, 25.4% of patients failed to receive their second prescription, 61.7% discontinued glaucoma therapy with their index medication, and 80% either discontinued or changed therapy.

Patients fail to persist with their treatment primarily because of debilitating or risky side effects1 and ineffectiveness,2 leading to the use of persistency as a surrogate marker for these clinical outcomes.3 In addition, high long-term cost1 and the inconvenience of the dosing regimens are often considerations.4 Dosing regimens can become particularly complex in patients with multiple comorbidities, many of whom are elderly5 and hindered by physical limitations that make it difficult for them to administer eyedrops.6

Well-motivated patients are more likely to continue their therapeutic regimens for extended periods—well beyond an initial prescription. Understanding the seriousness of glaucoma and the benefits of therapy, along with the positive reinforcement of having reached target IOP, encourages treatment persistence.1 In general, patients who continue to take their medication are more likely to comply with follow-up visits than patients who are not taking medication.2

Patients are more likely to persist with their treatment if they have reached their target IOP.1 Patients who see a benefit are more likely to continue, and physicians are less likely to change medications when progress is observed. Frequent office visits also promote persistence by reaffirming the severity of the disease and the benefits of the medical treatment.2

This section describes the pathophysiology of glaucoma, its prevalence, associated risk factors, and its impact on quality of life. This slide illustrates.

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This section describes the pathophysiology of glaucoma, its prevalence, associated risk factors, and its impact on quality of life. This slide illustrates.

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Presentation on theme: "This section describes the pathophysiology of glaucoma, its prevalence, associated risk factors, and its impact on quality of life. This slide illustrates."— Presentation transcript:

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