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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptNIH Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
J Pediatr. Author manuscript; available in PMC Nov 1, 2012.
Published in final edited form as:
PMCID: PMC3193560

Clinical Status and Cardiovascular Risk Profile of Adults with a History of Juvenile Dermatomyositis



A pilot study of adults who had onset of juvenile dermatomyositis (JDM) in childhood, before current therapeutic approaches, to characterize JDM symptoms and subclinical cardiovascular disease.

Study design

Eight adults who had JDM assessed for disease activity and 8 healthy adults (cardiovascular disease controls) were tested for carotid intima media thickness and brachial arterial reactivity. Adults who had JDM and 16 age-, sex-, and body mass index-matched healthy metabolic controls were evaluated for body composition, blood pressure, fasting glucose, lipids, insulin resistance, leptin, adiponectin, proinflammatory oxidized high-density lipoprotein (HDL), and nail-fold capillary end row loops.


Adults with a history of JDM, median age 38 years (24–44 years) enrolled a median 29 years (9–38 years) after disease onset, had elevated disease activity scores, skin (7/8), muscle (4/8), and creatine phosphokinase (2/8). Compared with cardiovascular disease controls, adults who had JDM were younger, had lower body mass index and HDL cholesterol (P = .002), and increased intima media thickness (P = .015) and their brachial arterial reactivity suggested impairment of endothelial cell function. Compared with metabolic controls, adults who had JDM had higher systolic and diastolic blood pressure, P = .048, P = .002, respectively; lower adiponectin (P = .03); less upper arm fat (P = .008); HDL associated with end row loops loss (r = −0.838, P = .009); and increased proinflammatory oxidized HDL (P = .0037).


Adults who had JDM, 29 years after disease onset, had progressive disease and increased cardiovascular risk factors.

Juvenile dermatomyositis (JDM) is characterized by symmetric proximal muscle weakness, a typical rash, and objective evidence of muscle inflammation.1 The hallmark of JDM is systemic microvascular injury to arterioles and capillaries, reflected in a decrease in the number of nail-fold capillary end row loops (ERL),2 the development of prominent cutaneous telangiectasia, as well as histologic evidence of intravascular and perivascular inflammation.1 The pathophysiology of JDM includes genetic susceptibility, environmental factors, and infectious triggers, with associated activation of complement and the cellular and humoral immune systems.1

The course of JDM can be either unicyclic or chronic, and the activity of persistent inflammation can be assessed by an elevated disease activity score3 and by quantitation of the number of nail-fold capillary ERL, which drop out with chronic inflammation.2 Risk factors for less-favorable outcomes and continued disease activity include a longer duration of untreated disease,4 younger age at presentation, and an A vs G polymorphism in the tumor necrosis factor-α (TNF-α)-308 promoter region.5

Cardiovascular involvement has rarely been documented in JDM, and most commonly includes cardiac arrhythmias in the child,6 or reports of myocardial infarction in adults.7 The physiology of the disease itself, with its metabolic abnormalities,8 as well as the treatment of JDM, which includes prolonged corticosteroid administration, may predispose to accelerated cardiovascular disease (CVD).

The presence of cardiovascular disease in adults who had JDM in childhood and, according to the standards of the time, were treated less aggressively at diagnosis, has not been evaluated. In this study, we tested the oldest patients who had been diagnosed with definite JDM for whom we had inception data. We recruited 8 adults diagnosed with JDM in childhood to evaluate the extent of disease activity and to assess their cardiovascular risk profiles.


All research complied with the Helsinki Declaration and was approved by the institutional review boards at Children’s Memorial Hospital (CMH), Chicago, Illinois (nos. 2002–12345, 2007–12974, GCRC 1037) and Northwestern University, Chicago, Illinois (STU00009196 to R.R-G.).

Twenty-five subjects of the more than 400 patients in our database qualified for the study. We sought adults who had JDM, who were 25–45 years old, and who had a definite or possible JDM diagnosis without overlap syndrome (such as antibody to UI-ribonucleoprotein or polymyositis-scleroderma antigens), or polymyositis. Of the 25 potential candidates, 8 were eligible and agreed to participate in this pilot study (JDM). Their previous CMH records were extracted for disease presentation. Adults who had JDM were assessed for disease activity, ERL, cardiovascular risk, and metabolic function. Two of the 8 smoked cigarettes (1 pack a week). Seven were not taking medications for the treatment of JDM or any other medications that interfere with glucose metabolism. Subject no. 7 was noncompliant in taking 5 mg/d (0.06 mg/kg) of oral prednisone for the 2 months preceding the study.

Sixteen healthy, nonsmoking participants (metabolic controls [Met-C]), matched 2:1 to adults who had JDM based on age, sex, and body mass index (BMI) enrolled. Historical data, anthropometric measurements, physical examination, blood sample (after an 8-hour fast), and ERL studies were obtained. A convenience sample was identified of 8 healthy subjects who had cardiovascular testing identical to the adults who had JDM in a concurrent rheumatologic research project (cardiovascular disease control [CVD-C]).

Disease Assessment

Adults who had JDM were evaluated by using a validated disease activity score of skin and muscle involvement,3 which were developed for children and used for comparison with previous diagnostic data. Eight fingers for each subject were studied for ERL, as previously described.2 Muscle enzymes were determined by standard methodology (aldolase, ultra-voilet kinetic assay; creatine kinase, alanine aminotransferase, aspartate aminotransferase by enzymatic rate method), Neopterin by immunoassay (DRG international, Mountainside, New Jersey), and von Willebrand factor antigen (vWF:Ag) in citrated plasma by using a turbidimetric assay.

Metabolic Assessment

Weight (kg) and height (cm) were rounded to the nearest tenth. BMI z score and height z score were calculated (Epi Info 2000; wwwn.cdc.gov/epiinfo/html/downloads.htm). Adult height z score were based on z scores for 20 year olds. Skin-fold data obtained by 1 of 2 experienced nutritionists (mid arm circumference, waist, and hips measured to 0.1 cm; triceps and subscapular to 0.1 mm) were compared with reference percentiles.9 Fasting glucose was determined by the hexokinase method, and insulin was determined by radioimmunoassay (cat. no. H1-14K; Millipore/Linco Research Inc, Billerica, Massachusetts). Cholesterol and triglycerides were determined by the timed-endpoint method, and high-density lipoprotein (HDL) was determined by the direct HDL-cholesterol method. Low-density lipoprotein–cholesterol was calculated by using total cholesterol – HDL – (triglycerides/5). Leptin and adiponectin were analyzed by radioimmunoassay (Millipore/Linco Research). Proinflammatory oxidized HDLs were evaluated in the laboratory of Navab and Fogelman by using previously published methodology.10

Fasting insulin and the homeostasis model assessment of insulin resistance (HOMA-IR: [glucose (mmol/L) × insulin (µU/mL)]/22.5) were used as markers of insulin resistance.11 Higher HOMA-IR reflected more insulin resistance. An approximate value of 4 represents insulin resistant state.12 The 75th percentile HOMA-IR in 5900 adults without diabetes >20 years of age was 2.86.13 Features of metabolic syndrome were based on the International Diabetes Federation and the American Heart Association/National Heart, Lung, and Blood Institute consensus.14

Subclinical Cardiovascular Assessment

The subjects underwent measurement of carotid intima media thickness (IMT) with a 8L5 linear transducer attached to a Sequoia 256 (Accuson Siemens, Mountain View, California) machine by using standard positioning and long-axis imaging planes. The B-mode imaging gain was set to allow optimal visualization of the intima-luminal interface.15 Images were obtained from the common carotid artery, carotid bulb, and internal carotid artery bilaterally, and measured (Image J [a public domain, Java-based image processing program developed at the National Institutes of Health]). The IMT was determined to be the largest value to the far wall of each segment.

Supine, fasting subjects for brachial arterial reactivity (BAR) were studied with a 8L5 linear transducer attached to an Sequoia 256 (Accuson Siemens) in a temperature-controlled environment between 7:30–9:30 a.m. A blood pressure cuff was placed distal to the elbow, and an imaging window for the brachial artery in long axis was obtained. The brachial arterial lumen equals the trailing edge of the intima to the leading edge of the opposite intima. The blood pressure cuff was inflated to 30 mm Hg over the systolic blood pressure, held for 5 minutes, and released. Images were reobtained in the same location at 60 and 90 seconds after cuff deflation and were measured offline by using Image J (www.rsbweb.nih.gov/ij/). The percentage change equals the greater of the percent changes from the 60 second or 90 second timepoints compared with baseline; values for a change less than 5% are considered abnormal, and 7%–10% change is normal.16 After a 5-minute rest, the adults who had JDM and the Met-C subjects had manual blood pressure performed, by using the correct-size cuff, in triplicate, and then averaged.

Statistical Analysis

HOMA-IR, insulin, and leptin results were log transformed for statistical analysis. Nonparametric tests were used due to the small sample size. Comparisons of adults who had JDM and healthy controls for CVD-C studies were performed (Mann-Whitley U test) (Table I). Adults who had JDM were compared with the closely matched Met-C subjects by using the Friedman test for continuous measures and Cochran Q for nominal measures (Table II). The Spearman rank correlation coefficients were used as appropriate. Adjustments for multiple comparisons were not made because this is a study with a modest sample size, the intent of which was to highlight those aspects that warrant further investigation. SPSS software version 12 (SPSS/IBM Corporation, Somers, New York) and SAS 9.1 (SAS Institute, Cary, North Carolina) were used for all analyses.

Table I
Cardiovascular studies of adults with a history of childhood JDM compared with controls
Table II
Metabolic features of adults with a history of childhood JDM compared with age-, sex-, BMI-matched controls


The initial disease characteristics of the 8 adults with a history of JDM, followed up for a median of 29 years (range, 9–38 years) after onset of disease are described in Table III. They had been diagnosed with JDM, from January 1968 to November 1997, and examined by 1 investigator (L.P.). Patient nos. 4, 5, and 6 were in treatment for 1.5, 2.8, and 2.3 years, respectively, before their first visit at CMH. At the time of the study, the subjects had not taken any medications for JDM for a median of 20 years (range, 0.1–30 years). Medication history included oral prednisone (8/8), methotrexate (4/8), intravenous methylprednisolone (4/8), hydroxychloroquine (2/8), azathioprine (1/8), cyclosporine (1/8).

Table III
Adults with childhood JDM: characteristics at initial presentation and follow-up

Physical and laboratory findings at follow-up are also listed in Table III. At the time of study, none of the adults who had JDM had been seen recently by a physician for JDM symptoms, despite the fact that all but one adult who had JDM had persistent skin erythema, which reflects disease activity or previous medication use, and 4 of 8 had weakness, which was severe in 2 cases, secondary to fixed flexion contractures after chronic damage and fibrosis. All of the ERL were less than the reference range, 3.1–6.0 (reference range, ≥6.8).2 In contrast, standard laboratory indicators of inflammation were negative. Two adults had a slightly elevated creatine phosphokinase (CPK), whereas both vWF:Ag, and neopterin (a marker of T-cell–dependent macrophage activation in JDM)1 were within normal limits. Of note, subject nos. 1, 5, 6, 7, and 8 had a family history of diabetes; subject nos. 5, 6, 7, and 8 also had a family history of coronary artery disease; and subjects 5 and 7 had a family history of hypertension.

Subject no. 4 had the highest CPK, severe disease activity, severe lipoatrophy, and decreased number of ERL (5.4). He also had metabolic derangements (insulin resistance, impaired glucose homeostasis, low adiponectin), hypertension, dyslipidemia, and extensive subclinical cardiovascular risks. This person had a normal BMI, normal waist circumference but an elevated waist-hip ratio, decreased upper arm fat area, and buccal fat loss typical of lipodystrophy in people with JDM.

The demographics and metabolic findings in the adults who had JDM and their closely matched controls are summarized in Table II. The adults who had JDM were shorter, despite similar BMI, and 63% had lipodystrophy. The adults who had JDM had significantly decreased triceps skin thickness and decreased upper arm fat area, which indicates loss of fat, and 4 of 8 had buccal fat wasting. Markers of insulin resistance were not significantly different, yet adiponectin and HDL-cholesterol were significantly lower in adults who had JDM (P = .03 for both). In addition, adults who had JDM had a higher prevalence of individual metabolic features, and 2 patients met the criteria for metabolic syndrome. The results of the assessment for subclinical cardiovascular disease in the adults who had JDM compared with CVD-C are presented in Table I. Adults who had JDM, despite being younger and having lower median BMI, had more evidence of disease than their healthy CVD-C. Indices of atherosclerotic burden, as assessed by IMT were worse in adults who had JDM compared with CVD-C. A greater proportion of adults who had JDM (5/8) compared with CVD-C (3/8) had a BAR less than 5%.16

There were no significant associations between the disease activity score of skin and markers of subclinical cardiovascular disease, blood pressure, or lipids. However, the 2 subjects with the most severe weakness also had the highest markers of insulin resistance and impaired fasting glucose. The number of ERL was not associated with indicators of subclinical cardiovascular disease but was negatively associated with fasting serum concentrations of HDL (r = −0.838, P = .009) (Figure, A).

Figure 1
A, Comparison of data from adults with JDM in childhood depicting nail-fold ERL and routine measurements of HDL. B, Box plot comparing data for the oxidized HDL inflammatory index for adults who had JDM and age-, sex-, race-, and BMI-matched controls. ...

CPK, one of the standard tests of inflammatory myopathies, was significantly associated with triglyceride-HDL ratio (r = 0.786, P = .021). The plasma level of vWF:Ag, although in the normal range, was positively associated with common carotid IMT (r = 0.814, P = .014) but negatively associated with the diagnosis of metabolic syndrome. Although the HDL-cholesterol was lower in adults who had JDM than in controls, the adults who had JDM had higher oxidized HDL inflammatory indices than metabolic controls (Figure, B).


There is a paucity of long-term follow-up studies of patients diagnosed with JDM in childhood, despite their apparent predisposition to increased traditional cardiovascular risk factors. The average duration of follow-up studies of children with inflammatory myopathy diagnosed in North America ranges from 7.2 years17 to 10.1 years.18 A recent case-control assessment of cardiac function in adults with JDM living in Norway for a median of 16.8 years after disease onset identified increased hypertension, as found in our eight adult patients who had JDM assessed for disease activity.19 They also documented left ventricular diastolic dysfunction on electrocardiogram, which indicates subclinical cardiovascular impairment.19

Many factors theoretically can contribute to increased cardiovascular risk in JDM. Children with JDM demonstrate a prothrombotic milieu mediated by thrombospondin-1,20 which was highly associated with the TNF-α-308 A polymorphism,21 present in twice as many JDM as ethnicity matched controls.5 JDM with active vasculopathy may have increased serum levels of vWF:Ag released from damaged endothelial cells.1 However, in this study, the vWF:Ag was within normal range for blood group antigen, as were the neopterin levels, which often are elevated in JDM at diagnosis1 and are considered a biomarker of inflammation in heart disease as well.22

The patients with JDM may have derangement of their lipid metabolism. A recent report demonstrated that the lipodystrophy associated with JDM in childhood is accompanied by hypertriglyceridemia and insulin resistance.23 However, we did not find similar associations in this small sample of adult patients. Pope et al24 also reported a lower frequency of metabolic abnormalities than expected in their patients with lipodystrophy, many of whom had JDM. Prevalence of metabolic abnormalities also may be related to type of lipodystrophy, focal, partial, or generalized, and are most common in those with generalized lipodystrophy.23 By inspection, 2 of 8 subjects had generalized lipodystrophy, 3 others had partial lipodystrophy.

In this study, half of the adults who had JDM had decreased muscle function, and all but one had some evidence of cutaneous inflammation. Despite this, traditional markers of inflammatory myositis were normal, except for 2 subjects, who had modestly elevated CPKs. The clinical abnormalities may be a result of flares of the myositis or may reflect residual deficits from previously treated flares. Our findings strongly suggest that the adults who had JDM have evidence of subclinical cardiovascular disease despite their relatively young age and low BMI. The increased IMT found in our adults who had JDM suggests an increased risk for atherosclerosis. It is increasingly recognized that atherosclerosis is an inflammatory process with many features in common with the rheumatologic diseases, and, conversely, chronic inflammatory rheumatic disease is associated with accelerated atherosclerosis, as is the case in patients with pediatric systemic lupus erythematosus.25 Some adult patients with JDM have evidence of calcium deposition in their carotid arteries. Although not part of this study protocol, two of the patients with JDM underwent coronary arterial computed tomography, a predictor of cardiovascular events, which showed extremely elevated calcium scores for age (patient nos. 5 and 6). There also was a trend toward evidence of endothelial dysfunction in patients with JDM, as suggested by the BAR. Although the percentage of BAR change did not quite reach statistical significance, the median BAR in the JDM group was abnormal (3.7%), whereas the BAR in the controls was within the reference limits (8.3%).

In other rheumatologic diseases, such as systemic lupus erythematosus, elevated levels of leptin and adiponectin have been reported and thought to be due to underlying inflammatory disease process.26 Leptin links metabolic status and the immune system, where it can augment autoimmunity. In this study, unlike individuals with other rheumatologic diseases, the leptin concentrations in adults who had JDM were not elevated. Inasmuch as leptin is usually positively correlated with adipose tissue, we speculate that the lack of elevation of leptin in adults with JDM in childhood is directly related to the decreased adipose tissue characteristic of lipodystrophy. In fact, both leptin deficiency and a low adiponectin have been identified in syndromes of lipodystrophy. In addition, the low adiponectin found in adults who had JDM compared with controls is similar to observations in obesity-related inflammatory processes that are associated with lower adiponectin.26 It is important to note that our adults who had JDM were not, in general, either insulin resistant or obese. An alternative explanation for the low adiponectin may be that adults who had JDM with at least one TNF-α-308 A allele may produce increased levels of TNF-α,5 which in vitro suppresses adiponectin production.26 Adiponectin is thought to be cardioprotective and plays a role in inhibiting inflammation and in promoting normal endothelial function.27 Therefore, low adiponectin may contribute to the cardiovascular risk identified in our subjects.

As expected, the adults who had JDM had lower HDL. However, within the JDM group, lower ERL was associated with higher HDL; the highly significant inverse correlation between ERL and HDL (r = −838, P = .009) was not expected (Figure, A). This paradox could be explained by the presence of a high-level of circulating proinflammatory HDL, as shown by the elevated oxidized HDL inflammatory index in adults who had JDM compared with their closely matched controls (P = .0037) (Figure, B). HDL therefore, may be deleterious in people with JDM, rather than protective, and may be associated with vascular damage. The presence of increased proinflammatory, oxidized HDL in patients with other rheumatologic diseases (systemic lupus erythematosus, rheumatoid arthritis) has previously been documented.28

Some of the acknowledged limitations of this pilot study are the small number of patients and that the study group was composed of more men than women, thus limiting detailed analyses. In addition, the majority of study subjects were diagnosed over 24 years ago, when indicators of inflammatory activity had not been identified and therapeutic intervention was not as aggressive as it currently is, or the medications were not available. It is clear that prospective patients will be needed to explore the natural course of JDM as treated youth progress through adulthood as well as to document evolution and burden of cardiovascular disease in adults treated for JDM in childhood. We suggest that childhood-onset JDM might be added to the list of conditions that appear to be associated with accelerated atherosclerosis in adulthood. The predisposition to cardiovascular disease in patients with JDM is most likely multifactorial in a setting of chronic inflammation.


We thank the adults who had JDM, as well as the control subjects who participated in this study. We are grateful to Gabrielle A. Morgan, MA, for her expert data collection and management. We also acknowledge Donald Zimmerman, MD, and Tamar Polonsky, MD, who reviewed the findings; Christine Sullivan, BS, for assistance with statistical review; Elisa Rhew, MD, for contributing healthy controls for CVD studies; Sue Cowen, RD, for skin-fold measurements; the laboratories of Drs Navab and Fogelman for the HDL inflammatory index assay, Maria Amoruso, MPH, for organizing the scheduling of patients; and Kelli Day and Pearon Hampton for expert manuscript assistance.

Supported in part by Northwestern University’s Clinical and Translational Science Award (1UL1RR025741-01), National Institutes of Health (5M01 RR00048 and R01-AR48289 to L.P., and K24 AR 002138, MO1 RR 00048, and P60 AR48098 to R.R-G.). Cure JM Foundation (to L.P.), Macy’s Miracle Foundation (to L.P.), and Mary Kirkland Center for Lupus Research and Rheuminations Inc (to R.R-G.).


Brachial arterial reactivity
Body mass index
Blood pressure
Children’s Memorial Hospital
Creatine phosphokinase
Cardiovascular disease
Cardiovascular disease controls
End row loops
High-density lipoprotein
Homeostasis model assessment of insulin resistance
Intima media thickness
Juvenile dermatomyositis
Metabolic controls
Tumor necrosis factor-a
von Willebrand factor antigen


Presented in part at the American College of Rheumatology (Emier M et al, “Abnormal Cardiovascular Risk Profile in Adult Patients with Juvenile Dermatomyositis” Arthritis Rheum 54:S 519, no. 1243,2006).


1. Feldman BM, Rider LG, Reed AM, Pachman LM. Juvenile dermatomyositis and other idiopathic inflammatory myopathies of childhood. Lancet. 2008;371:2201–2212. [PubMed]
2. Christen-Zaechs S, Seshadri R, Sundberg J, Paller AS, Pachman LM. Juvenile dermatomyositis: persistent association of nailfold capillaroscopy changes and skin involvement over 36 months with duration of untreated disease. Arthritis Rheum. 2008;58:571–576. [PMC free article] [PubMed]
3. Bode RK, Klein-Gitelman MS, Miller ML, Lechman TS, Pachman LM. Disease activity scores for children with juvenile dermatomyositis (JDM): reliability and validity evidence. Arthritis Care Res. 2003;49:7–15. [PubMed]
4. Pachman LM, Abbott K, Sinacore JM, Amoruso L, Dyer A, Lipton R, et al. Duration of illness is an important variable for untreated children with juvenile dermatomyositis. J Pediatr. 2006;148:247–253. [PubMed]
5. Pachman LM, Liotta-Davis M, Hong D, Kinsella TR, Mendez E, Kinder J, et al. TNF-α-308 A allele in juvenile dermatomyositis: association with increased TNFa production, disease duration, and pathological calcifications. Arthritis Rheum. 2000;43:2368–2377. [PubMed]
6. Pachman LM, Cooke N. Juvenile dermatomyositis: a clinical and immunological study. J Pediatr. 1980;96:226–234. [PubMed]
7. Lundberg IE. The heart in dermatomyositis and polymyositis. Rheumatology (Oxford) 2006;45 Suppl 4:iv18–iv21. [PubMed]
8. Coyle K, Rother KI, Weise M, Ahmed A, Miller FW, Rider LG. Metabolic abnormalities and cardiovascular risk factors in children with myositis. J Peds. 2009;155:882–887. [PMC free article] [PubMed]
9. Frisancho AR. Anthropometric Standards for the Assessment of Growth and Nutritional Status. Ann Arbor: University of Michigan Press; 1990.
10. Navab M, Imes SS, Hama SY, Hough G, Ross L, Bork R, et al. Monocyte transmigration induced by modification of low density lipoprotein in cocultures of human aortic wall cells is due to induction of monocyte chemotactic protein 1 synthesis and is abolished by high density lipoprotein. J Clin Invest. 1991;88:2039–2046. [PMC free article] [PubMed]
11. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412–419. [PubMed]
12. Quon MJ. Limitations of the fasting glucose to insulin ratio as an index of insulin sensitivity. J Clin Endocrinol Metab. 2001;86:4615–4617. [PubMed]
13. Chen J, Wildman RP, Hamm LL, Muntner P, Reynolds K, Whelton PK, et al. Association between inflammation and insulin resistance in U.S. nondiabetic adults: results from the Third National Health and Nutrition Examination Survey. Diabetes Care. 2004;27:2960–2965. [PubMed]
14. Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120:1640–1645. [PubMed]
15. El-Atrozy T, Nicolaides AN, Tegos T, Griffin M. The effect of B-mode ultrasonic image standardization on the echodensity of symptomatic and asymptomatic carotid bifurcation plaques. Int Angiol. 1998;17:179–186. [PubMed]
16. Taylor AJ, Merz CNB, Udelson JE. 34th Bethesda conference: “Can atherosclerosis imaging techniques improve the detection of patients at risk for ischemic heart disease?”; J Am Coll Cardiol; 2003. pp. 1855–1917. [PubMed]
17. Huber A, Feldman BM. Long-term outcomes in juvenile dermatomyositis: how did we get here and where are we going? Curr Rheumatol Rep. 2005;7:441–446. [PubMed]
18. Collison CH, Sinal SH, Jorizzo JL, Walker FO, Monu JU, Snyder J. Juvenile dermatomyositis and polymyositis: a follow-up study of long-term sequelae. South Med J. 1998;91:17–22. [PubMed]
19. Schwartz T, Sanner H, Husebye T, Flato B, Sjaastad I. Cardiac dysfunction in juvenile dermatomyositis: a case-control study. Ann Rheum Dis. 2011;70:766–771. [PubMed]
20. Isenberg JS, Martin-Manso G, Maxhimer JB, Roberts DD. Regulation of nitric oxide signaling by thrombospondin 1: implications for anti-angiogenic therapies. Nat Rev Cancer. 2009;9:182–194. [PMC free article] [PubMed]
21. Lutz J, Huwiler KG, Fedczyna T, Lechman TS, Crawford S, Kinsella TR, et al. Increased plasma thrombospondin-1 (TSP-1) levels are associated with the TNF α-308A allele in children with juvenile dermatomyositis. Clin Immunol. 2002;103:260–263. [PubMed]
22. Fuchs D, Avanzas P, Arroyo-Espliguero R, Jenny M, Consuegra-Sanchez L, Sanchez L, Kaski JC. The role of neopterin in atherogenesis and cardiovascular risk assessment. Curr Med Chem. 2009;16:4644–4653. [PubMed]
23. Bingham A, Mamyrova G, Rother KI, Oral E, Cochran E, Premkumar A, et al. Predictors of acquired lipodystrophy in juvenile-onset dermatomyositis and a gradient of severity. Medicine (Baltimore) 2008;87:70–86. [PMC free article] [PubMed]
24. Pope E, Janson A, Khambalia A, Feldman B. Childhood acquired lipodystrophy: a retrospective study. J Am Acad Dermatol. 2006;55:947–950. [PubMed]
25. Schanberg LE, Sandborg C, Barnhart HX, Ardoin SP, Yow E, Evans GW, et al. Premature atherosclerosis in pediatric systemic lupus erythematosus: risk factors for increased carotid intima-media thickness in the atherosclerosis prevention in pediatric lupus erythematosus cohort. Arthritis Rheum. 2009;60:1496–1507. [PMC free article] [PubMed]
26. Fantuzzi G. Adiponectin and inflammation: consenus and controversy. J Allergy Clin Immunol. 2008;121:326–330. [PubMed]
27. Shibata R, Ouchi N, Murohara T. Adiponectin and cardiovascular disease. Circ J. 2009;73:608–614. [PubMed]
28. McMahon M, Grossman J, Skaggs B, FitzGerald J, Sahakian L, Ragavendra N, et al. Dysfunctional proinflammatory high-density lipoproteins confer increased risk of atherosclerosis in women with systemic lupus erythematosus. Arthritis Rheum. 2009;60:2428–2437. [PMC free article] [PubMed]
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