Erythrocyte and Biochemical Abnormalities as Diagnostic Markers in Dogs With Hemangiosarcoma Related Hemoabdomen.

OBJECTIVE: To investigate: 1) acanthocytosis and presence of acanthocytes in peritoneal fluid as a diagnostic marker for hemangiosarcoma (HSA) in dogs with non-traumatic hemoabdomen; and 2) the association between other erythrocyte, biochemical, and hematologic abnormalities as a mean of differentiating HSA from other disease. STUDY DESIGN: Prospective double-blinded cohort study. ANIMALS: Dogs (n = 40) with non-traumatic hemoabdomen. METHODS: Dogs diagnosed with hemoabdomen (January 2012 to May 2013) had cytologic evaluation of abdominal effusion and peripheral blood smears. Peripheral blood CBC, PT, and aPTT, as well as blood and effusion acanthocytes, keratocytes, schistocytes, lactate, glucose, PCV, and TP results were compared using the paired t-test or Fisher's exact test. Based on histologic confirmation of HSA, dogs were divided into 2 groups (HSA, non-HSA) and variables compared. RESULTS: There was no significant difference in erythrocyte morphology in abdominal effusion or peripheral blood between dogs with HSA or non-HSA related hemoabdomen. Platelet concentration and peripheral blood PCV were significantly lower in the HSA group. CONCLUSIONS: A reliable preoperative biochemical or cytologic test to differentiate between HSA and non-HSA related hemoabdomen was not identified.

The McLeod syndrome without acanthocytes.

A 45-year-old man developed chorea, behavioural changes, moderate amyotrophy and polyneuropathy. Hypertrophic cardiomyopathy and increased serum lactate dehydrogenase and creatine kinase (CK) were found. Acanthocytes were not detected. The absence of XK protein and faintly expressed Kell antigens on erythrocytes were found. Genetic test revealed a R133X mutation of the XK gene, confirming the McLeod syndrome. After 7 years he suddenly developed delirium followed by severe hypoglycaemia, hyperthermia, rhabdomyolysis, hepatic and renal failure. Malignant arrhythmia caused death.

Dynamics of the structural and electrical characteristics of erythrocytes in men with metastatic adenocarcinoma of the prostate before and after plastic orchiectomy.

The changes of electrophoretic mobility of erythrocytes in the practically healthy men and in men with metastatic prostate cancer before and after castration were studied. The electrophoretic mobility of erythrocytes was investigated in laboratory conditions by Kharamanenko and Abramson micro methods. Experimental data were processed by means of standard variation statistics MINITAB (Basic statistic) p

Abetalipoproteinemia: a case report.

Abetalipoproteinemia is a rare autosomal recessive disorder characterized by steatorrhea, poor weight gain, acanthocytosis and retinitis pigmentosa. Here we peresent a six-month-old patient with abetaliporoteinemia. He had a history of chronic diarrhea from the first month of life. He was cachectic and his motor development was delayed. Microscopic examination of the stool revealed fat. Mild anemia with reticulocytosis, acanthocytosis, low triglyceride, low cholesterol, low-density lipoprotein, high-density lipoprotein, and apolipoprotein A and B were detected. Ophthalmological examination was normal. Peroral jejunal capsule biopsy revealed normal villi and significant lipid deposition in the cytoplasm of affected cells. The patient was given large doses of vitamins E and A.

Peripheral neuropathy in amyotrophic chorea-acanthocytosis.

We investigated involvement of the peripheral nervous system in 6 patients with amyotrophic chorea-acanthocytosis. Electromyographic and neurographic findings, and pathological changes as demonstrated by examination of biopsy specimens of muscle and sural nerve indicate that most patients had an axonal sensorimotor polyneuropathy with more pronounced involvement of the distal portion of the nerves. Results obtained in one patient raised the question of an anterior horn cell disorder.

Functional topography of band 3: specific structural alteration linked to functional aberrations in human erythrocytes.

Band 3 is the major anion transport polypeptide of erythrocytes. It appears to be the binding site of several glycolytic enzymes. Structurally, band 3 is the major protein spanning the erythrocyte membrane and connects the plasma membrane to band 2.1, which binds to the cytoskeleton. In the present study, we report an alteration of band 3 molecule that is associated with the following changes: erythrocyte shape change from discoid to "thorny cells" (acanthocytes), restriction of rotational diffusion of band 3 in the membrane, increase in anion transport, and decrease in the number of high-affinity ankyrin-binding sites. Changes in erythrocyte IgG binding, glyceraldehyde-3-phosphate dehydrogenase, fluorescence polarization (indicative of membrane fluidity), and other membrane proteins as determined by polyacrylamide gel electrophoresis were not detected. Cells containing the altered band 3 polypeptide were obtained from individuals with abnormal erythrocyte morphology. Two-dimensional peptide maps revealed differences in the Mr 17,000 anion transport segment of band 3 consistent with additions of tyrosines or tyrosine-containing peptides. The data suggest that (i) this alteration of band 3 does not result in accelerated aging as does cleavage and (ii) structural changes in the anion transport region result in alterations in anion transport.

Erythrocyte lipid alterations in pediatric cholestatic liver disease: spur cell anemia of infancy.

Spur cell anemia of liver disease is a hemolytic process characterized by spiculated erythrocytes and an elevated red cell membrane cholesterol/phospholipid (C/PL) molar ratio. This form of anemia is associated almost exclusively with adults in the advanced stages of alcoholic cirrhosis. We were therefore surprised to identify two unrelated infants with cholestatic liver disease and hemolytic anemia who had spiculated erythrocytes as the major abnormal cell form on peripheral smear. Erythrocyte membrane cholesterol and phospholipid determinations from these patients were compared with six infants with extrahepatic biliary atresia and target-shaped erythrocytes and with five normal adults. Erythrocyte C/PL molar ratio distinguished target cells from normal erythrocytes (p less than 0.01). The spur cell patients' erythrocyte C/PL molar ratios were clearly greater than either target cell patients or normal controls (1.30 vs. 1.02 vs. 0.84). Both patients' spur cell anemia resolved and target cells became the major abnormal erythrocyte form. These studies identify a transient form of spur cell anemia associated with infantile cholestatic liver disease. The factors leading to the formation of spur cell anemia in infancy require further investigation.

Lipid fluidity of the individual hemileaflets of human erythrocyte membranes.

The impermeant fluorescent probes (MIMAR reagents) described here permit the assessment of the lipid fluidity of individual membrane hemileaflets. They should also prove useful for examining the outer hemileaflets of the plasma membranes of intact cells. The observations, thus far, that normal human erythrocyte membranes have a characteristic asymmetry of fluidity, with the outer leaflet more fluid, correspond to prior findings with Mycoplasma, Newcastle Disease viral envelopes, and mouse LM cells. Hence, it is possible that the pattern is quite general in biological membranes. The particular lipid and protein components of the human-erythrocyte membrane that underly the fluidity asymmetry are unknown. The increased content of phosphatidylcholine in the outer leaflet and of the anionic phospholipids in the inner leaflet would be consonant with the fluidity difference. On the other hand, sphingomyelin, which tends to decrease fluidity, is localized mainly in the outer leaflet. Unknown at present is whether the cholesterol content of the two leaflets differs. From the results reported above, it is tempting to speculate that exogenously added cholesterol tends to localize in the outer leaflet, normally the more fluid leaflet, whereas endogenous cholesterol is more readily removed from the inner leaflet. This suggests, but clearly does not establish, that in the normal erythrocyte the cholesterol content of the inner leaflet exceeds that of the outer. Lastly, integral membrane proteins are expected to decrease lipid fluidity, and the usual pattern seen on freeze-fracture of large numbers of intra-membranous particles on the cytoplasmic face may signify a greater influence of protein in the inner leaflet. The hypothesis that perturbations of the fluidity of a given hemileaflet influence the membrane proteins (and their associated functions) in that leaflet is well-supported by the evidence described above. On the other hand, we understand less well the mechanisms by which lipid fluidity influences the proteins. For example, the decrease in sulfhydryl group reactivity of spectrin, actin, and Band 3 owing to cholesterol depletion (Table 7) may be due to a physical displacement of these proteins, as suggested by Borochov and Shinitzky. Why then does the reactivity of glyceraldehyde-phosphate dehydrogenase sulfhydryl groups increase under these conditions? There remains much to learn about membrane molecular mechanics and lipid-protein interactions. In such studies the impermeant MIMAR probes described here should prove useful.

Production of epidermal acantholysis in normal human skin in vitro by the IgG fraction from pemphigus serum.

Normal human skin was maintained in organ cultures for several days in Ham's F-10 medium with good preservation of the epidermal cells. When the partially purified IgG fraction from the pooled sera of patients with pemphigus vulgaris or pemphigus foliaceous was added to this culture system, after 24 hr some evidence of epidermal acantholysis was seen. By 72 hr, extensive suprabasilar epidermal acantholysis had occurred in which the acantholytic cells were indistinguishable histologically from the acantholytic cells in biopsies from skin lesions of patients with pemphigus vulgaris. In the control cultures (i.e., F-10 medium or F-10 medium + normal human serum IgG), none of these changes was seen. Direct immunofluorescent staining of these explants using fluorescein-labeled goat antihuman IgG showed that by 6 hr binding of the pemphigus IgG had occurred in the intercellular cement substance of the epidermis. The staining intensity was maximal by 18 to 20 hr. When the pemphigus serum was fractionated by DEAE-cellulose column chromatography, three major IgG-containing peaks (presumably IgG) were eluted which bound to the epidermoid intercellular substance and caused acantholysis in culture. The complement system did not play a role in the antibody-induced acantholysis since complement was not included in this system and heating the reconstituted F-10 + pemphigus IgG for 1 hr at 58 degrees C did not destroy the acantholytic activity. Autoradiographic experiments showed that after about 2 days in culture the rates of incorporation of RNA and protein precursors in the suprabasilar cells in the presence of pemphigus IgG were reduced to less than 10% of the normal IgG controls, whereas these synthetic activities of the basal cells were only slightly affected. These observations lead to the proposal that it is the interaction of the pemphigus autoantibody(s) with the suprabasilar epidermal cell which initiates and possibly substains the process(es) of acantholysis.