Erratum to “Prevalence of obesity/adiposity in Japanese psoriasis patients: Adiposity is correlated with the severity of psoriasis” [J. Dermatol. Sci. 54 (2009) 61–63]
2009; Elsevier BV; Volume: 55; Issue: 1 Linguagem: Inglês
10.1016/j.jdermsci.2009.04.003
ISSN1873-569X
AutoresHidetoshi Takahashi, Hitomi Tsuji, Ichiro Takahashi, Yoshio Hashimoto, Akemi Ishida‐Yamamoto, Hajime Iizuka,
Tópico(s)Adipokines, Inflammation, and Metabolic Diseases
ResumoAlthough epidemiologic survey revealed an association between psoriasis and obesity/adiposity [[1]Gisondi P. Tessari G. Conti A. Piaserico S. Schianchi S. Peserico A. et al.Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case–control study.Br J Dermatol. 2007; 157: 68-73Crossref PubMed Scopus (538) Google Scholar], no reports are present on the relationship in Japanese psoriasis patients. Obesity induces overproduction of inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin (IL)-6, and IL-8 in adipose tissue. The serum levels of TNF-α, IL-6, and IL-8 are increased in psoriasis and are associated with the disease severity [[2]Arican O. Aral M. Sasmaz S. Serum levels of TNF-α, IFN-7, IL-6, IL-8, IL-12, IL-17, and IL-18 in patients with active psoriasis and correlation with disease severity.Med Inflamm. 2005; 5: 273-279Crossref Scopus (632) Google Scholar]. Adipocytes also produce leptin, which acts primarily through the specific receptors at hypothalamus [[3]Campfleld L.A. Smith F.J. Guisez Y. Devos R. Bum P. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks.Science. 1995; 269: 546-549Crossref PubMed Scopus (3060) Google Scholar]. Leptin decreases appetite and increases energy expenditure and serum levels of leptin are known to reflect the body fat mass [[3]Campfleld L.A. Smith F.J. Guisez Y. Devos R. Bum P. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks.Science. 1995; 269: 546-549Crossref PubMed Scopus (3060) Google Scholar]. Adiponectin is another adipocyte-specific secretary protein abundantly present in circulation. Plasma levels of adiponectin are paradoxically decreased in obesity, insulin-resistance [[4]Matsuzaka Y. The metabolic syndrome and adipocytokines.FEBS Lett. 2006; 580: 2917-2921Abstract Full Text Full Text PDF PubMed Scopus (438) Google Scholar], and hypoadiponectinemia is closely associated with metabolic syndrome [[5]Hulthe J. Hulten L.M. Fagerberg B. Low adipocyte-derived plasma protein adiponectin concentration is associated with metabolic syndrome and small dense low-density lipoprotein particles: atherosclerosis and insulin resistance study.Metabolism. 2003; 52: 1612-1614Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar]. Recent study demonstrated that adiponectin and TNF-α suppress each other's production and also antagonize each other's function in their target cells [[6]Maeda M. Shimomura I. Kishida K. Nishizawa H. Matsuda M. Nagaretani H. et al.Diet-induced insulin resistance in mice lacking adipocectin/ACRP30.Nat Med. 2002; 8: 731-737Crossref PubMed Scopus (1798) Google Scholar]. We have shown the increased plasma leptin levels and decreased adiponectin levels in Japanese psoriasis patients [[7]Takahashi H. Tsuji H. Takahashi I. Hashimoto Y. Ishîda-Yamamoto A. Iizuka H. Plasma adiponectin and leptin levels in Japanese psoriasis patients.Br J Dermatol. 2008; 159: 1207-1208PubMed Google Scholar].Although the obesity or overweight usually means from increased fat of the body, there is some exception such as muscular athletes, and visceral adiposity persons who are within the normal range of body mass index (BMI). So we evaluated obesity/adiposity as BMI, %BF, and visceral adiposity and used the obesity as the term estimated by BMI. Adiposity was used as the term estimated by %BF and visceral adiposity. The aim of the present study is to investigate the association of psoriasis and obesity/adiposity and to dissect the relation between plasma levels of adipocytokines and adiposity in Japanese psoriasis patients.A total of 122 psoriasis patients, including 81 males and 41 females aged 25–72 (mean age 47.5), psoriasis area and severity index (PASI) 0.7–32.3 (mean 7.3), body surface area (BSA) 3–86 (mean 8.4), were enrolled. Seventy-eight control population (54 males and 24 females, mean age 38.6, 24–76) was also enrolled. Psoriasis severity was determined by PASI score. Weight and height of each patient were measured and BMI was calculated as the weight in kilograms divided by square of height in meters. Percent body fat (%BF) and visceral adiposity of each patient was measured by bioelectrical impedance analysis using body fat meter (TF-205), which is the product of Tanita Co., Inc. (Tokyo, Japan). Plasma was obtained fresh and centrifuged and was immediately frozen at −70 °C and stored until use. Plasma levels of TNF-α, adiponectin and leptin were measured by enzyme-linked immunosorbent assay (ELISA) kits, BioSource. These assays detected only human cytokines and the minimal detectable concentrations were 2.4 pg/ml for TNF-α, 0.1 IU/ml for adiponectin, and 1 fmol/ml for leptin, respectively.All these parameters of obesity were significantly increased in psoriasis compared with those of healthy controls (Table 1). There was the positive correlation between BMI, %BF and visceral adiposity level and the severity of psoriasis. The correlation of %BF (r = 0.52, P < 0.01) or visceral adiposity (r = 0.50, P < 0.01) with PASI was higher than that of BMI (r = 0.32, P < 0.05). Plasma levels of adiponectin in psoriasis were negatively correlated with BMI (r = −0.31, P < 0.05), %BF (r = −0.56, P < 0.01) and visceral adiposity (r = −0.76, P < 0.01) (Fig. 1A ). In contrast, plasma levels of TNF-α and leptin were positively correlated with BMI (r = 0.29, P < 0.05; r = 0.30, P < 0.05), %BF (r = 0.45, P < 0.01; r = 0.35, P < 0.05) and visceral adiposity (r = 0.54, P < 0.01; r = 0.39, P < 0.05) (Fig. 1B and C).Table 1BMI, percent body fat, and visceral adiposity in psoriasis and healthy control.PsoriasisHealthy controlP valueBMI26.2 ± 0.5224.5 ± 0.48<0.01%BF27.3 ± 1.2324.2 ± 1.45<0.01Visceral adiposity12.5 ± 0.749.78 ± 0.68<0.01 Open table in a new tab Hensler and Christophers (32) reported the positive correlation between psoriasis and obesity in Caucasians, which was confirmed by following studies [[1]Gisondi P. Tessari G. Conti A. Piaserico S. Schianchi S. Peserico A. et al.Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case–control study.Br J Dermatol. 2007; 157: 68-73Crossref PubMed Scopus (538) Google Scholar]. In the present study we firstly demonstrated that Japanese psoriasis patients also show a prevalence of obesity/adiposity. Recently metabolic syndrome, a cluster of central obesity, hypertension, hyperlipemia, and glucose intolerance, is shown to be a strong predictor of cardiovascular disease, diabetes mellitus, and coronary heart disease [[8]Sommer D.M. Jenisch S. Suchan M. Christophers E. Weichenthal M. Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis.Arch Dermatol Res. 2006; 298: 321-328Crossref PubMed Scopus (534) Google Scholar]. The prevalence of metabolic syndrome in U.S. and Western Europe is 25% and 35%, respectively, while that in Japanese population is 8%. This might be related to the lower incidence of Japanese psoriasis (0.01%) compared with Caucasians (2%).The relation between the metabolic syndrome and the severity of psoriasis is controversial. Sommer et al. [[8]Sommer D.M. Jenisch S. Suchan M. Christophers E. Weichenthal M. Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis.Arch Dermatol Res. 2006; 298: 321-328Crossref PubMed Scopus (534) Google Scholar] reported increased prevalence of metabolic syndrome in psoriasis with moderate to severe psoriasis. In contrast Gisondi et al. [[1]Gisondi P. Tessari G. Conti A. Piaserico S. Schianchi S. Peserico A. et al.Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case–control study.Br J Dermatol. 2007; 157: 68-73Crossref PubMed Scopus (538) Google Scholar] detected no correlation between the severity of psoriasis and the prevalence of metabolic syndrome [[1]Gisondi P. Tessari G. Conti A. Piaserico S. Schianchi S. Peserico A. et al.Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case–control study.Br J Dermatol. 2007; 157: 68-73Crossref PubMed Scopus (538) Google Scholar]. Although we could not detect the positive correlation between PASI score and the prevalence of metabolic syndrome, the correlation was clearly demonstrated between the PASI score and the prevalence of obesity, BMI, percent of body mass, and visceral adiposity. Among them visceral adiposity showed stronger association with PASI. Visceral adipose tissue is the major source of adipocytokines, such as adiponectin, TNF-α, and IL-6, and it is assumed that aberrant secretion of adipocytokines induces metabolic syndrome [[6]Maeda M. Shimomura I. Kishida K. Nishizawa H. Matsuda M. Nagaretani H. et al.Diet-induced insulin resistance in mice lacking adipocectin/ACRP30.Nat Med. 2002; 8: 731-737Crossref PubMed Scopus (1798) Google Scholar]. Increased visceral adiposity increases the secretion of TNF-α and IL-6, which might play an important role on the induction and the maintenance of psoriasis [[3]Campfleld L.A. Smith F.J. Guisez Y. Devos R. Bum P. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks.Science. 1995; 269: 546-549Crossref PubMed Scopus (3060) Google Scholar]. Consistent with this, the increased serum levels of TNF-α and IL-6 are correlated with psoriasis severity [[3]Campfleld L.A. Smith F.J. Guisez Y. Devos R. Bum P. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks.Science. 1995; 269: 546-549Crossref PubMed Scopus (3060) Google Scholar]. In contrast adiponectin is negatively correlated with visceral adiposity [[6]Maeda M. Shimomura I. Kishida K. Nishizawa H. Matsuda M. Nagaretani H. et al.Diet-induced insulin resistance in mice lacking adipocectin/ACRP30.Nat Med. 2002; 8: 731-737Crossref PubMed Scopus (1798) Google Scholar]. In our study the plasma adiponectin was negatively and the TNF-α was positively correlated with visceral adiposity, respectively. These findings are consistent with the view that obesity, especially visceral adiposity, correlates with psoriasis severity.In the present study we firstly demonstrated increased plasma levels of leptin in Japanese psoriasis patients. Activation of leptin receptor induces Janus kinase-signalling System and activates transcription-signalling cascade, STAT 3. Recent study of activated STAT 3 transgenic mice indicates that STAT 3 shows a critical role on the pathogenesis of psoriasis [[9]Sano S. Chan K.S. Carbajal S. Clifford J. Peavey M. Kiguchi K. et al.Stat3 links activated keratinocytes and immunocytes required for development of psoriasis in a novel transgenic mouse model.Nat Med. 2005; 11: 43-49Crossref PubMed Scopus (585) Google Scholar]. Increased leptin might play a role on the development of psoriasis through the STAT 3 System. Epidemiological investigation disclosed that diabetic mellitus, hypertension, hyperlipemia, and coronary artery sclerosis are prevalent in psoriasis [[8]Sommer D.M. Jenisch S. Suchan M. Christophers E. Weichenthal M. Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis.Arch Dermatol Res. 2006; 298: 321-328Crossref PubMed Scopus (534) Google Scholar]. Increased plasma levels of adiponectin show the lower risk of these disorders [[10]Nishida M. Funahashi T. Shimomura I. Pathophysiological significance of adiponectin.Med Mol Morphol. 2007; 40: 55-67Crossref PubMed Scopus (141) Google Scholar]. In our study we demonstrated lower plasma levels of adiponectin in psoriasis, which might be related to the increased prevalence of diabetic mellitus, hypertension, hyperlipemia, and coronary artery sclerosis in psoriasis. Although epidemiologic survey revealed an association between psoriasis and obesity/adiposity [[1]Gisondi P. Tessari G. Conti A. Piaserico S. Schianchi S. Peserico A. et al.Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case–control study.Br J Dermatol. 2007; 157: 68-73Crossref PubMed Scopus (538) Google Scholar], no reports are present on the relationship in Japanese psoriasis patients. Obesity induces overproduction of inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin (IL)-6, and IL-8 in adipose tissue. The serum levels of TNF-α, IL-6, and IL-8 are increased in psoriasis and are associated with the disease severity [[2]Arican O. Aral M. Sasmaz S. Serum levels of TNF-α, IFN-7, IL-6, IL-8, IL-12, IL-17, and IL-18 in patients with active psoriasis and correlation with disease severity.Med Inflamm. 2005; 5: 273-279Crossref Scopus (632) Google Scholar]. Adipocytes also produce leptin, which acts primarily through the specific receptors at hypothalamus [[3]Campfleld L.A. Smith F.J. Guisez Y. Devos R. Bum P. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks.Science. 1995; 269: 546-549Crossref PubMed Scopus (3060) Google Scholar]. Leptin decreases appetite and increases energy expenditure and serum levels of leptin are known to reflect the body fat mass [[3]Campfleld L.A. Smith F.J. Guisez Y. Devos R. Bum P. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks.Science. 1995; 269: 546-549Crossref PubMed Scopus (3060) Google Scholar]. Adiponectin is another adipocyte-specific secretary protein abundantly present in circulation. Plasma levels of adiponectin are paradoxically decreased in obesity, insulin-resistance [[4]Matsuzaka Y. The metabolic syndrome and adipocytokines.FEBS Lett. 2006; 580: 2917-2921Abstract Full Text Full Text PDF PubMed Scopus (438) Google Scholar], and hypoadiponectinemia is closely associated with metabolic syndrome [[5]Hulthe J. Hulten L.M. Fagerberg B. Low adipocyte-derived plasma protein adiponectin concentration is associated with metabolic syndrome and small dense low-density lipoprotein particles: atherosclerosis and insulin resistance study.Metabolism. 2003; 52: 1612-1614Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar]. Recent study demonstrated that adiponectin and TNF-α suppress each other's production and also antagonize each other's function in their target cells [[6]Maeda M. Shimomura I. Kishida K. Nishizawa H. Matsuda M. Nagaretani H. et al.Diet-induced insulin resistance in mice lacking adipocectin/ACRP30.Nat Med. 2002; 8: 731-737Crossref PubMed Scopus (1798) Google Scholar]. We have shown the increased plasma leptin levels and decreased adiponectin levels in Japanese psoriasis patients [[7]Takahashi H. Tsuji H. Takahashi I. Hashimoto Y. Ishîda-Yamamoto A. Iizuka H. Plasma adiponectin and leptin levels in Japanese psoriasis patients.Br J Dermatol. 2008; 159: 1207-1208PubMed Google Scholar]. Although the obesity or overweight usually means from increased fat of the body, there is some exception such as muscular athletes, and visceral adiposity persons who are within the normal range of body mass index (BMI). So we evaluated obesity/adiposity as BMI, %BF, and visceral adiposity and used the obesity as the term estimated by BMI. Adiposity was used as the term estimated by %BF and visceral adiposity. The aim of the present study is to investigate the association of psoriasis and obesity/adiposity and to dissect the relation between plasma levels of adipocytokines and adiposity in Japanese psoriasis patients. A total of 122 psoriasis patients, including 81 males and 41 females aged 25–72 (mean age 47.5), psoriasis area and severity index (PASI) 0.7–32.3 (mean 7.3), body surface area (BSA) 3–86 (mean 8.4), were enrolled. Seventy-eight control population (54 males and 24 females, mean age 38.6, 24–76) was also enrolled. Psoriasis severity was determined by PASI score. Weight and height of each patient were measured and BMI was calculated as the weight in kilograms divided by square of height in meters. Percent body fat (%BF) and visceral adiposity of each patient was measured by bioelectrical impedance analysis using body fat meter (TF-205), which is the product of Tanita Co., Inc. (Tokyo, Japan). Plasma was obtained fresh and centrifuged and was immediately frozen at −70 °C and stored until use. Plasma levels of TNF-α, adiponectin and leptin were measured by enzyme-linked immunosorbent assay (ELISA) kits, BioSource. These assays detected only human cytokines and the minimal detectable concentrations were 2.4 pg/ml for TNF-α, 0.1 IU/ml for adiponectin, and 1 fmol/ml for leptin, respectively. All these parameters of obesity were significantly increased in psoriasis compared with those of healthy controls (Table 1). There was the positive correlation between BMI, %BF and visceral adiposity level and the severity of psoriasis. The correlation of %BF (r = 0.52, P < 0.01) or visceral adiposity (r = 0.50, P < 0.01) with PASI was higher than that of BMI (r = 0.32, P < 0.05). Plasma levels of adiponectin in psoriasis were negatively correlated with BMI (r = −0.31, P < 0.05), %BF (r = −0.56, P < 0.01) and visceral adiposity (r = −0.76, P < 0.01) (Fig. 1A ). In contrast, plasma levels of TNF-α and leptin were positively correlated with BMI (r = 0.29, P < 0.05; r = 0.30, P < 0.05), %BF (r = 0.45, P < 0.01; r = 0.35, P < 0.05) and visceral adiposity (r = 0.54, P < 0.01; r = 0.39, P < 0.05) (Fig. 1B and C). Hensler and Christophers (32) reported the positive correlation between psoriasis and obesity in Caucasians, which was confirmed by following studies [[1]Gisondi P. Tessari G. Conti A. Piaserico S. Schianchi S. Peserico A. et al.Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case–control study.Br J Dermatol. 2007; 157: 68-73Crossref PubMed Scopus (538) Google Scholar]. In the present study we firstly demonstrated that Japanese psoriasis patients also show a prevalence of obesity/adiposity. Recently metabolic syndrome, a cluster of central obesity, hypertension, hyperlipemia, and glucose intolerance, is shown to be a strong predictor of cardiovascular disease, diabetes mellitus, and coronary heart disease [[8]Sommer D.M. Jenisch S. Suchan M. Christophers E. Weichenthal M. Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis.Arch Dermatol Res. 2006; 298: 321-328Crossref PubMed Scopus (534) Google Scholar]. The prevalence of metabolic syndrome in U.S. and Western Europe is 25% and 35%, respectively, while that in Japanese population is 8%. This might be related to the lower incidence of Japanese psoriasis (0.01%) compared with Caucasians (2%). The relation between the metabolic syndrome and the severity of psoriasis is controversial. Sommer et al. [[8]Sommer D.M. Jenisch S. Suchan M. Christophers E. Weichenthal M. Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis.Arch Dermatol Res. 2006; 298: 321-328Crossref PubMed Scopus (534) Google Scholar] reported increased prevalence of metabolic syndrome in psoriasis with moderate to severe psoriasis. In contrast Gisondi et al. [[1]Gisondi P. Tessari G. Conti A. Piaserico S. Schianchi S. Peserico A. et al.Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case–control study.Br J Dermatol. 2007; 157: 68-73Crossref PubMed Scopus (538) Google Scholar] detected no correlation between the severity of psoriasis and the prevalence of metabolic syndrome [[1]Gisondi P. Tessari G. Conti A. Piaserico S. Schianchi S. Peserico A. et al.Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case–control study.Br J Dermatol. 2007; 157: 68-73Crossref PubMed Scopus (538) Google Scholar]. Although we could not detect the positive correlation between PASI score and the prevalence of metabolic syndrome, the correlation was clearly demonstrated between the PASI score and the prevalence of obesity, BMI, percent of body mass, and visceral adiposity. Among them visceral adiposity showed stronger association with PASI. Visceral adipose tissue is the major source of adipocytokines, such as adiponectin, TNF-α, and IL-6, and it is assumed that aberrant secretion of adipocytokines induces metabolic syndrome [[6]Maeda M. Shimomura I. Kishida K. Nishizawa H. Matsuda M. Nagaretani H. et al.Diet-induced insulin resistance in mice lacking adipocectin/ACRP30.Nat Med. 2002; 8: 731-737Crossref PubMed Scopus (1798) Google Scholar]. Increased visceral adiposity increases the secretion of TNF-α and IL-6, which might play an important role on the induction and the maintenance of psoriasis [[3]Campfleld L.A. Smith F.J. Guisez Y. Devos R. Bum P. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks.Science. 1995; 269: 546-549Crossref PubMed Scopus (3060) Google Scholar]. Consistent with this, the increased serum levels of TNF-α and IL-6 are correlated with psoriasis severity [[3]Campfleld L.A. Smith F.J. Guisez Y. Devos R. Bum P. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks.Science. 1995; 269: 546-549Crossref PubMed Scopus (3060) Google Scholar]. In contrast adiponectin is negatively correlated with visceral adiposity [[6]Maeda M. Shimomura I. Kishida K. Nishizawa H. Matsuda M. Nagaretani H. et al.Diet-induced insulin resistance in mice lacking adipocectin/ACRP30.Nat Med. 2002; 8: 731-737Crossref PubMed Scopus (1798) Google Scholar]. In our study the plasma adiponectin was negatively and the TNF-α was positively correlated with visceral adiposity, respectively. These findings are consistent with the view that obesity, especially visceral adiposity, correlates with psoriasis severity. In the present study we firstly demonstrated increased plasma levels of leptin in Japanese psoriasis patients. Activation of leptin receptor induces Janus kinase-signalling System and activates transcription-signalling cascade, STAT 3. Recent study of activated STAT 3 transgenic mice indicates that STAT 3 shows a critical role on the pathogenesis of psoriasis [[9]Sano S. Chan K.S. Carbajal S. Clifford J. Peavey M. Kiguchi K. et al.Stat3 links activated keratinocytes and immunocytes required for development of psoriasis in a novel transgenic mouse model.Nat Med. 2005; 11: 43-49Crossref PubMed Scopus (585) Google Scholar]. Increased leptin might play a role on the development of psoriasis through the STAT 3 System. Epidemiological investigation disclosed that diabetic mellitus, hypertension, hyperlipemia, and coronary artery sclerosis are prevalent in psoriasis [[8]Sommer D.M. Jenisch S. Suchan M. Christophers E. Weichenthal M. Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis.Arch Dermatol Res. 2006; 298: 321-328Crossref PubMed Scopus (534) Google Scholar]. Increased plasma levels of adiponectin show the lower risk of these disorders [[10]Nishida M. Funahashi T. Shimomura I. Pathophysiological significance of adiponectin.Med Mol Morphol. 2007; 40: 55-67Crossref PubMed Scopus (141) Google Scholar]. In our study we demonstrated lower plasma levels of adiponectin in psoriasis, which might be related to the increased prevalence of diabetic mellitus, hypertension, hyperlipemia, and coronary artery sclerosis in psoriasis. Prevalence of obesity/adiposity in Japanese psoriasis patients: Adiposity is correlated with the severity of psoriasisJournal of Dermatological ScienceVol. 54Issue 1PreviewAlthough epidemiologic survey revealed an association between psoriasis and obesity/adiposity [1], no reports are present on the relationship in Japanese psoriasis patients. Obesity induces overproduction of inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin (IL)-6, and IL-8 in adipose tissue. The serum levels of TNF-α, IL-6, and IL-8 are increased in psoriasis and are associated with the disease severity [2]. Adipocytes also produce leptin, which acts primarily through the specific receptors at hypothalamus [3]. Full-Text PDF Introduction to ErratumJournal of Dermatological ScienceVol. 55Issue 1Preview Full-Text PDF
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