Erythrocyte aggregation in relation to diabetic retinopathy

Haeringen, N.J. van; Oosterhuis, J. A.; Terpstra, J.; Glasius, E.

doi:10.1007/bf01225995

Cited by 16 publications

(8 citation statements)

References 10 publications

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“…The alteration of plasma protein composition, including a decrease of albumin and an increase of the az-fraction and fibrinogen (and to a lesser extent, the changes of fl-and al-fractions), has been reported previously [1,4,10,12,13]. The percentage of the o-fraction (or the amount of fibrinogen) was positively correlated with the velocity of aggregation in our diabetic subjects (Table2).…”

Section: Discussionsupporting

confidence: 85%

“…If individual variation of the haematocrit is corrected, diabetic hyperviscosity may be caused by decreased erythrocyte deformability and/or by increased erythrocyte aggregation [8,9]. Although the increase of reversible aggregation in diabetes has been shown both in vitro [10][11][12] and in vivo [13], a quantitative study of erythrocyte aggregation, taking into account protein glycosylation, has not been made.…”

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confidence: 99%

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Increased erythrocyte aggregation in diabetes mellitus and its relationship to glycosylated haemoglobin and retinopathy

et al. 1984

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The velocity of erythrocyte aggregation in vitro was determined in 15 non-diabetic and 28 Type 1 (insulin-dependent) diabetic subjects, in autologous plasma under uniform shear flow using a rheoscope combined with a television image analyzer and a computer. In the diabetic subjects, the velocity of aggregation showed a significant correlation with the haemoglobin A1 level, and was significantly increased in the proliferative retinopathy group. An alteration of plasma protein composition in the diabetic subjects (increase of phi- and alpha 2-fractions) also influenced erythrocyte aggregation, being related to the haemoglobin A1 level. The percentage of the phi-fraction and a parameter, (alpha 2 + phi)/albumin, defined by plasma electrophoresis, showed a strong correlation with the velocity of aggregation.

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Section: Discussionsupporting

confidence: 85%

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confidence: 99%

Increased erythrocyte aggregation in diabetes mellitus and its relationship to glycosylated haemoglobin and retinopathy

et al. 1984

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“…In diabetic retinopathy as well, retinal vascular lesions similar to those seen in retinal vein occlusion are observed; here, in addition to a metabolic disorder of the retinal vessel wall, an increased erythrocyte aggregation tendency may be of importance ( Van Haeringen et al, 1973).…”

Section: Clinical Picturementioning

confidence: 92%

Photocoagulation in retinal vein occlusion

Sedney¹

1976

Doc Ophthalmol

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Recent studies, which will be discussed in detail in the chapters on pathology (chapter V), fluorescence angiography (chapter VII) and pathogenesis (chapter VIII), have considerably increased our insight into the development of retinal vein occlusion. CHAPTER III ANATOMICAL AND PHYSIOLOGICAL ASPECTS OF THE RETINAL CIRCULATIONMany factors can disturb the blood circulation in the eye. Morphologic changes of the vessel wall play an important role in retinal arteriosclerosis, hypertensive retinopathy, occlusion of the retinal veins and senile degeneration of the macula. In order to understand these processes it is necessary to have some knowledge of the anatomy and physiology of the retinal circulation.The metabolism of the retina is served by two vascular systems, i.e. the retinal and the choroidal system which, with the exception of capillary connections at the optic disc, are separate .The retinal vessels supply the inner layers of the retina from the internal limiting membrane to the outer plexiform layer. The choroidal network, which, by diffusion via Bruch's membrane, feeds the outer layers of the retina, i.e. the pigment epithelium, the layer of rods and cones, and the outer nuclear layer, arises from the short posterior ciliary arteries.Both vascular systems arise from the ophthalmic artery. After passing the lamina cribrosa the central retinal artery splits into 2 branches, i.e. the superior and inferior artery, which each split into a nasal and a temporal branch at or outside the margin of the optic disc. A cilio-retinal artery may exist, which arises directly from the choroidal circulation and feeds the papillo-macular area. Figures for the frequency of occurrence of this artery, which in one eye is seldom multiple, are variable. Hayreh (1963) found it in 25% of the eyes he examined, Seitz (1968) in 5-10% and Gass (1968) in 15-20%.The large retinal vessels lie between the nerve fibre layer and the inner plexiform layer of the retina. Each of the arterial branches divides into smaller vessels without anastomoses which finally end in a capillary bed. The retinal capillary bed is a complex network consisting of two layers throughout the greater part of the retina, viz. a superficial and a deep network (Michaelson, 1954). The superficial network lies between the nerve fibre layer and the inner plexiform layer, while the deeper network lies in the outer plexiform layer.In the peripapillary area, where the retina is thickest, three capillary networks are present; in the macular area, at the fovea where there are only three retinal layers (pigment epithelium, layer of rods and cones and outer nuclear layer) there is only one layer of capillaries, the deeper network;

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“…There are many clinical disorders in which rouleaux formation of red cells is recognized (Table 4). [33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50][51] Many of these disorders are known to be associated with increased risk of thrombosis. The thrombotic event may also be precipitated when a new hyperviscosity-inducing factor is added to an existing disorder.…”

Section: Hyperviscosity In Abnormal Red Blood Cell Aggregationmentioning

confidence: 99%

Hyperviscosity in Polycythemia Vera and Other Red Cell Abnormalities

Kwaan

Wang

2003

Semin Thromb Hemost

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Thrombosis is a major cause of mortality and morbidity in polycythemia vera (PV). The wide range of thrombotic events reflects the complex picture in PV. There are multiple factors involved in thrombogenesis in this disease, including increased hematocrit, thrombocytosis, impaired fibrinolytic activity, platelet activation, leukocyte activation, endothelial damage, interactions between platelets and endothelium, various modalities of therapy, and increased in whole-blood viscosity. Among them, the increase in blood viscosity, and hence the impairment of blood flow, is the major factor. In this article, the role of hyperviscosity in PV is reviewed. A high hematocrit occurs under PV and many other conditions with abnormal red blood cell aggregation. The impaired capillary blood flow results in neurological manifestations and increased bleeding risk in PV. Thrombotic complications can also occur in both arteries and veins and manifest as stroke, myocardial infarction, deep vein thrombosis, or pulmonary embolism. The hemodynamic principle is aptly applied in the management of PV. The most important objective is the reduction of the patient's hematocrit.

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Erythrocyte aggregation in relation to diabetic retinopathy

Cited by 16 publications

References 10 publications

Increased erythrocyte aggregation in diabetes mellitus and its relationship to glycosylated haemoglobin and retinopathy

Increased erythrocyte aggregation in diabetes mellitus and its relationship to glycosylated haemoglobin and retinopathy

Photocoagulation in retinal vein occlusion

Hyperviscosity in Polycythemia Vera and Other Red Cell Abnormalities

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