18 results match your criteria: "Healing Touch City Clinic[Affiliation]"

Cardiovascular (CV) disease is the leading cause of premature death in ankylosing spondylitis (AS). Atherosclerosis and AS share similar pathogenic mechanisms. The proven benefits of angiotensin-receptor blockers (ARBs) in atherosclerotic cardiovascular disease and their role in immune mediation provide strong rationale to investigate its impact with olmesartan on inflammation and endothelial dysfunction in AS.

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Background: Diabetic neuropathy increases risk of cardiovascular disease, peripheral artery disease, foot amputation and overall mortality. Not only hyperglycaemia induced nerve damage is harder to repair using currently approved medications, but also, the use of these agents is often limited by the extent of pain relief provided and side effects.

Methodology: In this prospective, open-label, pilot study, 20 type-2 diabetes mellitus patients (male/female=13/7, mean age- 56.

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Nitric Oxide: Link between Inflammation and Endothelial Dysfunction in Rheumatoid Arthritis.

Int J Angiol

September 2017

Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, India.

Nitric oxide (NO) plays an important role in inflammatory joint disease and endothelial function. Endothelial dysfunction has been attributed to a reduction in NO bioactivity in rheumatoid arthritis (RA). However, the relationship of NO with inflammation and endothelial dysfunction in RA has not yet been investigated.

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The main objective of the study was to perform the pharmacoeconomic analysis of synthetic disease-modifying anti-rheumatic drugs in rheumatoid arthritis patients. A prospective, observational study was conducted in 98 rheumatoid arthritis (RA) patients meeting 2010 Rheumatoid Arthritis Classification Criteria. Treatment-naive RA patients were initiated on synthetic disease-modifying anti-rheumatic drugs (DMARD/s) and followed up for 3 months.

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Objective: Cardiovascular (CV) disease is leading cause of mortality in rheumatoid arthritis (RA). Dysfunction of the vascular endothelium is a hallmark of most conditions that are associated with atherosclerosis and is therefore an early feature in atherogenesis. Biomarkers for rapid evolution of CV complications would be highly desirable for risk stratification.

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Endothelial progenitor cells (EPCs) have reparative potential in overcoming the endothelial dysfunction and reducing cardiovascular risk. EPC depletion has been demonstrated in the setting of established atherosclerotic diseases. We evaluated whether reduced EPCs population are associated with endothelial dysfunction, subclinical atherosclerosis, and inflammatory markers in ankylosing spondylitis (AS) patients without any known traditional cardiovascular risk factor.

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Cardiovascular disease is one of the leading causes of death in psoriatic arthritis (PsA). Pathogenesis of accelerated atherosclerosis in PsA remains to be elucidated. Endothelial dysfunction (ED) often precedes manifesting atherosclerosis.

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Peripheral artery disease (PAD) is the major risk factor for cardiovascular disease and lower extremity amputation in patients with diabetes. Autonomic neuropathy is a risk factor for cardiovascular-related morbidity and mortality. Sudomotor dysfunction is well established in type 2 diabetes mellitus (T2DM) and reflects small fibre neuropathy, cardiovascular autonomic neuropathy and peripheral sympathetic autonomic neuropathy.

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Objective: Accelerated atherosclerosis associated with an enhanced inflammatory state, which characterizes ankylosing spondylitis (AS), is the leading cause of increased cardiovascular risk. The objective of this study was to assess carotid intima-media thickness (CIMT) as a surrogate for subclinical atherosclerosis in AS patients and its possible correlation with disease-related clinical parameters.

Methods: We performed a prospective study of 30 consecutive patients meeting modified New York criteria for AS compared to 25 controls matched for age and sex.

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Predictors of autonomic neuropathy in rheumatoid arthritis.

Auton Neurosci

December 2016

Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, India.

Objective: Autonomic dysfunction occurs in rheumatoid arthritis (RA). However, the association between the autonomic dysfunction and inflammation has not been investigated in RA. We investigated the relationship between inflammation and ANS function in RA.

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Background: Cardiovascular autonomic neuropathy (CAN) is a significant risk predictor for sudden cardiac death in autoimmune rheumatic diseases. As yet, there is no therapeutic treatment of CAN in psoriatic arthritis (PsA). Even now, the impact of the most commonly employed disease-modifying antirheumatic drug (DMARD) therapy on CAN in PsA is not known.

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Article Synopsis
  • Autonomic neuropathy is a significant risk factor for sudden cardiac death in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS), but the effects of disease-modifying anti-rheumatic drugs (DMARDs) on this condition are not well understood.
  • A study assessing autonomic function in 60 RA and AS patients found that cardiovascular reflexes were notably impaired compared to healthy individuals, especially in those not on biologic treatments.
  • Treatment with synthetic DMARDs improved certain dysfunctions, but biologic DMARDs showed greater efficacy in enhancing autonomic function across all assessed areas in DMARD-naive RA and AS patients.
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Diabetic peripheral neuropathy and diabetic autonomic neuropathy are serious and common complications of diabetes associated with increased risk of mortality and cardiovascular disease. We sought to evaluate the safety and efficacy of minocycline in type 2 diabetic patients with diabetic peripheral and autonomic neuropathy. In a randomized placebo controlled study, 50 outpatients were randomly assigned to receive 100 mg minocycline or placebo.

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Autonomic dysfunction in psoriatic arthritis.

Clin Rheumatol

July 2013

Healing Touch City Clinic, no. 547, Sector 16-D, Chandigarh 160015, India.

Autonomic nervous system (ANS) involvement has been studied in systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, Sjogren's syndrome, and ankylosing spondylitis but still has not been studied in psoriatic arthritis (PsA). The aim of this study was to investigate the prevalence and the nature of autonomic neuropathy in patients with PsA. Sixteen patients of PsA and 15 age and sex matched control subjects were studied prospectively using a battery of noninvasive tests.

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Chronic inflammation in ankylosing spondylitis (AS) is associated with vascular endothelial dysfunction which leads to accelerated atherosclerosis. Accelerated atherosclerosis contributes to premature cardiovascular disease and increased cardiovascular mortality in AS. Spironolactone inhibits the production of proinflammatory cytokines and improves endothelial dysfunction in rheumatoid arthritis.

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Aim: Chronic inflammation in rheumatoid arthritis is associated with vascular endothelial dysfunction. The objective was to study the efficacy and safety of advanced glycation end products (AGEs) inhibitor (benfotiamine 50 mg + pyridoxamine 50 mg + methylcobalamin 500 μg, Vonder(®) (ACME Lifescience, Baddi, Himachal Pradesh, India)) on endothelial function in rheumatoid arthritis (RA).

Methods: Twenty-four patients with established active RA with high disease activity (Disease Activity Score of 28 joints [DAS28 score] > 5.

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Chronic inflammation in ankylosing spondylitis (AS) is associated with vascular endothelial dysfunction. Infliximab improves inflammatory disease activity in AS patients, but its effect on endothelial dysfunction has still not been tested in these patients. Twelve anti-TNF naive AS patients (mean age, 32.

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Objective: Chronic inflammation in rheumatoid arthritis (RA) is associated with vascular endothelial dysfunction. The aim of this study was to determine the effect of spironolactone on endothelial function in anti-tumour necrosis factor (TNF)-naive RA patients.

Methods: Twenty-four anti-TNF-naive RA patients (mean age 49 +/- 1.

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