Relationship between matrix metalloproteinase-3 serum level and pulmonary artery systolic pressure in patients with rheumatoid arthritis

2017 ◽  
Vol 33 (2) ◽  
pp. 191-197 ◽  
Author(s):  
Tetsuro Sugiura ◽  
Mikio Kamioka ◽  
Shigeo Yamanaka ◽  
Taisuke Hisahara ◽  
Yoko Hirakawa ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Serum Level ◽  
Pulmonary Artery ◽  
Matrix Metalloproteinase ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Matrix Metalloproteinase 3

AB1090 BIOMARKERS TO DIFFERENTIATE EARLY INDISTINGUISHABLE CASES OF OSTEOARTHRITIS AND RHEUMATOID ARTHRITIS.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1834.1-1834
Author(s):  
A. Elbeialy ◽  
H. El Abd ◽  
A. Shahin ◽  
R. Ibrahim
Keyword(s):  
Rheumatoid Arthritis ◽  
Serum Level ◽  
Matrix Metalloproteinase ◽  
Serum Levels ◽  
Significant Elevation ◽  
Control Groups ◽  
Matrix Metalloproteinase 3 ◽  
Early Stages ◽  
Early Ra ◽  
And Control

Background:Osteoarthritis (OA) and rheumatoid arthritis (RA) are the most frequent inflammatory diseases of the musculoskeletal system, which could not be differentiated in their early stages, and characterized by degradation of articular cartilage and impairment of joint function. Sometimes, criteria and radiography are not insufficient to distinguish early-stages of RA and OA and predict disease course, and therefor biomarkers that help clinicians to early diagnose disease are essential.Objectives:The aim of this study is to estimate serum level of Matrix metalloproteinase 3 (MMP3) and hrdroxyproline (HP) in early RA and OA patients to see if they can be used to differentiate both diseases at their early stagesMethods:The aim of this study is to estimate serum level of Matrix metalloproteinase 3 (MMP3) and hrdroxyproline (HP) in early RA and OA patients to see if they can be used to differentiate both diseases at their early stagesResults:We found a highly significant elevation of serum MMP3 in OA patients group compared to RA patients and control groups. We also found a highly significant elevation of MMP3 in RA patients than control group,(P < 0.001). Meanwhile, we found a highly significant elevation of HP in OA patients than in RA patients and control groups, (P < 0.001), whereas there was no significant difference between HP in RA patients and control groups (P > 0.05).Table 1.Demonstration of serum levels of MMP3 and HP in all groups.“Enzyme”OA(n=40)RA(n=40)Control(n=40)p-valueMMP3 pg/mL559.92±1112.84153.25±162.0559.79±63.54<0.001HPµg/mL12.87±18.754.81±6.894.52±1.55<0.001HPµg/mL4.81±6.894.52±1.55> 0.05Conclusion:Our results suggest that serum levels of Hydroxyproline (HP) rather than MMP3 could be used as a potential biomarker for early differentiation between osteoarthritis (OA) and rheumatoid arthritis (RA) when diagnostic criteria failed to be fulfilled.References:[1]Benedetti S, Canino C, Tonti G, Medda V, Calcaterra P, Nappi G, Salaffi F, Canestrari F. (2010): Biomarkers of oxidation, inflammation and cartilage degradation in osteoarthritis patients undergoing sulfur-based spatherapies. ClinBiochem.; 43: 973-8.[2]Fenton, S. A. M., Veldhuijzen van Zanten, J. J. C. S., Duda, J. L., Metsios, G. S., and Kitas, G. D. (2018). Sedentary behaviour in rheumatoid arthritis: definition, measurement and implications for health. Rheumatology. (Oxford) 57(2), 213-226.[3]Murphy, G., and Nagase, H. (2008). Progress in matrix metalloproteinase research. Mol. Aspects Med. 29(5), 290-308.[4]Bonnans, C., Chou, J., and Werb, Z. (2014). Remodelling the extracellular matrix in development and disease. Nat. Rev. Mol. Cell Biol. 15(12), 786-801.[5]Hofman, K., Hall, B., Cleaver, H., & Marshall, S. (2011): High-throughput quantification of hydroxyproline for determination of collagen. Analytical biochemistry, 417(2), 289-291.[6]Barranco, C. (2015): Osteoarthritis: activate autophagy to prevent cartilage degeneration? Nat. Rev. Rheumatol. 11, 127.[7]M.S. Radha and Dr. M.R. Gangadhar (2015), Serum enzyme of matrix metalloproteinase-3 in patients with knee osteoarthritis, International Journal of Recent Scientific Research Vol. 6, Issue, 6, pp.4457-4460, June, 2015.[8]Bassiouni, H. M., El-Deeb, M., Kenawy, N., Abdul-Azim, E., & Khairy, M. (2011). Phonoarthrography, musculoskeletal ultrasonography, and biochemical biomarkers for the evaluation of knee cartilage in osteoarthritis. Modern rheumatology, 21(5), 500-508.[9]Ahmed, U., Anwar, A., Savage, R. S., Costa, M. L., Mackay, N., Filer, A., Raza, K., Watts, R. A., Winyard, P. G., Tarr, J., Haigh, R. C., Thornalley, P. J., and Rabbani, N. (2015). Biomarkers of early stage osteoarthritis, rheumatoid arthritis and musculoskeletal health. Sci. Rep. 5, 9259.Acknowledgments:We are indebted to Dr El Shaimaa Abdel Hakim, and Dr Asmaa Fouaad for their great help in this studyDisclosure of Interests:None declared

Effect of acute lower respiratory tract infection on pulmonary artery pressure in children with post-tricuspid left-to-right shunt

2021 ◽  
pp. 1-5
Author(s):  
Sakshi Sachdeva ◽  
Shyam S. Kothari ◽  
Saurabh K. Gupta ◽  
Sivasubramanian Ramakrishnan ◽  
Anita Saxena
Keyword(s):  
Tract Infection ◽  
Pulmonary Artery ◽  
Respiratory Tract ◽  
Respiratory Tract Infection ◽  
Lower Respiratory Tract Infection ◽  
Pulmonary Artery Pressure ◽  
Lower Respiratory Tract ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Artery Pressure

Abstract We sought to examine the influence of clinically severe lower respiratory tract infection on pulmonary artery pressure in children having CHD with post-tricuspid left-to-right shunt, as it may have physiological and clinical implications. In a prospective single-centre observational study, 45 children with post-tricuspid left-to-right shunt and clinically severe lower respiratory tract infection were evaluated during the illness and 2 weeks after its resolution. Pulmonary artery systolic pressure was estimated non-invasively using shunt gradient by echocardiography and systolic blood pressure measured non-invasively. Median pulmonary artery systolic pressure during lower respiratory tract infection was only mildly (although statistically significantly) elevated during lower respiratory tract infection [60 (42–74) versus 53 (40–73) mmHg, (p < 0.0001)]. However, clinically significant change in pulmonary artery systolic pressure defined as the increase of >10 mmHg was present in only 9 (20%) patients. In the absence of hypoxia or acidosis, only a small minority (9%, n = 4) showed significant pulmonary artery systolic pressure rise >10 mmHg. In the absence of hypoxia or acidosis, severe lower respiratory tract infection in patients with acyanotic CHD results in only mild elevation of pulmonary artery systolic pressure in most of the patients.

scholarly journals Serum-Free Thyroxine Levels Were Associated with Pulmonary Hypertension and Pulmonary Artery Systolic Pressure in Euthyroid Patients with Coronary Artery Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-8
Author(s):  
Bingjie Wu ◽  
Jingjing Jiang ◽  
Minghui Gui ◽  
Lin Liu ◽  
Qiqige Aleteng ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Pulmonary Hypertension ◽  
Regression Analysis ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Systolic Pressure ◽  
Free Thyroxine ◽  
Pulmonary Artery Systolic Pressure ◽  
Serum Free ◽  
Artery Disease

The aim of this study was to evaluate the association between thyroid hormone levels, pulmonary hypertension (PH), and pulmonary artery systolic pressure (PASP) in euthyroid patients with coronary artery disease (CAD). A cross-sectional study was conducted in individuals who underwent coronary angiography and were diagnosed as CAD from March 2013 to November 2013. 811 subjects (185 women and 626 men) were included in this study. PASP was measured by transthoracic Doppler echocardiography. 86 patients were diagnosed as PH and had significantly higher free thyroxine (FT4) levels than those without PH. Multiple logistic regression analysis demonstrated an independent association of FT4 levels with PH after adjustment of gender, age, body mass index, systolic blood pressure, left ventricular ejection fraction, hypertension, and medication use of calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists, and nitrates. Serum-free triiodothyronine (FT3) and thyroid-stimulating hormone (TSH) were not associated with PH. Furthermore, multivariate linear regression analysis showed that FT4 levels emerged as an independent predictor for PASP, while FT3 and TSH levels were not associated with PASP. Our study demonstrated that, in euthyroid patients with CAD, FT4 was an independent risk factor for PH, and FT4 levels were independently associated with PASP.

Abstract 15388: Persistent Pulmonary Hypertension After Transcatheter Aortic Valve Implantation: Impact on Mortality

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Maria Drakopoulou ◽  
Konstantinos Stathogiannis ◽  
Konstantinos Toutouzas ◽  
George Latsios ◽  
Andreas Synetos ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Aortic Stenosis ◽  
Pulmonary Artery ◽  
Severe Aortic Stenosis ◽  
Systolic Pressure ◽  
Right Atrial ◽  
Pulmonary Artery Systolic Pressure ◽  
End Point ◽  
The Right ◽  
The Impact

Objective: Severe aortic stenosis leads to increased pulmonary arterial systolic pressure. A controversy still remains regarding the impact of persistent pulmonary hypertension (PHT) on prognosis of patients undergoing transcatheter aortic valve implantation (TAVI). We sought to investigate the impact of persistent PHT on 2-year all-cause mortality of patients with severe aortic stenosis following TAVI. Methods: Patients with severe and symptomatic aortic stenosis (effective orifice area [EOA]≤1 cm 2 ) who were scheduled for TAVI with a self-expanding valve at our institution were prospectively enrolled. Prospectively collected echocardiographic data before and after TAVI were retrospectively analyzed in all patients. Pulmonary artery systolic pressure was estimated as the sum of the right ventricular to the right atrial gradient during systole and the right atrial pressure. PHT following TAVI was classified as absent if <35 mmHg and persistent if ≥35 mmHg. Primary clinical end-point was 2-year all-cause mortality defined according to the criteria proposed by the Valve Academic Research Consortium-2. Results: Hundred and forty patients (mean age: 82±9 years) were included in the study. The primary clinical end point occurred in 17 patients (12%) during a median follow-up period of 2 years. Mean pulmonary artery systolic pressure was reduced in all patients following TAVI (45±9 versus 41±6 mmHg, p<0.01). Mortality rate was higher in patients with persistent PHT compared to patients with normal pulmonary artery systolic pressure following TAVI (26% versus 14 %, p<0.01). Patients that reached the primary clinical end point had a higher post procedural mean systolic pulmonary pressure (43±9 versus 39±6 mmHg, p=0.02). In multivariate regression analysis, persistence of PHT (OR: 2.51, 95% CI: 1.109-7.224, p=0.01) was an independent predictor of long-term mortality. Conclusions: The persistence of pulmonary hypertension after TAVI is associated with long term mortality. Identifying the population that will clearly benefit from TAVI is still need to be validated by larger trials.

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