The mean red cell volume in diabetes mellitus

Davidson, R. J. L.; Evan-Wong, L. A.; Stowers, J. M.

doi:10.1007/bf00252770

Cited by 16 publications

(11 citation statements)

References 6 publications

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“…In severe diabetic decompensation, however, Davidson and Evan-Wong [3] have failed to find macrocytosis, as judged by "spun" MCV. Water deficiency in diabetic pre-coma is the most probable explanation: with clouding of consciousness, patients fail to drink adequately to replace their fluid losses.…”

Section: Discussionmentioning

confidence: 99%

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Real and artefactual erythrocyte swelling in hyperglycaemia

1985

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Summary.The mean erythrocyte volume of ~ patients with acute diabetic decompensation was determined by Coulter measurement and found to be elevated above normal (mean increase 5.5 Ix3). Experiments in vitro revealed this to be an artefact associated with Coulter determination. A more reliable estimate of in vivo erythrocyte volume can be obtained from centrifugated haematocrit and erythrocyte count. With this method, true erythrocyte swelling parallel to glucose concentration was observed when erythrocytes were exposed to isotonic glucose-NaC1 solutions. This volume increase resulted from decreased sodium concentration and was in the order of 0.5-1.0 ix 3 per mmol/1 of sodium. Glucose was osmotically ineffective. Similar volume changes were documented in a diabetic patient parallel to his daily variations of blood glucose. In severe diabetic decompensation, dehydration usually prevents an increase in erythrocyte volume. We conclude that hyperglycaemia is associated with erythrocyte swelling if total serum tonicity remains within the normal range.

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Section: Discussionmentioning

confidence: 99%

“…Erythrocytes from patients with diabetic decompensation have been reported to have an increased mean corpuscular volume (MCV) [1][2][3][4][5]. However, the aetiology and even existence of this phenomenon remain controversial.…”

mentioning

confidence: 99%

Real and artefactual erythrocyte swelling in hyperglycaemia

1985

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“…Increased red call aggregation in diabetes is associated with raised fibrinogen levels (259) and reduced erythrocyte size (260,261). Activated white cells exhibit a further reduction in their deformability in diabetes (262).…”

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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“…The deformability of diabetic RBCs has been extensively investigated using various experimental approaches including optical microscopy 2 , Coulter counter 3 , and laser diffraction ektacytometry 4 . In particular, the main cytoplasmic alteration in diabetic RBCs caused by hyperglycaemia, the glycation of haemoglobin (Hb), has gained increasing attention because the relative amount of glycated Hb, mainly consisting of HbA1c to total Hb, reflects the mean plasma glucose concentration of the previous three months 5 .…”

Section: Introductionmentioning

confidence: 99%

Refractive index tomograms and dynamic membrane fluctuations of red blood cells from patients with diabetes mellitus

Lee

Park

et al. 2017

Sci Rep

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In this paper, we present the optical characterisations of diabetic red blood cells (RBCs) in a non-invasive manner employing three-dimensional (3-D) quantitative phase imaging. By measuring 3-D refractive index tomograms and 2-D time-series phase images, the morphological (volume, surface area and sphericity), biochemical (haemoglobin concentration and content) and mechanical (membrane fluctuation) parameters were quantitatively retrieved at the individual cell level. With simultaneous measurements of individual cell properties, systematic correlative analyses on retrieved RBC parameters were also performed. Our measurements show there exist no statistically significant alterations in morphological and biochemical parameters of diabetic RBCs, compared to those of healthy (non-diabetic) RBCs. In contrast, membrane deformability of diabetic RBCs is significantly lower than that of healthy, non-diabetic RBCs. Interestingly, non-diabetic RBCs exhibit strong correlations between the elevated glycated haemoglobin in RBC cytoplasm and decreased cell deformability, whereas diabetic RBCs do not show correlations. Our observations strongly support the idea that slow and irreversible glycation of haemoglobin and membrane proteins of RBCs by hyperglycaemia significantly compromises RBC deformability in diabetic patients.

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The mean red cell volume in diabetes mellitus

Cited by 16 publications

References 6 publications

Real and artefactual erythrocyte swelling in hyperglycaemia

Real and artefactual erythrocyte swelling in hyperglycaemia

Complications: Neuropathy, Pathogenetic Considerations

Refractive index tomograms and dynamic membrane fluctuations of red blood cells from patients with diabetes mellitus

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