Chicken anemia virus

Chicken anemia virus is commonly found in commercially produced chickens and has a worldwide distribution. It is difficult to inactivate thermally or with common disinfectants, which limits the utility of normal sanitization practices. The virus is important because of the disease it produces following transovarian transmission and because of its potential for inducing immunosuppression alone or in combination with other infectious agents. Control measures are directed at limiting vertical transmission and preventing coinfections with other lymphocidal agents.     

Sickle cell anemia

Sickle cell disease is a hereditary chronic hemolytic anaemia mostly found in negroes. The blood of these patients contains hemoglobin S. Absence of oxygen determines the sickling to the red blood cells. In the heterozygous state clinical manifestations usually are absent. The homozygous form shows different symptoms. The progressive course with hemolytic, aplastic or thrombotic crises mostly ends in an early death in infancy or childhood. Treatment is largely palliative. Transfusions, treatment of the crises and general measures play the most essential role.     

Pernicious anemia in childhood

Two children from different families with pernicious anemia are described. The defect appears to be the lack of intrinsic factor in the acid gastric juice. The correct diagnosis and proper therapy are essential for insuring a normal growth and development. Studies performed in other members of both families failed to reveal any hematologic disorder. The prolonged and close follow-up of the first case enabled the authors to assist in the birth of a normal offspring.     

Megaloblastic anemia in pregnancy

Megaloblastic anemia is one of the acquired nutritional anemias that may complicate pregnancy. It is most often secondary to folic acid deficiency because folate requirements are increased during gestation. When the diagnosis of megaloblastic anemia is confirmed, appropriate therapy will initiate a rapid reversal of the anemia process. Because of the association between neural tube defects and folate deficiency, it is recommended that women of reproductive age take folic acid supplementation.     

Sulindac-induced immune hemolytic anemia

BACKGROUND: Sulindac, a nonsteroidal, anti-inflammatory, indene-derived drug, caused life-threatening immune hemolytic anemia in an individual with back pain. CASE REPORT: A patient was admitted to the hospital with immune hemolytic anemia and kidney and liver failure after several days ingestion of sulindac. The direct antiglobulin test was positive with polyspecific and monospecific anti-IgG but not with anti-C3. The eluate did not react in routine tests but reacted strongly after the addition of sulindac. The serum contained a sulindac-dependent antibody reacting to a titer of 32. The sulindac-dependent antibody was of both IgG and IgM classes and had no apparent blood group specificity. The antibody agglutinated red cells from humans and chimpanzees but not from chickens, rabbits, or sheep, which implied that a specific component on human and chimpanzee red cells was needed for reactivity. The antibody reacted with red cells treated with trypsin, papain, pronase, dithiothreitol, and sialidase. With aggressive medical care, the patient's condition improved. CONCLUSION: These findings appear compatible with the so-called immune complex mechanism for drug-induced immune hemolytic anemia. Physicians are alerted to the severe nature of this syndrome.     

Refractory anemia with severe dysplasia: clinical significance of morphological features in refractory anemia

Refractory anemia (RA) in myelodysplastic syndromes (MDS) are very heterogeneous diseases regarding their morphology, clinical features and survival. We proposed the new designations 'RA with severe dysplasia (RASD)' and 'RA with minimal dysplasia (RAminiD)'. In our criteria, RASD is considered present if a bone marrow (BM) examination shows Pseudo-Pelger-Huet anomalies of mature neutrophils > or =3% and/or micromegakaryocytes (mMgk) of megakaryocytes > or =10% in RA patients. RAminiD is defined as RA cases other than RASD. After the reclassification of 58 primary RA patients, the group was composed of 45 RAminiD and 13 RASD patients. The blast percentage in the BM and the frequency of cytogenetic abnormalities observed in the RASD patients were intermediate between those in the RAminiD and RAEB patients. The analysis of survival curves revealed differences among the three groups; the RASD patients had lower survival probabilities than those of the RAminiD group, and significantly higher probabilities than those of the RAEB group. (RAminiD vs RASD, P=0.06; RASD vs RAEB, P=0.004.) Our data indicate that in RA patients, RASD is a distinct subset of RA with an unfavorable clinical outcome.