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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 31  |  Issue : 3  |  Page : 928-934

Evaluation of pentraxin-3 level in patients with diabetic retinopathy


1 Department of Internal Medicine, Faculty of Medicine, Menoufia University, Al Minufiyah, Egypt
2 Department of Clinical Pathology, Faculty of Medicine, Menoufia University, Al Minufiyah, Egypt
3 Department of Internal Medicine, Ministry of Health, Cairo, Egypt

Date of Submission21-Feb-2017
Date of Acceptance18-Apr-2017
Date of Web Publication31-Dec-2018

Correspondence Address:
Mohammed Mogahed
Department of Internal Medicine, Ministry of Health, Cairo
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_140_17

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  Abstract 


Objective
The aim of this study was to evaluate serum pentraxin-3 (PTX3) levels as an indicator of diabetic retinopathy (DR) in patients with type 2 diabetes mellitus (T2DM).
Background
DR is responsible for 10.2% of worldwide visual loss. Pentraxin-3 is an acute phase protein secreted by different types of cells and correlates with the disease activity.
Patients and methods
A total of 80 individuals were included in the study. They were divided into three groups. Group 1 included 30, type 2 diabetic patients without retinopathy, group 2 included 30, type 2 diabetic patients with retinopathy, and group 3 included 20 apparently healthy individuals. Group 2 was subdivided into 20 patients with nonproliferative and 10 patients with proliferative DR. Serum glycated hemoglobin, C-reactive protein (CRP), lipid profile, liver function tests, renal function tests, serum PTX3 level, and fundus examination were measured in all the patients.
Results
Serum PTX3 was significantly elevated in T2DM with retinopathy than T2DM without retinopathy and control group. There is no statistical difference between proliferative and nonproliferative DR regarding PTX3. Serum PTX3 was significantly positively correlated with age and high-sensitivity CRP in the proliferative DR group and cholesterol, low-density lipoprotein and high-sensitivity CRP in the proliferative DR group.
Conclusion
PTX3 levels were significantly higher in T2DM with retinopathy than those without retinopathy and control group, and positively correlated with inflammatory marker. Thus, it might be used in the prognosis of DR.

Keywords: diabetes mellitus, diabetic retinopathy, pentraxin-3, prognosis


How to cite this article:
Nouh MZ, Sonbol A, Mogahed M. Evaluation of pentraxin-3 level in patients with diabetic retinopathy. Menoufia Med J 2018;31:928-34

How to cite this URL:
Nouh MZ, Sonbol A, Mogahed M. Evaluation of pentraxin-3 level in patients with diabetic retinopathy. Menoufia Med J [serial online] 2018 [cited 2019 Sep 15];31:928-34. Available from: http://www.mmj.eg.net/text.asp?2018/31/3/928/248721




  Introduction Top


Diabetes mellitus (DM) is an epidemic disease that accounts for high rate of morbidity and mortality. This is due to the high rate of occurrence of complications that lead to health burden both for patients and countries[1]. Death from cardiovascular complications affects nearly 50% of type 2 diabetes mellitus (T2DM) patients[2].

Diabetic complications include both microvascular and macrovascular. Retinopathy, nephropathy, and neuropathy are microvascular complications[3].

DM microvascular complications are caused by systemic inflammatory reaction[4],[5]. The relationship between increased plasma concentration of acute phase biomarkers such as C-reactive protein (CRP) and T2DM has been reported by several studies[6],[7].

Singh et al.[8] stated that diabetic retinopathy (DR) is a microangiopathy affecting all of the small retinal vessels, such as arterioles, capillaries, and venules. DR is characterized by increased vascular permeability, ocular hemorrhages, and lipid exudate. DR is responsible for a higher percentage of patients with visual loss[9]. Recently, DR is classified as either nonproliferative or proliferative[10].

Pentraxin-3 (PTX3) is an acute phase reactant released by peripheral tissues in response to endothelial dysfunction[11]. PTX3 promotes restenosis, inhibits angiogenesis, and increases the formation of advanced atherosclerotic lesions, typically by inhibiting the fibroblast growth factor (FGF2) reaction of angiogenesis[12],[13]. Recently, PTX3 has been shown to be a sensitive biomarker of localized inflammatory reactions and innate immunity in cardiovascular and renal diseases[14],[15],[16].

Elevated levels of plasma CRP and short pentraxin are more frequently observed in both DM and DR patients[17],[18].

There are very few studies on PTX3 in DR[19], so the aim of our study was to determine the PTX3 level in T2DM patients with retinopathy and use it as a diagnostic and prognostic tool among those patients.


  Patients and Methods Top


This study was carried out at the Internal Medicine Department, Menoufia University Hospitals and Ahmed Maher Teaching Hospital. We divided the patients into three groups: group 1 included 30 T2DM patients without retinopathy (16 men and 14 women); group 2 included 30 T2DM patients with retinopathy (17 men and 13 women); and group 3 included 20 apparently healthy volunteers as a control (10 men and 10 women). Group 2 is subdivided into 20 patients with nonproliferative diabetic retinopathy (NPDR) and 10 patients with proliferative diabetic retinopathy (PDR).

All patients underwent full history taking and clinical examination was performed. Blood pressure measurements were taken using sphygmomanometer as a mean on three times at different occasions in sitting position: diastolic pressure (DP), systolic pressure (SP) measured, and mean arterial pressure = DP + 1/3(SP − DP), (normally 70–110 mmHg)[20]. Also, BMI was calculated as the weight in kilograms divided by the square of the height in meters (kg/m2)[21].

Patients with the following criteria were excluded: patients with a history of hypertension, patients with any form of chronic infection or current or past history of receiving any immune modulating drugs, patients with malignancy, renal impairment, intravenous drug abusers, patients with severe eye disease, and retinal detachment.

The protocol for this study followed the ethical standards and approved by the ethical committee of our institution and all patients gave informed consent to participate in this study.

Laboratory assessment

Blood samples for hematological and biochemical measurements were obtained from the forearm after overnight fasting. Serum glycated hemoglobin (HA1C), CRP, liver function tests, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and renal function tests (urea, creatinine) were measured by standard methods in the routine clinical laboratory.

Serum PTX3 levels were determined by an enzyme-linked immunoassay using PTX3 ELISA kits from Shanghai Sunred Biological Technology Company (Shanghai, China), according to the manufacturer's instructions.

Fundus examination

Fundus examination was carried out by slit lamp biomicroscope and indirect ophthalmoscopy, fundus color photograph centered on the macula and fundus fluorescein angiography wherever indicated.

Statistical analysis

Data were analyzed using the Program for Social Science, version 20.0 for windows (SPSS Inc., Chicago, Illinois, USA) and MedCalc 13 for windows (MedCalc Software BVBA, Ostend, Belgium). Data were analyzed using statistical quantitative data and were expressed as mean ± SD. Qualitative data were expressed as frequency and percentage. The following statistical tests were used as appropriate: χ2-test, Student's t-test. Correlations between variables were done using Spearman's rank correlation coefficient (r). Values of P less than 0.05 were taken as statistically significant.


  Results Top


Sixty diabetic patients were included in our study. They were divided into two groups; group 1 diabetic without retinopathy (30 patients), group 2 included 30 T2DM patients with retinopathy (17 men and 13 women); group 3 included 20 apparently healthy volunteers as a control (10 men and 10 women); besides group 2 was subdivided into NPDR (20 patients) and PDR (10 patients). Mean age of the groups were 55.03 ± 7.44,58 ± 6.68 and 66 ± 5.14 years, respectively, and the female: male ratios were 14: 16, 8: 12, and 5: 5, respectively [Table 1].
Table 1: Comparison between studied groups according to demographic and clinical data

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HA1C was highly significant in diabetes with normal fundus and retinopathy groups than in the control group (P = 0.000), whereas there was no significant difference between retinopathy group and diabetes with normal fundus group (P = 0.914) [Table 1].

As regards PTX3 and high-sensitivity C-reactive protein (hsCRP) levels, there were highly significant increase in NPDR group than in diabetes with normal fundus group (P = 0.000); there was also significant difference between PDR and diabetes with normal fundus group (P = 0.001 and 0.002, respectively) and no significant difference between PDR and NPDR (P = 0.891 and 0.981v) [Table 2] and [Figure 1] and [Figure 2].
Table 2: Comparison between diabetes without retinopathy group and retinopathy subgroups (nonproliferative diabetic retinopathy and proliferative diabetic retinopathy) according to demographic and clinical data

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Figure 1: Comparison between log PTX3 and log hsCRP in the studied groups. DM, diabetes mellitus; log hsCRP, log-transformed value of high-sensitivity C-reactive protein; PTX3, Pentraxin-3.

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Figure 2: Comparison between levels of log hsCRP and log PTX3 in the patient group. DM, diabetes mellitus; log hsCRP, log-transformed value of high-sensitivity C-reactive protein; NPDR, nonproliferative diabetic retinopathy; PDR, proliferative diabetic retinopathy; PTX3, Pentraxin-3.

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In diabetes with normal fundus group PTX3 was positively correlated with hsCRP and age, significant with systolic blood pressure and not significant with duration, aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatinine, cholesterol, diastolic blood pressure, LDL, HDL, and HA1C [Table 3].
Table 3: Correlation between log Pentraxin-3 and other measured laboratory parameters

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In NPDR group, PTX3 did not correlate with duration, blood pressure, AST, ALT, creatinine, cholesterol, blood pressure, LDL, HDL, and HA1C. However, PTX3 is highly significant with age, with significant correlation with hsCRP [Table 3].

In the PDR group, PTX3 did not correlate with age, duration, blood pressure, AST, ALT, creatinine, cholesterol, blood pressure, HDL, and HA1C). In contrast, PTX3 was significant with (log hsCRP, cholesterol, LDL) [Table 3] and [Figure 3].
Figure 3: Correlation between log hsCRP and log PTX3 in diabetes with retinopathy. log hsCRP, log-transformed value of high-sensitivity C-reactive protein; PTX3, Pentraxin-3.

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The cutoff point for PTX3 was 1150 pg/ml that has sensitivity 93.3% and specificity 72%, and cutoff point of CRP was 760 pg/ml has sensitivity 93.3% and specificity 68%. Combined use of PTX3 and CRP decrease sensitivity to 76.7%, but increase specificity to 90% [Figure 4].
Figure 4: Receiver operating characteristic curve for detection of the best cutoff point of serum PTX3 and hsCRP in diabetic retinopathy. log hsCRP, log-transformed value of high-sensitivity C-reactive protein; PTX3, Pentraxin-3.

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  Discussion Top


The most common microvascular complication of DM is DR that leads to preventable visual loss in diabetic patients[22],[23]. The percentage of DR in T2DM after a duration of 20 years is estimated at about 60%[24]. The increased incidence of DR is due to many factors such as poor glycemic control and long duration of diabetes, associated hypertension, hyperlipidemia, nephropathy, pregnancy, and anemia[10].

Many factors have involved in the pathogenesis of DR such as chronic hyperglycemia, increased polyol and protein kinase C pathway activity[25],[26], increased vascular endothelial growth factor[25], production of advanced glycation end products[27], chronic oxidative damage[28], increased activation of the renin angiotensin system, and chronic inflammation and leukostasis[10].

PTX3 is a 200 amino acid protein that is secreted from the endothelium, macrophages, myeloid cells, dendritic cells, and many other cells in response to cytokines and endotoxins such as bacterial products, interleukin-1, and tumor necrosis factor[29].

PTX3 plays many biological roles such as in the regulation of inflammatory reaction, innate immunity, and female fertility[11]. The expression of PTX3 is increased in acute coronary syndromes[30], and it is a predictor of poor outcome in congestive heart failure patients[31]. PTX3 is also increased in many other diseases such as sleep apnea syndrome[32], pulmonary infection[33], rheumatoid arthritis, progressive systemic sclerosis, and in other rheumatologic diseases[34].

Both PTX3 and CRP are acute phase reactants known to be involved in inflammation, endothelial dysfunction, and atherosclerosis[35],[36],[37],[38],[39]. As they are increased in DM, they can be used as prognostic factors for vascular complications such as DR[5],[38],[39].

In our study, plasma levels of PTX3 and CRP were significantly higher in both NPDR and PDR than in diabetes with normal fundus group and with normal individuals, whereas there was no significant difference between both groups of diabetic retinopathy. This reflects that DR in T2DM is an inflammatory process associated with increase inflammatory reactants.

PTX3 and CRP, in our study as well as in the study by Zhou et al.[19] and Yang et al.[40], showed significant increase in their levels with the development and progression of DR, with a cutoff value of 1150 pg/ml and sensitivity 93.3% and specificity 72% for PTX3, and with a cutoff value of 760 pg/ml and sensitivity 93.3% and specificity 68% for CRP. The combined use of PTX3 and CRP decreases the sensitivity to 76.7%, but increases specificity to 90%.

Similar results regarding elevated PTX3 and CRP in DR were documented by Yang et al.[40] and Woo et al.[40],[41], who reported that the retinal pigment epithelium and vascular tissues can express PTX3 locally reflecting that it can be used as a biomarker of vascular inflammation. Yang et al.[40] stated that PTX3 levels are associated with the development and progression of DR in Korean patients with T2DM. This was a case–control study which recruited 163 individuals – 92 diabetic patients with DR, 30 diabetics without DR, and 41 healthy controls whose plasma levels of PTX3 and hsCRP were measured and compared. The proportion of higher-degree retinal complications increased in direct correlation with log PTX3 levels with a P trend less than 0.001 whereas a similar analysis based on log hsCRP values had a P trend of 0.006. On the basis of the PTX3 and hsCRP levels selected based on receiver operating curves, the diagnostic sensitivity of PTX3 for DR was 53.3% and the sensitivity was 91.7% while for hsCRP it was 51.1 and 70.8%, respectively. The authors therefore suggested that PTX3 may be a more accurate predictor of DR development than hsCRP. The presence of elevated PTX3 levels from early disease and its progressive elevation with increasing disease severity seem to suggest it has potential as a screening marker.

Nowak et al.[17] reported similar results regarding CRP whereas other studies such as that of Cai et al.[42] and Nguyen et al.[43], did not show significant association between CRP and DR. Few studies have reported lower serum levels of CRP in T2DM with DR compared with those without DR as in Lim et al.[44] and Tsunoda et al.[45]. Yang et al.[40] assumed that this discrepancy could be due to differences in the sites of inflammation and production of inflammatory cytokines or the effects of confounding factors such as drugs or liver disease.

Possible explanations of this association are that DM microangiopathy is associated with endothelial dysfunction and neutrophil adhering to the damaged endothelium and inducing local vascular and tissue injury[46]. This leukocyte–endothelial interaction produces PTX3 that is believed to be involved in innate immunity and tissue remodeling.[47]. This supports the hypothesis that T2DM may be a manifestation of ongoing cytokine-mediated acute-phase response, initiated by the innate immune system[48].


  Conclusion Top


PTX3 as well as CRP are acute phase reactants that can be used as markers of progression of retinopathy in T2DM and they are increased with disease duration. Moreover, poor glycemic control was significantly associated with higher incidence and severity of diabetic retinopathy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Elgart JF, Caporale JE, Asteazarán S, Jorge L, Fuente DL, Camillucci C, et al. Association between socioeconomic status, type 2 diabetes and its chronic complications in Argentina. Diabetes Res Clin Pract 2014; 104:241–247.  Back to cited text no. 1
    
2.
Neutzsky-Wulff AV, Andreassen KV, Hjuler ST, Feigh M, Bay-Jensen A, Zheng Q, et al. Future detection and monitoring of diabetes may entail analysis of both β-cell function and volume: how markers of β-cell loss may assist. J Transl Med 2012; 10:214–229.  Back to cited text no. 2
    
3.
American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2014; 37 (Suppl 1):S81–S90.  Back to cited text no. 3
    
4.
Goksen D, Levent E, Kar S, Özen S, Darcan S. Serum adiponectin and hsCRP levels and non-invasive radiological methods in the early diagnosis of cardiovascular system complications in children and adolescents with type 1 diabetes mellitus. J Clin Res Pediatr Endocrinol 2013; 5:174–181.  Back to cited text no. 4
    
5.
Yu HI, Sheu WH, Song YM, Liu HC, Lee WJ, Chen YT. C reactive protein and risk factors for peripheral vascular disease in subjects with type 2 diabetes mellitus. Diabet Med 2004; 21:336–341.  Back to cited text no. 5
    
6.
McMillan DE. Increased levels of acute-phase serum proteins in diabetes. Metabolism 1989; 38:1042–1046.  Back to cited text no. 6
    
7.
Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 2001; 286:327–334.  Back to cited text no. 7
    
8.
Singh R, Ramasamy K, Abraham C, Gupta V, Gupta A. Diabetic retinopathy: an update. Indian J Ophthalmol 2008; 56:178–188.  Back to cited text no. 8
    
9.
Kumari S, Panda S, Mangaraj M, Mandal MK, Mahapatra PC. Plasma MDA and antioxidant vitamins in diabetic retinopathy. Indian J Clin Biochem 2008; 23:158–162.  Back to cited text no. 9
    
10.
Sayin N, Kara N, Pekel G. Ocular complications of diabetes mellitus. World J Diabetes 2015; 6:92–108.  Back to cited text no. 10
    
11.
Mantovani A, Garlanda C, Doni A, Bottazzi B. Pentraxins in innate immunity: from C-reactive protein to the long pentraxin PTX3. J Clin Immunol 2008; 28:1–13.  Back to cited text no. 11
    
12.
Shindo A, Tanemura H, Yata K, Hamada K, Shibata M, Ymeda Y, et al. Inflammatory biomarkers in atherosclerosis: pentraxin 3 can become a novel marker of plaque vulnerability. PLoS One 2014; 9:e100045.  Back to cited text no. 12
    
13.
Leali D, Bianchi R, Bugatti A, Nicoli S, Mitola S, Ragona L, et al. Fibroblast growth factor 2-antagonist activity of a long-pentraxin 3-derived anti-angiogenic pentapeptide. J Cell Mol Med 2010; 14:2109–2121.  Back to cited text no. 13
    
14.
Hamad RR, Eriksson MJ, Berg E, Larsson A, Bremme K. Impaired endothelial function and elevated levels of pentraxin3 in early-onset preeclampsia. Acta Obstet Gynecol Scand 2012; 91:50–56.  Back to cited text no. 14
    
15.
Zhou Y, Ni Z, Zhang J, Zhang W, Wu Q, Shen G, et al. Plasma pentraxin 3 may be a better marker of peripheral artery disease in hemodialysis patients than C-reactive protein. Vasc Med 2013; 18:85–91.  Back to cited text no. 15
    
16.
Hudzik B, Szkodzinski J, Pietka-Rzycka A, Danikiewicz A, Wojnar R, Lekston A, et al. Plasma pentraxin 3 may be a more sensitive marker of inflammatory response than high-sensitivity C-reactive protein after bare metal stent compared to drug-eluting stent implantation. J Interferon Cytokine Res 2013; 33:280–284.  Back to cited text no. 16
    
17.
Nowak M, Wielkoszynski T, Marek B, Kos-Kudła B, Swietochowska E, Siemińska L, et al. Antioxidant potential, paraoxonase 1, ceruloplasmin activity and C-reactive protein concentration in diabetic retinopathy. Clin Exp Med 2010; 10:185–192.  Back to cited text no. 17
    
18.
Muni RH, Kohly RP, Lee EQ, Manson JE, Semba RD, Schaumberg DA. Prospective study of inflammatory biomarkers and risk of diabetic retinopathy in the diabetes control and complications trial. JAMA Ophthalmol 2013; 131:514–521.  Back to cited text no. 18
    
19.
Zhou W, Hu W. Serum and vitreous pentraxin 3 concentrations in patients with diabetic retinopathy. Genet Test Mol Biomarkers 2016; 20:149–153.  Back to cited text no. 19
    
20.
Meaney E, Alva F, Moguel R, Meaney A, Alva J, Webel R. Formula and nomogram for the sphygmomanometric calculation of the mean arterial pressure. Heart 2000; 84:64.  Back to cited text no. 20
    
21.
WHO. Physical status: the use and interpretation of anthropometry. Report of a WHO expert consultation. WHO technical report series number 854. Geneva: World Health Organization; 1995.  Back to cited text no. 21
    
22.
Antonetti, DA, Klein, R, Gardner, TW. Diabetic retinopathy. N Engl J Med 2012; 366:1227–1239.  Back to cited text no. 22
    
23.
Kajiwara A, Miyagawaa H, Saruwatari J, Kita A, Sakata M, Kawata Y, et al. Gender differences in the incidence and progression of diabetic retinopathy among Japanese patients with type 2 diabetes mellitus: a clinic-based retrospective longitudinal study. Diabetes Res Clin Pract 2014; 103:e7–e10.  Back to cited text no. 23
    
24.
Garg S, Davis RM. Diabetic retinopathy screening update. Clin Diabetes 2009; 4:140–145.  Back to cited text no. 24
    
25.
Kowluru RA. Diabetic retinopathy: mitochondrial dysfunction and retinal capillary cell death. Antioxid Redox Signal 2005; 7:1581–1587.  Back to cited text no. 25
    
26.
Naruse K, Nakamura J, Hamada Y, Nakayama M, Chaya S, Komori T, et al. Aldose reductase inhibition prevents glucose-induced apoptosis in cultured bovine retinal microvascular pericytes. Exp Eye Res 2000; 71:309–315.  Back to cited text no. 26
    
27.
Chu J, Ali Y. Diabetic retinopathy: a review. Drug Dev Res 2008; 69:1–14.  Back to cited text no. 27
    
28.
Kowluru RA, Tang J, Kern TS. Abnormalities of retinal metabolism in diabetes and experimental galactosemia. VII. Effect of long-term administration of antioxidants on the development of retinopathy. Diabetes 2001; 50:1938–1942.  Back to cited text no. 28
    
29.
Bottazzi B, Bastone A, Doni A, Garlanda C, Valentino S, Deban L, et al. The long pentraxin PTX3 as a link among innate immunity, inflammation, and female fertility. J Leukoc Biol 2006; 79:909–912.  Back to cited text no. 29
    
30.
Peri G, Introna M, Corradi D, Iacuitti G, Signorini S, Avanzini F, et al. PTX3, a prototypical long pentraxin, is an early indicator of acute myocardial infarction in humans. Circulation 2000; 102:636–641.  Back to cited text no. 30
    
31.
Matsubara J, Sugiyama S, Nozaki T, Sugamura K, Konishi M, Ohba K, et al. Pentraxin 3 is a new inflammatory marker correlated with left ventricular diastolic dysfunction and heart failure with normal ejection fraction. J Am Coll Cardiol 2011; 57:861–869.  Back to cited text no. 31
    
32.
Maugeri N, Rovere-Querini P, Slavich M, Coppi G, Doni A, Bottazzi B, et al. Early and transient release of leukocyte pentraxin 3 during acute myocardial infarction. J Immunol 2011; 187:970–979.  Back to cited text no. 32
    
33.
Medzhitov R. Toll-like receptors and innate immunity. Nat Rev Immunol 2001; 1:135–145.  Back to cited text no. 33
    
34.
Iwata Y, Yoshizaki A, Ogawa F, Komura K, Hara T, Muroi E, et al. Increased serum pentraxin 3 in patients with systemic sclerosis. J Rheumatol 2009; 36:976–983.  Back to cited text no. 34
    
35.
Garlanda C, Bottazzi B, Bastone A, Mantovani A. Pentraxins at the crossroads between innate immunity, inflammation, matrix deposition, and female fertility. Annu Rev Immunol 2005; 23:337–366.  Back to cited text no. 35
    
36.
Manfredi AA, Rovere-Querini P, Bottazzi B, Garlanda C Mantovani A. Pentraxins, humoral innate immunity and tissue injury. Curr Opin Immunol 2008; 20:538–544.  Back to cited text no. 36
    
37.
Kocyigit I, Eroglu E, Orscelik O, Unal A, Gungor O, Ozturk F, et al. Pentraxin 3 as a novel bio-marker of inflammation and endothelial dysfunction in autosomal dominant polycystic kidney disease. J Nephrol 2014; 27:181–186.  Back to cited text no. 37
    
38.
Kume N, Mitsuoka H, Hayashida K, Tanaka M. Pentraxin 3 as a biomarker for acute coronary syndrome: comparison with biomarkers for cardiac damage. J Cardiol 2011; 58:38–45.  Back to cited text no. 38
    
39.
Lee DH, Jeon HK, You JH, Park MY, Lee SJ, Kim SS. Pentraxin 3 as a novel marker predicting congestive heart failure in subjects with acute coronary syndrome. Korean Circ J 2010; 40:370–376.  Back to cited text no. 39
    
40.
Yang HS, Woo JE, Lee SJ, Park SH, Woo JM. Elevated plasma pentraxin 3 levels are associated with development and progression of diabetic retinopathy in Korean patients with type 2 diabetes mellitus. Invest Ophthalmol Vis Sci 2014; 55:5989–5997.  Back to cited text no. 40
    
41.
Woo JM, Kwon MY, Shin DY, Kang YH, Hwang N, Chung SW. Human retinal pigment epithelial cells express the long pentraxin PTX3. Mol Vis 2013; 19:303–310.  Back to cited text no. 41
    
42.
Cai XL, Wang F, Ji LN. Risk factors of diabetic retinopathy in type 2 diabetic patients. Chin Med J (Engl) 2006; 119:822–826.  Back to cited text no. 42
    
43.
Nguyen TT, Alibrahim E, Islam FM, Klein R, Klein BE, Cotch MF, et al. Inflammatory, hemostatic, and other novel biomarkers for diabetic retinopathy: the multi-ethnic study of atherosclerosis. Diabetes Care 2009; 32:1704–1709.  Back to cited text no. 43
    
44.
Lim LS, Tai ES, Mitchell P, Wang JJ, Tay WT, Lamoureux E, et al. C-reactive protein, body mass index, and diabetic retinopathy. Invest Ophthalmol Vis Sci 2010; 51:4458–4463.  Back to cited text no. 44
    
45.
Tsunoda K, Arita M, Yukawa M, Ueyama M, Furuta M, Nakagawa T. Retinopathy and hypertension affect serum high-sensitivity C-reactive protein levels in type 2 diabetic patients. J Diabetes Complications 2005; 19:123–127.  Back to cited text no. 45
    
46.
Segel GB, Halterman MW, Lichtman MA. The paradox of the neutrophil's role in tissue injury. J Leukoc Biol 2011; 89:359–372.  Back to cited text no. 46
    
47.
Inforzato A, Jaillon S, Moalli F, Barbati E, Bonavita E, Bottazzi B. The long pentraxin PTX3 at the crossroads between innate immunity and tissue remodeling. Tissue Antigens 2011; 77:271–282.  Back to cited text no. 47
    
48.
Crook M. Type 2 diabetes mellitus: a disease of the innate immune system? An update. Diabet Med 2004; 21:203–207.  Back to cited text no. 48
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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