the impact of outpatient diabetes

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The Impact of Outpatient DiabetesManagement on Serum Lipids in Urban

African-Americans With Type 2 DiabetesDIANE M. ERDMAN, PHARMD1

CURTISS B. COOK, MD2

KURT J. GREENLUND, PHD3

WAYNE H. GILES, MD3

IMAD EL-KEBBI, MD2

GINA J. RYAN, PHARMD4

DANIEL L. GALLINA, MD2

DAVID C. ZIEMER, MD2

VIRGINIA G. DUNBAR, BS1

LAWRENCE S. PHILLIPS, MD2

OBJECTIVE Treating dyslipidemia in diabetic patients is essential, particularly amongminority populations with increased risk of complications. Because little is known about theimpact of outpatient diabetes management on lipid outcomes, we examined changes in lipidprofiles in urban African-Americans who attended a structured diabetes care program.

RESEARCH DESIGN AND METHODS A retrospective analysis of initial and 1-yearfollow-uplipidvalues was conductedamong patients selected from a computerizedregistry of anurban outpatient diabetes clinic. The independent effects of lipid-specific medications, glycemiccontrol, and weight loss on serum total cholesterol, LDL cholesterol, HDL cholesterol, andtriglyceride levels were evaluated by analysis of covariance and multiple linear regression.

RESULTS In 345 patients (91% African-American and 95% with type 2 diabetes), HbA1c

decreased from 9.3% at the initial visit to 8.2% at 1 year (P 0.001); total and LDL cholesteroland triglyceride levels were significantly lower, and HDL cholesterol was higher. After stratifyingbased on use of lipid-specific therapy, different outcomes were observed. In 243 patients nottaking dyslipidemia medications, average total cholesterol, LDL cholesterol, and triglycerideconcentrations at 1 year were similar to initial values, whereas in 102 patients receiving phar-macotherapy, these lipid levels were all lower at 1 year relative to baseline ( P 0.001). MeanHDL cholesterol increased regardless of lipid treatment status (P 0.001). After adjusting forother variables, changes in LDL cholesterol concentration were associated only with use oflipid-specific agents (P 0.003), whereas improved HbA

1cand weight loss had no independent

effect.Lipidtherapy,improvedglycemic control, andweight loss were not independently relatedto changes in HDL cholesterol andtherefore could notaccount for thepositive changes observed.Use of lipid-directed medications, improvement in glycemic control, and weight loss all resultedin significant declines in triglyceride levels but only improved HbA

1cand weight loss had an

independent effect.

CONCLUSIONS Among urban African-Americans, diabetes management led to favor-able changes in HDL cholesterol and triglyceride levels, but improved glycemic control andweight loss had no independent effect on LDL cholesterol concentration. Initiation of pharma-cologic therapy to treat high LDL cholesterol levels should be considered early in the course ofdiabetes management to reach recommended targets and reduce the risk of cardiovascular

complications in this patient population.

Diabetes Care 25:915, 2002

Diabetes is recognized as an indepen-dent risk factor for cardiovasculardisease (CVD) (1), and cardiovas-

cular outcomes are less favorable thanin those without diabetes (26). How-ever, little progress has been made in re-ducing heart disease mortality in diabeticpatients when compared with the nondi-abetic U.S. population (7). The pathogen-esis of heart disease in individuals withdiabetes is complex, but serum lipids are

frequently abnormal and likely contributeto the increased risk of CVD (8,9). Be-cause use of medications that improvelipid profiles can also reduce CVD riskamong individuals with diabetes (1012), aggressive intervention is recom-mended when dyslipidemia is detected(13).

Recent data indicate that recom-mended clinical targets for lipids are notbeing achieved among patients at highrisk for CVD (14). Structured diabetesprograms have been shown to improveglycemic control, but there is actually lit-tle information about the impact of suchprograms on the severity of dyslipidemiain type 2 diabetes, particularly in popula-tions enriched in ethnic groups at in-creased risk of diabetes-related CVDmortality (1519).

In our setting, which serves primarilyAfrican-Americans with type 2 diabetes,patients typically have LDL cholesterollevels that fall outside of American Diabe-tes Association (ADA) clinical targets,with an average value of 140 mg/dl at pre-sentation (20). Low HDL cholesterol is

less common, and only a low percentageof patients have hypertriglyceridemia(20). Therefore, interventions directedat lowering LDL cholesterol and raisingHDL cholesterol should take priority indecisions about the choice of therapyfor dyslipidemia. To determine the im-pact of diabetes care on serum lipids inthis population, we examined the inde-pendent effects of lipid-directed phar-macotherapy, glycemic control, andweight loss on lipid outcomes after 1year of treatment.

From the 1Grady Health System Atlanta, and the 2Division of Endocrinology and Metabolism, Departmentof Medicine, Emory University School of Medicine; the 3Division of Adult and Community Health, NationalCenter for Chronic Disease Prevention and Health Promotion, the Centers for Disease Control and Preven-tion; and the 4Department of Pharmacy Practice, Mercer University, Atlanta, Georgia.

Address correspondence and reprint requests to Curtiss B. Cook, MD, Diabetes Unit, Emory UniversitySchool of Medicine, 69 Butler St., S.E., Atlanta, GA 30303. E-mail: [email protected].

Received for publication 12 April 2001 and accepted in revised form 21 September 2001.Abbreviations:ADA, American Diabetes Association; ANCOVA, analysis of covariance; CVD, cardiovas-

cular disease; HMG, hydroxymethylglutaryl.A table elsewhere in this issue shows conventional and Systeme International (SI) units and conversion

factors for many substances.

C l i n i c a l C a r e / E d u c a t i o n / N u t r i t i o n

O R I G I N A L A R T I C L E

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RESEARCH DESIGN AND

METHODS

Overview of treatment programThe diabetes treatment program has beendescribed previously (17,18). Briefly, in-tensive education in lifestyle modifica-tion, self-management training, and diet,coupled with intensification of medicaltherapy when needed to control hyper-glycemia, have been integral parts of ourstructured care program. The overalltreatment approach has been shown toresult in significantly lower HbA

1clevels

(17,18).

Patient selectionPatients who initially presented to theprogram between 1991 and 1998 wereselected from a computerized registry if

they had a 1-year (52 10 weeks) fol-low-up visit andif serum total cholesterol,HDL cholesterol, LDL cholesterol, andtriglyceride levels were measured at boththe initial (baseline) and 1-year visits. Wechose a 1-year follow-up because we be-lieved this would be a sufficient amountof time to expect life-style and pharmaco-logic interventions to take effect or be ini-tiated. Data on lipid-specific medicationsfor these patients were obtained from thecomputerized Pharmacy and Drug Infor-mation system maintained by the healthsystem.

Laboratory studies andmeasurementsSerum total cholesterol, HDL cholesterol,and triglyceride levels were determinedon fasting blood samples using standardtechniques as described previously (21).Because LDL cholesterol levels were de-termined using the Friedewald equation,patients with triglyceride levels 400mg/dl were not included in the analysis(22); only 4% of African-American pa-tients in our setting have triglyceride lev-

els400 mg/dl (20).

AnalysesPatients were stratified into individuals re-ceiving medical therapy for dyslipidemiaat 1 year (pharmacotherapy group) andindividuals not receiving lipid-directedtherapy (nonpharmacotherapy group),and lipid outcomes were examined sepa-rately for each category. Pharmacother-apy patients included individuals inwhom medication was maintained or in-creased during the 1-year follow-up as

well as individuals for whom therapy wasinitiated. Statistical differences betweengroups were tested on log-transformeddata using either paired or unpaired Stu-dents t tests, and 2 analysis was used forproportions.

To evaluate the impact of care onreaching lipoprotein targets, we exam-ined LDL cholesterol, HDL cholesterol,and triglyceride distributions using ADAclinical guidelines applicable to the timeencompassed by the data set. Before1998, the recommended goal for LDLcholesterol was 130 mg/dl, and drugtreatment was suggested for values 160mg/dl. The proportion of patients meet-ing the ADA definition of an HDL choles-terol level at high risk for CVD was alsodetermined, using sex-specific criteria(35 mg/dl in men and 45 mg/dl inwomen). Finally, we determined the per-centage of patients at goal (200 mg/dl)for triglyceride levels (23).

We next determined the independenteffects of lipid-directed therapy, im-proved glycemic control, and weight losson changes in LDL cholesterol, HDL cho-lesterol, and triglyceride concentrationsusing both analysis of covariance (AN-COVA) and multiple linear regression.For the ANCOVA, patients were stratifiedaccording to lipid therapy status (therapyversus no therapy), whether they had a

reduction in HbA1c level (HbA1c im-proved versus not improved), and byweight loss (weight loss versus no weightloss). HbA

1cwas defined as improved if

there was a decrease of0.5% at 1 year;the HbA

1c not improved group was ex-pected to include individuals in whomHbA1c values were similar or higher thanbaseline. Weight loss was defined as a de-crease of1.0 kg at 1 year; it was antici-pated that the no weight loss categorywould incorporate individuals whoseweight was either unchanged or increased

compared with their initial visit. A changein lipoprotein concentration relative tobaseline was considered significant if the95% CI did not cross zero. Statistical dif-ferences in the changes in lipid levels be-tween categories were tested afteradjusting for patient age, duration of dia-betes, sex, race, baseline lipid levels,mode of treatment for hyperglycemia,and year of initial visit.

Using multiple linear regressionmodels, we separately evaluated the inde-pendent effect of lipid therapy, weight

change, and HbA1c

change on change inLDL cholesterol, HDL cholesterol, andtriglyceride levels (all defined as year mi-nus baseline values). Analyses were ad-

justed as for the ANCOVA.

RESULTS

Patient characteristicsWe identified 345 patients in whom totalcholesterol, LDL cholesterol, HDL choles-terol, and triglyceride levels were mea-sured at the initial and 1-year visits. Atpresentation, the mean age of this studygroup was 57 years, mean weight was89.6 kg, and mean BMI was 32.6 kg/m2;68% were women, 91% were African-

American, and 95% had type 2 diabetes.The mean duration of diabetes was 5.4years. Average HbA1c declined from 9.3

to8.2%(P 0.001) by 1 year in the studygroup. Patients not included in the anal-yses (n 5,728) were slightly younger(52 years, P 0.001) at presentation, hada similar duration of diabetes (5.4 years),had a comparable weight (88.0 kg) butslightly lower BMI (31.6 kg/m2, P 0.019), and similar HbA

1c(9.3%) relative

to those studied. The proportion ofwomen and African-Americans were sim-ilar.

Among study patients, there were de-creases in total cholesterol (219 to 212mg/dl, P 0.001), LDL cholesterol (148to 139mg/dl, P0.001), and triglyceride(148 to 142 mg/dl, P 0.007) concentra-tions and an increase in HDL cholesterollevel (47 to 50 mg/dl, P 0.001). Com-pared with the study patients at the initialvisit, those not analyzed had lower totalcholesterol, LDL cholesterol, and HDLcholesterol values (207, 136, and 46 mg/dl, respectively; P 0.04) and higher butnot significantly different triglyceride lev-els (167 mg/dl, P 0.94). Subsequentanalyses focused on those in the studygroup.

Lipid profiles innonpharmacotherapy patientsThe mean HbA

1clevel of nonpharmaco-

therapy patients (n 243) declined sig-nificantly (P 0.001) relative to theinitial visit, with an average decrease of1.0% (Table 1). Despite the improvementin HbA

1c, the total cholesterol, LDL cho-

lesterol, and triglyceride concentrationsat 1 year were comparable to levels foundat the initial visit (all P 0.28).

LDL cholesterol distributions of non-

Diabetes care and lipids in African-Americans

10 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002


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lipid levels (Table2). Use of lipid-directedtherapy was associated with a significantdecline in LDL cholesterol level, whichwas statistically greater than that detectedin individuals not given lipid-directedtherapy (P 0.003). Improved HbA1cwas also associated with a significant de-crease in LDL cholesterol, but this was notdifferent from that in individuals with noimprovement in HbA

1c(P 0.47). Los-

ing1 kg body weight was not associatedwith a significant decrease in LDL choles-terol concentration, and changes werecomparable between weight-loss catego-ries (P 0.86). Therefore, only use oflipid-directed therapy was independentlyassociated with decrease in LDL choles-terol levels.

HDL cholesterol concentrations in-creased significantly in most categories,but changes were similar regardless of

lipid therapy status (P 0.80), HbA1coutcome (P 0.44), or weight loss (P 0.82). Lipid therapy, improvement inHbA

1c, andweight loss were allassociated

with significant decreases in triglyceridelevels, but only weight loss demonstratedan independent effect (P 0.035) (Table2). Results of ANCOVA analyses werecomparable if stricter definitions wereused for improvement in HbA

1c(1.0%)

or weight loss (decrease 2.5 kg) (notshown).

Using multiple linear regression, re-

sults mostly agreed with the ANCOVA.Lipid therapy was significantly associated(P 0.028) with change in LDL choles-terol, whereas change in HbA

1cand

weight had no independent effect (bothP 0.43); HbA1c, use of lipid therapy,and weight did not significantly impactHDL cholesterol (all P 0.50). Weightchange was related to change in triglycer-ides (P 0.0085), whereas use of lipidtherapy had no effect (P0.76). Theonly

exception to the ANCOVA results wasthat change in HbA

1cwas significantly re-

lated to change in triglyceride level (P 0.027).

After 1994, our program becamemore aggressive in intensifying therapyfor hyperglycemia, which resulted in bet-ter HbA1c outcomes compared with ear-lier years (24). Therefore, we performedthe above analyses on the subset of pa-tients seen between 1995 and 1998. The1-year HbA1c outcome for 19951998was 7.9%, compared with 8.6% for19911994 (P 0.013). Despite the bet-ter HbA

1coutcome for 19951998, re-

peat ANCOVA and multiple l inearregression analyses of this patient subsetshowed the relationships between HbA

1c,

weight, and lipid medications with lipidlevels the same as for the whole study pe-

riod of 19911998 (data not shown).

CONCLUSIONS The 345 patientsin this study had significant reductions inlevels of HbA1c, total cholesterol, LDLcholesterol, and triglycerides as well as anincrease in HDL cholesterol, which is ev-idence that the diabetes management pro-gram improved both glycemic controland serum lipids. However, lipid out-comes were not affected uniformly by tra-ditional program components such asglycemic control, weight loss, and lipid-directed pharmacotherapy.

We detected significant reductions inLDL cholesterol only in patients given lip-id-directed pharmacotherapy. Patients

Figure 2LDL cholesterol distribution for patients on lipid pharmacotherapy at 1 year.

Table 2Effect of lipid therapy, glyemic control, and weight loss on LDL cholesterol, HDLcholesterol, and triglyceride changes (mg/dl)

Change

in LDL

Change

in HDL

Change in

triglycerides

Lipid pharmacotherapy at 1 year

No 2 (7 to 3) 3 (15) 1 (9 to 8)

Yes 27 (38 to 16)* 2 (05) 17 (31 to3)HbA

1cat 1 year

Not improved 6 (13 to 0) 2 (1 to 4) 1 (9 to 12)

Improved (decrease 0.5%) 12 (20 to 5) 3 (15) 11 (20 to1)

Weight change at 1 year

No weight loss 11 (17 to 4) 2 (14) 1 (10 to 8)

Lost weight (decrease 1.0 kg) 8 (15 to 0) 3 (16) 14 (26 to 3)

Data are means (95% CI). Changes in lipids de fined as 1 year minus initial values. Negative changes denotea decrease and positive changes an increase in lipid concentration compared with initial visit. Analyses wereconducted by ANCOVA and were adjusted for other variables in the table plus patient age, duration ofdiabetes,race (African-Americanversus other), sex, hyperglycemia treatment (diet, oral agents, insulin),yearof initial visit, and initial lipid values. *Significantly different from those not on therapy (P 0.003);significantly different from baseline (CI does not cross zero); significantly different from those withoutweight loss (P 0.035).




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classifiedas improved HbA1c

had a sub-stantial decrease in HbA

1cand achieved

an average level of 7.4% after 1 year and avalue close to national standards (13).Individuals classified as not improvedhad an increase in HbA

1c, but the change

in LDL cholesterol was comparable re-gardless of final glycemic status. Simi-larly, patients with weight loss lost anaverage of 5.6 kg, whereas individualsclassified as no weight loss gained 4.0kg, and changes in LDL cholesterol werealso comparable between groups. This isconsistent with findings from anotherstudy, in which intensive versus nonin-tensive lifestyle modification resulted insimilar declines in LDL cholesterol among

African-American patients with type 2 di-abetes (25). Our results suggest that al-though glycemic control and weight

management are cornerstones of diabetestherapy, neither intervention may play amajor role in improving LDL cholesterolin populations comparable to ours. Life-style modification must continually beemphasized and reinforced in overall di-abetes care and may lower cardiovascularrisk through factors not examined here.Our finding that LDL cholesterol declinedeven among individuals who did not ex-perience HbA

1cimprovement or weight

loss may be explained by other manage-ment elements such as lifestyle modifica-tion (changes in diet composition and/orphysical activity). Because we do not cap-ture data on exercise or dietary habits, weare unable to retrospectively assess the ef-fects of these interventions on lipid pro-files. Because the decrease in LDLcholesterol was highly associated with useof lipid-specific pharmacotherapy, our re-sults indicate that early introduction oflipid-modifying agents into the treatmentprogram should be given strong consid-eration for patients with high LDL choles-terol levels.

Recent data indicate that detection

and treatment of high LDL cholesterol of-ten falls short of national recommenda-tions (14,26,27). Although this study wasnot designed to examine practice pat-terns, our data also indicatethat providerswere not sufficiently aggressive in theirmanagement when high LDL cholesterolconcentrations were found. Guidelinesoperating during 1998 and earlier sug-gested institution of pharmacotherapy foran LDL cholesterol value 160 mg/dl(23), but in our study, 25% of the un-treated patients had levels higher than

this threshold and remained withouttherapy at 1 year. Moreover, nearly one-third of treated patients still had LDLcholesterol levels 160 mg/dl at 1 year,implying delayed or insufficient inten-sification of therapy. Since 1998, a morestringent clinical target for LDL choles-terol in diabetes, with a goal of100mg/dl, has been suggested by the ADA,and it is a goal now recommended by theNational Cholesterol Education Program(28). It is not yet known whether practi-tioners have responded to the recom-mended lower targets for LDL cholesterolwith more aggressive use of medicationtherapy.

We have defined previously clinicalinertia as a failure to intensify therapywhen such action is needed and not oth-erwise contraindicated. Studying the ba-

sis for clinical inertia and implementingmeasures to overcome it can result in ad-ditional improvement in glycemic controlof a population (24). Successful diabetesmanagement requires attention to multi-ple metabolic parameters. When practi-tioners are focused on a single healthproblem, other processes of care may notbe delivered (29). It is possible that theintense concentration on treating hy-perglycemia may have detracted fromaggressively managing dyslipidemia. Ex-amination of potential barriers in themanagement of dyslipidemia requiresfurther investigation and is underway(30).

Although the diabetes care programled to an increase in HDL cholesterol con-centrations, an encouraging observationindicating the benefit of the program onthis lipoprotein, definite variables that ac-counted for this change were not identi-fied. The therapies examined here(glycemic control, weight loss, and lipidpharmacotherapy) were not indepen-dently associated with changes in HDLcholesterol. Other components of the ed-

ucation and treatment paradigms mayhave resulted in higher HDL cholesterol.Nevertheless, despite improvement in theHDL cholesterol profile after 1 year ofmanagement, a substantial proportion ofpatients still had levels that would conferincreasedcardiovascular risk. In this anal-ysis, there was a predominant use ofHMG-CoA reductase inhibitors, whichtypically have only a modest effect onHDL cholesterol levels (13,23). These ob-servations suggest that HDL cholesterolmay have been underemphasized as an

independent target of intervention whenpractitioners made therapeutic decisionsand indicates a potential need to increaseawareness of the benefits of increasingHDL cholesterol (31) during the course ofdiabetes care.

Although use of lipid medication sig-nificantly reduced triglyceride concentra-tion relative to baseline, this effect wasstatistically similar to the change seenamong patients not on lipid therapy. Thedecrease in triglyceride level with im-proved HbA

1cwas also significant com-

pared with baseline. Although the resultsof the ANCOVA indicated that improvedHbA1c did not have an independent effecton triglyceride change, multiple linear re-gression confirmed the effect of glycemiccontrol on this lipoprotein. Weight lossalso independently affected triglyceride

levels; the average change in the weight-loss category was significantly greaterthan in the noweight-loss group and in-dicates that even the modest weight de-crease detected here would likely bebeneficial in the management of hypertri-glyceridemia.

Certain limitations to the study mustbe noted. Because LDL cholesterol levelstended to be high and triglyceride levelstended to be low in our patient popula-tion, LDL cholesterol was of primary in-terest to us. Therefore, we retrospectivelyselected patients according to whetherlevels of this lipoprotein were available.This led to statistical differences in somecharacteristics between the study popula-tion and those not included in the analy-ses. Although the clinical significance ofthese small differences is unclear, thestudy sample size, although still informa-tive about the results of care, may not re-flect eventual changes in the lipid profilesof the larger patient base. A recent studysupports findings from the Diabetes Con-trol and Complications Trial that achiev-ing glycemic control improves lipid status

among patients with type 1 diabetes(32,33). Studies examining the relation-ship between achieving normal bloodglucose levels and the effect it has on se-rum lipids among patients with type 2 di-abetes have yielded inconsistent results(25,34). For instance, in contrast to otherdata, our educational program resulted ina significant improvement in HDL choles-terol levels (25). The findings here mightbe specific to our clinic population, whichis enriched in African-Americans, whotypically have a lipid profile different

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from that of Caucasians (20). Additionalstudies are required to determine whetherour observations can be generalized toother clinical settings and whether indi-vidual lipoproteins remain at target overlonger follow-up periods. Studies focus-ing on lipid levels rather than just glyce-mic control as primary outcomes of careare needed in diabetes.

Our analysis shows how serum lipidsare likely to respond within the context ofroutine diabetes care. Standard ap-proaches to managing diabetes will likelybenefit HDL cholesterol and triglyceridelevels, even without use of lipid-directedmedications, but glycemic control andweight management may provide littlebenefit in reducing high LDL cholesterollevels. In accordance with what is becom-ing recognized increasingly (35), our re-

sults indicate that patients with elevatedLDL cholesterol concentrations may needearly introduction of lipid-specific agentsinto their treatment programs rather thanwait a long period to observe effects ofnonpharmacologic approaches. More-over, education programs aimed at lipid-related decision-making by providersmay be needed to increase attention tomanagement of all aspects of diabetic dys-lipidemia beyond improving LDL cho-lesterol alone. Establishing the mosteffective methods of achieving recom-mended lipid targets will be needed toreduce the morbidity and mortality ofCVD in diabetic patients at high risk.

Acknowledgments This study was sup-ported by awards from the Agency for Health-care Research andQuality (HS-09722)and theNational Institutes of Health (DK-33475 andDK-48124).

References1. Barrett-Connor E, Wingard DL:Heart dis-

ease and diabetes. In Diabetes in America.

Washington, DC, U.S. Govt. Printing Of-fice, 1995, p. 429 456 (NIH publ. no.95-1468)

2. Stamler J, Vaccaro O, Neaton J, Went-worth D: Diabetes, other risk factors, and12-year cardiovascular mortality for menscreened in the Multiple Risk Factor In-tervention Trial. Diabetes Care 16:434 444, 1993

3. Haffner SM, Lehto S, Ronnemaa T,Pyorala K, Laakso M: Mortality from cor-onary heart disease in subjects with type 2diabetes and in nondiabetic subjects withand without prior myocardial infarction.

N Engl J Med 339:229 234, 19984. Abbott RD, Donahue RP, Kannel WB,

Wilson PW: The impact of diabetes onsurvival following myocardial infarctionin men vs women: the FraminghamStudy. JAMA 260:3456 3460, 1988

5. Herlitz J, Karlson BW, Edvardsson N,

Emanuelsson H, Hjalmarson A: Prognosisin diabetics with chest pain or othersymptoms suggestive of acute myocardialinfarction. Cardiology 80:237245, 1992

6. Miettinen H, Lehto S, Salomaa V, Ma-honen M, Niemela M, Haffner SM,Pyorala K, Tuomilehto J: Impact of diabe-tes on mortality after the first myocardialinfarction: the FINMONICA MyocardialInfarction Register Study Group. DiabetesCare 21:69 75, 1998

7. Gu K, Cowie CC, Harris MI: Diabetes anddecline in heart disease mortality in USadults. JAMA 281:12911297, 1999

8. Steiner G: Risk factors for macrovascular

disease in type 2 diabetes: classic lipid ab-normalities. Diabetes Care 22 (Suppl. 3):C6 C9, 1999

9. Laakso M: Lipids and lipoproteins as riskfactors for coronary heart disease in non-insulin-dependent diabetes mellitus. AnnMed 28:341345, 1996

10. Pyorala K, Pedersen TR, Kjekshus J,Faergeman O, Olsson AG, ThorgeirssonG: The Scandinavian Simvastatin Sur-vival Study (4S): cholesterol loweringwith simvastatin improves prognosis ofdiabetic patients with coronary artery dis-ease: a subgroup analysis of the Scandina-vian Simvastatin Survival Study (4S).

Diabetes Care 20:614 620, 199711. Goldberg RB,Mellies MJ, Sacks FM,Moye

LA, Howard BV, Howard WJ, Davis BR,Cole TG, Pfeffer MA, Braunwald E: Car-diovascular events and their reductionwith pravastatin in diabetic and glucose-intolerant myocardial infarction survivorswith average cholesterol levels: subgroupanalyses in the cholesterol and recurrentevents (CARE) trial: the Care Investiga-tors. Circulation 98:25132519, 1998

12. Haffner SM, Alexander CM, Cook TJ,Coccuzzi SJ, Musliner TA, Pederson TR,Kjekshus J, Pyorala K, for the Scandina-vian Simvistatin Survival Study Group:

Reduced coronary events in simvastatin-treated patients with coronary heart dis-ease and diabetes or impaired fastingglucose levels: subgroup analysis in theScandinavian Simvastatin Survival Study.Arch Intern Med 159:26612667, 1999

13. American Diabetes Association: Manage-ment of dyslipidemia in adults with dia-betes. Diabetes Care 22:S56 S59, 1999

14. Pearson TA, Laurora I, Chu H, Kafonek S:The Lipid Treatment Assessment Project(L-TAP): a multicenter survey to evaluatethe percentages of dyslipidemic patientsreceiving lipid-lowering therapy and

achieving low-density lipoprotein choles-terol goals. Arch Intern Med 160:459 467, 2000

15. Peters AL, Davidson MB: Application of adiabetes managed care program. DiabetesCare 21:10371043, 1998

16. de Sonnaville JJ, Bouma M, Colly LP, Dev-

ille W, Wijkel D, Heine RJ: Sustainedgood glycaemic control in NIDDM pa-tients by implementation of structuredcare in general practice: 2-year follow-upstudy. Diabetologia 40:1334 1340, 1997

17. Ziemer DC, Goldschmid M, Musey VC,Domin WS, Thule PM, Gallina DL, Phil-lips LS: Diabetes in urban African Ameri-cans. III. Management of type II diabetesin a municipal hospital setting. Am J Med101:2533, 1996

18. Cook CB, Ziemer DC, El-Kebbi I, GallinaDL, Dunbar VG, Ernst KL, Phillips LS: Di-abetes in urban African Americans. XVI.Overcoming clinical inertia improves gly-

cemic control in patients with type 2 dia-betes. Diabetes Care 22:1494 1500, 1999

19. Centers for Disease Control and Preven-tion: Diabetes Surveillance, 1997. Atlanta,GA, U.S. Department of Health and Hu-man Services, 1997

20. Cook CB, Erdman DM, Ryan GJ, Green-lund KJ, Giles WH, Gallina DL, El-KebbiI, Ziemer DC, Ernst KL, Dunbar VG, Phil-lips LS: The pattern of dyslipidemia amongurban African Americans with type 2 dia-betes. Diabetes Care 23:319 324, 2000

21. Kahn HS, Dunbar VG, Ziemer DC, Phil-lips LS: Diabetes in urban African Ameri-

cans. XII. Anthropometry for assessingmunicipal hospital outpatients recentlydiagnosed with type 2 diabetes. ObesityRes 6:247254, 1998

22. Friedewald WT, Levy RI, FredericksonDS: Estimation of low-density lipoproteincholesterol in plasma without use of thepreparative ultracentifuge. Clin Chem 18:499 502, 1972

23. American Diabetes Association:Detectionand management of lipid disorders in di-abetes. Diabetes Care 19 (Suppl. 1):S96 S102, 1996

24. Cook CB, Ziemer DC, El-Kebbi I, GallinaDL, Dunbar VG, Ernst KL, Phillips LS: Di-

abetes in urban African Americans. XVI.Overcoming clinical inertia improves gly-cemic control in patients with type 2 dia-betes. Diabetes Care 22:1494 1500, 1999

25. Agurs-Collins TD, Kumanyika SK, TenHave TR, Adams-Campbell LL: A random-ized controlled trial of weight reductionand exercise for diabetes management inolder African-American subjects. DiabetesCare 20:15031511, 1997

26. Giles WH, Anda RF, Jones DH, SerdulaMK, Merritt RK, DeStefano F: Recenttrends in the identification and treatmentof high blood cholesterol by physicians:




7/7

progress and missed opportunities. JAMA269:11331138, 1993

27. Frolkis JP, Zyzanski SJ, Schwartz JM, Su-han PS: Physician noncompliance withthe 1993 National Cholesterol EducationProgram (NCEP-ATPII) guidelines. Circu-lation 98:851 855, 1998

28. Expert Panel on Detection, Evaluation,and Treatment of High Blood Cholesterolin Adults: Executive summary of theThird Report of the National CholesterolEducation Program (NCEP) Expert Panelon Detection, Evaluation, and Treatmentof High Blood Cholesterol in Adults(Adult Treatment Panel III). JAMA 285:2486 2497, 2001

29. Fontana SA, Baumann LC, Helberg C,Love RR: The delivery of preventive ser-vices in primary care practices according

to chronic disease status. Am J PublicHealth 87:1190 1196, 1997

30. Sciutto C, Phillips LS, Miller CD, CookCB, Dunbar V, Gallina DL, El-Kebbi IM:Barriers to management of hypercholes-terolemia in patients with type 2 diabetes(Abstract). Diabetes 50:1047-P, 2001

31. Rubins HB, Robins SJ, Collins D, Fye CL,Anderson JW, Elam MB, Faas FH, LinaresE, Schaefer EJ, Schectman G, Wilt TJ, Wittes J, for the Veterans Affairs High-Density Lipoprotein Cholesterol Inter-vention Trial Study Group: Gemfibrozilfor the secondary prevention of coronaryheart disease in men with low levels ofhigh density lipoprotein cholesterol.N Engl J Med 341:410 418, 1999

32. The Diabetes Control and ComplicationsTrial Research Group: Effect of intensive

diabetes management on macrovascularevents and risk factors in the DiabetesControl and Complications Trial. Am JCardiol 75:894 903, 1995

33. Perez A, Wagner AM, Carreras G, Gime-nez G, Sanchez-Quesada JL, Rigla M, Go-mez-Gerique JA, Pou JM, de Leiva A:

Prevalence and phenotypic distributionof dyslipidemia in type 1 diabetes mel-litus. Arch Intern Med 160:2756 2762,2000

34. Purnell JQ,BrunzellJD: Effect of intensivediabetes therapy on diabetic dyslipide-mia. Diabetes Reviews 5:434 444, 1997

35. Dyslipidemia and diabetes mellitus: path-ophysiology and treatment [article on-line]. Available from http://www.ndei.org/patient/clinical_commandments. Accessed27 August 2001.

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