focal areas of edema within the inner retinal layers, cystoidspaces, small hemorrhages, and disruption of the photorecep-tors.6 Acute pancreatitis may also be associated with otherfactors that may contribute to the development of retinopa-thy such as fat embolization, increased venous pressure,retinal arteriolar spasm, fluctuations in blood pressure, andanemia.

This report describes a case of Purtscher-like retinopathyoccurring in association with pancreatic adenocarcinoma.The pathophysiologic mechanism for this association isnot clear. The condition may represent a paraneoplasticsyndrome. It may have been associated with subclinicalpancreatitis or alternatively may have been a precedingsign of pancreatitis.7 It is also possible that pancreaticinsult, such as invasion by a tumor, results in the release ofactivated protease enzymes, setting off a cycle of comple-ment activation and microvascular occlusion. Pancreaticadenocarcinoma should be included in the list of systemicconditions associated with Purtscher-like retinopathy.

REFERENCES

1. Purtscher O. Angiopathia retinae traumatica. Lymphor-rhagien des Augengrundes. Albrecht von Graefes Arch Oph-thalmol 1912;82:347–371.

2. Gass JDM. Stereoscopic atlas of macular diseases: diagnosisand treatment. St Louis: Mosby-Year Book, Inc, 1997.

3. Inkeles DM, Walsh JB, Matz R. Purtscher’s retinopathy inacute pancreatitis. Am J Med Sci 1976;272:335–338.

4. Kelley JS. Purtscher’s retinopathy related to chest compression

by safety belts: fluorescein angiographic findings. Am J Oph-thalmol 1972;74:278–283.

5. Snady ML, Morse PH. Retinopathy associated with acutepancreatitis. Am J Ophthalmol 1985;100:246–251.

6. Kincaid MC, Green WR, Knox DL, Mohler C. A clinicopath-ological case report of retinopathy of pancreatitis. Br J Oph-thalmol 1982;66:219–226.

7. Sanders RJ, Brown GC, Brown A, Gerner EW. Purtscher’sretinopathy preceding acute pancreatitis. Ann Ophthalmol1992;24:19–21.

Is Serum Cholesterol Associated WithProgression of Diabetic Retinopathyor Macular Edema in Persons WithYounger-Onset Diabetes ofLong Duration?Barbara E. K. Klein, MD, Ronald Klein, MD, andScot E. Moss, MA

Accepted for publication June 23, 1999.From the Department of Ophthalmology and Visual Sciences, Univer-

sity of Wisconsin Medical School, Madison, Wisconsin (B.E.K.K., R.K.,S.E.M.). This study was supported by grant EY03083 from the NationalInstitutes of Health, Bethesda, Maryland (R.K., B.E.K.K.), and in part byResearch to Prevent Blindness, Inc, New York, New York (R.K.; SeniorScientific Investigator Award).

Inquiries to Barbara E. K. Klein, MD, MPH, Department of Ophthal-mology and Visual Sciences, University of Wisconsin–Madison, 610North Walnut St, 460 WARF, Madison, WI 53705-2397; fax: (608)263-0279; e-mail: kleinb@epi.ophth.wisc.edu

FIGURE 2. Axial computed tomography of the abdomen shows a large mass in the tail of the pancreas with direct extension to theperipancreatic fat (open arrowhead) and metastasis to the portal nodes and liver (arrow).

AMERICAN JOURNAL OF OPHTHALMOLOGY652 NOVEMBER 1999

PURPOSE: To quantitate the relationships of total choles-terol and high-density lipoprotein cholesterol to theincidence and progression of diabetic retinopathy andmacular edema 5 years later in those with younger-onsetdiabetes of long duration.METHODS: Casual serum specimens for lipid values andfundus photography at the time of the lipid determina-tions were evaluated with regard to retinal lesions inphotographs taken 5 years later during the course of apopulation-based cohort study.RESULTS: Univariable associations were significant forassociations of incident retinal lesions with total choles-terol/high-density lipoprotein cholesterol, but multi-variable associations considering covariates were notsignificant.CONCLUSION: Our data suggest that lowering cholesterolby therapeutic means may not be indicated for the solepurpose of decreasing the incidence or progression ofthese retinal lesions. (Am J Ophthalmol 1999;128:652–654. © 1999 by Elsevier Science Inc. All rightsreserved.)

SERUM LIPIDS HAVE BEEN SUSPECTED TO BE RISK FAC-

tors for diabetic retinopathy and macular edema. Chewand associates1 reported that in the Early Treatment ofDiabetic Retinopathy Study cohort there was a relation-ship of total and of low-density lipoprotein cholesterol andretinal hard exudates. The association of lipid-loweringagents and retinopathy is being evaluated in clinical trials.In a subset of persons participating in the WisconsinEpidemiologic Study of Diabetic Retinopathy (WESDR),Klein and associates2 reported a cross-sectional relation-ship between total cholesterol and the prevalence of hardexudates in the macula but no relationship of these lipidlevels to the severity of diabetic retinopathy.

We report total cholesterol and high-density lipoprotein(HDL) cholesterol determinations on serum samples of theentire participating cohort of the younger-onset group inthe WESDR population to determine whether a relation-ship exists among these lipid fractions and the severity ofdiabetic retinopathy, retinal hard exudates, and macularedema 5 years later.

The population has been described3,4 and the cohort has

FIGURE 1. Progression and incidence of retinal lesions in younger-onset persons with diabetes of 10 years’ duration or longer,1990–1992 to 1995–1996.

BRIEF REPORTSVOL. 128, NO. 5 653

been followed since 1980. The examinations relevant tothis report occurred in 1990–1992 in persons with 10 ormore years of type 1 diabetes, with further follow-up in1995–1996. Differences between participants and nonpar-ticipants have been described.3,4 Lipid determinationswere performed on a casual serum specimen.2 Severity ofretinopathy was assigned on the basis of gradings of fundusphotographs.4

In univariable analyses, direct relationships of totalcholesterol and inverse relationships of HDL cholesterol toprogression of retinopathy, progression to proliferativeretinopathy, incidence of macular edema, incidence ofhard exudates, and progression of hard exudates werefound, but in most cases the relationships were notsignificant. However, the ratio of total to HDL cholesterolwas significant (test for trend) for all end points (Figure 1).The relative risks comparing the highest with the lowestquartile for each end point were progression of retinopa-thy, 1.51 (95% confidence interval [CI], 1.10, 2.06);progression to proliferative retinopathy, 3.01 (95% CI,1.24, 7.32); incidence of macular edema, 4.27 (95% CI,1.58, 11.56); incidence of hard exudates, 1.74 (95% CI,1.07, 2.85); and progression of hard exudates, 1.79 (95%CI, 0.92, 3.48). When these relationships were analyzedwith multivariable models in which we consideredduration of diabetes, glycosylated hemoglobin, diastolicblood pressure, proteinuria, and body mass index ascovariates, these relationships were no longer statisti-cally significant.

The relationships of total and HDL cholesterol todiabetic retinal lesions initially suggested that these lipids,especially when combined as a ratio, were predictive.However, when taking other covariates into account, therelationships were diminished so that they were no longersignificant. Thus these data suggest that altering these lipidlevels by diet or pharmacologic means is not indicated forthe sole purpose of reducing the incidence or severity ofthese retinal lesions.

REFERENCES

1. Chew EY, Klein ML, Ferris FL III, et al. Association ofelevated serum lipid levels with retinal hard exudate indiabetic retinopathy: Early Treatment Diabetic RetinopathyStudy (ETDRS) Report 22. Arch Ophthalmol 1996;114:1079–1084.

2. Klein BEK, Moss SE, Klein R, Surawicz TS. The WisconsinEpidemiologic Study of Diabetic Retinopathy. XIII. Relation-ship of serum cholesterol to retinopathy and hard exudate.Ophthalmology 1991;98:1261–1265.

3. Klein R, Klein BEK, Moss SE, Cruickshanks KJ. The Wiscon-sin Epidemiologic Study of Diabetic Retinopathy. XIV. Ten-year incidence and progression of diabetic retinopathy. ArchOphthalmol 1994;112:1217–1228.

4. Klein R, Klein BEK, Moss SE, Cruickshanks KJ. The Wiscon-sin Epidemiologic Study of Diabetic Retinopathy. XVII. The14-year incidence and progression of diabetic retinopathy andassociated risk factors in type 1 diabetes. Ophthalmology1998;105:1801–1815. Brief Reports

Retinal Detachment AssociatedWith a Macular Hole in SeverelyMyopic EyesJun Akiba, MD, Suguru Konno, MD, andAkitoshi Yoshida, MD

PURPOSE: To investigate factors associated with extensiveretinal detachment in severely myopic eyes with a mac-ular hole.METHOD: Fifty-two consecutive eyes with a macular holeand severe myopia were retrospectively studied.RESULTS: An extensive retinal detachment, defined asextending beyond the cuff of subretinal fluid, was ob-served in 37 eyes (71%). Extensive retinal detachmentdeveloped in 36 (95%) of 38 eyes with a posteriorstaphyloma and in one (7%) of 14 eyes without aposterior staphyloma (P < .0001). Extensive retinaldetachment also developed in 32 (89%) of 36 eyes withcomplete posterior vitreous detachment and in five(31%) of 16 eyes without posterior vitreous detachment(P < .0001).CONCLUSION: Posterior staphyloma rather than antero-posterior vitreomacular traction may contribute to thedevelopment of retinal detachment associated with amacular hole in severely myopic eyes. (Am J Ophthal-mol 1999;128:654–655. © 1999 by Elsevier ScienceInc. All rights reserved.)

AMACULAR HOLE IN SEVERELY MYOPIC EYES OFTEN IS

associated with an extensive retinal detachment definedas extending beyond the cuff of subretinal fluid. However,such retinal detachments rarely develop in idiopathic macularhole cases, most of which have mild to moderate refractiveerrors. Tangential vitreous traction is thought to play animportant role in macular hole formation, but little is knownabout why a macular hole in severely myopic eyes tends todevelop an extensive retinal detachment.

To analyze factors associated with extensive retinal detach-ment, we retrospectively studied 52 consecutive eyes with amacular hole and severe myopia (.26 diopters of sphericalequivalent) in 50 Japanese patients (41 women, nine men;aged 36 to 78 years). The refractive errors ranged from 27 to226 diopters of spherical equivalent. The axial lengthsranged from 26.30 to 30.77 mm. The vitreous condition wasstudied biomicroscopically with a fundus preset lens. Statisti-cal analysis was performed with the chi-square test with Yatescorrection and Fisher exact test.

The macular holes ranged in size from one fifth to half ofa disk diameter. In 44 (85%) of the 52 eyes, the holes were

Accepted for publication July 7, 1999.From the Department of Ophthalmology, Asahikawa Medical College,

Asahikawa, Japan.Inquiries to Jun Akiba, MD, Department of Ophthalmology, Asa-

hikawa Medical College, 4-5-3-11 Nishikagura, Asahikawa 078-8510,Japan; fax: 81-166-68-2549; e-mail: jakiba@asahikawa-med.ac.jp

AMERICAN JOURNAL OF OPHTHALMOLOGY654 NOVEMBER 1999