P2748Lipoprotein(a) and autotaxin in patients with stenotic atherosclerosis of coronary arteries and aortic valve stenosis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
O Afanasieva ◽  
N Tmoyan ◽  
O Razova ◽  
E Klesareva ◽  
M Afanasieva ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Aortic Valve Stenosis ◽  
Odds Ratio ◽  
Control Group ◽  
Elevated Concentration ◽  
Oxidized Phospholipids ◽  
Lipoprotein A ◽  
Group I ◽  
Group Ii

Abstract Background Lipoprotein(a) [Lp(a)] is an independent risk factor of coronary heart disease (CHD) and calcific aortic valve stenosis (CAVS). It has been recently shown that autotaxin (ATX), which breaks down lysophosphatidylcholine, derived from oxidized phospholipids, to lysophosphatidic acid, was strongly associated with CAVS. Purpose The aim of the study was to investigate the role of Lp(a) and ATX in CHD patients with and without CAVS. Methods The study included 438 patients (average age 66±11 years, men 310), 332 had CHD with ≥50% stenosis in at least one coronary artery according to angiography. CAVS was diagnosed with ultrasound. The control group consisted of 106 patients without CHD and CAVS. The concentrations of Lp(a), ATX, lipids and blood cells were measured for all the patients. Results CHD without CAVS (group I) was diagnosed in 287 patients, 45 patients had CHD and CAVS (group II). Patients in both groups were older than patients in the control group (75±8, 66±10 and 61±13 years respectively). ATX level was lower in group I (median [25; 75%]: 493 [406; 583] ng/ml) than in control group (544 [412; 655] ng/ml, p=0.02) or group II (553 [475; 609] ng/ml, p=0.003). Lp(a) was lower in control group (14.5 [5.5; 36.0] mg/dl) than in group I (25.6 [9.7; 58.5] mg/dl, p=0.0004) and group II (23.8 [9.9; 79.1] mg/dl, p=0.02). Elevated level of ATX was positively associated with CAVS in CHD patients, but negatively with CHD in patients without CAVS. We have shown that age, glucose level and neutrophil-lymphocytes index (NLI) could be predictors of CAVS in patients with CHD according to results of logistic regression analysis. Odds ratio of high (QIV) vs. low (QI) Odds ratio (95% confidence interval) Groups Autotaxin Lipoprotein(a) Neutrophil-lymphocytes index I vs. control 0.5 (0.3–0.9)* 2.7 (1.3–5.2)** 2.4 (1.3–4.6)* II vs. control 8.6 (1.1–70.1)* 3.4 (1.2–9.4)* 6.2 (2.2–16.9)** II vs. I 16.6 (2.1–131.1)** 1.3 (0.5–3.2) 2.5 (1.0–6.37)* *p<0.05, **p<0.005. Conclusion Elevated Lp(a) level is a predictor of CHD regardless of calcific aortic valve stenosis, whereas elevated concentration of autotoxin in CHD patients was associated with calcific aortic valve stenosis.

The Prevalence of Lipoprotein(a) Measurement and Degree of Elevation Among 2710 Patients With Calcific Aortic Valve Stenosis in an Academic Echocardiography Laboratory Setting

Angiology ◽  
2017 ◽  
Vol 68 (9) ◽  
pp. 795-798 ◽  
Author(s):  
Michael J. Wilkinson ◽  
Gary S. Ma ◽  
Calvin Yeang ◽  
Lawrence Ang ◽  
Monet Strachan ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Aortic Valve Stenosis ◽  
Control Group ◽  
Oxidized Phospholipids ◽  
Lipoprotein A ◽  
Causal Risk Factor ◽  
Echocardiography Laboratory ◽  
Ongoing Development ◽  
Independent Assay

Lipoprotein(a; Lp[a]) and its associated oxidized phospholipids are causal, genetic risk factors for calcific aortic valve stenosis (CAVS). We determined the prevalence of Lp(a) measurement among 2710 patients with CAVS and 1369 control patients (∼50% of study group) without CAVS with an echocardiogram between January 2010 and February 2016 in an academic echocardiography laboratory. Lipoprotein(a) measurements were performed at a referral laboratory using an isoform-independent assay. The prevalence of any Lp(a) measurement was 4.6% (124 of the 2710) in patients with CAVS and 3.1% (42 of the 1369) in the control group ( P = .021). In patients with CAVS, mean (standard deviation) Lp(a) levels were 38 (54) mg/dL and median (interquartile range) Lp(a) levels were 14 (6-48) mg/dL. Of the 124 patients with CAVS having Lp(a) measurements, 83 (66.9%) had Lp(a) <30 mg/dL and 41 (33.1%) had Lp(a) ≥30 mg/dL. This study reflects low physician testing of Lp(a) levels in CAVS. Given the role of Lp(a) as a causal risk factor for CAVS, and the ongoing development of therapies to normalize Lp(a) levels, our results suggest that Lp(a) measurements in CAVS should be more widely obtained in clinical practice.

scholarly journals Lipoprotein(a) and oxidized phospholipids in calcific aortic valve stenosis

2016 ◽  
Vol 31 (4) ◽  
pp. 440-450 ◽  
Author(s):  
Calvin Yeang ◽  
Michael J. Wilkinson ◽  
Sotirios Tsimikas
Keyword(s):  
Aortic Valve ◽  
Aortic Valve Stenosis ◽  
Oxidized Phospholipids ◽  
Lipoprotein A

Role of lipoprotein (a) and LPA KIV2 repeat polymorphism in bicuspid aortic valve stenosis and calcification: a proof of concept study

2018 ◽  
Vol 14 (1) ◽  
pp. 45-50 ◽  
Author(s):  
Elena Sticchi ◽  
Betti Giusti ◽  
Antonella Cordisco ◽  
Anna Maria Gori ◽  
Alice Sereni ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Bicuspid Aortic Valve ◽  
Aortic Valve Stenosis ◽  
Proof Of Concept ◽  
Repeat Polymorphism ◽  
Lipoprotein A ◽  
Concept Study

Kringle IV Encoding Domains in the Apo(a) Gene and Serum Lipoprotein(a) Level Do Not Contribute to Avascular Necrosis of Bone (AVN) in Acute Lymphoblastic Leukemia.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4440-4440
Author(s):  
Désirée D.L. Bezemer ◽  
Robert D. van Beek ◽  
Jules P.P. Meijerink ◽  
Sabine M.P.F. de Muinck Keizer-Schrama ◽  
Rob Pieters ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Mononuclear Cells ◽  
Lymphoblastic Leukemia ◽  
Serum Lipoprotein ◽  
Control Group ◽  
Lipoprotein A ◽  
Group Iii ◽  
Group I ◽  
Group Ii ◽  
The Difference

Abstract Introdution Symptomatic AVN occurs as a serious complication of treatment in 4%–12.5% of pediatric cases with ALL. The final common pathway for the development of AVN involves a compromise in the blood flow, leading to infarction. The pathogenesis is multifactorial, including elevated intracortical pressure, vascular occlusion, altered lipid metabolism/fat emboli, hemostatic abnormalities and inhibition of angiogenesis. The difference in incidence of AVN in patients treated according to one and the same protocol suggests a genetic variation as a contribution to the biology of AVN. In one report, familial occurence of bone marrow edema syndrome (early phase of AVN) was associated with elevated levels of lipoprotein(a)[Lp(a)]. Lp(a) is a complex of low-density lipoprotein (LDL) and a high molecular weight glycoprotein called apolipoprotein(a)[apo(a)]. The Lp(a) level is inversely correlated with the kringle IV repeat number in apo(a), that is present as a naturally variation in the population. Methods We investigated the Lp(a) levels and the genetic variation in the Apo(a) gene in pediatric patients with and without AVN. DNA from mononuclear cells was isolated from 10 ALL patients with AVN (group I) and 12 patients without AVN (group II), all matched for age, gender and protocol. AVN is defined as pain of the extremities, not related to treatment with vincristine, confirmed by finding typical abnormalities on MRI. The control group consisted of 13 healthy Caucasian subjects (group III). To detect the number of kringle IV repeats pulsed field gel elctrophoresis (PFGE) and Southern blot of genomic DNA was performed. Serum Lp(a) levels were determined by immuno-nefelometric detection method. Results The median number of kringle IV repeats (mean of both alleles) did not significantly differ between the three groups: 25 (range 16–37, group I), 24 (range 13–32, group II), 21 (range 10–36, group III). The median Lp(a) levels in ALL patients with AVN versus ALL patients without AVN were respectively 0.085 g/L (range &lt;0.02–0.848) and 0.067 g/L (range &lt;0.02–0.362). Again the difference was not significant. Conclusion Our results suggest that Lp(a) and genetic polymorphism of apo(a) do not play a mayor role in the pathogenesis of AVN in pediatric ALL.

scholarly journals Efficacy of Physiotherapy for Urinary Incontinence following Prostate Cancer Surgery

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Elżbieta Rajkowska-Labon ◽  
Stanisław Bakuła ◽  
Marek Kucharzewski ◽  
Zbigniew Śliwiński
Keyword(s):  
Prostate Cancer ◽  
Urinary Incontinence ◽  
Odds Ratio ◽  
Prostatic Carcinoma ◽  
Rehabilitation Program ◽  
Control Group ◽  
Group I ◽  
Significant Difference ◽  
Group Ii ◽  
The Difference

The study enrolled 81 with urinary incontinence following radical prostate-only prostatectomy for prostatic carcinoma. The patients were divided into two groups. The patients in Group I were additionally subdivided into two subgroups with respect to the physiotherapeutic method used. The patients of subgroup IA received a rehabilitation program consisting of three parts. The patients of subgroup IB rehabilitation program consist of two parts. Group II, a control group, had reported for therapy for persistent urinary incontinence following radical prostatectomy but had not entered therapy for personal reasons. For estimating the level of incontinence, a 1-hour and 24-hour urinary pad tests, the miction diary, and incontinence questionnaire were used, and for recording the measurements of pelvic floor muscles tension, the sEMG (surface electromyography) was applied. The therapy duration depended on the level of incontinence and it continued for not longer than 12 months. Superior continence outcomes were obtained in Group I versus Group II and the difference was statistically significant. The odds ratio for regaining continence was greater in the rehabilitated Group I and smaller in the group II without the rehabilitation. A comparison of continence outcomes revealed a statistically significant difference between Subgroups IA versus IB. The physiotherapeutic procedures applied on patients with urine incontinence after prostatectomy, for most of them, proved to be an effective way of acting, which is supported by the obtained results.

scholarly journals The association of lipoprotein(a) and apolipoprotein(a) phenotypes with peripheral artery disease

2018 ◽  
Vol 90 (9) ◽  
pp. 31-36 ◽  
Author(s):  
N A Tmoyan ◽  
M V Ezhov ◽  
O I Afanasieva ◽  
E A Klesareva ◽  
O A Razova ◽  
...  
Keyword(s):  
Peripheral Artery Disease ◽  
Group Iv ◽  
Control Group ◽  
Peripheral Artery ◽  
Lipoprotein A ◽  
Group Iii ◽  
Apolipoprotein A ◽  
Group I ◽  
Artery Disease

Aim. Lipoprotein(a) [Lp(a)] is an independent risk factor of coronary heart disease (CHD) and myocardial infarction. Data about the role of Lp(a) in the development of peripheral artery disease (PAD) is controversial and uncertain. The aim of the study was to evaluate the association between Lp(a), apolipoprotein(a) [apo(a)] phenotypes and PAD. Materials and methods. The study included 998 patients (707 male and 291 female, average age 60±12). The patients were divided into 4 groups depending on the presence or absence PAD and CHD: group I (n=188, PAD+CHD+), group II (n=78, PAD+CHD-), group III (n=407, PAD-CHD+), group IV (n=325, PAD-CHD-). Results. The level of Lp(a) was significantly higher in groups I, II, III in comparison with patients of control group (group IV): 34 [15; 80], 30 [10; 49], 22 [8; 60] mg/dl vs. 15 [6; 35] mg/dl respectively, p

scholarly journals Oxidized Phospholipids, Lipoprotein(a), and Progression of Calcific Aortic Valve Stenosis

2015 ◽  
Vol 66 (11) ◽  
pp. 1236-1246 ◽  
Author(s):  
Romain Capoulade ◽  
Kwan L. Chan ◽  
Calvin Yeang ◽  
Patrick Mathieu ◽  
Yohan Bossé ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Aortic Valve Stenosis ◽  
Oxidized Phospholipids ◽  
Lipoprotein A

scholarly journals ISONIAZID INDUCED LIVER DAMAGE

2018 ◽  
Vol 25 (07) ◽  
pp. 1124-1128
Author(s):  
Naveed Ahsan ◽  
Sarwat Jahan ◽  
Sana Imran ◽  
Naveed Ahsan
Keyword(s):  
Histopathological Examination ◽  
Portal Tract ◽  
Group Iv ◽  
Control Group ◽  
Hepatic Lobule ◽  
Group Iii ◽  
Liver Histopathology ◽  
Group I ◽  
Group Ii

Objectives: To observe healthy effects of silymarin on liver histopathology againstliver damage, caused by isoniazid in rabbits. Study Design: Interventional study. Setting:Animal House of Jinnah Postgraduate Medical Centre, Karachi. Period: April to September2013. Methods: Total 28 rabbits of weight 1-1.5kg of either sex were used in this study. Whichwere divided randomly into four equal groups: Group I was control group. In group II silymarin(50mg/kg/day orally) was administered, in group III isoniazid (50mg/kg/dayorally) was given;and in group IV, effects of combination therapy of isoniazid and silymarin were observed. Beforestarting the drug therapy, at day 0 and one day after the end of study period i.e., at day 19, bodyweight of each animal was recorded. Rabbits were sacrificed on 19th day and the required liversample was taken for histopathological examination. The data feeding and analysis at the endof study was done on computer package SPSS (Statistical packages of social science) version16. Results: No mortality was recorded in any group. In group II (silymarin treated) animals inthis group exhibited no any histological changes in the hepatic lobule except few inflammatorycells 28.5% were seen in the portal tract. The liver microscopic examination in group III(Isoniazid treated), animals showed the disturbed architecture of the lobule. There were no fattychanges, whereas ballooning degeneration was 42.9%, hepatocytes necrosis was 71% andportal inflammation was 71.4% which was very severe. Animals in group IV, given combinationof silymarin and isoniazid showed the intact architecture of the hepatic lobule, in which 14.29%ballooning degeneration, whereas necrosis of hepatocytes and portal inflammation was mildin nature which may be due to hepatoprotective role of silymarin. Conclusion: Silymarin hashepatoprotective effects when given in combination with isoniazid.

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