scholarly journals Adalékok az időskori maculadegeneráció – etiopatogeneziséből fakadó – nem gyógyszeres intervenciójához

2015 ◽  
Vol 156 (28) ◽  
pp. 1128-1132 ◽  
Author(s):  
Tamás Fischer

It has a great therapeutic significance that the disorder of the vascular endothelium, which supplies the affected ocular structures, plays a major role in the development of age-related macular degeneration. Chronic inflammation is closely linked to diseases associated with endothelial dysfuncition and age-related macular degeneration is accompanied by a general inflammatory response. The vascular wall including those in chorioids may be activated by several repeated and/or prolonged mechanical, physical, chemical, microbiological, immunologic and genetic factors causing a protracted host defence response with a consequent vascular damage, which leads to age-related macular degeneration. Based on this concept, age-related macular degeneration is a local manifestation of the systemic vascular disease. This recognition should have therapeutic implications because restoration of endothelial dysfunction can stabilize the condition of chronic vascular disease including age-related macular degeneration, as well. Restoration of endothelial dysfunction by non-pharmacological or pharmacological interventions may prevent the development or improve endothelial dysfunction resulting in prevention or improvement of age-related macular degeneration. Non-pharmacological interventions which may have beneficial effect in endothelial dysfunction include (1) smoking cessation; (2) reduction of increased body weight; (3) adequate physical activity; (4) appropriate diet (a) proper dose of flavonoids, polyphenols and kurcumin; (b) omega-3 long-chain polyunsaturated fatty acids: docosahexaenoic acid and eicosapentaenoic acid; (c) carotenoids, lutein and zeaxanthins), (d) management of dietary glycemic index, (e) caloric restriction, and (5) elimination of stressful lifestyle. Non-pharmacological interventions should be preferable even if medicaments are also used for the treatment of endothelial dysfunction. Orv. Hetil., 2015, 156(28), 1128–1132.

2015 ◽  
Vol 156 (9) ◽  
pp. 358-365 ◽  
Author(s):  
Tamás Fischer

The wall of blood vessels including those in choroids may be harmed by several repeated and/or prolonged mechanical, physical, chemical, microbiological, immunologic, and genetic impacts (risk factors), which may trigger a protracted response, the so-called host defense response. As a consequence, pathological changes resulting in vascular injury (e. g. atherosclerosis, age-related macular degeneration) may be evolved. Risk factors can also act directly on the endothelium through an increased production of reactive oxygen species promoting an endothelial activation, which leads to endothelial dysfunction, the onset of vascular disease. Thus, endothelial dysfunction is a link between the harmful stimulus and vascular injury; any kind of harmful stimuli may trigger the defensive chain that results in inflammation that may lead to vascular injury. It has been shown that even early age-related macular degeneration is associated with the presence of diffuse arterial disease and patients with early age-related macular degeneration demonstrate signs of systemic and retinal vascular alterations. Chronic inflammation, a feature of AMD, is tightly linked to diseases associated with ED: AMD is accompanied by a general inflammatory response, in the form of complement system activation, similar to that observed in degenerative vascular diseases such as atherosclerosis. All these facts indicate that age-related macular degeneration may be a vascular disease (or part of a systemic vasculopathy). This recognition could have therapeutic implications because restoration of endothelial dysfunction may prevent the development or improve vascular disease resulting in prevention or improvement of age-related macular degeneration as well. Orv. Hetil., 2015, 156(9), 358–365.


2015 ◽  
Vol 156 (46) ◽  
pp. 1847-1858 ◽  
Author(s):  
Tamás Fischer

It is of great therapeutic significance that disordered function of the vascular endothelium which supply the affected ocular structures plays a major role in the pathogenesis and development of age-related macular degeneration. Chronic inflammation is closely linked to diseases associated with endothelial dysfunction, and age-related macular degeneration is accompanied by a general inflammatory response. According to current concept, age-related macular degeneration is a local manifestation of systemic vascular disease. This recognition could have therapeutic implications because restoration of endothelial dysfunction can restabilize the condition of chronic vascular disease including age-related macular degeneration as well. Restoration of endothelial dysfunction by pharmaacological or non pharmacological interventions may prevent the development or improve endothelial dysfunction, which result in prevention or improvement of age related macular degeneration as well. Medicines including inhibitors of the renin-angiotensin system (converting enzyme inhibitors, angiotensin-receptor blockers and renin inhibitors), statins, acetylsalicylic acid, trimetazidin, third generation beta-blockers, peroxisome proliferator-activated receptor gamma agonists, folate, vitamin D, melatonin, advanced glycation end-product crosslink breaker alagebrium, endothelin-receptor antagonist bosentan, coenzyme Q10; “causal” antioxidant vitamins, N-acetyl-cysteine, resveratrol, L-arginine, serotonin receptor agonists, tumor necrosis factor-alpha blockers, specific inhibitor of the complement alternative pathway, curcumin and doxycyclin all have beneficial effects on endothelial dysfunction. Restoration of endothelial dysfunction can restabilize chronic vascular disease including age-related macular degeneration as well. Considering that the human vascular system is consubstantial, medicines listed above should be given to patients (1) who have no macular degeneration but have risk factors for the disease and are older than 50 years; (2) who have been diagnosed with unilateral age-related macular degeneration in order to prevent damage of the contralateral eye; (3) who have bilateral age-related macular degeneration in order to avert deterioration and in the hope of a potential improvement. However, randomised prospective clinical trials are still needed to elucidate the potential role of these drug treatments in the prevention and treatment of age-related macular degeneration. Orv. Hetil., 2015, 156(46), 1847–1858.


2014 ◽  
Vol 55 (1) ◽  
pp. 492 ◽  
Author(s):  
Sheldon Rowan ◽  
Karen Weikel ◽  
Min-Lee Chang ◽  
Barbara A. Nagel ◽  
Jeffrey S. Thinschmidt ◽  
...  

2006 ◽  
Vol 83 (4) ◽  
pp. 880-886 ◽  
Author(s):  
Chung-Jung Chiu ◽  
Larry D Hubbard ◽  
Jane Armstrong ◽  
Gail Rogers ◽  
Paul F Jacques ◽  
...  

2021 ◽  
Vol 11 (7) ◽  
Author(s):  
Niyazi Acar ◽  
Bénédicte M. J. Merle ◽  
Soufiane Ajana ◽  
Zhiguo He ◽  
Stéphane Grégoire ◽  
...  

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 111-111
Author(s):  
Kingsley Kalu ◽  
Angelica Ly ◽  
Charles McMonnies ◽  
Jayashree Arcot

Abstract Objectives The aim of this study was to assess the dietary intakes of lutein, zeaxanthin (L + Z) and omega-3-essential fatty acid(EFA) among a selected population of Australian based adults and to examine the effect of specified risk factors for age-related macular degeneration(AMD) on those levels. Methods A cross-sectional study involving 70 adults aged 19–52 years was carried out. Demographic data were obtained using an online self-administered questionnaire while dietary intakes were estimated using USDA's 24 hours recall questionnaire, the Victorian Cancer Council(Australia) food frequency questionnaire and anthropometric characteristics were obtained using a body composition analyzer. Dietary intakes of lutein, zeaxanthin, omega-3-EFA and anthropometric indices against the risk of AMD were established using descriptive statistics and Spearman correlation. Results The mean age of the population was 29.9 ± 8.1years with 51% men and 49% women. Women had a higher intake of L + Z (1908.6 μg/day versus 1032.8 μg/day) and alpha-linolenic acid(ALA) compared to men(1.7 ± 1.1 g/day versus 1.6 ± 1.2 g/day). Men consumed more omega-3-EFA than women (433 ± 397.1 mg/day versus 365 ± 210.7 mg/day). L + Z levels were higher among people of Middle Eastern and South Asian origin (>4000 μg/day) in the 19–25years age group. People of Middle Eastern, South East Asian and South Asian had the highest intake of omega-3-EFA(>500 mg/day) at ages 19–25, 26–32 and 34–52years respectively. Women aged 34–52years with a family history of AMD had higher levels of L + Z(>2500 μg/day) while women aged 26–32years with a family history of AMD had higher levels of ALA(>3 g/day). Ethnicity and L + Z were correlated (P = −0.456, P < 0.02). Higher levels of intake of L + Z (>4000 μg/day) were seen in participants aged 34–52years with a 5–10years residence in Australia. Participants who had less than 5–10years of residency had higher levels of omega-3-EFA(>500 mg/day) for ages 26–32years while those aged 34–52years who had less than 5years of residency had higher ALA(>4 g/day). Conclusions Intake levels for L + Z vary significantly among participants. Culturally specific dietary habits could feasibly influence the levels of intake of L + Z. Intake levels of omega-3-EFA were met. This study provides detailed intake levels of L + Z and omega-3-EFA for the ‘at-risk’ AMD group. Funding Sources No funding source.


Sign in / Sign up

Export Citation Format

Share Document