Amniotic membrane transplantation for ocular surface reconstruction in neurotrophic corneal ulcera.

The purpose of this study is to analyze clinical experience about the effects of human amniotic membrane transplantation in eyes with neurotrophic ulcers. In 11 eyes the application of amniotic membrane was performed since January 1999 because of neurotrophic ulcers. The follow up period was longer than 12 months: 19.7+/-6.0 months. The average healing period after the surgery was 1.6+/-0.6 weeks. All corneas were fluorescein negative even 12 months after operation. Visual acuity after the transplantation was similar to the one before the surgery in 8 eyes. In 3 eyes the visual acuity after the surgery was better than before. Amniotic membrane transplantation can be considered an effective alternative for treating persistent epithelial defects such as neurotrophic ulcers. It has some advantages over corneal transplantation: a relatively simple procedure, no allograft rejection and it could be particularly beneficial in countries where cornea shortage is apparent.

Is lipoprotein(A) a risk factor for atherosclerosis of the retinal arteries?

Elevated plasma Lp(a) has been linked to development of coronary artery disease (CAD). There is no data about plasma Lp(a) and atherosclerosis of the retinal arteries. Therefore the purpose of this study was to assess the risk of retinal vessels atherosclerosis conferred by elevated plasma Lp(a) levels in 73 adult males. The results were compared with those in 45 matched apparently healthy males with no retinal vessel changes. The atherosclerotic changes of the retinal vessels were determined by direct ophthalmoscopy and graded (1-4) according to Scheie. Plasma levels of Lp(a) were measured by radial immunodiffusion. The results were compared using chi-square test. Although a very weak correlation between plasma Lp(a) levels and the incidence of retinal atherosclerosis was found, no significant association between the degree of atherosclerotic changes and plasma Lp(a) levels could be proven. Thus it could be concluded that plasma Lp(a) level is not a significant risk factor for atherosclerosis of the retinal arteries.

Plasma cortisol in men--relationship with atherosclerosis of retinal arteries.

The production of cortisol increases in acute stress but the effects of chronic stress on plasma cortisol are still controversial. Stress on the other hand plays a role in coronary artery disease (CAD) and carotid atherosclerosis. Since there is no data about plasma cortisol and atherosclerosis of the retinal arteries, the purpose of this study was to explore the relationship between plasma cortisol in 101 adult males with the degree of their retinal vessels atherosclerosis. The results were compared with those in 47 matched apparently healthy men with no retinal vessels changes. The atherosclerotic changes of retinal vessels were determined by direct ophthalmoscopy and graded (1-4) according to Scheie. Morning plasma cortisol levels were determined by radioimmunoassay using commercial kits. The results were compared by using chi-square test. No association between morning plasma cortisol concentrations and retinal vessels atherosclerosis could be found. The results of this study do not support a role for physiological levels of plasma cortisol in the development of atherosclerosis, at least of the retinal arteries, in men.

Amniotic membrane transplantation for ocular surface reconstruction.

The purpose of this study is to analyze the clinical experience and the effect of human amniotic membrane transplantation on pterygium excision and bullous keratopathy. From January 1999 to January 2001 at University Hospital "Sestre milosrdnice" amniotic membrane transplantation was performed consecutively in 21 eyes: 11 eyes with bullous keratopathy and 10 with recurrent pterygia. In the group with bullous keratopathy epithelization took place in 19.6 days in 72.7% and the reduction of pain was satisfactory. Recurrence rate in group with recurrent pterygia was 20%. Based on the presented results it could be concluded that amniotic membrane transplantation can be considered as an effective alternative for treating severe ocular surface diseases and as an alternative for penetrating keratoplasty if there is a lack of grafts.

[Estrogens and risks for onset of atherosclerosis]. / Estrogeni i rizik nastanka ateroskleroze.

There are many evidences suggesting that estrogens prevent atherosclerosis and its consequences such as coronary heart disease (CHD) in women. The risk for CHD is less in premenopausal women when compared with age-matched men, but the protective effect of estrogens is lost with menopause. A part of this beneficial effect may be ascribed to the ability of estrogens to favorably alter the plasma lipoproteins profile, i.e. increase HDL and decrease LDL and Lp(a). However, the changes in the lipid profile do not fully account for the protective effect afforded by estrogens, indicating that other mechanisms are likely to be involved. One of these mechanisms may include estrogens ability to prevent oxidative modification of LDL. A number of animal and human studies strongly suggest also a direct effect on the vascular endothelium, decreasing the expression of adhesion molecules involved in monocyte adhesion such as VCAM-1. It seems that estrogens also cause by increasing the synthesis of NO a decrease in chemokines involved in monocyte migration into the subendothelial space (TNF alpha, IL-1 and MCP-1) and growth factors influencing the migration of smooth muscle cells (PDGF). They also decrease fibrinogen and homocysteine, and these substances when increased are considered independent risk factors for CHD. However, the results of the first randomised controlled trial of hormone replacement therapy (HRT) with estrogens concerning the CHD published recently differ from previous observational epidemiological studies in both primary and secondary intervention, which showed beneficial effect of HRT. The final answer about the effects of HRT on CHD is expected from several ongoing trials.

[New information on the pathophysiology of atherosclerosis]. / Novije spoznaje o patofiziologiji ateroskleroze.

The past decade has witnessed enormous progress in our understanding of the nature of this process. The development of an atherosclerotic plaque is a complex process which begins with endothelial dysfunction, the trigger for which are factors such as hypercholesterolemia, smoking, hypertension, hyperhomocysteinemia and impaired glucose metabolism. This dysfunction includes increased endothelial permeability to lipoproteins and other plasma constituents, which is mediated by NO, PDGF, prostacyclin, angiotensin II and endothelin; up-regulation of endothelial adhesion molecules including VCAM-1, ICAM-1, and selectins and migration of leukocytes and monocytes-macrophages in the subendothelial space mediated by oxidized LDL, MCP-1, PDGF and MCSF. The next step includes smooth-muscle cells migration (stimulated by PDGF and TGF-beta), T-cell activation (mediated by TNF-alpha and IL-2), formation of foam-cells from macrophages (mediated by oxidized LDL, MCSF, TNF-alpha and IL-1) and platelet adherence and aggregation (stimulated by thromboxane A2, tissue factor etc). The smooth muscle cells form a fibrous cap which confers mechanical stability of the plaque and separates the lipid rich thrombogenic core from the lumen and circulating blood. Whether a plaque will remain intact and therefore stable or rupture and lead to thrombosis causing an acute coronary syndrome (MI, unstable angina pectoris) depends upon a number of factors, the most important of which is its composition. Plaque size plays only a minor role in determining risk of an acute coronary syndrome. Rupture of the fibrous cap occurs due to thinning of the cap caused by an influx and activation of macrophages which release metalloproteinases and other proteolytic enzymes (stimulated by inflammatory cells, particularly T-lymphocytes). These enzymes cause degradation of the fibrous tissue of the cap which can result in thrombous formation and occlusion of the artery. Stable plaques have a thick fibrous cap, a small lipid core, and few inflammatory cells. In contrast, vulnerable plaques have a high lipid content, numerous inflammatory cells, and a thin fibrous cap with reduced collagen and vascular smooth muscle cells in it. Although vulnerable plaques are believed to account for only a small number of all coronary atheromas, they are responsible for most acute coronary events.

[Pathophysiology of atherosclerosis. II. Etiopathogenic mechanisms and risk factors]. / Patofiziologija ateroskleroze. II. Etiopatogenetski mehanizmi i faktori rizika.

The authors present an up-to-date review on etiopathogenesis of atherosclerosis. Theories of etiology of atherosclerosis are described: response-to-injury hypothesis, lipid deposition hypothesis, lysosome hypothesis, encrustation hypothesis, mural thrombi hypothesis, monoclonal and clonal senescence hypothesis. The role of endothelial injury and platelet adhesion as well as smooth muscle cells proliferation due to these events, their growth control and the role of macrophages in atherogenesis are explained thoroughly. Special attention is focused on the interaction of arterial cells and lipoproteins at sites of vessel injury, lipid metabolism of the lesion and on synergy of arterial injury caused by various injury mechanisms and hypercholesterolemia in atherogenesis. Atherosclerotic risk factors and their impact on atherogenesis are discussed as well (e.g. hyperlipoproteinemia, hypertension, tobacco smoking, diabetes and abnormal glucose tolerance, gout, obesity, menopause and oral contraceptives, diminished physical activity, type A of personality behavior etc.). The possibilities of regression or reversal of ateromatous plaques are presented too.

[Pathophysiology of atherosclerosis. I. The morphology and developmental levels of atherosclerotic changes]. / Patofiziologija ateroskleroze. I. Oblici i stupnjevi razvoja aterosklerotickih promjena.

The authors present an up-to-date review on natural history of atherosclerosis. After a short introduction dealing with history of atherosclerosis research, data about morphology and pathology of the normal arterial wall are presented. Special attention is focused on structural differences of arteries in different body districts as well as vascular endothelium and smooth muscle cells and their role in atherogenesis. Pathogenetic mechanisms in the evolution of lesions and morphology of different types of atherosclerotic lesions based on cellular and metabolic changes are explained in details: early lesions such as gelatinous elevations-insudative lesions, fetty dots and streaks and microthrombi; advanced lesions such as fibromusculoelastic lesions, pearly-white fibrous atherosclerotic plaques and atheromatous plaques; and complicated lesions with calcifications, ulcerations, thrombosis and hemorrhage.