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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Marked spiculation of red blood cells was observed in a young dog with severe hepatic disease. The resulting anemia was similar to spur cell anemia associated with hepatocellular disease in man. Though the exact cause of spur cell formation is not known, abnormalities in serum lipids and red cell membrane lipids are likely involved. A peculiar pattern of serum lipoproteins may have been involved in formation of this dog's spur cells.
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PMID:Spur cell anemia in a dog. 72 79

A 29-year-old male who had a 15-year history of alcohol drinking was admitted with a 5-month history of jaundice in July 1989. Laboratory examinations revealed that he had hemolytic anemia and severe liver damage. Erythrocytes of peripheral blood showed typical spiculated cells on light microscopic and scanning electron microscopic studies. Free-cholesterol/phospholipid ratio of the erythrocyte membrane was elevated, and the level of chenodeoxycholic acid increased in serum. The patient was diagnosed as having advanced alcoholic cirrhosis associated with spur cell anemia. Two months after admission, he was complicated with chronic disseminated intravascular coagulopathy (DIC). Anemia, hepatic failure and DIC progressed, and the patient died six months after admission. The mechanism of the formation of spur cells was discussed.
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PMID:[Severe alcoholic cirrhosis associated with spur cell anemia and DIC]. 188 27

Thirteen members of a family carrying a gene for pedigree of hypobetalipoproteinemia were analyzed for lipoprotein compositions, apolipoprotein (apo) B levels, and apo B isoforms. Judging from low density lipoprotein (LDL)-cholesterol (Chol) and apo B levels, a 75-year-old proband, a father who died of unknown fever, thrombopenia, and anemia, and his wife were heterozygous for hypobetalipoproteinemia. The proband had ataxic movement of hands and gait disturbance in later life. Three of four living siblings had extremely low levels of LDL-Chol (6 mg/dL) and LDL-apo B (2 mg/dL), and were postulated to have homozygous hypobetalipoproteinemia. Electrophoresis revealed marked deficiency of apo B-100, although trace amounts were noted in LDL. In contrast, apo B-48 was present in chylomicrons obtained after a fatty meal in the two patients with homozygous hypobetalipoproteinemia, indicating a selective deficiency of apo B-100 but not apo B-48. The defect in these patients seemingly is different from abnormal apo B-37 reported recently for a family with hypobetalipoproteinemia. Clinically, acanthocytotic red blood cells (8% to 12%), fatty liver, and low levels of serum lipid-soluble vitamins A and D were noted in homozygotes. One heterozygous sibling had 26 mg/dL LDL-Chol and 5 mg/dL LDL-apo B levels. All seven subjects in the third generation had low levels of Chol (85 to 140 mg/dL), LDL-Chol (40 to 63 mg/dL) and LDL-apo B (10 to 20 mg/dL). They also showed mild acanthocytosis (0.5% to 2%) and a decrease of fat-soluble vitamins in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Homozygous hypobetalipoproteinemia with spared chylomicron formation. 290 27

We describe a new family with hereditary choreo-acanthocytosis. Two members of this family were affected; neither of them suffered from anaemia or signs of haemolysis. The acanthocytes showed an impaired deformability with an increase in whole blood viscosity. The composition of the plasma and erythrocyte membrane lipids was normal, as was the fatty acid composition of the erythrocyte ghost membranes. The only alteration found was a decrease in the fluidity of the erythrocytic membrane.
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PMID:A new family with hereditary choreo-acanthocytosis. 311 32

Anemia, edema, and length and weight below the 10th tile were the presenting signs in an infant with cystic fibrosis. She had a peripheral blood smear characterized by poikylocytosis, acanthocytosis and anisocytosis; low serum total proteins, albumin, and tocopherol/total lipid ratio. Following two months of treatment with oral pancreatic replacement therapy and tocopherol, her hemoglobin concentration, serum proteins and tocopherol/total lipid ratio returned to normal. The peripheral blood smear showed normal red cell morphology and her length and weight were above the 50th percentile. The mechanisms of anemia in cystic fibrosis patients are discussed.
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PMID:Anemia and edema as presenting signs in cystic fibrosis: case report. 347 59

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.
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PMID:Erythrocyte lipid alterations in pediatric cholestatic liver disease: spur cell anemia of infancy. 403 66

A 38-year-old male chronic alcoholic developed spur-cell anemia during an episode of non-A, non-B hepatitis. Lipid evaluation showed a marked decrease in cholesterol (1.98 mmol/l), in triglycerides (0.41 mmol/l) and in phospholipids (1.38 mmol/l) in total serum as well as in VLDL and LDL. Serum apolipoprotein B was also low. Cholesterol (C) and phospholipid (PH) content of the erythrocytic membrane was increased, as was the intraerythrocytic C/PH ratio. Hemolysis ceased with correction of the hypobetalipoproteinemia. The relationship between acquired acanthocytosis and lipid disorders is discussed.
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PMID:[Reversible acquired acanthocytosis and hemolytic anemia associated with hypobetalipoproteinemia in a chronic alcoholic]. 641 78

The authors report the cases of 3 patients with severe alcoholic cirrhosis and spur cell anemia. The spur cell anemia must be suspected when there is haemolytic anemia, highly macrocytic with normal serum level of cholesterol and without fatty liver. The cytologic confirmation is difficult even with a phase contrast microscope. The evolution did not exceed 7 and 8 months in 2 cases; the third patient is still alive but quite sick after 1.5 year. These data lead us to point out the difficulty of the diagnosis by routine light microscopy and to remind the poor prognosis after the spur cell anemia is discovered, as documented in the literature.
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PMID:[Anemia caused by acanthocytosis in the cirrhotic patient: diagnosis and prognostic significance. 3 cases]. 666 2

The clinical and laboratory findings in eight patients with spur cell anemia are presented and compared with other cases gathered from the literature. Although there is no specific clinical or laboratory abnormality, the condition can be recognized by a constellation of findings. The majority of patients have a long history of ethanol abuse with clinical and laboratory manifestations of hepatocellular dysfunction. All patients have anemia, a reticulocyte count usually greater than 5%, and indirect hyperbilirubinemia. The sine qua non for the diagnosis of spur cell anemia is an increased percentage (usually greater than 20%) of acanthocytes on a peripheral smear. The prognosis of spur cell anemia is poor, the majority of patients dying within a year. From our study, spur cell anemia appears to be more prevalent than is generally reported.
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PMID:Spur cell anemia. 712 89

A retrospective study of red blood cell parameters in 53 dogs with experimental radiation-induced hemangiosarcoma showed 24 had anemia. Morphologic alterations in red blood cells in peripheral blood films from anemic dogs included signs of regeneration (anisocytosis and polychromasia), hypochromasia, red cell fragmentation and acanthocytosis. The degree and type of red cell changes varied from dog to dog and generally correlated with the principal site of tumor involvement. Blood from dogs with tumors principally involving liver had red cell regeneration, fragmentation and acanthocytosis. Blood from dogs with tumors primarily involving the heart had only red cell fragmentation. Blood films from dogs with skeletal and pulmonary hemangiosarcomas were similar to blood films from dogs with hepatic hemangiosarcoma except that red cell alterations generally were less severe. Scanning and transmission electron micrographic evaluation of neoplastic tissue showed large amounts of fibrin within neoplastic vascular sinuses and disruption and distortion of red blood cells traversing these abnormal vascular beds. The red blood cell fragmentation syndrome associated with radiation-induced hemangiosarcomas therefore was considered to be a microangiopathic hemolytic anemia of localized origin.
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PMID:Microangiopathic hemolytic anemia associated with radiation-induced hemangiosarcomas. 718 20


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