AI Article Synopsis
- The study aimed to assess the effectiveness of systemic beta-blockers in lowering eye pressure in primary open-angle glaucoma (POAG) patients who also have arterial hypertension.
- 29 patients participated, receiving a combination of treatments including beta-blockers, with significant follow-ups to measure intraocular pressure (IOP) changes over one year.
- Results showed a notable decrease in IOP, with the worst affected eyes showing reductions of 14% at 4 weeks and up to 26% at one year, suggesting beta-blockers can be a viable option for managing both conditions and minimizing medication side effects.
Article Abstract
Aim: to evaluate the ocular hypotensive efficacy of systemic beta-blockers in primary glaucoma patients suffering from arterial hypertension (AH).
Material And Methods: The study included 29 patients with POAG (58 eyes) aged from 47 to 83 years. Patients with stage I-III POAG received instillations of prostaglandin analogs and carbonic anhydrase inhibitors. All POAG patients also suffered from arterial hypertension and were prescribed selective beta-blockers (metoprolol, bisoprolol, or nebivalol) as monotherapy or as part of combination therapy (if the target arterial pressure had not been achieved under the initial treatment). After the start of oral beta-blockers therapy, the patients were re-examined at 2 and 4 weeks, 3 months, 6 months, and 1 year.
Results: A clinically significant reduction of IOP in the most seriously affected eye - by 3.3 mmHg (p<0.05), or 14% - occurred four weeks after the start of selective beta-blockers. Over three months of combination therapy, IOP in the 'worst' eye decreased by 4.4 mmHg (18.5%). At 1 year, IOP in the 'worst' eye was 6.2 mmHg (26%) lower than at baseline (p<0.05).
Conclusion: Aged and senile patients with primary glaucoma usually suffer from polypathy (on average, they have 6.3±0.6 concurrent somatic diseases). To reduce the risk of polypharmacy and the frequency of side effects in the treatment of POAG and AH patients, it is advised that the treatment includes oral selective beta-blockers able to provide target levels of arterial pressure and IOP. In this study, oral beta-blockers in POAG and AH patients enabled IOP reduction as great as 18.5%-26% of baseline values over a 1-year follow-up period.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.17116/oftalma2017133246-50 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Joint Group and Multi Institutional Position Opinion: Cirrhotic Cardiomyopathy-From Fundamentals to Applied Tactics.
Medicina (Kaunas)
December 2024
Clinic for Gastroenterology and Hepatology, University Clinical Centre of Serbia, 11 000 Belgrade, Serbia.
Cirrhotic cardiomyopathy (CCM) is a diagnostic entity defined as cardiac dysfunction (diastolic and/or systolic) in patients with liver cirrhosis, in the absence of overt cardiac disorder. Pathogenically, CCM stems from a combination of systemic and local hepatic factors that, through hemodynamic and neurohormonal changes, affect the balance of cardiac function and lead to its remodeling. Vascular changes in cirrhosis, mostly driven by portal hypertension, splanchnic vasodilatation, and increased cardiac output alongside maladaptively upregulated feedback systems, lead to fluid accumulation, venostasis, and cardiac dysfunction.
View Article and Find Full Text PDFProgressive systemic inflammation precedes decompensation in compensated cirrhosis.
JHEP Rep
February 2025
Department of Gastroenterology and Hepatology, Hospital Universitario Ramón y Cajal, Instituto Ramon y Cajal de Investigación Sanitaria (IRYCIS), Universidad de Alcalá, Madrid, Spain.
Background & Aims: Systemic inflammation is a driver of decompensation in cirrhosis with unclear relevance in the compensated stage. We evaluated inflammation and bacterial translocation markers in compensated cirrhosis and their dynamics in relation to the first decompensation.
Methods: This study is nested within the PREDESCI trial, which investigated non-selective beta-blockers for preventing decompensation in compensated cirrhosis and clinically significant portal hypertension (CSPH: hepatic venous pressure gradient ≥10 mmHg).
Nonselective beta blockade enhances gut microbiome diversity in a rodent model of trauma, hemorrhage, and chronic stress.
J Trauma Acute Care Surg
February 2025
From the Department of Surgery and Sepsis and Critical Illness Research Center (J.A.M., L.S.K., E.E.P., C.G.A., K.B.K., L.E.B., P.A.E., A.M.M.), University of Florida College of Medicine, Gainesville; and The Gut Biome Lab, Department of Health, Nutrition, and Food Sciences (G.P., R.N.), Florida State University College of Education, Health, and Human Sciences, Tallahassee, Florida.
Background: Traumatic injury leads to gut dysbiosis with changes in microbiome diversity and conversion toward a "pathobiome" signature characterized by a selective overabundance of pathogenic bacteria. The use of non-selective beta antagonism in trauma patients has been established as a useful adjunct to reduce systemic inflammation. We sought to investigate whether beta-adrenergic blockade following trauma would prevent the conversion of microbiome to a "pathobiome" phenotype.
View Article and Find Full Text PDFEmergency medicine updates: Sympathetic crashing acute pulmonary edema.
Am J Emerg Med
January 2025
Department of Emergency Medicine, Rush University Medical Center, Chicago, IL, USA.
Introduction: Patients with heart failure exacerbation can present in a variety of ways, including sympathetic crashing acute pulmonary edema (SCAPE). Emergency physicians play a key role in the diagnosis and management of this condition.
Objective: This narrative review evaluates key evidence-based updates concerning the diagnosis and management of SCAPE for the emergency clinician.
Paroxysmal sympathetic hyperactivity: A common consequence of traumatic brain injury.
Auton Neurosci
February 2025
Department of Medicine, Jinnah Sindh Medical University, Rafiqi H J Shaheed Road, Karachi, Pakistan. Electronic address:
Paroxysmal Sympathetic Hyperactivity (PSH) is a challenging and often underrecognized syndrome, commonly arising after a traumatic brain injury (TBI). Characterized by episodic bursts of heightened sympathetic activity, PSH presents with a distinct constellation of symptoms including hypertension, tachycardia, hyperthermia, and diaphoresis. While the exact pathophysiology remains elusive, current evidence suggests that the syndrome results from an imbalance between excitatory and inhibitory neuronal pathways within the central nervous system, leading to dysregulated autonomic responses.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!