Related Experiment Video
Updated: May 8, 2026
09:37
A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging
Published on: July 14, 2016
Activated protein C resistance in Behcet's disease
Hoda Abdel Badaee1, Amr Edrees, Sherif Amin
1Department of Internal Medicine, University of Missouri-Kansas City, Kansas, USA. edreesa@umkc.edu.
Thrombosis Journal
|September 6, 2013
Summary
This study found no significant difference in activated protein C resistance (APC-R) in Behcet's disease patients with or without vascular issues. However, high homocysteine levels showed a trend towards increased ocular lesions.
Area of Science:
- Vascular Medicine
- Rheumatology
- Hematology
Background:
- Behcet's disease is a chronic, multi-system inflammatory disorder with unknown causes.
- Thromboembolism, particularly venous, is a common complication, often linked to endothelial dysfunction.
- Existing explanations for hypercoagulability in Behcet's disease are incomplete.
Purpose of the Study:
- To determine the prevalence of activated protein C resistance (APC-R) in Egyptian patients with Behcet's disease.
- To investigate hyperhomocysteinemia in patients with vascular complications and its relation to thromboembolic events.
Main Methods:
- Assessed APC resistance ratio in Behcet's disease patients with and without vascular involvement.
- Measured homocysteine levels in patients with vascular complications.
- Analyzed the association between APC resistance, homocysteine levels, and thromboembolic/ocular complications.
Main Results:
- The mean APC resistance ratio was similar between patients with (2.6±0.8) and without (2.8±0.6) vascular involvement (P=0.5).
- A trend was observed for a higher incidence of ocular lesions in patients with elevated homocysteine levels (P=0.08).
Conclusions:
- Activated protein C resistance does not appear to be a significant risk factor for vascular complications in this cohort of Egyptian Behcet's disease patients.
- Hyperhomocysteinemia may be associated with specific complications like ocular lesions in Behcet's disease, warranting further investigation.
Related Concept Videos
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
01:25Antihypertensive Drugs: Direct Renin Inhibitors
The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
01:26Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers
Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
01:01Hypersensitivity Reactions: Cytolytic Reactions
Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...