Commentary
Inflammatory markers of cardiovascular disease risk in Portuguese psoriatic patients: relation with narrow-band ultraviolet B and psoralen plus ultraviolet A Susana Coimbra1,2, PhD, Hugo Oliveira3, MD, Maria J. Neuparth2,4, PhD, Ame´rico Figueiredo3, MD, PhD, Petronila Rocha-Pereira1,5, PhD, and Alice Santos-Silva2,6, PhD
1 Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, Portugal, 2CESPU, Instituto de Investigac¸a˜o e Formac¸a˜o Avanc¸ada em Cieˆncias e Tecnologias da Sau´de, Gandra-PRD, Portugal, 3Servic¸o de Dermatologia, Centro Hospitalar e Universita´rio de Coimbra, Universidade de Coimbra, Coimbra, Portugal, 4Centro de Investigac¸a˜o em Actividade Fı´sica, Sau´de e Lazer (CIAFEL), Universidade do Porto, Porto, Portugal, 5 Centro de Investigac¸a˜o em Cieˆncias da Sau´de (CICS), Universidade da Beira Interior, Covilha˜, Portugal, and 6Laborato´rio de Bioquı´mica, Departamento de Cieˆncias Biolo´gicas, Faculdade de Farma´cia (FFUP), Universidade do Porto, Porto, Portugal
Correspondence Susana Coimbra or Alice Santos-Silva Instituto de Biologia Molecular e Celular da Universidade do Porto Rua do Campo Alegre 823 4150-180 Porto, Portugal E-mail: [email protected] or [email protected]
Psoriasis is known to associate with cardiovascular disease (CVD) events, and patients with psoriasis present a high prevalence of CVD risk factors.1 Patients with high levels of C-reactive protein (CRP), a short-chain pentraxin produced in the liver, have an increased risk for adverse cardiovascular outcome.2 Increased CRP has been recognized as a direct contributor to atherosclerosis, and it is one of the strongest predictors of coronary artery disease and mortality risk.3 Pentraxin 3 (PTX3) is a long-chain pentraxin produced by macrophages, dendritic cells, and endothelial cells, in response to inflammatory signals. High PTX3 levels have been associated with cardiovascular events.4,5 The association of PTX3 with CVD and with all causes of death is independent of CRP and other CVD risk factors; indeed, PTX3 seems to reflect aspects of the inflammatory process that are different for CRP.5 Increased
levels of both inflammatory markers, PTX3 and CRP, have been reported in patients with psoriasis.6–8 Indeed, Bevelacqua et al.7 and Ctirad et al.8 reported that CRP and PTX3 are increased at psoriasis exacerbation stage. However, their data concerning correlation of Psoriasis Area and Severity Index (PASI) with PTX3 was not consensual; the first group found a positive significant correlation between PTX3 levels and PASI, but the second did not observe any correlation between them. Ctirad et al.8 found that Goeckermans therapy, the combination of coal tar with ultraviolet B (UVB), decreased PTX3 and CRP levels significantly. We aimed to clarify these findings by studying the effect of narrow-band UVB (NB-UVB) and psoralen plus UVA (PUVA) therapies on PTX3 and CRP levels. Thirty patients (18 women/12 men; 48.3 ± 14.7 years old), presenting moderate to severe psoriasis vulgaris 393
ª 2013 The International Society of Dermatology
International Journal of Dermatology 2014, 53, 393–396
394
Commentary
PTX3 and CRP relation with NB-UVB and PUVA therapy
(a)
(b)
(c)
International Journal of Dermatology 2014, 53, 393–396
Coimbra et al.
Figure 1 Pentraxin 3 (a), C-reactive protein (b), and Psoriasis Area and Severity Index (PASI; c) values for controls and patients with psoriasis before (T0) and after (T12) narrowband ultraviolet light B (NB-UVB) and psoralen plus UVA (PUVA) therapy. Comparisons between groups were performed using Student’s unpaired t-test or Mann–Whitney U-test, and differences between data, before and after treatment, were evaluated by Student’s paired t-test or Wilcoxon signed-rank test (according to Gaussian distribution of the substances). Statistically significant: P < 0.05
(PASI: 21.8 ± 9.7; PASI range: 7.2–42.7; disease duration: 23.1 ± 11.9 years), attending the Dermatology Department of the University Hospitals of Coimbra, and 20 healthy volunteers, matched with patients for age (42.4 ± 16.3 years old; P = 0.190) and gender (11 women/nine men), were enrolled in this study after informed consent. Considering other CVD risk factors besides these two inflammatory markers, patients and controls were matched for obesity (body mass index [BMI] – values were 28.6 [24.9–29.8] and 25.6 [23.5– 29.6] kg/m2, respectively; P = 0.255) and smoking history (23.3% and 25.0% smokers, respectively; P = 0.894). Patients were analyzed before starting treatment (T0) and after 12 weeks (T12) of therapy with NB-UVB (n = 15) or with PUVA (n = 15). For BMI values, the PUVA (28.7 (26.7–29.7) kg/m2) and the NB-UVB (28.6 [21.5– 30.1] kg/m2) groups did not differ between them (P = 0.436) and from the control (P = 0.093 and P = 0.831, respectively); the patients’ weight did not change after treatment. Patient’s in the PUVA and NBUVB groups had similar smoking habits (26.7% and 20.0% smokers, respectively, P = 0.775) and were similar to controls (P = 0.805 and P = 0.934, respectively). The type of treatment was decided by the patients’ dermatologist, according to severity of disease presentation and to clinical and therapeutic history of patients. NB-UVB initial dose was 0.1–0.3 J/cm2, with an increase of 0.1 J/cm2 in every session (three per week) until a maximum dose of 2.5 J/cm2. For PUVA treatment, two hours before UVA irradiation 8-methoxypsoralen (0.6 mg/kg body weight) was administered; the initial dose of UVA was 2–3 J/cm2 with an increase of 0.5 J/cm2 in every session (three per week) until a maximum dose of 12 J/cm2. None of the patients received any antipsoriatic treatment for at least one month before blood collection; moreover, patients did not use any topical antipsoriatic therapy during the study, and they were not under any other regular treatment. PTX3 was evaluated by enzyme-immunoassay (Quantikine Human Pentraxin 3/TSG-14 Immunoassay; R&D Systems, Minneapolis, MN, USA) and CRP by im-
ª 2013 The International Society of Dermatology
Coimbra et al.
PTX3 and CRP relation with NB-UVB and PUVA therapy
munoturbidimetry (CRP [latex] High-Sensitivity; Roche Diagnostics, Basel, Switzerland). Compared to controls, patients presented at significantly higher PTX3 (0.266 [0.168–0.382] and 0.575 [0.375–0.980] ng/ml, respectively; P < 0.001] and CRP levels (1.63 [1.08–2.66] and 4.18 [1.93–10.04] mg/l, respectively; P = 0.001). At T12, PTX3 (0.385 [0.238– 0.558] ng/ml) and CRP values (2.82 [1.69–5.81] mg/l) diminished significantly (P < 0.001 and P = 0.001, respectively), but, compared to controls, their values remained increased (P = 0.041 and P = 0.020, respectively). At T0, PTX3 correlated significantly and positively with PASI (r = 0.376; P = 0.040). In multiple linear regression analysis, PASI remained significantly associated with Log10 PTX3 (P = 0.033). When compared to controls, NB-UVB and PUVA patients presented at T0 statistically significant increased values of PTX3 (T0: 0.476 [0.350–0.941] and 0.617 [0.378– 1.619] ng/ml, respectively; Fig. 1a) and CRP (T0: 4.20 [1.90–8.00] and 4.16 [1.94–13.80] mg/l, respectively; Fig. 1b). PTX3 (T12 NB-UVB: 0.336 [0.196–0.491] ng/ ml; T12 PUVA: 0.420 (0.252–0.589 ng/ml) and CRP (T12 NB-UVB: 3.83 [1.16–5.66] mg/l; T12 PUVA: 2.69 [1.70–6.50] mg/l) diminished significantly after NB-UVB and PUVA therapy. However, for PUVA patients, both PTX3 and CRP values remained significantly higher, as compared to controls (Fig. 1a,b). At T0, PUVA patients presented significantly higher PASI values than NB-UVB (25.3 ± 10.7, PASI range: 10.0–42.7, and 18.3 ± 7.4, PASI range: 7.2–30.0, respectively; Fig. 1c); in both treatments, PASI diminished significantly after therapy (NB-UVB: 4.8 ± 5.2, PASI range: 0.8–21.4; PUVA: 4.8 ± 6.7, PASI range: 0.0–21.6; Fig. 1c). In accordance with Bevelacqua et al. and Ctirad et al.,7,8 we found that at the active stage of the disease, the inflammatory markers, PTX3 and CRP, were significantly increased, confirming psoriasis as an inflammatory condition. Patients with psoriasis are known to present several CVD risk factors, such as oxidative stress, hypertension, abnormal lipid profile, overweight, and obesity with altered adipokine secretion and inflammation. The raised levels of CRP and PTX3, independent inflammatory markers of CVD risk, might contribute to the increased risk of CVD events in patients with psoriasis. In accordance with Bevelacqua et al.7 and in opposition to Ctirad et al.,8 we found that PTX3 levels correlated positively and significantly with PASI. Moreover, multiple linear regression analysis showed that PTX3 is an important determinant of PASI and may work as a good marker of psoriasis severity, as was proposed for CRP.6 PTX3, together with PASI and CRP, may therefore be useful to monitor psoriasis and its treatment.
Ctirad et al.8 found that PTX3 and CRP levels decreased significantly after Goeckerman therapy. PUVA and NBUVB therapies, usually used to treat moderate to severe forms of psoriasis vulgaris, are known to present antiinflammatory and immunomodulatory activities.9 Concerning the different type of treatments, NB-UVB and PUVA, they were clearly successful therapies, as confirmed by the significant decrease in PASI. For PUVA and NBUVB, we observed similar modifications, a decrease in CRP and PTX3 levels, inducing a significant reduction in the inflammatory state. However, after PUVA therapy a residual inflammation persists, as shown by the values of PTX3 and CRP that, compared to controls, remained higher in patients with psoriasis. In the active stage of the disease, before starting a therapy, PUVA patients, as shown by PASI, presented more severe forms of psoriasis, as compared to NB-UVB patients. In accordance with our results, Ctirad et al. found that after Goeckerman therapy, PTX3 and CRP remained significantly increased for patients with PASI values of 20.9 ± 8.4. Our data suggest that for the more severe forms of psoriasis, even after successful treatment, residual inflammation persists, with PTX3 and CRP levels remaining higher. This may imply that patients with severe forms of psoriasis present higher risk of CVD events, as a residual inflammation persists after therapy. In summary, PTX3, together with PASI and CRP, seems to be useful to monitor psoriasis and its treatment. PUVA and NB-UVB decreased CRP and PTX3 levels, inducing a significant reduction in the inflammatory state. Data show that PTX3 and CRP, independent inflammatory markers of CVD risk, are high in the active stage of the disease and, in the severe forms of psoriasis, their values remain higher than the control values, even after treatment that is usually considered as successful according to PASI values. These patients are, therefore, at higher risk for CVD events, as a residual inflammation persists.
ª 2013 The International Society of Dermatology
Commentary
Acknowledgments This study was supported by FCT (POCI/SAU – OBS/ 58600/2004) and FEDER, and by CITS (06-2011-CITS/ CESPU). References 1 Neimann AL, Shin DB, Wang X, et al. Prevalence of cardiovascular risk factors in patients with psoriasis. J Am Acad Dermatol 2006; 55: 829–835. 2 Celik T, Iyisoy A, Celik M, et al. C-reactive protein in chronic heart failure: a new predictor of survival. Int J Cardiol 2009; 135: 396–397. 3 Boekholdt SM, Hack CE, Sandhu MS, et al. C-reactive protein levels and coronary artery disease incidence and
International Journal of Dermatology 2014, 53, 393–396
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396
Commentary
PTX3 and CRP relation with NB-UVB and PUVA therapy
mortality in apparently healthy men and women: the EPIC-Norfolk prospective population study 1993-2003. Atherosclerosis 2006; 187: 415–422. 4 Liu Q, Tu T, Bai Z, et al. Elevated plasma pentraxin 3: a potential cardiovascular risk factor? Med Hypotheses 2011; 77: 1068–1070. 5 Jenny NS, Arnold AM, Kuller LH, et al. Associations of pentraxin 3 with cardiovascular disease and all-cause death: the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol 2009; 29: 594–599. 6 Coimbra S, Oliveira H, Reis F, et al. C-reactive protein and leucocyte activation in psoriasis vulgaris according to
International Journal of Dermatology 2014, 53, 393–396
Coimbra et al.
severity and therapy. J Eur Acad Dermatol Venereol 2010; 24: 789–796. 7 Bevelacqua V, Libra M, Mazzarino MC, et al. Long pentraxin 3: a marker of inflammation in untreated psoriatic patients. Int J Mol Med 2006; 18: 415– 423. 8 Ctirad A, Lenka B, David P, et al. Goeckermans therapy for psoriasis with special reference to serum pentraxin 3 level. Int J Dermatol 2008; 47: 1011–1014. 9 Lebwohl M, Ali S. Treatment of psoriasis. Part 1. Topical therapy and phototherapy. J Am Acad Dermatol 2001; 45: 487–498; quiz 99–502.
ª 2013 The International Society of Dermatology
Inflammatory markers of cardiovascular disease risk in Portuguese psoriatic patients: relation with narrow-band ultraviolet B and psoralen plus ultraviolet A Susana Coimbra1,2, PhD, Hugo Oliveira3, MD, Maria J. Neuparth2,4, PhD, Ame´rico Figueiredo3, MD, PhD, Petronila Rocha-Pereira1,5, PhD, and Alice Santos-Silva2,6, PhD
1 Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, Portugal, 2CESPU, Instituto de Investigac¸a˜o e Formac¸a˜o Avanc¸ada em Cieˆncias e Tecnologias da Sau´de, Gandra-PRD, Portugal, 3Servic¸o de Dermatologia, Centro Hospitalar e Universita´rio de Coimbra, Universidade de Coimbra, Coimbra, Portugal, 4Centro de Investigac¸a˜o em Actividade Fı´sica, Sau´de e Lazer (CIAFEL), Universidade do Porto, Porto, Portugal, 5 Centro de Investigac¸a˜o em Cieˆncias da Sau´de (CICS), Universidade da Beira Interior, Covilha˜, Portugal, and 6Laborato´rio de Bioquı´mica, Departamento de Cieˆncias Biolo´gicas, Faculdade de Farma´cia (FFUP), Universidade do Porto, Porto, Portugal
Correspondence Susana Coimbra or Alice Santos-Silva Instituto de Biologia Molecular e Celular da Universidade do Porto Rua do Campo Alegre 823 4150-180 Porto, Portugal E-mail: [email protected] or [email protected]
Psoriasis is known to associate with cardiovascular disease (CVD) events, and patients with psoriasis present a high prevalence of CVD risk factors.1 Patients with high levels of C-reactive protein (CRP), a short-chain pentraxin produced in the liver, have an increased risk for adverse cardiovascular outcome.2 Increased CRP has been recognized as a direct contributor to atherosclerosis, and it is one of the strongest predictors of coronary artery disease and mortality risk.3 Pentraxin 3 (PTX3) is a long-chain pentraxin produced by macrophages, dendritic cells, and endothelial cells, in response to inflammatory signals. High PTX3 levels have been associated with cardiovascular events.4,5 The association of PTX3 with CVD and with all causes of death is independent of CRP and other CVD risk factors; indeed, PTX3 seems to reflect aspects of the inflammatory process that are different for CRP.5 Increased
levels of both inflammatory markers, PTX3 and CRP, have been reported in patients with psoriasis.6–8 Indeed, Bevelacqua et al.7 and Ctirad et al.8 reported that CRP and PTX3 are increased at psoriasis exacerbation stage. However, their data concerning correlation of Psoriasis Area and Severity Index (PASI) with PTX3 was not consensual; the first group found a positive significant correlation between PTX3 levels and PASI, but the second did not observe any correlation between them. Ctirad et al.8 found that Goeckermans therapy, the combination of coal tar with ultraviolet B (UVB), decreased PTX3 and CRP levels significantly. We aimed to clarify these findings by studying the effect of narrow-band UVB (NB-UVB) and psoralen plus UVA (PUVA) therapies on PTX3 and CRP levels. Thirty patients (18 women/12 men; 48.3 ± 14.7 years old), presenting moderate to severe psoriasis vulgaris 393
ª 2013 The International Society of Dermatology
International Journal of Dermatology 2014, 53, 393–396
394
Commentary
PTX3 and CRP relation with NB-UVB and PUVA therapy
(a)
(b)
(c)
International Journal of Dermatology 2014, 53, 393–396
Coimbra et al.
Figure 1 Pentraxin 3 (a), C-reactive protein (b), and Psoriasis Area and Severity Index (PASI; c) values for controls and patients with psoriasis before (T0) and after (T12) narrowband ultraviolet light B (NB-UVB) and psoralen plus UVA (PUVA) therapy. Comparisons between groups were performed using Student’s unpaired t-test or Mann–Whitney U-test, and differences between data, before and after treatment, were evaluated by Student’s paired t-test or Wilcoxon signed-rank test (according to Gaussian distribution of the substances). Statistically significant: P < 0.05
(PASI: 21.8 ± 9.7; PASI range: 7.2–42.7; disease duration: 23.1 ± 11.9 years), attending the Dermatology Department of the University Hospitals of Coimbra, and 20 healthy volunteers, matched with patients for age (42.4 ± 16.3 years old; P = 0.190) and gender (11 women/nine men), were enrolled in this study after informed consent. Considering other CVD risk factors besides these two inflammatory markers, patients and controls were matched for obesity (body mass index [BMI] – values were 28.6 [24.9–29.8] and 25.6 [23.5– 29.6] kg/m2, respectively; P = 0.255) and smoking history (23.3% and 25.0% smokers, respectively; P = 0.894). Patients were analyzed before starting treatment (T0) and after 12 weeks (T12) of therapy with NB-UVB (n = 15) or with PUVA (n = 15). For BMI values, the PUVA (28.7 (26.7–29.7) kg/m2) and the NB-UVB (28.6 [21.5– 30.1] kg/m2) groups did not differ between them (P = 0.436) and from the control (P = 0.093 and P = 0.831, respectively); the patients’ weight did not change after treatment. Patient’s in the PUVA and NBUVB groups had similar smoking habits (26.7% and 20.0% smokers, respectively, P = 0.775) and were similar to controls (P = 0.805 and P = 0.934, respectively). The type of treatment was decided by the patients’ dermatologist, according to severity of disease presentation and to clinical and therapeutic history of patients. NB-UVB initial dose was 0.1–0.3 J/cm2, with an increase of 0.1 J/cm2 in every session (three per week) until a maximum dose of 2.5 J/cm2. For PUVA treatment, two hours before UVA irradiation 8-methoxypsoralen (0.6 mg/kg body weight) was administered; the initial dose of UVA was 2–3 J/cm2 with an increase of 0.5 J/cm2 in every session (three per week) until a maximum dose of 12 J/cm2. None of the patients received any antipsoriatic treatment for at least one month before blood collection; moreover, patients did not use any topical antipsoriatic therapy during the study, and they were not under any other regular treatment. PTX3 was evaluated by enzyme-immunoassay (Quantikine Human Pentraxin 3/TSG-14 Immunoassay; R&D Systems, Minneapolis, MN, USA) and CRP by im-
ª 2013 The International Society of Dermatology
Coimbra et al.
PTX3 and CRP relation with NB-UVB and PUVA therapy
munoturbidimetry (CRP [latex] High-Sensitivity; Roche Diagnostics, Basel, Switzerland). Compared to controls, patients presented at significantly higher PTX3 (0.266 [0.168–0.382] and 0.575 [0.375–0.980] ng/ml, respectively; P < 0.001] and CRP levels (1.63 [1.08–2.66] and 4.18 [1.93–10.04] mg/l, respectively; P = 0.001). At T12, PTX3 (0.385 [0.238– 0.558] ng/ml) and CRP values (2.82 [1.69–5.81] mg/l) diminished significantly (P < 0.001 and P = 0.001, respectively), but, compared to controls, their values remained increased (P = 0.041 and P = 0.020, respectively). At T0, PTX3 correlated significantly and positively with PASI (r = 0.376; P = 0.040). In multiple linear regression analysis, PASI remained significantly associated with Log10 PTX3 (P = 0.033). When compared to controls, NB-UVB and PUVA patients presented at T0 statistically significant increased values of PTX3 (T0: 0.476 [0.350–0.941] and 0.617 [0.378– 1.619] ng/ml, respectively; Fig. 1a) and CRP (T0: 4.20 [1.90–8.00] and 4.16 [1.94–13.80] mg/l, respectively; Fig. 1b). PTX3 (T12 NB-UVB: 0.336 [0.196–0.491] ng/ ml; T12 PUVA: 0.420 (0.252–0.589 ng/ml) and CRP (T12 NB-UVB: 3.83 [1.16–5.66] mg/l; T12 PUVA: 2.69 [1.70–6.50] mg/l) diminished significantly after NB-UVB and PUVA therapy. However, for PUVA patients, both PTX3 and CRP values remained significantly higher, as compared to controls (Fig. 1a,b). At T0, PUVA patients presented significantly higher PASI values than NB-UVB (25.3 ± 10.7, PASI range: 10.0–42.7, and 18.3 ± 7.4, PASI range: 7.2–30.0, respectively; Fig. 1c); in both treatments, PASI diminished significantly after therapy (NB-UVB: 4.8 ± 5.2, PASI range: 0.8–21.4; PUVA: 4.8 ± 6.7, PASI range: 0.0–21.6; Fig. 1c). In accordance with Bevelacqua et al. and Ctirad et al.,7,8 we found that at the active stage of the disease, the inflammatory markers, PTX3 and CRP, were significantly increased, confirming psoriasis as an inflammatory condition. Patients with psoriasis are known to present several CVD risk factors, such as oxidative stress, hypertension, abnormal lipid profile, overweight, and obesity with altered adipokine secretion and inflammation. The raised levels of CRP and PTX3, independent inflammatory markers of CVD risk, might contribute to the increased risk of CVD events in patients with psoriasis. In accordance with Bevelacqua et al.7 and in opposition to Ctirad et al.,8 we found that PTX3 levels correlated positively and significantly with PASI. Moreover, multiple linear regression analysis showed that PTX3 is an important determinant of PASI and may work as a good marker of psoriasis severity, as was proposed for CRP.6 PTX3, together with PASI and CRP, may therefore be useful to monitor psoriasis and its treatment.
Ctirad et al.8 found that PTX3 and CRP levels decreased significantly after Goeckerman therapy. PUVA and NBUVB therapies, usually used to treat moderate to severe forms of psoriasis vulgaris, are known to present antiinflammatory and immunomodulatory activities.9 Concerning the different type of treatments, NB-UVB and PUVA, they were clearly successful therapies, as confirmed by the significant decrease in PASI. For PUVA and NBUVB, we observed similar modifications, a decrease in CRP and PTX3 levels, inducing a significant reduction in the inflammatory state. However, after PUVA therapy a residual inflammation persists, as shown by the values of PTX3 and CRP that, compared to controls, remained higher in patients with psoriasis. In the active stage of the disease, before starting a therapy, PUVA patients, as shown by PASI, presented more severe forms of psoriasis, as compared to NB-UVB patients. In accordance with our results, Ctirad et al. found that after Goeckerman therapy, PTX3 and CRP remained significantly increased for patients with PASI values of 20.9 ± 8.4. Our data suggest that for the more severe forms of psoriasis, even after successful treatment, residual inflammation persists, with PTX3 and CRP levels remaining higher. This may imply that patients with severe forms of psoriasis present higher risk of CVD events, as a residual inflammation persists after therapy. In summary, PTX3, together with PASI and CRP, seems to be useful to monitor psoriasis and its treatment. PUVA and NB-UVB decreased CRP and PTX3 levels, inducing a significant reduction in the inflammatory state. Data show that PTX3 and CRP, independent inflammatory markers of CVD risk, are high in the active stage of the disease and, in the severe forms of psoriasis, their values remain higher than the control values, even after treatment that is usually considered as successful according to PASI values. These patients are, therefore, at higher risk for CVD events, as a residual inflammation persists.
ª 2013 The International Society of Dermatology
Commentary
Acknowledgments This study was supported by FCT (POCI/SAU – OBS/ 58600/2004) and FEDER, and by CITS (06-2011-CITS/ CESPU). References 1 Neimann AL, Shin DB, Wang X, et al. Prevalence of cardiovascular risk factors in patients with psoriasis. J Am Acad Dermatol 2006; 55: 829–835. 2 Celik T, Iyisoy A, Celik M, et al. C-reactive protein in chronic heart failure: a new predictor of survival. Int J Cardiol 2009; 135: 396–397. 3 Boekholdt SM, Hack CE, Sandhu MS, et al. C-reactive protein levels and coronary artery disease incidence and
International Journal of Dermatology 2014, 53, 393–396
395
396
Commentary
PTX3 and CRP relation with NB-UVB and PUVA therapy
mortality in apparently healthy men and women: the EPIC-Norfolk prospective population study 1993-2003. Atherosclerosis 2006; 187: 415–422. 4 Liu Q, Tu T, Bai Z, et al. Elevated plasma pentraxin 3: a potential cardiovascular risk factor? Med Hypotheses 2011; 77: 1068–1070. 5 Jenny NS, Arnold AM, Kuller LH, et al. Associations of pentraxin 3 with cardiovascular disease and all-cause death: the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol 2009; 29: 594–599. 6 Coimbra S, Oliveira H, Reis F, et al. C-reactive protein and leucocyte activation in psoriasis vulgaris according to
International Journal of Dermatology 2014, 53, 393–396
Coimbra et al.
severity and therapy. J Eur Acad Dermatol Venereol 2010; 24: 789–796. 7 Bevelacqua V, Libra M, Mazzarino MC, et al. Long pentraxin 3: a marker of inflammation in untreated psoriatic patients. Int J Mol Med 2006; 18: 415– 423. 8 Ctirad A, Lenka B, David P, et al. Goeckermans therapy for psoriasis with special reference to serum pentraxin 3 level. Int J Dermatol 2008; 47: 1011–1014. 9 Lebwohl M, Ali S. Treatment of psoriasis. Part 1. Topical therapy and phototherapy. J Am Acad Dermatol 2001; 45: 487–498; quiz 99–502.
ª 2013 The International Society of Dermatology
