Chapter 54A
Lens-Related Glaucomas
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The lens-related glaucomas, a heterogeneous group of uncommon maladies, can develop through either open-angle or angle-closure mechanisms (Table 1). Correct identification of the mechanism underlying intraocular pressure elevation in suspected lensrelated disorders is essential for appropriate management. Differentiation of phacolytic, phacoanaphylactic, and infectious processes solely based on clinical examination is occasionally difficult.1,2 Cytologic, histologic, and microbiologic evaluation of ocular fluids and tissues can contribute greatly to the management of affected eyes and also potentially to fellow eyes. One should always consider the possibility of mixed mechanisms of intraocular pressure elevation (e.g., the frequent coexistence of traumatic recession of the anterior chamber angle with phacolytic glaucoma or lens subluxation).3,4


TABLE 1. Lens-Related Glaucomas

EntityAngle StatusMechanism
Phacolytic glaucomaOpenOutflow obstruction by lens protein and macrophages
Lens-particle glaucomaOpenOutflow obstruction by lens particles, possibly inflammatory cells
Glaucoma-associated with retained intravitreal lens fragmentsOpenOutflow obstruction by lens particles, lens protein, inflammatory cells (vitreous component?)
Glaucoma associated with phacoanaphylactic uveitisOpen or closedOutflow obstruction due to inflammation; pupillary block
Phacomorphic glaucomaClosedPupillary block; rarely direct compression of angle by intumescent lens
Glaucoma secondary to ectopia lentisClosedPupillary block


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Phacolytic glaucoma is a distinctive syndrome of elevated intraocular pressure occurring in an eye with a mature or hypermature cataract.5,6 The clinical history usually reveals the acute onset of pain and redness in an eye that has exhibited poor vision for a long time. Intraocular pressure commonly exceeds 35 mmHg, and the anterior chamber angle is open. Corneal edema often makes examination of the anterior segment difficult. The anterior chamber cell response is variable and heavy flare is typical but extensive keratitic precipitates and hypopyon are uncommon (Fig. 1). The refractile crystals that are occasionally visible in the anterior chamber may be composed of cholesterol or calcium oxalate.7–9

Fig. 1. Hypopyon in phacolytic glaucoma. Note the large white patches on the anterior lens capsule. (Courtesy of David M. Meisler, MD)

Posterior synechiae do not tend to form, unlike the case with phacoanaphylactic uveitis. White flocculant material may be observed floating in the anterior chamber or in the vitreous cavity.9,10 A similar material adherent to the lens capsule in the form of white patches is characteristic of phacolytic glaucoma (see Figs. 1 and 2). Epstein11 has emphasized the diagnostic importance of this finding, particularly in cases of dislocation of the lens into the vitreous cavity. Retinal perivasculitis has been observed in phacolytic glaucoma.10

Fig. 2. Small white patches on the anterior lens capsule in phacolytic glaucoma.

Histopathologic examination of eyes enucleated for phacolytic glaucoma (an outcome that should be rare) reveals liquefaction of the lens cortex and attenuation of the lens capsule, most notably the posterior capsule.5 Rupture of the capsule may be present more often than is clinically suspected. The inflammatory cell population is almost exclusively composed of bloated macrophages that appear to have engulfed lens material. The absence of significant levels of lymphocytes, plasma cells, and polymorphonuclear leukocytes is an important feature that differentiates phacolytic glaucoma from other forms of intraocular inflammation. Aqueous humor specimens obtained through diagnostic paracentesis or during cataract surgery may be evaluated by cytologic examination of material collected in a millipore filter or by phase-contrast microscopy.8,11,12 Observation of characteristic macrophages (Fig. 3) can provide confirmatory evidence but failure to identify cells does not rule out phacolytic glaucoma.13

Fig. 3. Lens-laden macrophages from aqueous aspirate in phacolytic glaucoma. (Courtesy of David M. Meisler, MD)

It is believed that heavy molecular-weight protein becomes soluble as liquefaction of the lens cortex develops. Most often, this protein diffuses into the anterior chamber through an intact (although possible rarefied) lens capsule but phacolytic glaucoma can develop after traumatic or spontaneous rupture of the capsule.14 The vitreous opacities that sometimes develop may represent protein leakage through the posterior capsule.9 Although infiltration of the aqueous outflow pathways with bloated macrophages may contribute to intraocular pressure elevation,5 Epstein and colleagues15,16 have presented clinical and experimental evidence that lens protein plays a more important role in outflow obstruction.

The definitive treatment for phacolytic glaucoma is cataract extraction, which eliminates the source of the outflow-obstructing lens protein. Medical therapy for glaucoma may help reduce intraocular pressure in preparation for surgery. During an extracapsular or phacoemulsification procedure, visualization of the anterior capsular flap is difficult because of the absence of a red reflex and the intense white background of the lens. Turning down the microscope illumination and obliquely illuminating the eye with an external light source may facilitate the safe completion of the anterior capsulotomy or capsulorhexis.17 The surgeon should remain mindful of the propensity for rupture of the posterior capsule during manipulation of a hypermature cataract. If this complication occurs, it is essential that all residual cortical and nuclear material be removed, using automated vitrectomy techniques if necessary. The prognosis for reduction of intraocular pressure and restoration of good visual acuity after prompt cataract surgery is generally good, even if limited vision and faulty light projection were present preoperatively.13,18,19 Vitreous opacities due to phacolytic glaucoma resolve after removal of the cataract without the need for vitrectomy.9

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Intraocular pressure elevation with uveitis may occur subsequent to release of lens material into the anterior chamber through a surgically or traumatically created opening in the lens capsule.11,20 Because this can occur years after an incomplete extracapsular cataract extraction—at a time when soluble lens protein has presumably been reabsorbed—it has been inferred that insoluble lens particles are responsible for outflow obstruction in this entity. The observation that irrigation of the anterior chamber to remove lens particles helps to control the glaucoma lends support to this theory. A cellular role in outflow obstruction is suggested by the report of bloated macrophages in the aqueous humor of a patient who developed this syndrome 67 years after incomplete extracapsular cataract extraction.21

The degree of intraocular pressure elevation and inflammation partially depends on the amount and physical state of the lens material liberated. Other factors, such as pre-existing outflow facility and individual immunologic differences, may explain why substantial amounts of retained lens cortex often are harbored by eyes that do not develop this syndrome. Cases involving relatively small amounts of lens material may be managed with corticosteroids and glaucoma medicines while allowing absorption of lens material. If the amount of dispersed lens substance is large, however, or the intraocular pressure elevation and inflammation are severe or protracted, surgical removal of the lens material by irrigation or aspiration, extraction, or automated vitrectomy techniques is indicated.


A secondary glaucoma that shares some features of both phacolytic glaucoma and lens particle glaucoma may result from intraoperative loss of lens material into the vitreous cavity through a posterior capsular rent or an area of zonular dialysis.22–27 The result tends to be a syndrome of poor vision, uveitis, corneal edema, and acute glaucoma in the early postoperative period. The knowledge that such a course may lie ahead could tempt the cataract surgeon to make a deep incursion into the vitreous cavity in an attempt to retrieve the dislocated lens fragments through the cataract incision. Such temptations are best resisted to avoid injury to the retina.28 Contemporary pars plana automated vitrectomy techniques in the hands of an experienced vitreoretinal surgeon offer the best chance for a successful outcome. Concomitant retinal endolaser or cryopexy, internal gas tamponade, or scleral buckling may be needed to treat retinal tears or detachment, which often complicate this syndrome. It is often possible for the anterior segment surgeon to primarily insert an intraocular lens during the cataract surgery without adversely affecting the ultimate visual outcome.24–27

Intravitreal lens cortex is better tolerated by the eye than nuclear material. If only a small amount of cortical material remains in the vitreous after cataract surgery, annoying floaters may be the only aftermath. Larger amounts of cortical material and even modest amounts of nuclear material tend to cause substantial uveitis and intraocular pressure elevation. In this case, occasionally it may be possible to weather the storm with corticosteroids and medical glaucoma therapy but most often vitrectomy is necessary. The optimal timing of vitrectomy has been the subject of some controversy. Blodi and colleagues23 reported that the incidence of chronic glaucoma is lower if vitrectomy is performed within 3 weeks of the cataract operation than when it is performed later. Other authors have been unable to confirm a correlation between the timing of vitrectomy and the incidence of chronic glaucoma after vitrectomy.25,26 In addition to chronic glaucoma, causes of visual loss despite vitrectomy include corneal decompensation, chronic uveitis, cystoid macular edema, proliferative vitreoretinopathy, and late retinal detachment. The greater the trauma to the eye during the cataract operation, the poorer the ultimate visual outcome is likely to be.

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Phacoanaphylactic uveitis (phacoanaphylactic endophthalmitis,29 phacoantigenic uveitis30) is a rarely diagnosed inflammatory condition believed to be the result of altered tolerance to lens proteins. The classic clinical presentation of this disease is a chronic granulomatous uveitis with onset 1 to 14 days after extracapsular cataract surgery or trauma to the crystalline lens.30,31 Latent periods between the presumed inciting event and the onset of uveitis have been reported to extend up to a year or more.32–34 In a large series of histopathologically confirmed cases, 20% of eyes had no history of trauma or evidence of a penetrating wound.35 This is in agreement with case reports of phacoanaphylactic uveitis after spontaneous rupture of the lens capsule or that occurring without clinical evidence of violation of the lens capsule.1,36 Mutton-fat keratitic precipitates and extensive synechia formation are typical findings, and hypopyon is sometimes observed. The fellow eye may exhibit a “sympathizing” uveitis that responds to bilateral lensectomy.37

In contrast to phacolytic glaucoma, phacoanaphylactic uveitis is usually not associated with glaucoma except occasionally in advanced stages. In a large series of confirmed cases, hypotony was diagnosed clinically in 58% of cases but glaucoma was diagnosed in only 17% of cases.35 If unchecked, phacoanaphylaxis may result in secondary open-angle glaucoma due to obstruction of outflow channels by inflammatory cells and debris.38 Angle closure can develop with pupillary block (due to posterior synechiae) or without pupillary block (due to inflammatory or neovascular peripheral anterior synechiae). Endstage disease may involve formation of a cyclitic membrane, retinal detachment, and phthisis bulbi, resulting in enucleation.

The most definitive diagnostic feature of phacoanaphylactic uveitis—a zonal type of granulomatous inflammation centered around residual lens material—has been observable only in enucleated eyes.39,40 The zone adjacent to the lens is composed of polymorphonuclear leukocytes, with epithelioid and giant cells making up the next zone. Lymphocytes and plasma cells occupy the zone most distant from the lens and also diffusely infiltrate the uveal tract. Foamy macrophages similar to those seen in phacolytic glaucoma have been observed.41

Phacoanaphylaxis is believed to be an immune complex disease that develops when the normal tolerance to lens proteins is abrogated.29 The mechanisms of sensitization to lens proteins after injury to the lens are poorly understood. Induction of autoimmunity to lens protein in an animal model requires coadministration of an adjuvant or use of a T-cell stimulating agent. The finding of bacteria in only 5% of specimens with phacoanaphylactic uveitis argues against a significant role of bacterial products as adjuvants in producing clinical disease.35

When granulomatous uveitis occurs after cataract surgery or lens injury, the clinical differentiation of phacoanaphylaxis from other causes of inflammation can prove difficult.29 This probably explains the low rate (5%) of correct clinical diagnosis of phacoanaphylaxis before enucleation in a large retrospective series.35 Fulminant uveitis occurring within the first 2 weeks after intraocular surgery or penetrating injury always requires consideration of infectious endophthalmitis, which is probably far more common than phacoanaphylactic uveitis.

Cases with a more indolent course or delayed onset may represent chronic infectious endophthalmitis caused by organisms of lesser virulence, such as Propionibacterium acnes, Candida species, Streptococcus epidermidis, or others.42–45 Aerobic and anaerobic vitreous cultures are crucial. Removal of any residual lens material using automated vitrectomy may be necessary if inflammation cannot be controlled medically. Removal of the posterior capsule may be required to control recalcitrant cases of chronic postoperative endophthalmitis.44 Histopathologic and microbiologic evaluation of excised tissue should be performed.41,46,47 If contemporary methods of diagnosis and treatment for infectious endophthalmitis after surgery or trauma are used and corticosteroids and vitrectomy are judiciously used, any clinically unsuspected phacoanaphylaxis is likely to be managed successfully.

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Increasing lens thickness due to growth of the lens cortex is a well-recognized factor in the development of primary angle-closure glaucoma.48 Other factors such as short axial length of the eye, pre-existing individual differences in the anatomy of the anterior segment, and zonular relaxation may also contribute variably. When angle-closure glaucoma develops due to intumescence of the lens that can be distinguished from normal lens growth, the term phacomorphic glaucoma is applied.49

Rapidly developing mature cataracts and cataracts caused by trauma or inflammation may involve sufficient swelling of the lens to induce phacomorphic glaucoma. The diagnosis of phacomorphic glaucoma should be entertained when unilateral or asymmetric cataract is associated with shallowing of the anterior chamber angle not explained by other factors. (e.g., miotic therapy, lens subluxation, or uveal effusion). It is wise to rule out a posterior segment mass in an eye with unilateral phacomorphic glaucoma, using ultrasonography if necessary.50

The differentiation of phacomorphic glaucoma from primary angle-closure glaucoma is sometimes difficult. Both conditions respond to laser iridotomy (unless extensive peripheral anterior synechiae exist), indicating a common mechanism of pupillary block. The uncommon development of phacomorphic glaucoma despite adequate iridotomy suggests that with extreme degrees of lens enlargement in small eyes, the peripheral iris may be directly pushed against the trabecular meshwork by the lens without pupillary block.51

The definitive treatment of phacomorphic glaucoma in eyes with potential for visual improvement is cataract surgery.19 Because angle-closure glaucoma can be precipitated or worsened by the mydriasis required for lens removal,52 laser iridotomy should be considered before cataract surgery to avoid the hazards of intraocular surgery in an eye with severe pressure elevation.51 The creation of a safe and controlled capsulorhexis during the cataract procedure may be facilitated by prior aspiration of liquid cortex from the lens using a 30-gauge needle.53

Just as angle closure can result from crowding of the anterior chamber angle by an enlarged lens, a similar process can occur with an average-sized lens in an extraordinarily small (nanophthalmic) eye. The nanophthalmic eye has been described as “a small eye with a small cornea, shallow anterior chamber, marked iris convexity, moderate to high hypermetropia, thick sclera, a normal or thick lens with a high lens/eye volume ratio, a high propensity for angle closure glaucoma, more frequently observed with increasing age, and often complicated by the presence of thickened choroid and /or nonrhegmatogenous retinal detachment.”54 The axial length of the globe is generally 20.5 mm or less. Although the lens is thicker than normal in some nanophthalmic eyes, lens extraction is not the procedure of choice for controlling angle-closure glaucoma because of the high incidence of intractable exudative detachment of the choroid and ciliary body with nonrhegmatogenous retinal detachment after intraocular surgery in this condition.54,55 Safer measures include medical therapy for glaucoma, laser iridotomy to relieve pupillary block, and laser iridoplasty to pull the peripheral iris away from the trabecular meshwork.56 The unusually thick nanophthalmic sclera may promote uveal effusion by compressing the vortex veins or by preventing normal transscleral diffusion of protein from the suprachoroidal space, resulting in accumulation of suprachoroidal fluid due to increased colloid osmotic pressure.57 Resolution of uveal effusion after vortex vein decompression, posterior sclerotomy to drain suprachoroidal fluid (with or without topical mitomycin C to prevent closure of the sclerotomy), or partial thickness sclerectomy has been reported.56–59 Performance of one or more of these procedures should be strongly considered before or during any intraocular surgery that becomes absolutely necessary in a nanophthalmic eye.

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Heritable abnormalities or acquired disruption of zonular support may allow the lens to decenter within the normal plane of its equator or to luxate anteriorly or posteriorly. Anterior movement of the lens, herniation of vitreous in areas of zonular deficiency, or both can lead to angle-closure glaucoma due to pupillary block. Although other mechanisms should be considered when managing patients with ectopia lentis60 (e.g., traumatic recession of the anterior chamber angle, phacolytic glaucoma, angle anomalies in aniridia), only pupillary block is considered here.

Ectopia lentis may present as an isolated disorder, accompany other ocular abnormalities, or be associated with systemic syndromes, many of which involve skeletal dysplasia (Table 2). In a Danish national study, the cause could be established in 69% of 396 cases of congenital extopia lentis.61 Of the identifiable causes, 68% of cases were due to Marfan's syndrome, 21% to ectopia lentis et pupillae, 8% to simple dominant ectopia lentis, 1.1% to homocyctinuria, 0.7% to Weill-Marchesani syndrome, and 0.7% to sulfite oxidase deficiency. When all cases are considered—including acquired ectopia lentis—trauma is probably the most common cause (Fig 4).62–64 Spontaneous lens dislocation is observed commonly in aniridia and rarely in exfoliation syndrome and buphthalmos. Syphilis should be included in the differential diagnosis of systemic conditions causing ectopia lentis.


TABLE 2. Conditions Associated With Ectopia Lentis

  Systemic Disorders
  Marfan's syndrome
  Marfan-like syndrome
  Familial pseudomarfanism
  Stickler's syndrome
  Vitreoretinopathy-encephalocele syndrome
  Weill-Marchesani syndrome
  Sulfite oxidase deficiency
  Sturge-Weber syndrome
  Crouzon's syndrome
  Pfandler's syndrome
  Ehlers-Danlos syndrome
  Refsum's syndrome
  Kniest syndrome and variants
  Klippel-Feil syndrome
  Wildervanck's syndrome
  Alport's syndrome
  Focal dermal hypoplasia syndrome
  Sprengel's deformity
  Cross-Khodadoust syndrome
  Primordial dwarfism
  Klinefelter's syndrome
  Lenz microphthalmia syndrome
  Rieger's syndrome
  Mandibulofacial dysostosis
  Ocular Disorders
  Trauma (including surgical)
  Familial simple ectopia lentis
  Genetic spontaneous late subluxation of the lens
  Ectopia lentis et pupillae
  Congenital glaucoma/buphthalmos
  Mature or hypermature cataract
  Exfoliation syndrome
  Cornea plana
  Blepharoptosis—high myopia syndrome
  Persistent hyperplastic primary vitreous
  Intraocular pentastomid larva
  Intraocular tumor
  Chronic uveitis

(Modified with permission from Ritch R: Glaucoma secondary to lens intumescence and dislocation. In Ritch R, Shield MB [eds]: The Secondary Glaucomas, p 134. St. Louis, CV Mosby, 1982)


Fig. 4. Traumatic cataract dislocated into the anterior chamber.

Lens dislocation is an important feature of several heredofamilial syndromes that also include skeletal dysplasias. Marfan's syndrome is the most prevalent of these. Characteristics of this dominantly inherited condition include long thin limbs (arachnodactyly), joint hyperextensibility, pectus excavatus, scoliosis, and premature death due to cardiovascular disease (primarily aortic dissection or cardiac valvular dysfunction). Enlargement of the globe and retinal detachment may occur. Bilateral lens dislocation occurs in 50% to 80% of patients but only a minority of those with ectopia lentis (8% in one series65) develop glaucoma. Dislocation of the lens into the anterior chamber is less common in Marfan's syndrome than in homocystinuria.65,66

Homocystinuria results from a variety of recessively inherited enzymatic deficiencies affecting the metabolism of homocysteine and methionine. Serum levels of these amino acids may improve with pyridoxine therapy and dietary modification in some patients. Tall, thin body habitus similar to that seen in Marfan's syndrome and generalized osteoporosis are common. About half of homocystinuria patients develop mental retardation. Progressive zonular degeneration results in lens dislocation in about 90% of patients. A tendency for thromboembolic events may cause death at an early age, posing a particular risk during and after general anesthesia. For this reason—and to make available intervention at the earliest possible time—biochemical screening for homocystinuria should be performed in all cases of nontraumatic lens dislocation without an obvious cause.67 Vascular occlusions in the retina and optic nerve have been reported in homocystinuria. Glaucoma developed in 24% of those with ectopia lentis in one series.65

Weill-Marchesani syndrome is characterized by brachymorphia (short digits and short stocky build), limited joint mobility, and microspherophakia transmitted in either a dominant or a recessive fashion. Micropherophakia occasionally occurs in association with other heritable syndromes or as an isolated abnormality. Microspheric lenses are larger in anteroposterior dimension and smaller in equatorial dimension than normal. The increased curvature of the lens surfaces and frequent occurrence of lens dislocation contribute to severe myopia and a high risk of angle closure glaucoma due to pupillary block.68–70

Several signs may be helpful in identifying subtle lens subluxation. Progressive myopia or noncorneal astigmatism may result from anterior displacement or tilting of the lens. Phacodonesis is most readily appreciated by observation of the lens while delivering a firm downward rap to the slit-lamp table or while the patient rapidly centers gaze from an eccentric position. Gonioscopy affords an excellent means of identifying iridodnesis in areas of zonular deficiency. Asymmetry of the depth of the anterior chamber angle between the two eyes or marked variations in depth from one quadrant to another in an affected eye can be helpful clues. Pupillary block due to ectopia lentis imparts a “volcano crater” contour to the central iris.71 Careful biomicroscopy may disclose a small bead of vitreous issuing through the pupil. At times, pupillary block may be position-dependent,72 and tonometry in various eye positions may reveal significant differences.

Pupillary block glaucoma associated with ectopia lentis is often best managed with laser iridotomy or surgical iridectomy. More than one laser iridotomy may be required to find a location where the vitreous is not adherent to the posterior iris. An iridotomy is less likely to become blocked by vitreous if performed over an area of intact zonules. Prophylactic iridotomy in Weill-Marchesani syndrome has been advocated.73 Miotic therapy may exacerbate pupillary block by allowing anterior movement of the lens in cases where partial zonular integrity remains. Worsening of angle-closure glaucoma is particularly likely when eyes with microspherophakia are treated with miotics.68 Iridectomy eliminates this problem, allowing safe use of miotics to prevent dislocation of the lens into the anterior chamber. Cycloplegia can help break an angle-closure attack in eyes with some residual zonular function by pulling the lens posteriorly. This approach increases the risk of dislocation of a freely mobile lens into the anterior chamber, however.71 Cycloplegia-induced angle closure without ectopia lentis in WeillMarchesani syndrome has been reported.74 Lens extraction is usually not the procedure of choice for managing angle-closure glaucoma due to ectopia lentis because of the associated vitreoretinal complications. Many of the conditions listed in Table 2 are accompanied by high degrees of axial myopia or peripheral retinal degeneration. Modern automated lensectomy-vitrectomy techniques allow removal of a dislocated lens with a lower incidence of retinal detachment than that encountered with older techniques.75–78 Lensectomy may be indicated if ectopia lentis is complicated by uncorrectable optical problems (especially in young children at risk for amblyopia), phacolytic glaucoma, suspected phacoanaphylaxis, pupillary block unresponsive to iridotomy, or cases of lens dislocation into the anterior chamber that fail to reverse with mydriasis and supine positioning.

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49. Appleton B, Lowrey A: Phacogenic glaucoma. Am J Ophthalmol 47:682, 1959

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52. Civerchia LL, Balent A: Intraocular lens implantation in acute angle closure glaucoma associated with cataract. Am Intraocular Implant Soc J 11:171, 1985

53. Rao SK, Padmanabhan P: Capsulorhexis in eyes with phacomorphic glaucoma. J Cataract Refract Surg 24:882, 1998

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55. Ryan EA, Zwaan J, Chylak LT: Nanophthalmos with uveal effusion: Clinical and embryologic considerations. Ophthalmology 89:1013, 1982

56. Jin JC, Anderson DR: Laser and unsutured sclerotomy in nanophthalmos. Am J Ophthalmol 109:575, 1990

57. Brockhurst RJ: Cataract surgery in nanophthalmic eyes. Arch Ophthalmol 108:965, 1990

58. Kocak I, Altintas AGK, Yalvac IS et al: Treatment of glaucoma in young nanophthalmic patients. Int Ophthalmol 20:107, 1997

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