Serum Pentraxin 3 and hs-CRP Levels in Children with Severe Pulmonary Hypertension

Year 2014, Volume: 31 Issue: 3, 219 - 223, 01.07.2014

Cemşit Karakurt Fazlı Serkan Çelik Osman Başpınar Aydın Derya Şahin Çağatay Taşkapan Saim Yoloğlu

Abstract

Background: Pulmonary arterial hypertension secondary to untreated left-to-right shunt defects leads to increased pulmonary blood
flow, endothelial dysfunction, increased pulmonary vascular resistance, vascular remodelling, neointimal and plexiform lesions. Some
recent studies have shown that inflammation has an important role in
the pathophysiology of pulmonary arterial hypertension.
Aims: The aim of this study is to evaluate serum pentraxin 3 and high
sensitive (hs)-C reactive protein (hs-CRP) levels in children with severe pulmonary arterial hypertension (PAH) secondary to untreated
congenital heart defects and evaluate the role of inflammation in pulmonary hypertension.
Study Design: Cross sectional study.
Methods: After ethics committee approval and receiving consent
from parents, there were 31 children were selected for the study
with severe PAH, mostly with a left-to-right shunt, who had been
assessed by cardiac catheterisation and were taking specific pulmonary vasodilators. The control group consisted of 39 age and gender
matched healthy children. After recording data about all the patients
including age, gender, weight, haemodynamic studies and vasodilator testing, a physical examination was done for all subjects. Blood
was taken from patients and the control group using peripheral veins
to analyse serum Pentraxin 3, N-terminal pro-Brain Natriuretic Peptide (NT-ProBNP) and hs-CRP levels. Serum Pentraxin-3 levels were
measured by enzyme linked immunosorbent assay (ELISA) and
expressed as ng/mL. Serum hs-CRP levels were measured with an
immunonephelometric method and expressed as mg/dL. The serum
concentration of NT-proBNP was determined by a chemiluminescent
immunumetric assay and expressed as pg/mL.
Results: Serum Pentraxin- 3 levels were determined to be 1.28±2.12
(0.12-11.43) in the PAH group (group 1) and 0.40±0.72 (0.07-3.45)
in group 2. There was a statistically significant difference between
the two groups (p<0.01). Serum hs-CRP levels were measured as
2.92±2.12 (0.32-14.7) mg/dL in group 1 and 0.35±0.16 (0.07-3.45)
mg/dL in group 2. The hs-CRP level was increased in the PAH group
to a significant degree (p<0.01).
Conclusion: Our study showed that pentraxin 3 and hs-CRP levels
were increased significantly in the PAH group. We consider that inflammation plays an important role in severe pulmonary hypertension and progressive pulmonary arterial hypertension in children
with PAH.
(Balkan Med J 2014;31:219-23)

Keywords

hs-CRP, inflammation, pentraxin 3, pulmonary arterial hypertension

References

• 1. Ivy D. Advances in pediatric pulmonary arterial hypertension. Curr Opin Cardiol 2012;27:70-81. [CrossRef]
• 2. Moledina S, Hislop AA, Foster H, Schulze-Neick I, Haworth SG. Childhood idiopathic pulmonary arterial hypertension: A national cohort study. Heart 2010;96:1401-6. [CrossRef]
• 3. Fraisse A, Jais X, Schleich JM, di Filippo S, Maragnes P, Beghetti M, et al. Characteristics and prospective 2-year follow-up of children with pulmonary arterial hypertension in France. Arch Cardiovasc Dis 2010;103:66-74. [CrossRef]
• 4. Beghetti M, Tissot C. Pulmonary hypertension in congenital shunts. Rev Esp Cardiol 2010;63:1179-93. [CrossRef]
• 5. Rabinovitch M, Keane JF, Norwood WI, Castaneda AR, Reid L. Vascular structure in lung biopsy tissue correlated with pulmonary hemodynamic findings after repair of congenital heart defects. Circulation 1984;69:655-67. [CrossRef]
• 6. Rabinovitch M, Keane JF, Fellows KE, Castaneda AR, Reid L. Quantitative analysis of the pulmonary wedge angiogram in congenital heart defects: correlation with hemodynamic data and morphometric findings in lung biopsy tissue. Circulation 1981;63:152-64. [CrossRef]
• 7. Heath D, Edwards JE. The pathology of hypertensive pulmonary vascular disease. Circulation 1958;18:533-47. [CrossRef]
• 8. Maciocia PM. Inflammatory signaling in pulmonary hypertension:the controversial role of CRP, and the search for new therapies. Cardiovasc Ther 2010;28:1-4. [CrossRef]
• 9. Doni A, Peri G, Chieppa M, Allavena P, Pasqualini F, Vago L, et al. Production of the soluble pattern recognition receptor ptx3 by myleoid, but not plasmacytoid, dendtritic cells. Eur J Immunol 2003;33:2886-93. [CrossRef]
• 10. Mantovani A, Garlanda C, Doni A, Botazzi B. Pentraxins in innate immunity: From c-reactive protein to the long pentraxin ptx3. J Clin Immunol 2008;28:1-13. [CrossRef]
• 11. Abman SH, Ivy DD. Recent progress in understanding pediatric pulmonary hypertension. Curr Opin Pediatr 2011;23:298-304. [CrossRef]
• 12. Haworth SG, Beghetti M. Assessment of endpoints in the pediatric population: congenital heart disease and idiopathic pulmonary arterial hypertension. Curr Opin Pulm Med 2010;16(Suppl 1):S35-41. [CrossRef]
• 13. van Loon RL, Roofthooft MT, van Osch-Gevers M, Delhaas T, Strengers JL, Blom NA, et al. Clinical characterization of pediatric pulmonary hypertension: complex presentation and diagnosis. J Pediatr 2009;155:176-82. [CrossRef]
• 14. Fasnacht MS, Tolsa JF, Beghetti M. The Swiss registry for pulmonary arterial hypertension: The paediatric experience. Swiss Med Wkly 2007;137:510-3.
• 15. Celermajer DS, Cullen S, Deanfield JE. Impairment of endotheliumdependent pulmonary artery relaxation in children with congenital heart disease and abnormal pulmonary hemodynamics. Circulation 1993;87:440-6. [CrossRef]
• 16. Giaid A, Saleh D. Reduced expression of endothelial nitric oxide synthase in the lungs of patients with pulmonary hypertension. N Engl J Med 1995;333:214-21. [CrossRef]
• 17. Giaid A, Yanagisawa M, Langleben D, Michel RP, Levy R, Shennib H, et al. Expression of endothelin-1 in the lungs of patients with pulmonary hypertension. N Engl J Med 1993;328:1732-9. [CrossRef]
• 18. Price LC, Wort SJ, Perros F, Dormüller P, Huertas A, Montani D, et al. Inflammation in pulmonary arterial hypertension. Chest 2012;41:210-21. [CrossRef]
• 19. Nicolls MR, Taraseviciene-Stewart L, Rai PR, Badesch DB, Voelkel NF. Autoimmunity and pulmonary hypertension: A perspective. Eur Respir J 2005;26:1110-8. [CrossRef]
• 20. Price LC, Wort SJ, Perros F, Dormüller P, Huertas A, Montani D, et al. Inflammation in pulmonary arterial hypertension. Chest 2012;141:210-21. [CrossRef]
• 21. Tuder RM, Voelkel NF. Pulmonary hypertension and inflammation. J Lab Clin Med 1998;132:16-24. [CrossRef]
• 22. Ramakrishnan S, Kukreti BB, Salahudin S, Pendharkar A, Karthikeyan G, Bhargava B, et al. Inflammatory markers are elevated are in Eisenmenger syndrome. Pediatr Cardiol 2013;34:1791-6. [CrossRef]
• 23. Tamura Y, Ono T, Kuwana M, Inoue K, Takei M, Yamamoto T, et al. Human Pentraxin 3 (PTX3) as novel biomarker for the diagnosis of pulmonary hypertension. PLOS One 2012;7:1-5. [CrossRef