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Keywords:

  • Juvenile arthritis;
  • Nutritional status;
  • Body mass index;
  • Lean body mass;
  • DEXA

Abstract

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. REFERENCES

Objective

Growth abnormalities and poor nutritional status have been reported in children with juvenile idiopathic arthritis (JIA). The aim of this study was to evaluate the impact of juvenile chronic rheumatic disease on current nutritional status in adult patients in remission or with active disease.

Methods

One hundred thirty-eight women and 82 men, aged >20 years, with JIA were studied after a mean disease duration of 15.5 ± 2.3 years. Eighty-four (61%) of the women and 49 (60%) of the men were in remission. Forty-one healthy women and 54 healthy men served as a reference group. Body composition was analyzed by dual-energy x-ray absorptiometry.

Results

There was no difference in height or body mass index (BMI) between patients and healthy subjects. However, female patients with systemic disease had significantly reduced BMI compared with those with pauciarticular JIA (P < 0.001), and female patients who used or had been using corticosteroids had significantly lower weight, height, and BMI compared with the patients who had never used corticosteroids (P < 0.05). Female patients in remission had significantly more lean body mass compared with healthy controls (P < 0.05) and significantly less body fat was found in both women and men (P < 0.01 for both). Patients with active disease had the same amount of lean body mass as the healthy controls, but significantly less body fat (P < 0.05 for women and P < 0.01 for men).

Conclusion

Adult patients with JIA had attained normal height, weight, and BMI, with the exception of women with systemic JIA and those who were using or had used corticosteroids. Patients with JIA in remission seemed to have a better nutritional status than healthy subjects.


INTRODUCTION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. REFERENCES

Juvenile idiopathic arthritis (JIA) is a chronic inflammatory process that affects the joints, synovial tissue, and bursa. Concomitant poor nutritional status has been reported, which is indicated by reduced muscle mass, low serum albumin concentration, unbalanced iron metabolism, and reduced antioxidant defense (1–4). These features have been shown to be the results of increased production of tumor necrosis factor α and interleukin-1 (4, 5). In addition, it is possible that reduced physical activity during childhood affects the anthropometric variables in children with JIA (6).

Because childhood and adolescence are the periods of body growth, interference with nutritional status during these years may have implications for height, weight, and body composition in adulthood. The aim of this study was to evaluate the influence of juvenile chronic rheumatic disease during childhood and adolescence on current nutritional status in adult patients in remission or with active disease.

PATIENTS AND METHODS

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. REFERENCES

Patients.

The patients included in the present study had previously been diagnosed with idiopathic arthritis of at least 6 weeks' duration and met the criteria for JIA (Table 1) (7). All patients had been hospitalized for the first time at the Center for Rheumatic Diseases at Rikshospitalet, Oslo, Norway between January 1980 and September 1985. Of 400 total patients with JIA diagnosed during this period, 336 (84%) participated in the study, which was conducted in 1997. Of the 64 patients (16%) who did not take part, 8 had died, 12 chose not to participate, 5 had left the country, and the addresses of 39 could not be found. The findings in patients < 20 years of age were excluded from this report, because there were no age-matched controls. The final number of participants was 220: 138 women and 82 men. Mean age (± SD) and mean disease duration (± SD) were 24.9 ± 2.9 and 15.6 ± 2.4 years in the women and 25.2 ± 3.1 and 14.1 ± 2.1 years in the men.

Table 1. Subgroups of patients with juvenile arthritis (JA)*
 All JA patientsActive diseaseIn remission
  • *

    Data presented as number (%) unless otherwise noted.

Women   
 Number1385484
 Pauciarticular66 (48)20 (37)46 (55)
 Polyarticular42 (30)21 (38)21 (25)
 Systemic6 (4)1 (2)5 (6)
 Psoriatic arthritis13 (9)6 (11)7 (8)
 Juvenile ankylosing spondylitis2 (1)2 (4) 
 Syndrome of seronegative enthesopathy and arthropathy6 (4)2 (4)4 (5)
 Arthritis in inflammatory bowel disease3 (2)2 (4)1 (1)
Men   
 Number823349
 Pauciarticular29 (35)9 (27)20 (41)
 Polyarticular18 (22)9 (27)9 (18)
 Systemic8 (10)3 (9)5 (10)
 Psoriatic arthritis11 (13)3 (10)8 (16)
 Juvenile ankylosing spondylitis8 (10)5 (15)3 (6)
 Syndrome of seronegative enthesopathy and arthropathy8 (10)4 (12)4 (8)

At the time of investigation, 84 (61%) of the women and 49 (60%) of the men had a history of JIA. This was defined as being in remission, with no disease activity, and these subjects had not taken medication for the previous 6 months (Table 2). The mean duration of remission (± SD) was 8.2 ± 4.5 years and 10.2 ± 4.2 years in the women and men, respectively. The mean duration of active disease (± SD) in these patients was 7.3 ± 4.9 years for the women and 4.8 ± 4.0 years for the men. Patients with persistent JIA were defined as having active disease at the time of investigation. In the groups of patients with active disease, the mean (± SD) disease duration was 15.7 ± 2.7 years in women and 15.0 ± 2.1 years in men. Eight male and 20 female patients had high disease activity at the time of investigation, which was defined as having > 5 swollen joints and/or an erythrocyte sedimentation rate (ESR) > 28 mm/hour.

Table 2. Characteristics of patients with juvenile arthritis (JA) and healthy subjects*
 Active diseaseIn remissionHealthy subjects
  • *

    Data presented as mean ± SD unless otherwise noted. NR = not relevant.

Women   
 Number548441
 Age at inclusion, years24.9 ± 2.825.4 ± 2.727.3 ± 3.2
 Age at disease onset, years9.5 ± 3.19.8 ± 3.1NR
 Disease duration, years15.7 ± 2.77.3 ± 4.9NR
 Arthritis severity index, median (range)13 (0–160)0 (0–52)NR
 Use of steroids   
  Never used, n (%)32 (59)73 (87) 
  Used earlier, n (%)13 (24)11 (13) 
  Current medication, n (%)9 (17)  
Men   
 Number334954
 Age at inclusion, years25.5 ± 3.425.2 ± 2.925.8 ± 2.9
 Age at disease onset, years9.8 ± 3.310.3 ± 3.3NR
 Disease duration, years15.0 ± 2.14.8 ± 4.1NR
 Arthritis severity index, median (range)7 (0–52)0 (0–61)NR
 Use of steroids   
  Never used, n (%)19 (58)38 (78) 
  Used earlier, n (%)5 (15)11 (22) 
  Current medication, n (%)9 (27)  

Ninety-five (41 females, 54 males) healthy subjects were recruited from 2 military camps in the Oslo area. The subjects had no known disease that was ascertained by a physical exam. Seventeen (41%) of the female group were military employees and 50 (93%) of the male group were military employees. The mean ages (± SD) were 27.4 ± 3.2 years for the women and 25.8 ± 2.9 years for the men (Table 2).

The study was approved by the Regional Ethics Committee for Medical Research, and informed consent was obtained from all the participants.

Measurements.

Estimated body fat and estimated lean mass were evaluated by means of dual-energy x-ray absorptiometry (DEXA; Lunar Expert, Lunar Radiation Corporation, Madison, WI). Daily quality tests were run with a phantom, and only 2 technicians were used. The coefficient of variation of bone mineral density measurements was <1.5% at the setting we used. The same technician and physician certified all scans.

Because some of the patients had had prosthetic replacements in different joints, these measurements were only made in 77 of the male patients and 128 female patients. All the participants were weighed (W) on a digital scale to the nearest kilogram, and the height (H) was measured to the nearest centimeter. Body mass index (BMI) was calculated by W/H2. Underweight was defined as BMI < 20 for men and BMI < 19 for women. Overweight was defined as BMI > 25 for men and BMI > 24 for women, and obese was defined as BMI > 30 for both women and men (8).

The Westergren ESR, hemoglobin concentration, serum albumin, and total serum calcium were measured by routine laboratory methods. Serum 25-hydroxyvitamin D was measured by means of a competitive protein-binding assay. The arthritis severity index was calculated on the basis of a clinical examination. This index, which is the sum of the graded values for joint swelling, tenderness, and limited range of motion, has been found to be a good predictor of the development of severe disease (9).

Food and nutrient intake were estimated by means of a quantitative food frequency questionnaire, which has been validated for this age group (10, 11). The questionnaire was optically read and the calculations fully computerized in accordance with the Norwegian Food Composition Table (12). Physical activity was quantified on a 6-part scale, in which daily physical activity for 20 minutes or more was rated 6 and none or very rare physical activity was rated 1. Physical activity in this context was defined as perspiring and becoming short of breath.

Statistical analysis.

Statistical analysis was performed with the SPSS for Windows statistical package, 8th edition (SPSS Inc., Chicago, IL). The data are given as means ± SD. The Kolmogorov–Smirnov test was used to determine the normality of the data before statistical tests that require a Gaussian distribution were performed. One-way analysis of variance with Bonferroni corrections was run to evaluate group differences of patients with active disease, in remission, and healthy subjects in variables with a Gaussian distribution. Independent sample t-tests were then used to compare groups. Kruskal–Wallis test was run to evaluate differences between groups of patients with active disease, in remission, and healthy subjects of variables of non-normality, and Mann–Whitney U test was used to test differences between groups. The latter test was also used for measurements on ordinal scale (physical activity). The Pearson correlation coefficient was calculated to test the association between 2 variables with a Gaussian distribution, and Spearman's rank correlation coefficient was used in cases of non-normal distribution.

RESULTS

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. REFERENCES

There was no statistically significant difference between the patient groups with high and low disease activity, the patients in remission, and the healthy controls in mean height and BMI, (Table 3). However, the female patients with systemic JIA had significantly lower weight and BMI compared with the pauciarticular JIA group (P < 0.001, data not shown). The female patients who were using or had used corticosteroids had significantly lower weight, height, and BMI compared with patients who had never used corticosteroids (P < 0.05 for all). The same findings were seen in the men, but the differences were not statistically significant. Six male patients (7.5%) and 15 female patients (11%) were classified as underweight, whereas none of the healthy subjects were underweight (Figure 1).

Table 3. Anthropometric and laboratory measurements in adults with juvenile arthritis and healthy subjects*
 Active diseaseIn remissionHealthy subjects
  • *

    Data presented as mean ± SD, unless otherwise noted. BMI = body mass index; ESR = erythrocyte sedimentation rate.

  • P < 0.05 between patient groups and healthy subjects.

  • P < 0.01 between patient groups and healthy subjects.

  • §

    P < 0.05 between patients in remission and patients with active disease.

  • P < 0.001 between patients in remission and patients with active disease.

Women   
 Number548441
 Height, cm166.8 ± 6.6167.2 ± 5.5168.6 ± 6.8
 BMI, kg/cm223.0 ± 4.123.7 ± 4.723.8 ± 3.6
 Lean body mass, kg42.7 ± 5.545.1 ± 6.142.1 ± 5.0
 Body fat, %28.4 ± 9.626.2 ± 11.433.3 ± 7.9
 ESR, mm/hour20 ± 19§9 ± 68 ± 5
 Hemoglobin, gm/liter1.23 ± 0.121.32 ± 0.091.25 ± 0.08
 Albumin, gm/liter41.0 ± 4.3§43.6 ± 3.041.4 ± 2.2
Men   
 Number334954
 Height, cm179.8 ± 5.9180.7 ± 7.8181.0 ± 6.2
 BMI, kg/cm223.5 ± 2.624.4 ± 3.824.8 ± 2.4
 Lean body mass, kg61.9 ± 6.564.0 ± 6.761.0 ± 5.5
 Body fat, %13.7 ± 7.312.9 ± 11.020.1 ± 6.5
 ESR, mm/hour14 ± 20§4 ± 33 ± 2
 Hemoglobin, gm/liter1.46 ± 0.121.50 ± 0.091.46 ± 0.08
 Albumin, gm/liter43.9 ± 5.2§47.1 ± 2.944.6 ± 2.3
thumbnail image

Figure 1. Percentage of underweight, normal weight, overweight, and obese in patients with juvenile idiopathic arthritis and in healthy subjects.

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Female patients in remission had significantly more total lean body mass than healthy subjects (P < 0.05). This difference was still significant when adjusted for height. The percentage of total body fat was significantly higher in the healthy subjects compared with the patients in remission (P < 0.001) and those with active disease (P < 0.01 in the female and P < 0.001 in the male groups; Table 3).

The female patients in remission had significantly higher hemoglobin concentrations and serum concentrations of albumin than the healthy controls and the patients with active disease (Table 3). The same was seen in the male group, but results did not reach statistical significance for the hemoglobin concentration. The serum concentration of calcium was higher in the patient groups than in the healthy subjects. The potassium concentration was significantly higher in the patients with active disease than in the healthy controls (P < 0.05).

The energy intake per kilogram body weight was higher in the patient groups than in the healthy subjects, but this was not statistically significant (Table 4). In the male group, fat intake was significantly higher in the patients with active disease than in the healthy subjects. In addition, the percentage of unsaturated fat was higher in the patients with active disease than in the healthy subjects (P < 0.05). The same was seen in the female group, but the difference was not statistically significant. The patients with active disease had a significantly higher intake of whole-fat milk and mayonnaise than the controls, whereas the healthy subjects had a higher intake of skim milk. As a consequence of the higher fat intake, vitamin D and vitamin E intake was also higher in the patients with active disease than in the healthy subjects. Mean sugar intake constituted 9–10% of the total energy intake in all groups.

Table 4. Energy and nutrient intake in patients with juvenile arthritis compared with healthy subjects*
 Active diseaseIn remissionHealthy subjects
  • *

    Data presented as mean ± SD, unless otherwise noted.

  • P ≤ 0.05.

Women   
 Number507040
 Energy intake, kcal2,132 ± 7042,259 ± 8362,049 ± 591
 Energy intake, kcal per kg body weight35 ± 1436 ± 1530 ± 8
 Protein intake, gm per kg body weight1.2 ± 0.51.2 ± 0.51.1 ± 0.3
 Fat intake, gm (% of energy intake)79 ± 32 (33)80 ± 31 (32)73 ± 19 (32)
  Saturated fatty acids, gm31 ± 1432 ± 1429 ± 14
  Monoeneic fatty acids, gm27 ± 1128 ± 1125 ± 9
  Polyunsaturated fatty acids, gm14 ± 614 ± 612 ± 5
  Polyunsaturated fatty acids, % of total energy intake5.9 ± 2.05.6 ± 1.75.2 ± 1.6
 Sugar, gm60 ± 6070 ± 8353 ± 31
 Fiber, gm21 ± 922 ± 920 ± 6
 Vitamin C, mg109 ± 68128 ± 64106 ± 52
 Retinol, equivalents1,327 ± 8061,314 ± 5621,048 ± 376
 Vitamin D, μg4.5 ± 3.04.1 ± 2.43.9 ± 2.2
 Vitamin E, mg7 ± 38 ± 37 ± 2
 Calcium, mg817 ± 268859 ± 378813 ± 364
 Magnesium, mg292 ± 95311 ± 92292 ± 77
 Iron, mg10 ± 310 ± 310 ± 2
Men   
 Number263951
 Energy intake, kcal3,161 ± 1,1793,229 ± 8222,892 ± 694
 Energy intake, kcal per kg body weight43 ± 2042 ± 1336 ± 9
 Protein intake, gm per kg body weight1.5 ± 0.51.4 ± 0.41.3 ± 0.3
 Fat intake, gm (% of energy intake)129 ± 64 (36)121 ± 39 (34)103 ± 32 (32)
  Saturated fatty acids, gm50 ± 2847 ± 1641 ± 13
  Monoeneic fatty acids, gm45 ± 2342 ± 1336 ± 12
  Polyunsaturated fatty acids, gm25 ± 1323 ± 1118 ± 8
  Polyunsaturated fatty acids, % of total energy intake7.1 ± 2.56.3 ± 2.45.4 ± 1.8
 Sugar, gm83 ± 5290 ± 5471 ± 38
 Fiber, gm24 ± 1026 ± 925 ± 9
 Vitamin C, mg108 ± 58144 ± 71135 ± 55
 Retinol, equivalents1,699 ± 7441,606 ± 6811,609 ± 682
 Vitamin D, μg6.8 ± 3.65.9 ± 2.95.3 ± 2.5
 Vitamin E, mg11 ± 611 ± 39 ± 3
 Calcium, mg1,217 ± 5691,263 ± 4731,205 ± 398
 Magnesium, mg422 ± 153429 ± 108404 ± 96
 Iron, mg13 ± 414 ± 314 ± 4

Supplementation was as common in the healthy subjects as in the patient groups. About 20% supplemented their daily intake with cod liver oil, and 50% of the females and 35% of the males with minerals and/or vitamins.

Fifty-five percent of the women and 67% of the men with active disease smoked every day as compared with 44% of the healthy subjects and patients in remission. However, the difference was not statistically significant. The healthy subjects reported a significantly higher frequency of physical activity than the patient groups (P < 0.05 for the men and P < 0.01 for the women, Kruskal-Wallis test).

DISCUSSION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. REFERENCES

JIA is a heterogeneous group of chronic inflammatory disorders in which poor nutritional status is often seen (13–16). Studies have revealed protein energy malnutrition and low lean body mass with normal to increased fat mass in children with active disease. A more recent study showed reduced fat-free mass and a significantly higher resting energy expenditure (REE) per kilogram body weight in patients with systemic juvenile rheumatoid arthritis (17). The same study indicated increased REE in patients with oligo- and polyarticular juvenile rheumatoid arthritis, but the difference was not statistically significant. Nutritional supplementation with nocturnal nasogastric tube feeding has been shown to improve growth and nutritional status in children with JRA, which means that a greater awareness of healthy eating habits might benefit patients with active disease (18).

Our aim in this study was to investigate nutritional status in young adult patients with JIA to evaluate the impact of the disease during childhood and adolescence. We did not find that the patients were any less tall than the healthy subjects. Increased prepubertal growth has also been reported prior to disease debut in patients with juvenile chronic arthritis compared with healthy peers (19). Although the patients had a drop in growth velocity the first year with disease, growth velocity was increased again after 1 year with treatment. This finding supports our results. Weight was lower in patients with active disease, but BMI was similar in patients and healthy subjects (due to a nonsignificantly lower height). Between 5% and 10% of the female patients and 6% and 12% of the male patients were underweight, whereas none of the healthy subjects were underweight. Obesity was as common in the healthy subjects as in the patients. A most interesting finding was that lean body mass, measured by DEXA, was significantly higher in patients in remission than healthy subjects and patients with active disease. Furthermore, patients with active disease had similar lean body mass compared with the healthy subjects. Our material might have been biased, because 16% of the total population did not participate in this study. There was, however, no difference in sex, onset type, age of diagnosis, or disease duration between those who chose to participate and those who did not participate. On the other hand, 5 male and 10 female patients were not measured by DEXA scanning because of prosthetic replacements in different joints. These patients were shorter and weighed less than the rest of the patients, although the differences were not statistically significant.

Our findings are encouraging, because most studies have shown that children with active disease have less muscle mass (4, 5). Our results may indicate that once the period of active disease has ended, body growth manages to catch up. However, patients with systemic disease during adolescence and those using corticosteroids appear to suffer from sequelae into adulthood.

The healthy subjects who volunteered to participate in this study were recruited from 2 military bases, and although most of them were doing office work at the time of investigation, most of the males had had training as military officers. We therefore assumed that our reference group would be at least as physically fit as our patients, and they did in fact report a higher frequency of physical activity than the patients.

Our method evaluating lean body mass by means of DEXA has been shown to be satisfactory compared with standard methods, although it may underestimate fat mass (20, 21). Our results are supported by the fact that we found high lean body mass in patients in remission in both the female and the male populations. The fact that the patients in remission had higher lean body mass than either the controls or patients with active disease fits with the higher serum albumin and hemoglobin concentrations that were found in this group, although no significant correlations were found between lean body mass and either serum albumin or hemoglobin concentration.

The patients with high disease activity had a higher energy intake per kilogram body weight, though this was not statistically significant. This agrees with an earlier study where we reported a higher energy intake per kilogram body weight in patients with high disease activity compared with patients with low disease activity and healthy controls (16). It has been shown that patients with high disease activity have a higher REE, which would agree with our finding that energy intake has to be increased in this patient group to obtain a normal body weight (17).

Several earlier studies have documented a reduced concentration of unsaturated fatty acids, especially linoleic acid, in the phospholipid fraction in patients with active rheumatic disease (22–28). In our study we found that the patients with high disease activity had a higher total intake of unsaturated fat, and this represented a higher percentage of the energy intake. This might mean that patients with active disease have an unconscious desire for fat, which could have implications both for studies of supplementation with omega-3 fatty acids and for the development of atherosclerosis (29–31).

Because both the female and the male patients in remission had a higher lean body mass and less fat than healthy subjects, it is possible that having a disease during childhood and adolescence increases the individual's health awareness. The patient groups are also in frequent contact with the public health team. However, at the time of this investigation none of the acquired health variables, such as physical activity, smoking, and nutrient intake, indicated healthier living habits among patients in remission than among healthy subjects. On the other hand, adolescents with juvenile chronic arthritis report more overprotection from parents than adolescents in the general population, which indicates closer parental followup (32). This may lead to a more favorable health outcome later in life.

From this study, conducted on Norwegian patients with JIA, it seems that having a chronic rheumatic disease during late childhood and puberty had little impact on nutritional status. However, the patients with the highest disease activity had reduced height and weight, but patients with a disease activity that did not require use of corticosteroids seemed to have benefited anthropometrically from the disease, having less body fat and greater muscle mass. This is an interesting observation that might inspire further investigations.

REFERENCES

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. REFERENCES
  • 1
    Helliwell M, Coombes EJ, Moody BJ, Batstone GF, Robertson JC. Nutritional status in patients with rheumatoid arthritis. Ann Rheum Dis 1984; 43: 38690.
  • 2
    Araujo V, Arnal C, Boronat M, Ruiz E, Dominguez C. Oxidant-antioxidant imbalance in blood of children with juvenile rheumatoid arthritis. Biofactors 1998; 8: 1559.
  • 3
    Helgeland M, Svendsen E, Forre O, Haugen M. Dietary intake and serum concentrations of antioxidants in children with juvenile arthritis. Clin Exp Rheumatol 2000; 18: 63741.
  • 4
    Roubenoff R, Roubenoff RA, Ward LM, Holland SM, Hellmann DB. Rheumatoid cachexia: depletion of lean body mass in rheumatoid arthritis: possible association with tumor necrosis factor. J Rheumatol 1992; 19: 150510.
  • 5
    Roubenoff R, Roubenoff RA, Cannon JG, Kehayias JJ, Zhuang H, Dawson-Hughes B, et al. Rheumatoid cachexia: cytokine-driven hypermetabolism accompanying reduced body cell mass in chronic inflammation. J Clin Invest 1994; 93: 237986.
  • 6
    Henderson CJ, Lovell DJ, Specker BL, Campaigne BN. Physical activity in children with juvenile rheumatoid arthritis: quantification and evaluation. Arthritis Care Res 1995; 8: 1149.
  • 7
    Petty RE, Southwood TR, Baum J, Bhettay E, Glass DN, Manners P, et al. Revision of the proposed classification criteria for juvenile idiopathic arthritis: Durban, 1997. J Rheumatol 1998; 25: 19914.
  • 8
    World Health Organization. Physical status: the use and interpretation of anthropometry. Geneva: World Health Organization; 1995.
  • 9
    Ruperto N, Ravelli A, Levinson JE, Shear ES, Murray K, Link TB, et al. Long-term health outcomes and quality of life in American and Italian inception cohorts of patients with juvenile rheumatoid arthritis. II. Early predictors of outcome. J Rheumatol 1997; 24: 9528.
  • 10
    Solvoll K, Lund-Larsen K, Søyland E, Sanstad B, Drevon Ch A. A quantitative food frequency questionnaire evaluated in a group of dermatologic outpatients. Scand J Nutr 1993; 37: 1505.
  • 11
    Andersen LF, Nes M, Lillegaard IT, Sandstad B, Bjorneboe GE, Drevon CA. Evaluation of a quantitative food frequency questionnaire used in a group of Norwegian adolescents. Eur J Clin Nutr 1995; 49: 54354.
  • 12
    Haga Rimestad A, Blaker B, Flåten A-M, Nordbotten A. Food composition table. Oslo: Universitetsforlaget; 1995.
  • 13
    Johansson U, Portinsson S, Åkesson A, Svantesson H, Öckerman P-A, Åkesson B. Nutritional status in girls with juvenile chronic arthritis. Hum Nutr Clin Nutr 1986; 40C: 5767.
  • 14
    Henderson CJ, Lovell DJ. Comprehensive nutritional assessment of children and adolescents with juvenile rheumatoid arthritis (JRA) [abstract]. Arthritis Rheum 1987; 30 Suppl 4: S202.
  • 15
    Bacon MC, White PH, Raiten DJ, Craft N, Margolis S, Levander OA, et al. Nutritional status and growth in juvenile rheumatoid arthritis. Semin Arthritis Rheum 1990; 20: 97106.
  • 16
    Haugen M, Høyeraal HM, Larsen S, Gilboe I-M, Trygg K. Nutrient intake and nutritional status in children with juvenile chronic arthritis. Scand J Rheumatol 1992; 21: 16570.
  • 17
    Knops N, Wulffraat N, Lodder S, Houwen R, de Meer K. Resting energy expenditure and nutritional status in children with juvenile rheumatoid arthritis. J Rheumatol 1999; 26: 203943.
  • 18
    Lovell DJ, White PH. Growth and nutrition in juvenile rheumatoid arthritis. In: WooP, WhiteP, AnsellB, editors. Pediatric rheumatology update. New York: Oxford University Press; 1990. p. 4756.
  • 19
    Saha MT, Verronen P, Laippala P, Lenko HL. Growth of prepubertal children with juvenile chronic arthritis. Acta Paediatrica 1999; 88: 7248.
  • 20
    Elowsson P, Forslund AH, Mallmin H, Feuk U, Hansson I, Carlsten J. An evaluation of dual-energy x-ray absorptiometry and underwater weighing to estimate body composition by means of carcass analysis in piglets. J Nutrition 1998; 128: 15439.
  • 21
    Ellis KJ. Human body composition: in vivo methods. Physiological Rev 2000; 80: 64980.
  • 22
    Hagenfeldt L, Wennmalm A. Turnover of a prostaglandin precursor arachidonic acid in rheumatoid arthritis. Europ J Clin Invest 1975; 5: 2359.
  • 23
    Bruderlein H, Daniel R, Boismenu D, Julien N, Couture F. Fatty acid profiles of serum phospholipids in patients suffering rheumatoid arthritis. Prog Lipid Res 1981; 20: 62531.
  • 24
    Haataja M, Niemien A-L, Mäkisara P, Kalliomæki JL. Prostaglandin precursors in rheumatoid arthritis. J Rheumatol 1982; 9: 913.
  • 25
    Johansson U, Portinsson S, Åkesson A, Svantesson H, Åkesson B. Fatty acid composition of plasma phosphatidylcholine and erythrocyte lipids, and dietary fat intake in juvenile chronic arthritis. Prog Lipid Res 1986; 25: 57982.
  • 26
    Jacobsson L, Lindgärde R, Manthorpe R, Åkesson B. Correlation of fatty acid composition of adipose tissue lipids and serum phosphatidylcholine and serum concentrations of micronutrients with disease duration in rheumatoid arthritis. Ann Rheum Dis 1990; 49: 9015.
  • 27
    Suryaprabha P, Das UN, Ramesh G, Vijay Kumar K, Stravan Kumar G. Reactive oxygen species, lipid peroxides and essential fatty acids in patients with rheumatoid arthritis and systemic lupus erythrematosus. Prostaglandins Leukot Essent Fatty Acids 1991; 43: 2515.
  • 28
    Jira W, Spiteller G. Dramatic increase of linoleic acid peroxidation products by aging, atherosclerosis, and rheumatoid arthritis. Adv Exp Med Biol 1999; 469: 47983.
  • 29
    Kremer JM, Lawrence DA, Jubiz W, DiGiacomo R, Rynes R, Bartholomew LE, et al. Dietary fish oil and olive oil supplementation in patients with rheumatoid arthritis: clinical and immunologic effects. Arthritis Rheum 1990; 33: 81020.
  • 30
    Pasceri V, Yeh ET. A tale of two diseases: atherosclerosis and rheumatoid arthritis. Circulation 1999; 100: 21246.
  • 31
    Park YB, Lee SK, Lee WK, Suh CH, Lee CW, Lee CH, et al. Lipid profiles in untreated patients with rheumatoid arthritis. J Rheumatol 1999; 26: 17014.
  • 32
    Aasland A, Nøvik TS, Flato B, Vandvik IH. A multimodal, prospective assessment of outcome in families of children with early onset of juvenile chronic arthritis. Families Systems Health 1998; 16: 26780.