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At least 19 recordsLinked to original sources
PubMed1989

Red cell deformability and lipid composition in two forms of acanthocytosis: enrichment of acanthocytic populations by density gradient centrifugation.

Whole cell deformability and lipid determinations were performed on red cells from two patients who had acanthocytes in the peripheral blood (10% and 20% to 30%) and normal serum lipoprotein levels. One patient had typical chorea-acanthocytosis and the other had no clinical abnormalities associated with acanthocytosis. Red cells from the patient with chorea-acanthocytosis showed reduced deformability, as measured by a visco-diffractometric method (ektacytometry), which could be explained by the presence of increased numbers of dehydrated cells containing high concentrations of hemoglobin. The total cell population showed a modest increase in potassium efflux, which may be responsible for reduced cation content and dehydration in a subpopulation of cells. When the patients' red cells were separated into different density populations by centrifugation on density gradients, the cells of classic acanthocyte morphology were concentrated in the high-density layers. This was true for both patients, although the subject with acanthocytes and no clinical disorder had a normal red cell density distribution. Lipid analysis of both types of acanthocytes showed an increase in the relative proportion of sphingomyelin with respect to the glycerophospholipids. Total cholesterol and phospholipid levels were reduced in the chorea-acanthocytosis red cells, but the other acanthocytes did not differ significantly in total lipid content from normal control samples. Thus, the one common abnormal feature in these two forms of acanthocytosis is the increase in the proportion of red cell sphingomyelin. Because this is a very stable, immobile component of the membrane, we suggest that its relative enrichment could result from a defect in the transport and maintenance of glycerophospholipids. Further study of the dynamics of glycerophospholipid organization in acanthocytes may be useful in increasing our understanding of the genesis of abnormal, acanthocytic morphology.

Acanthocytes↗
PubMed1991

[Hypothyroidism and acanthocytes: diagnostic significance of blood smear].

We report on 3 cases of hypothyroidism in which the diagnoses were suspected after having observed acanthocytes on the blood film. The diagnostic value of this erythrocyte change has been neglected, although the results of studies have shown a test specificity of 87-99%, other diseases related to acanthocytes being very rare. After an analysis of the studies and case reports dealing with acanthocytes we conclude that hypothyroidism must be excluded in all cases where acanthocytes are observed on the blood film.

Acanthocytes↗
PubMed1989

Effect of phosphatidylserine on the shape of McLeod red cell acanthocytes.

The rare McLeod blood group phenotype is characterized by weak Kell antigens, lack of the common Kx antigen, and acanthocytic morphology. Previous studies that did not detect membrane or cytoskeletal protein abnormalities suggested a lipid disturbance. In normal red cells, dimyristoyl phosphatidylserine (DMPS) is transported across the membrane by an enzymatic process and accumulates in the inner leaflet of the membrane bilayer causing discocyte to stomatocyte shape changes. Scanning electron microscopy of McLeod red cells shows a mixture comprised of 15% discocytes, 51% with irregular surfaces, and 34% acanthocytes. On incubation with various concentrations of DMPS at 37 degrees C for periods up to two hours, McLeod red cells transported DMPS across the membrane and caused irregularly shaped and acanthocytic McLeod red cells to attain normal discocyte shape and later to become stomatocytes. Chlorpromazine, which at 0 degrees C preferentially partitions into the inner monolayer of the membrane, had a similar effect on the shape of McLeod red cells. This suggests that in McLeod cells acanthocytosis is due to a lack of lipid in the inner leaflet of the membrane bilayer but that the imbalance is not caused by defective transport of phosphatidylserine across the membrane.

Acanthocytes↗
PubMed1993

Choreo-acanthocytosis like phenotype without acanthocytes: clinicopathological case report. A contribution to the knowledge of the functional pathology of the caudate nucleus.

Detailed clinical and neuropathological findings in two unrelated patients with a chorea-acanthocytosis-like phenotype (CA) are reported. One case met all the diagnostic criteria of CA and had a deceased brother with the same disease. The second case had a virtually identical phenotype to the former but without acanthocytes. These findings suggest that both patients are affected by the same disease and that acanthocytes are not essential to the diagnosis. Neuropathological autopsy studies on the brain of the second case showed selective atrophy of the caudate nucleus that seemed to correspond to the movement disorder and behavioural abnormalities prominent in this patient. In both subjects, morphometric and ultrastructural examination of the peripheral nerve showed loss of myelinated fibres, more accentuated distally, and cytoskeletal changes in the axoplasm. These findings support the hypothesis that peripheral neuropathy in CA is caused by distal axonopathy.

Acanthocytes↗
PubMed1999

Late appearance of acanthocytes during the course of chorea-acanthocytosis.

A case of chorea-acanthocytosis (CA) syndrome is described. The presence of acanthocytes has usually been considered an important diagnostic marker of CA. However, it is not specific and other neurological diseases have to be considered. In the present report we rule out other diagnostic possibilities and show that the acanthocytes in the peripheral blood smears can appear even later during the course of the disease.

Acanthocytes↗
PubMed1989

Tris acetylacetonate aluminium(III) induces osmotic fragility and acanthocyte formation in suspended erythrocytes.

Tris acetylacetonate aluminium(III) (Al(acac)3), dissolved in water, is effective in producing osmotic fragility in suspended erythrocytes in the concentration range of 0.034-0.34 mmol/l. Water solutions of Tris maltolate aluminium(III) (Al(malt)3) and aluminium lactate (Al(lac)3) are also effective but the dose-response behavior is less pronounced. Moreover, only Al(acac)3 induces a prominent generation of acanthocytes. The stronger effects of Al(acac)3 on membrane stability are attributed to the greater solubility of this complex in the cell membrane.

Acanthocytes↗
PubMed1994

Irregular distortion of the erythrocytes (acanthocytes, spur cells) in senile dementia.

An excess of irregularly distorted red cells with spiked forms (acanthocytes, spur cells) has been found in a substantial minority of patients with senile dementia of Alzheimer type (7 of 50 patients, 3 of 21 men and 4 of 29 women). Of 100 control patients, 42 men and 58 women), 5 (3 men and 2 women) showed comparable distortion, but, of these, one man may well have incipient dementia and the others had serious organic diseases which may be associated with comparable erythrocytic changes. The cause of the distortion is not yet clear, but the presence of occasional giant erythrocytes in the absence of general macrocytosis suggests a possible abnormality of cell-membrane synthesis. This distortion may be a useful marker in patients with loss of memory. Whether it is a manifestation of a haemopoietic clone or a constitutional anomaly associated with Alzheimer's disease remains to be seen.

ABO Blood-Group System↗
PubMed1989

Shape determinants of McLeod acanthocytes.

We have sought to elucidate the spiculated shape of McLeod erythrocytes. Red cells from a normal donor and from a McLeod patient were incubated in phosphate-buffered saline containing 0, 0.05, or 0.1 mM chlorpromazine at 0 degrees C for 5 min, then glutaraldehyde-fixed, and examined by scanning electron microscopy. The normal red cells were biconcave disks in which chlorpromazine induced inward (negative) curvature: deep cupping (stomatocytosis) and multiple invaginations. The McLeod cells were mostly spiculated. Chlorpromazine at lower concentration converted them into biconcave disks and, at higher concentration, into stomatocytes. These results support the hypothesis that the spiculation of McLeod cells is the result of an imbalance of surface area between the two lipid leaflets of the membrane; that is, a bilayer couple effect. We determined the numerical density of intramembrane particles (IMP) in replicas of both fracture faces of red cells subjected to freeze fracture and rotary shadowing. These values were as follows (expressed per microns 2 of membrane +/- SD): the normal protoplasmic fracture face had 2200 +/- 306 and the McLeod had 2300 +/- 250. The normal exoplasmic fracture face had 388 +/- 75 and the McLeod had 330 +/- 59. We conclude that there is no evidence for derangement of band 3, the principal protein in the IMP, in McLeod erythrocytes.

Acanthocytes↗
PubMed1983

Benign X-linked myopathy with acanthocytes (McLeod syndrome). Its relationship to X-linked muscular dystrophy.

Two healthy men with McLeod syndrome, a rare X-linked recessive phenotype characterized by acanthocytosis and weakened red blood cell antigenicity in the Kell blood group system, have been investigated. Both men showed raised blood creatine kinase levels, with myopathic EMG abnormalities. Biopsies of the quadriceps muscle showed the features of an active myopathy although there was no clinical evidence of muscular abnormality. The combination of the association of membrane abnormalities in red blood cells and a myopathy in both McLeod phenotype and Duchenne muscular dystrophy suggests that these syndromes may be due to related genetic abnormalities. The genetic locus for McLeod phenotype is situated near the end of the short arm of the X chromosome. The locus for Duchenne muscular dystrophy is unknown but it has been postulated that it is also situated on the short arm of the X chromosome at Xp 21. The occurrence of a subclinical X-linked myopathy with acanthocytosis (McLeod phenotype) thus raises the possibility of a new approach to genetic investigations in Duchenne muscular dystrophy, and in the related milder forms of this disease.

Acanthocytes↗
PubMed1995

Liver alcoholic cirrhosis and spur-cell (acanthocytic) anaemia. A study of erythrocyte ghost composition and fluidity.

BACKGROUND: The occurrence of spur-cell anaemia in the course of cirrhosis is rare. Alterations of the lipid composition and fluidity of erythrocyte (RBC) ghosts may be present and participate in the phenomenon. METHODS: A 59-year-old male patient with alcoholic cirrhosis developed severe spur-cell haemolytic anaemia before death. We compared his RBC ghosts with those of 10 cirrhotic patients and used a group of 9 healthy subjects as controls. RESULTS: The cholesterol to protein ratio was higher in cirrhotic patients; besides, they had less unsaturated fatty acid. The ratio of phospholipid phosphorus to protein did not change; yet, the distribution of phosphorus among phospholipid classes was altered. No difference in 1,6-diphenyl-1,3,5-hexatriene fluorescence anisotropy (membrane fluidity) was observed between the ghosts of cirrhotic patients and those of healthy people. However, the ghosts of the patient with spur-cell anaemia were more rigid than those of either group. CONCLUSIONS: The values of most variables of cirrhotic patients' ghosts lay between those of healthy subjects and those of the one who developed spur-cell anaemia. It is concluded that some homeostatic mechanisms must control fluidity during cirrhosis; in some cases alterations are particularly great, and fluidity cannot be maintained.

Acanthocytes↗