PubMed · 8918646
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E Wandel. 1996. Dysmorphic erythrocytes.. https://pubmed.ncbi.nlm.nih.gov/8918646/
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We studied cerebral perfusion and oxygen metabolism in three patients with chorea-acanthocytosis using positron-emission tomography and oxygen-15 labeled O2 and CO2. High-field magnetic resonance imaging also was performed. Regional cerebral blood flow (rCBF) and oxygen metabolism (rCMRO2) were significantly reduced in the caudate and putamen when compared with seven control subjects. Mild but significant reductions of rCBF (lower than the normal control values -2 SD) were found in the bilateral frontal, left temporal and parietal, and bilateral thalamic areas; rCMRO2 was reduced in the bilateral frontal and left temporal areas. Magnetic resonance imaging showed increased signal intensity accompanied by scattered bright spots in the caudate head and putamen on T2-weighted images; decreased signal intensity was shown at these sites on T1-weighted images. These findings were not observed in 10 neurologically normal volunteers and are rare in the common hyperkinetic form of Huntington's disease. Reduced cerebral perfusion and oxygen metabolism seem to be related to the intellectual and personality changes that occur in chorea-acanthocytosis. Combined positron-emission tomography and magnetic resonance imaging studies may improve diagnostic accuracy in patients with chorea-acanthocytosis and related disorders.
Poikilocytosis of red blood cells (RBCs) was observed to be associated with anemia in rats given subcutaneous injections of cadmium (Cd). Phase-contrast light and scanning electron microscopic examinations revealed that acanthocytes appeared in the early stages of administration, and that the number of RBC fragments increased later. Ultrastructural analysis of RBC ghosts by negative staining demonstrated that the normal lattice structure of the membrane skeleton was abolished. The osmotic fragility curve of the Cd-exposed RBCs disclosed that most of the cells were less fragile than control RBCs. These data indicate that the RBC membrane skeleton is initially altered by Cd-exposure, followed by deformation of the cell, thus promoting intrasplenic hemolysis, and resulting in anemia.
A 30-year-old woman presented with a progressive neurologic disorder characterized by seizures, buccolingual dyskinesias, orofacial tics, choreiform movements, atrophy, and areflexia. Investigations revealed normal lipid profile except for aprebetalipoproteinemia. Phase-contrast and electron microscopy showed 35 to 40% acanthocytes. MRI and 18fluorodeoxyglucose-PET studies showed caudate atrophy and hypometabolism. The phenotype of this patient is neuroacanthocytosis and its association with aprebetalipoproteinemia may represent a new subentity of the disorder.