bs_bs_banner

Australasian Journal of Dermatology (2013) 54, 259–263

doi: 10.1111/ajd.12044

ORIGINAL RESEARCH

Weight gain and tumour necrosis factor-alpha inhibitors in patients with psoriasis Eugene Tan,1 Christopher Baker1,2,3 and Peter Foley1,2,3 1

Skin and Cancer Foundation Victoria, Carlton, 2St. Vincent’s Hospital Melbourne, Fitzroy, and 3The University of Melbourne, Melbourne, Victoria, Australia

ABSTRACT Objectives: To compare the effect of anti-tumour necrosis factor (TNF)-a therapies with agents that do not target TNF-a on bodyweight and body mass index (BMI) in patients with psoriasis. Methods: A retrospective analysis of patients from the Skin and Cancer Foundation and St Vincent’s Hospital Melbourne. Bodyweight and BMI were compared at baseline and weeks 12, 24 and 48. Results: A total of 143 patients were studied, equating 286 treatment courses in all. Of these, 178 courses were with an anti-TNFa agent (54 on adalimumab, 61 on etanercept and 63 on infliximab) and 108 courses were on non-anti-TNFa agents (73 on efalizumab and 35 on ustekinumab). Anti-TNFa therapy with adalimumab and infliximab resulted in weight gain from week 12 until week 48. At week 12 the infliximab group gained 1.7 ⫾ 4.7 kg and adalimumab group gained 1.5k ⫾ 4.5 kg. This effect persisted at week 24 (infliximab: 3.4 ⫾ 5.7 kg; adalimumab: 2.2 ⫾ 4.4 kg)

Correspondence: Dr Eugene Tan, Skin & Cancer Foundation Victoria, 1/80 Drummond Street, Melbourne, Vic. 3125, Australia. Email: [email protected] Eugene Tan, FRACP Christopher Baker, FACD. Peter Foley, FACD. Conflict of interest: P Foley has served as a paid investigator for clinical trials in psoriasis by Amgen, Wyeth/Pfizer, ScheringPlough/MSD, Novartis, GlaxoSmithKleine, Bristol-Myers Squibb, Sanofi-Aventis, Actelion and Celgene. From Abbott, Wyeth/Pfizer, Schering-Plough/MSD, Janssen-Cilag and Merck Serono he has received speaker’s honoraria for presentations. He has served as a paid member of Australian, Asia Pacific and/or global medical advisory boards for Amgen, Abbott, Janssen-Cilag, Schering-Plough/ MSD, Wyeth/Pfizer, GlaxoSmithKleine and Leo Pharma. He has received unrestricted research and education support from Wyeth/ Pfizer, Abbott, Schering-Plough/MSD, and Janssen-Cilag. C Baker has received clinical research and education grants from Abbott, Janssen-Cilag and Pfizer. Submitted 12 June 2012; accepted 10 February 2013.

until the end of the study (infliximab: 1.3 ⫾ 2.9 kg; adalimumab: 2.4 ⫾ 6.4 kg). There was a trend for weight gain in the etanercept group that did not reach statistical significance. Therapy with ustekinumab and efalizumab did not result in weight gain. Conclusion: Therapy with adalimumab and infliximab is associated with a significant increase in bodyweight and BMI. Key words: adalimumab, anti-TNFa, biologics, body mass index, etanercept, infliximab, PASI75, psoriasis, ustekinumab.

INTRODUCTION Chronic plaque psoriasis affects 1–3 per cent of the general population, and in Australia the prevalence is estimated to be about 2 per cent.1 While topical therapy remains the first-line treatment, up to 25 per cent of patients have moderate to severe psoriasis requiring systemic therapy.2,3 The advent of biological therapy allows a more effective and targeted approach to the treatment of psoriasis with the selective blockade of T-lymphocyte-mediated inflammation, which is central to the pathogenesis of psoriasis.4 Antitumour necrosis factor (TNF)a agents such as etanercept, infliximab and adalimumab have been successfully used in the treatment of moderate to severe psoriasis.5–10 In the authors’ experience, weight gain has been noted in psoriasis patients in whom an anti-TNFa agent has been commenced. This has not been observed with other biological agents that do not interfere with the function of TNFa, such as efalizumab, which impairs leukocyte migration and function. This weight gain is significant, considering the association of psoriasis with the metabolic syndrome and risk of cardiovascular disease with chronic inflammatory conditions.11–15 Abbreviations: BMI TNF PASI75-A

© 2013 The Authors Australasian Journal of Dermatology © 2013 The Australasian College of Dermatologists

body mass index tumour necrosis factor 75% reduction in the psoriasis area and severity index score.

260

E Tan et al.

In this study an analysis of changes in bodyweight and body mass index (BMI) was undertaken on patients who have been commenced on a biological agent. The aim of the study was to determine whether a difference exists between patients on an anti-TNFa agent compared to those on nonanti-TNFa agents.

METHODS AND MATERIALS A retrospective analysis was performed on patients from the Skin and Cancer Foundation Victoria and St Vincent’s Hospital, Melbourne. Data were extracted from the Australasian Psoriasis Registry Database (https://www.psoriasis. asn.au/default.aspx). This database was first developed in 2006 and continues to collect data on psoriasis patients treated with a biological agent from Australia and New Zealand. Information such as the patients’ basic characteristics, weight and BMI were analysed at intervals of 12 weeks until week 48. The analysis included patients who had received a particular biological agent as well as those who are currently receiving that agent, as some cross-over occurred between biological agents. No patient ever received two biologics simultaneously at any point and an interval of at least 1 month was observed before the initiation of the other biological agent.

Statistical analysis Differences at baseline for mean age, weight and BMI was calculated using a one-way ANOVA to allow the means of five groups to be compared. A paired t-test was used to calculate the differences in mean weight and BMI at discrete time points (weeks 0, 12, 24 and 48). The paired t-test was chosen as it allowed the means of two groups (separated by time points) to be compared. Fischer’s exact test was used to determine whether a difference existed in the proportion of patients who achieved a 75% reduction in the psoriasis area and severity index score (PASI75) and did (or did not) gain weight and also in patients who gained weight and did (or did not) achieve PASI75. The Fischer’s test was used in this setting as it permits an examination of the association

Table 1

between two categorical data (weight gain and PASI75) in a small sample size. All statistical analyses were performed using PASW/SPSS Statistics 18 for Windows, Release 18.0.0 (SPSS, Chicago, IL, USA).

RESULTS In total, 286 treatment courses were undertaken in 143 patients with a biological agent. Of these treatments, 54 courses used adalimumab, 73 used efalizumab, 61 used etanercept, 63 used infliximab and 35 used ustekinumab. The patients’ characteristics are presented in Table 1. There were no statistically significant differences in age, bodyweight and BMI among the groups of patients at baseline (ANOVA; P < 0.05: detailed analysis is not shown). Of patients given adalimumab, 28 per cent changed to another biological agent (Table 2) compared with 34 per cent for infliximab, 49 per cent for etanercept, 9 per cent for ustekinumab and 97 per cent for efalizumab (efalizumab was officially withdrawn from Australia in March 2009). There was an increase in bodyweight and BMI in patients commenced on infliximab and adalimumab (Tables 3–5) compared to at baseline, which was apparent from week 12 and continued until week 48. The mean bodyweight increment was 1.7 kg for infliximab and 1.5 kg for adalimumab at week 12 (Table 3). The weight gain was most marked at week 24 with 3.2 kg gained in the infliximab group and 2.2 kg for adalimumab compared to baseline. When weight gain was compared in pairs of week 12 versus 24 and week 24 versus week 48, the patients were found to have gained the most weight between the interval of week 12 and 24 (Table 4). Weight gain was not significant from week 24 to week 48 (Table 4). Although there was no significant weight gain for patients in the etanercept group, a trend existed for weight gain and two patients gained 8 kg and 12 kg, respectively. No trend or significant weight gain was noted in patients treated with efalizumab or ustekinumab. There was no relationship between PASI75 response and weight gain (data not shown) across all biological agents. The increase in weight did not influence clinical response. Similarly, there was no relation-

Patients’ characteristics Biological agent

Number†

Adalimumab 54

Infliximab 63

Etanercept 61

Ustekinumab 35

Efalizumab 73

Sex (male: female) Mean age (years) Psoriatic arthritis Smokers (current: former: not recorded) Body mass index at baseline Weight at baseline (kg) Mean duration of therapy (weeks) Median duration of therapy (weeks)

36:18 49.0 ⫾ 11.7 31 20 (6:10:4) 29.5 ⫾ 5.2 88.7 ⫾ 16.2 49.7 ⫾ 30.7 47.0

51:12 49.7 ⫾ 11.8 32 25 (9:7:9) 30.5 ⫾ 6.6 91.7 ⫾ 21.4 100.0 ⫾ 58.7 105.2

45:16 52. 3 ⫾ 11.3 35 18 (8:4:6) 30.7 ⫾ 5.6 93.6 ⫾ 19.2 62.6 ⫾ 31.3 46.6

24:11 47.5 ⫾ 11.3 18 17 (9:7:1) 33.8 ⫾ 6.8 101.3 ⫾ 21.8 52.9 ⫾ 23.8 52.2

53:20 51.5 ⫾ 11.8 35 25 (12:6:7) 30.3 ⫾ 5.9 91.7 ⫾ 20.8 72.5 ⫾ 51.3 60.9

† Includes those who have received the particular biological agent as well as those who are currently on the agent, as some cross-over occurred between biological agents.

© 2013 The Authors Australasian Journal of Dermatology © 2013 The Australasian College of Dermatologists

261

ship amongst weight gainers and whether or not they achieved PASI75 (data not shown). 39 41 31 32 0

Current patients

Weight gain and TNF

Number of patients who have been on the biological agent = current patients + total who have changed. ‡Two patients are no longer on any biological therapy.

1 (1) 1 (33) 33 (47)

12 (40) 0 23 (32)

Adalimumab Infliximab Etanercept Ustekinumab Efalizumab



54 62 61 35 73 15 (28) 21 (34) 30 (49) 3 (9) 71‡ (97) 0 0 0 0 7 (47) 9 (43) 8 (27) 5 (33) 2 (10)

10 (48) 10 (33) 2 (67) 14 (20)

Changed to →

3 (20)

Adalimumab (n, % of total changed)

Table 2

Cross-over of biological agents

Infliximab (n, % of total changed)

Etanercept (n, % of total changed)

Ustekinumab (n, % of total changed)

Efalizumab (n, % of total changed)

Total changed (n, % of total patients)

Total patients (n)†

DISCUSSION This study shows that therapy with adalimumab and infliximab is associated with weight gain. Weight gain is not significant in psoriasis patients treated with etanercept, efalizumab and ustekinumab. The increase in weight occurred as early as 12 weeks and continued up to 48 weeks of treatment. Weight gain was most apparent from week 12 until week 24. Thereon, the patients’ weight seemed to have stabilized, although it was still elevated compared to the baseline. Weight gain was not associated with lack of efficacy and likewise, PASI response could not be used to predict patients who did or did not gained weight. The impact of weight gain and PASI response appear to be independent. Our results are in agreement with publications of antiTNFa agent use in patients with psoriasis with the exception of etanercept.16–20 Two recent studies assessing infliximab in psoriasis patients found a significant weight gain of 1.6–2.5 kg in one year.19,20 Men and patients with severe psoriasis are at higher risk for weight gain.19 Two retrospective analyses concurred with the above findings and noted an average increase of 1.5–2.5 kg at 24 weeks.16,17 Gisondi and colleagues examined the effects of infliximab and etanercept on bodyweight and BMI compared to methotrexate. A significant weight gain of 1.5 ⫾ 2.7 kg and 2.5 ⫾ 3.3 kg (mean ⫾ SD) was observed in patients treated with etanercept and infliximab, respectively, after 24 weeks.16 Saraceno and colleagues also observed a significant increase in bodyweight for etanercept, adalimumab and infliximab compared to efalizumab and methotrexate. At week 24, 1.66 kg was gained in the etanercept group, 2.23 kg in the adalimumab group and 1.08 kg in the infliximab group.17 Similar findings have also been reported with the use of anti-TNFa agents in rheumatoid arthritis and inflammatory bowel disease.18,21–24 Total bodyweight is composed of fat mass and fatfree mass (muscle and bone mass). TNF-a is believed to promote loss of fat-free mass by shifting protein metabolism towards net catabolism.25,26 In addition, high levels of TNFa are thought to antagonise insulin, which is a hormone with anabolic effects. Hence, weight gain with a TNF-a blockade could be due to an increase in muscle or fat-free mass: a positive effect. However, if the gain in weight is due to an increase in fat mass this could increase cardiovascular risk. No study to date has addressed this issue in psoriasis patients. In a prospective study of infliximab therapy in patients with Crohn’s disease, an 18 per cent increase in total abdominal fat was noted on magnetic resonance imaging but there was no associated change in lipid profile or glycaemia HbA1c.24 Broit and colleagues also found an increase in fat mass in spondyloarthropathy patients receiving an anti-TNFa agent but this was associated with a concomitant increase in lean muscle mass.21 More studies are needed to explore the physiological parameters involved in this weight gain, particularly in the psoriasis group. © 2013 The Authors Australasian Journal of Dermatology © 2013 The Australasian College of Dermatologists

262 Table 3

E Tan et al. Mean and (median) weight gained (kg) from baseline for weeks 12, 24 and 48

Therapy

Week 12

P-value

Week 24

P-value

Week 48

P-value

Adalimumab Infliximab Etanercept Ustekinumab Efalizumab

1.5 ⫾ 4.5 (1.0) 1.7 ⫾ 4.7 (0.0) 0.4 ⫾ 1.8 (0.0) -0.4 ⫾ 3.6 (-0.5) 0.0 ⫾ 3.6 (0.0)

P < 0.05 P < 0.02 P > 0.1 P > 0.1 P > 0.1

2.2 ⫾ 4.4 (1.5) 3.2 ⫾ 4.9 (2.0) 0.3 ⫾ 3.4 (0.0) -1.1 ⫾ 5.4 (-0.4) -0.3 ⫾ 5.9 (0.0)

P < 0.01 P < 0.001 P > 0.1 P > 0.1 P > 0.1

2.4 ⫾ 6.4 (4.5) 2.5 ⫾ 5.4 (1.9) -0.1 ⫾ 6.3 (0.8) -1.0 ⫾ 5.7 (0.5) 0.4 ⫾ 3.4 (0.0)

P < 0.05 P < 0.005 P > 0.1 P > 0.1 P > 0.1

Table 4

Mean and (median) weight gained (kg)

Therapy

Week 12 versus 24

P-value

Week 24 versus 48

P-value

Adalimumab Infliximab Etanercept Ustekinumab Efalizumab

1.3 ⫾ 2.5 (0.3) 1.8 ⫾ 3.9 (0.3) -0.1 ⫾ 4.2 (0.0) 0.1 ⫾ 4.1 (0.0) -0.3 ⫾ 4.9 (0.0)

P < 0.03 P < 0.03 P > 0.1 P > 0.1 P > 0.1

-0.2 ⫾ 3.2 (0.0) 0.2 ⫾ 3.4 (0.0) -0.6 ⫾ 2.7 (0.1) -0.9 ⫾ 4.1 (0.0) -0.9 ⫾ 3.2 (0.0)

P > 0.1 P > 0.1 P > 0.1 P > 0.1 p = 0.1

Table 5

Mean body mass index at weeks 0, 12, 24 and 48

Therapy

Week 0

Week 12

P-value

Week 24

P-value

Week 48

P-value

Adalimumab Infliximab Etanercept Ustekinumab Efalizumab

30.0 ⫾ 5.41 29.9 ⫾ 6.68 30.9 ⫾ 5.86 33.7 ⫾ 6.73 29.5 ⫾ 5.68

30.5 ⫾ 5.36 30.5 ⫾ 6.85 31.1 ⫾ 5.88 33.6 ⫾ 6.86 29.7 ⫾ 5.54

P < 0.05 P < 0.02 P > 0.1 P > 0.1 P > 0.1

31.0 ⫾ 3.51 31.3 ⫾ 7.44 30.4 ⫾ 5.30 35.2 ⫾ 6.92 29.8 ⫾ 5.16

P < 0.05 P < 0.001 P > 0.1 P > 0.1 P > 0.1

29.9 ⫾ 4.70 30.7 ⫾ 7.63 29.6 ⫾ 4.99 35.6 ⫾ 7.03 29.9 ⫾ 4.70

P < 0.05 P < 0.002 P > 0.1 P > 0.1 P > 0.1

Cross-over of biological therapy is a potential confounder and is a reality in clinical practice. However, no patient ever received two biologics simultaneously at any point and an interval of at least 1 month was observed before the initiation of another biological agent. With the exception of ustekinumab, the half-lives of the other biological therapies are short: efalizumab – 5 days, etanercept – 3 to 6 days, infliximab – 7 to 12 days and adalimumab – 14 days. Furthermore, most of the weight gain tended to occur at weeks 12–24 after initiation of the biological agent. A limitation of our study is its retrospective nature. There was no specific analysis of diet or exercise-related factors. Hence, other factors such as changes in lifestyle could account for weight gain. No body composition measures were performed and hence we are unable to determine which physiological parameter accounted for weight gain. Nonetheless, the weight gain is statistically significant and in accordance with earlier reports.16–18 We are also unable to comment on weight change after 48 weeks as that was the extent of our study duration. Independent of its effect on weight, the blockade of TNFa has been reported to exert positive metabolic effects. In rheumatoid arthritis patients, infliximab significantly increased serum levels of adiponectin, an important adipocyte-derived hormone with anti-arthrogenic properties.22,27 In a prospective study anti-TNFa therapy was associated with a reduction in carotid intima-media thickness.28 Other studies have noted a reduction in insulin resistance of rheumatoid arthritis patients treated with infliximab using surrogate measures such as fasting insulin, homeostasis model of insulin resistance, quantitative insulin sensitivity

check index and hyperinsulinemic-euglycaemia clamp test – the gold standard for measurement of insulin resistance.29–34 It is postulated that high levels of TNFa inhibits insulin receptor activity and contributes to insulin resistance.35 This increased glucose sensitivity is present in spite of increased bodyweight, suggesting that the effects of TNFa inhibition could be independent of any potential increase in adiposity.32 Studies of weight gain and metabolic effects of anti-TNFa therapy in psoriasis patients are limited. Most of the evidence is extrapolated from patients with rheumatological diseases or inflammatory bowel disease. Moreover, longterm follow up is lacking.17 Clinicians and patients need to be aware of the possibility of weight gain with an anti-TNFa agent. Until large-scale studies with a long follow up are conducted, the cardiovascular risk of weight gain cannot be understated. In the Framingham Heart Study, a small increase in weight of 2.25 kg in healthy individuals was associated with a 21–45 per cent increase in the risk for developing the metabolic syndrome.36 In addition, psoriasis is frequently associated with the metabolic syndrome and has been identified as an independent risk factor for diabetes and hypertension.14 Psoriasis patients who gain weight on an anti-TNFa agent will need to be screened carefully for the presence of the metabolic syndrome (if not previously identified) and have modifiable cardiovascular risk factors addressed. In summary, therapy with an anti-TNFa agent is associated with weight gain. Whether this is due to an increase in fat mass or fat-free mass has yet to be fully elucidated. It is possible that any deleterious effects of weight gain could be

© 2013 The Authors Australasian Journal of Dermatology © 2013 The Australasian College of Dermatologists

Weight gain and TNF counterbalanced by the positive metabolic effects of the TNFa blockade. However, with the current evidence this weight gain will need to be addressed within the context of other cardiovascular risk factors.

REFERENCES 1.

2.

3. 4. 5.

6.

7.

8.

9.

10.

11. 12.

13.

14.

15.

16.

17.

18. 19.

20.

21.

Australian Institute of Health and Welfare. Australia’s Health 2004. (2004). Available from URL: http://www.aihw.gov.au/ publication-detail/?id=6442467608 (Accessed 5 March 2013). Huerta C, Rivero E, Rodriguez LA. Incidence and risk factors for psoriasis in the general population. Arch. Dermatol. 2007; 143: 1559–65. Naldi L. Epidemiology of psoriasis. Curr. Drug Targets Inflamm. Allergy 2004; 3: 121–8. Woodley DT, Kim GH. Potential new insight into the pathogenesis of psoriasis. Arch. Dermatol. 2009; 145: 713–4. Gottlieb AB, Evans R, Li S et al. Infliximab induction therapy for patients with severe plaque-type psoriasis: a randomized, double-blind, placebo-controlled trial. J. Am. Acad. Dermatol. 2004; 51: 534–42. Iyer S, Yamauchi P, Lowe NJ. Etanercept for severe psoriasis and psoriatic arthritis: observations on combination therapy. Br. J. Dermatol. 2002; 146: 118–21. Leonardi CL, Powers JL, Matheson RT et al. Etanercept as monotherapy in patients with psoriasis. N. Engl. J. Med. 2003; 349: 2014–22. Reich K, Nestle FO, Papp K et al. Infliximab induction and maintenance therapy for moderate-to-severe psoriasis: a phase III, multicentre, double-blind trial. Lancet 2005; 366: 1367–74. Weisman MH, Moreland LW, Furst DE et al. Efficacy, pharmacokinetic, and safety assessment of adalimumab, a fully human anti-tumor necrosis factor-alpha monoclonal antibody, in adults with rheumatoid arthritis receiving concomitant methotrexate: a pilot study. Clin. Ther. 2003; 25: 1700–21. Saurat JH, Stingl G, Dubertret L et al. Efficacy and safety results from the randomized controlled comparative study of adalimumab vs. methotrexate vs. placebo in patients with psoriasis (CHAMPION). Br. J. Dermatol. 2008; 158: 558–66. Gelfand JM, Neimann AL, Shin DB et al. Risk of myocardial infarction in patients with psoriasis. JAMA 2006; 296: 1735–41. Prodanovich S, Kirsner RS, Kravetz JD et al. Association of psoriasis with coronary artery, cerebrovascular, and peripheral vascular diseases and mortality. Arch. Dermatol. 2009; 145: 700–3. Friedewald VE, Cather JC, Gelfand JM et al. AJC editor’s consensus: psoriasis and coronary artery disease. Am. J. Cardiol. 2008; 102: 1631–43. Qureshi AA, Choi HK, Setty AR et al. Psoriasis and the risk of diabetes and hypertension: a prospective study of US female nurses. Arch. Dermatol. 2009; 145: 379–82. Ludwig RJ, Herzog C, Rostock A et al. Psoriasis: a possible risk factor for development of coronary artery calcification. Br. J. Dermatol. 2007; 156: 271–6. Gisondi P, Cotena C, Tessari G et al. Anti-tumour necrosis factor-alpha therapy increases body weight in patients with chronic plaque psoriasis: a retrospective cohort study. J. Eur. Acad. Dermatol. Venereol. 2008; 22: 341–4. Saraceno R, Schipani C, Mazzotta A et al. Effect of anti-tumor necrosis factor-alpha therapies on body mass index in patients with psoriasis. Pharmacol. Res. 2008; 57: 290–5. Stamp L, Cross N, O’Donnell J. Weight gain with tumour necrosis factor-alpha inhibitors. Intern. Med. J. 2005; 35: 267. Mahe E, Reguiai Z, Barthelemy H et al. Evaluation of risk factors for body weight increment in psoriatic patients on inf-

22.

23.

24.

25. 26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

36.

263

liximab: a multicentre, cross-sectional study. J. Eur. Acad. Dermatol. Venereol. 2012; doi: 10.1111/jdv.12066. [Epub ahead of print]. Florin V, Cottencin AC, Delaporte E et al. Body weight increment in patients treated with infliximab for plaque psoriasis. J. Eur. Acad. Dermatol. Venereol. 2013; 27: e186–90. Briot K, Gossec L, Kolta S et al. Prospective assessment of body weight, body composition, and bone density changes in patients with spondyloarthropathy receiving anti-tumor necrosis factor-alpha treatment. J. Rheumatol. 2008; 35: 855–61. Engvall IL, Tengstrand B, Brismar K et al. Infliximab therapy increases body fat mass in early rheumatoid arthritis independently of changes in disease activity and levels of leptin and adiponectin: a randomized study over 21 months. Arthritis Res. Ther. 2010; 12: R197. Koutroubakis IE, Oustamanolakis P, Malliaraki N et al. Effects of tumor necrosis factor alpha inhibition with infliximab on lipid levels and insulin resistance in patients with inflammatory bowel disease. Eur. J. Gastroenterol. Hepatol. 2009; 21: 283–8. Parmentier-Decrucq E, Duhamel A, Ernst O et al. Effects of infliximab therapy on abdominal fat and metabolic profile in patients with Crohn’s disease. Inflamm. Bowel Dis. 2009; 15: 1476–84. Walsmith J, Roubenoff R. Cachexia in rheumatoid arthritis. Int. J. Cardiol. 2002; 85: 89–99. Roubenoff R, Roubenoff RA, Ward LM et al. Rheumatoid cachexia: depletion of lean body mass in rheumatoid arthritis. Possible association with tumor necrosis factor. J. Rheumatol. 1992; 19: 1505–10. Nishida K, Okada Y, Nawata M et al. Induction of hyperadiponectinemia following long-term treatment of patients with rheumatoid arthritis with infliximab (IFX), an anti-TNF-alpha antibody. Endocr. J. 2008; 55: 213–6. Del Porto F, Lagana B, Lai S et al. Response to anti-tumour necrosis factor alpha blockade is associated with reduction of carotid intima-media thickness in patients with active rheumatoid arthritis. Rheumatology (Oxford) 2007; 46: 1111–5. Kiortsis DN, Mavridis AK, Filippatos TD et al. Effects of infliximab treatment on lipoprotein profile in patients with rheumatoid arthritis and ankylosing spondylitis. J. Rheumatol. 2006; 33: 921–3. Yazdani-Biuki B, Stelzl H, Brezinschek HP et al. Improvement of insulin sensitivity in insulin resistant subjects during prolonged treatment with the anti-TNF-alpha antibody infliximab. Eur. J. Clin. Invest. 2004; 34: 641–2. Seriolo B, Ferrone C, Cutolo M. Longterm anti-tumor necrosis factor-alpha treatment in patients with refractory rheumatoid arthritis: relationship between insulin resistance and disease activity. J. Rheumatol. 2008; 35: 355–7. Oguz FM, Oguz A, Uzunlulu M. The effect of infliximab treatment on insulin resistance in patients with rheumatoid arthritis. Acta Clin. Belg. 2007; 62: 218–22. Gonzalez-Gay MA, De Matias JM, Gonzalez-Juanatey C et al. Anti-tumor necrosis factor-alpha blockade improves insulin resistance in patients with rheumatoid arthritis. Clin. Exp. Rheumatol. 2006; 24: 83–6. Huvers FC, Popa C, Netea MG et al. Improved insulin sensitivity by anti-TNFalpha antibody treatment in patients with rheumatic diseases. Ann. Rheum. Dis. 2007; 66: 558–9. Hotamisligil GS, Peraldi P, Budavari A et al. IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNFalpha- and obesity-induced insulin resistance. Science 1996; 271: 665–8. Wilson PW, Kannel WB, Silbershatz H et al. Clustering of metabolic factors and coronary heart disease. Arch. Intern. Med. 1999; 159: 1104–9.

© 2013 The Authors Australasian Journal of Dermatology © 2013 The Australasian College of Dermatologists

Weight gain and tumour necrosis factor-alpha inhibitors in patients with psoriasis.

To compare the effect of anti-tumour necrosis factor (TNF)-α therapies with agents that do not target TNF-α on bodyweight and body mass index (BMI) in...
90KB Sizes 0 Downloads 0 Views