Abnormal Blood Rheology in Young Male Diabetics With and Without Retinopathy

Lowe, G. D. O.; Belch, J J F; Lowe, Julia; MacCuish, A C; Manderson, W. G.

doi:10.1055/s-0038-1665792

Cited by 15 publications

(18 citation statements)

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“…Raised plasma viscosity associated with increased fibrinogen and globulin levels has been observed in diabetes by many (241,(244)(245)(246)(247) but not all (248)(249)(250) investigators, and has been invoked as a cause for increased susceptibility to thrombosis in diabetes. Whole-blood viscosity appears to be increased in diabetes (245, 251), and it has been attributed to increased circulating fibrinogen levels (251)(252)(253), decreased erythrocyte deformability (245,253,254) (a finding disputed by some [249,255,256]), and/or leukocytosis (247,249,256) (which may occur in diabetes without infection [241,257]). Hyperviscosity in diabetes appears to reflect the degree of metabolic control (258).…”

Section: Contribution Of Abnormal Rheology To Diabetic Neuropathymentioning

confidence: 99%

Complications: Neuropathy, Pathogenetic Considerations

et al. 1992

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The most common form of neuropathy associated with diabetes mellitus is distal symmetric sensorimotor polyneuropathy, often accompanied by autonomic neuropathy. This disorder is characterized by striking atrophy and loss of myelinated and unmyelinated fibers accompanied by Wallerian degeneration, segmental, and paranodal demyelination and blunted nerve fiber regeneration. In both humans and laboratory animals, this progressive nerve fiber damage and loss parallels the degree and/or duration of hyperglycemia. Several metabolic mechanisms have been proposed to explain the relationship between the extent and severity of hyperglycemia and the development of diabetic neuropathy. One mechanism, activation of the polyol pathway by glucose via AR, is a prominent metabolic feature of diabetic rat peripheral nerve, where it promotes sorbitol and fructose accumulation, myo-inositol depletion, and slowing of nerve conduction by alteration of neural Na(+)-K(+)-ATPase activity or perturbation of normal physiological osmoregulatory mechanisms. ARIs, which normalize nerve myo-inositol and nerve conduction slowing, are currently the focus of clinical trials. Other specific metabolic abnormalities that may play a role in the pathogenesis of diabetic neuropathy include abnormal lipid or amino acid metabolism, superoxide radical formation, protein glycation, or potential blunting of normal neurotrophic responses. Metabolic dysfunction in diabetic nerve is accompanied by vascular insufficiency and nerve hypoxia that may contribute to nerve fiber loss and damage. Although major questions about the pathogenesis of diabetic neuropathy remain unanswered and require further intense investigation, significant recent progress is pushing us into the future and likely constitutes only the first of many therapies directed against one or more elements of the complex pathogenetic process responsible for diabetic neuropathy.

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Section: Contribution Of Abnormal Rheology To Diabetic Neuropathymentioning

confidence: 99%

Complications: Neuropathy, Pathogenetic Considerations

et al. 1992

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“…An impairment of the red blood cell deformability (RBCD) results in an increase in blood viscosity, which is affected not only by the haematocrit and the plasma proteins such as fibrinogen {Lowe, Lowe, Drummond, Reith, Belch, Kesson, Wylie, Foulds, Forbes, Mac Cuish and Manderson 1980) but by the rigid RBCs as well {Juhan, Bayle, Vague and Juhan 1978). On the other hand it has been demonstrated that the increase of RBCD may improve blood viscosity (Dintenfass 1976;Leonhardt and Grigoleit 1977).…”

Section: Introductionmentioning

confidence: 99%

Red Blood Cell Deformability Index in Diabetic Retinopathy

Diamantopoulos

Raptis²,

Moulopoulos³

1987

Horm Metab Res

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In order to investigate the relationship between haemorheological disturbances and diabetic microangiopathy we have studied the red blood cell deformability index (RBCD-index) by means of a filtration technique in 69 diabetics, aged 49-83 years, and in 40 non diabetic healthy controls (group A) of respective age and sex. The diabetics were classified into the following groups, according to the findings of a thorough clinical and laboratory investigation. Twenty patients (group B) were free of vascular complications, whereas 9 (group C) suffered from background retinopathy, 27 (group D) background retinopathy and ischaemic cardiopathy or peripheral arterial occlusive disease and 13 (group E) of proliferative retinopathy with diffuse micro- and macroangiopathy. The RBCD-index was significantly (P less than 0.001) decreased in diabetics with retinopathy compared to the diabetic and non diabetic controls. The lowest RBCD-index was observed in diabetics with proliferative retinopathy and in those with diffuse micro- and macrovascular complications (RBCD-index, means +/- SDM ml/min: A 0.68 +/- 0.15; B 0.64 +/- 0.08; C 0.60 +/- 0.08; D 0.49 +/- 0.09; E 0.48 +/- 0.09). These findings suggest that the RBCD is impaired in diabetics with retinopathy, especially in those with severe vascular complications, and that this abnormal rheological behavior of erythrocytes can be found even in the early stages of diabetic microangiopathy.

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“…the body's prevailing biochemistry influences their absorption and/or reaction. In addition increased PG and levels of fatty acids will increase blood viscosity which in turn will influence the dissociation of reagents, metabolites and toxins to and from reactive sites thereby influencing the rate at which proteins react and alter cell function[24–27]. …”

Section: Physiological Systemsmentioning

confidence: 99%

The multi-systemic nature of diabetes mellitus: Genotype or phenotype?

Ewing

Parvez

2010

NAJMS

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Background:This article discusses factors which materially influence the diagnosis, prevention and treatment of diabetes mellitus but which may be overlooked by the prevailing biomedical paradigm. That cognition can be mathematically linked to the function of the autonomic nervous system and physiological systems casts new light upon the mechanisms responsible for homeostasis and origins of disease. In particular, it highlights the limitations of the reductionist biomedical approach which considers mainly the biochemistry of single pathologies rather than considering the neural mechanisms which regulate the function of physiological systems, and inherent visceral organs; and which are subsequently manifest as biochemistries of varying degrees of complexity and severity. As a consequence, histopathological tests are fraught with inherent limitations and many categories of drugs are significantly ineffective.Aims:Such limitations may be explained if disease (in particular diabetes mellitus) has multiple origins, is multi-systemic in nature and, depending upon the characteristics of each pathology, is influenced by genotype and/or phenotype.Results:This article highlights the influence of factors which are not yet considered re. the aetiology of diabetes mellitus e.g. the influence of light and sensory input upon the stability of the autonomic nervous system; the influence of raised plasma viscosity upon rates of reaction; the influence of viruses and/or of modified live viruses given in vaccinations; systemic instability, in particular the adverse influence of drinks and lack of exercise upon the body's prevailing pH and its subsequent influence upon levels of magnesium and other essential trace elements.Conclusions:This application of the top-down systems biology approach may provide a plausible and inclusive explanation for the nature and occurrence of diabetes mellitus.

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Abnormal Blood Rheology in Young Male Diabetics With and Without Retinopathy

Cited by 15 publications

References 0 publications

Complications: Neuropathy, Pathogenetic Considerations

Complications: Neuropathy, Pathogenetic Considerations

Red Blood Cell Deformability Index in Diabetic Retinopathy

The multi-systemic nature of diabetes mellitus: Genotype or phenotype?

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