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

The dramatic advances that have taken place in recent years in the care of sick and premature infants also have been matched by a similar increase in the use of blood transfusion therapy. Haematological features indicate that a newborn has a blood volume of 85-125 ml/kg the foetal haemoglobin is 60-85% and average Hb in full term infant is 18 gm/dl. By 2-3 months it falls to 11-12 g/dl the main cause of anemia are iron poor diet, weaning diets recurrent or chronic infections and hemolytic episodes in malarious areas. The red cells transfusions are usually top up transfusions, exchange transfusions, partial exchange transfusions. Top up- are for investigational losses and correction of mild degrees of anemias, upto to 5-15 ml/kg. They comprise 90% of all neonatal transfusions and are used in low birth babies in special care units for a maximum of 9-10 episodes. The walk in donor programs once popular are not much in vogue. The threshold for transfusion is 8-10 g/dl Hb for upto 5 weeks. Exchange transfusions are done for correction of anemia, removal of bilirubin, removal of antibodies and replacement of red cells. Ideally plasma reduced red cells that are not older than 5 days are used. It is prepared by removal of 120 ml of standard whole blood donation. The advantage of fresh cells is that hyperkalemia is avoided and good post transfusion survival acceptable red cell oxygen affinity. However it has to be screened for sickle cell disease and G6PD deficiency. Indications for exchange transfusion are kernicterus, neonatal hemolysis, G6PD deficiency, ARDS, neonatal sepsis, DIC and neonatal isoimmune thrombocytopaenia. Complications include over transfusion, perforation of major vessels, hypocalcaemia, citrate toxicity, hypothermia, hypoglycaemia, thrombocytopenia, necrotizing enterocolitis, GVHD, bacterial, viral infections. Partial exchange transfusions are done for symptomatic anemia, where Hb<10 g/dl, it is indicated in polycythemia and hyperviscosity syndromes. Exchange volume = Blood volume x (observed Hct-Desired HCt) divided observed Hct. Points to consider-there is weak expression of ABO antigens so particular care while grouping. Transfusing volumes should be 2-5 ml/kg/hour in paediatric bags of 50-100 ml with infusion devices. Platelet transfusion are indicated in neonatal throbocytopaenia, thrombocytopaenia due to sepsis, DIC, bacterial pathogens, CMV, TORCHS, Obstetric conditions such as pre eclampsia, intrauterine death abruption placenta birth injury hypoxia schock neonatal iso immune thrombocytopaenia and maternal ITP. Administration 1 RDE/pack per 2.5 kg single dose of fresh platelets less than 24hrs which contains 55 x 10(9) cells. This also contributes fresh plasma so is useful for coagulation defects also, though there is a risk of CMV and GVHD due to leucocyte contamination. Granulocyte concentrate; Gravity leucopheresis-1:8 ratio of 60 ml of 6% HES made to stand for 1hr.
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PMID:Component therapy. 1451 88

Hemolysis after renal transplantation in some cases is clearly related to hemolytic-uremic syndrome (HUS) and usually attributed to cyclosporine (CsA) treatment. Acute hemolysis in other recipients is related to anti-erythrocyte autoantibodies. In most cases these patients have received ABO-compatible, although ABO-nonidentical, organs, mostly from O blood group donors. We report three cases of autoimmune hemolytic anemia after renal transplantation. Two patients (patients: 1 and 2; ABO-compatible, but nonidentical kidneys) suffered acute hemolysis in the third week after transplantation. One patient (patient 3: ABO-identical kidney) suffered a chronic, subclinical course of disease beginning 5 months after transplantation. The clinical picture of this disease was completely different from HUS. The existence of severe anemia (patients 1 and 2), hyperbilirubinemia (particularly high in patient 3), increased serum lactic dehydrogenase levels, and decreased serum haptoglobin in the presence of good graft function suggested an hemolytic anemia. In all patients the direct antiglobulin test was positive. The acute or chronic symptoms of hemolysis disappeared, at 2 and 5 weeks, respectively, after conversion from CsA to tacrolimus. Hemolysis in these patients probably relates to alloantibodies derived from passenger B lymphocytes transplanted with the organs. Because hemolysis has been most frequently related to CsA therapy, it is suggested that B lymphocytes proliferated and produced antibodies because CsA effects to inhibit T-cell function generally spares B-cell activity. It is proposed that a subtype of B cells, which are resistant to CsA, produces anti-A and/or anti-B antibodies. Treatment with tacrolimus appears to be successful, probably due to its alternate, and likely more effective, manner of B-cell suppression.
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PMID:Hemolytic anemia after renal transplantation: analysis of case reports. 1452 99

The differential diagnosis of anemia must consider immune hemolytic anemias as a frequent cause. Whereas detection of anti-red blood cell (RBC) alloantibodies frequently induced by immunogenic stimuli (transfusion, pregnancy) is performed by routine serology, diagnosing autoimmune hemolytic anemias or drug-induced hemolytic anemias remains a challenge, usually requiring close collaboration of a number of disciplines. Positive direct antiglobulin test (Coombs' test) represents a central criterion in diagnosing immune hemolytic anemias, leading to further detailed analyses. The most-severe type of immune-mediated hemolysis is acute intravascular hemolysis after ABO incompatible RBC transfusion. This review highlights underlying biochemical aspects, immunohematological diagnostics, and the clinical relevance of RBC allo- and autoantibodies, including paroxysmal nocturnal hemoglobinemia and drug-induced hemolysis. Finally, current and partly experimental therapeutic strategies of immune hemolytic anemias are summarized.
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PMID:Immune hemolysis-serological and clinical aspects. 1459 82

We report the case of an ABO-incompatible kidney transplant recipient who died suddenly following a good transplant course of 12 years. For 10 years after transplantation, the graft function had been stable (s-Cr: 1.0-1.5 mg/dL), although chronic hepatitis C had developed, with elevation of transaminase. In the 11th year, he was admitted into the hospital with low-grade fever and general fatigue. Jaundice and anaemia progressed, and he died 2 months after admission. The autopsy diagnosis was: (1) post-renal transplantation state, (2) phlegmonous enterocolitis with septic infarction, (3) cellulitis and necrotic myositis, and (4) sepsis. The transplanted kidney graft showed well-preserved glomeruli and tubules, corresponding to chronic allograft nephropathy (CAN) grade Iota (ci1, ct1, cv1), according to the Banff classification. The pathological changes observed in this long-surviving ABO-incompatible kidney graft were similar to those of an ABO-compatible graft, although its degree was milder.
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PMID:An autopsy case of bacterial septic shock 12 years following ABO-incompatible renal transplantation. 1519 73

We report the case of a 62-year-old woman who developed an autoanti-D after cladribine treatment. In May 2000, the patient underwent splenectomy for a stage IV-B lymphoplasmocytic lymphoma. She was transfused with ABO- and Rh(D)-matched blood. A month later, she received chemotherapy with cladribine. In February 2001, blood grouping showed her to be AB, D+ and the direct antiglobulin test was positive for IgG. An autoanti-D was identified in the eluate. Genotypic analysis confirmed the Rh phenotype of the patient as ccDEe. No hemolysis was evident, as judged by the absence of anemia, a bilirubin of 15.7 micromol/L, and lactic dehydrogenase of 412 IU/L. When an anti-D is identified in a D+ blood recipient, a passive transfer of anti-D, and an alloimmunization in a recipient with a weak D phenotype, should be ruled out. Finally, as in our case, an autoantibody is an additional possibility.
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PMID:Autoanti-D in a patient after cladribine treatment for lymphoplasmocytic lymphoma. 1537 70

To evaluate the dynamic changes of erythropoietin (EPO) and its significance following ABO-incompatible allogeneic hematopoietic stem cell transplantation (allo-HSCT), sequential changes in serum EPO levels were measured by enzyme linked immunosorbent assay (ELISA) in 11 patients receiving allo-HSCT from ABO-incompatible donors. The results showed that the mean EPO level was markedly elevated and reached to its highest level at 0 day-2 week after allo-HSCT (233.73 +/- 81.95 mU/ml and 226.07 +/- 113.87 mU/ml respectively, P >0.05). Although the EPO levels were significantly lower at 1 month (128.49 +/- 108.92 mU/ml, P <0.05) and after the reversion of blood type (73.07 +/- 68.85 mU/ml, P <0.05), they were still elevated up to 2 months after allo-HSCT. The EPO levels always had significant positive correlation with the RBC transfusions. At 0 day and 4 week after allo-HSCT, the EPO levels had significant negative correlation with the Hb levels; at 6 and 8 week after allo-HSCT, the EPO levels had no relation with the Hb levels, they had significant positive correlation with the time of erythrocyte recovery and anti-A isoagglutinin titers at the same time. It is concluded that serum erythropoietin levels continuously increasing following ABO-incompatible allogeneic allo-HSCT suggest that exogenous recombinant human erythropoietin treatment for anemia may not be beneficial.
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PMID:[Dynamic examination of the serum erythropoietin levels following ABO-incompatible allogeneic hematopoietic stem cell transplantation and its implications]. 1549 30

Effective prenatal care should integrate the best available evidence into a model of shared decision making. Pregnant women should be counseled about the risks of smoking and alcohol and drug use. Structured educational programs to promote breastfeeding are effective. Routine fetal heart auscultation, urinalysis, and assessment of maternal weight, blood pressure, and fundal height generally are recommended, although the evidence for these interventions is variable. Women should be offered ABO and Rh blood typing and screening for anemia during the first prenatal visit. Genetic counseling and testing should be offered to couples with a family history of genetic disorders, a previously affected fetus or child, or a history of recurrent miscarriage. All women should be offered prenatal serum marker screening for neural tube defects and aneuploidy. Women at increased risk for aneuploidy should be offered amniocentesis or chorionic villus sampling. Counseling about the limitations and risks of these tests, as well as their psychologic implications, is necessary. Folic acid supplementation beginning in the preconception period reduces the incidence of neural tube defects. There is limited evidence that routine use of other dietary supplements may improve outcomes for the mother and infant.
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PMID:Evidence-based prenatal care: Part I. General prenatal care and counseling issues. 1583 31

With the shortage of lung donors, we have performed 28 living donor lobar lung transplantations (LDLLTs) since October 1998. Although lungs from ABO-identical donors were used if available, lungs were transplanted from donors showing minor ABO mismatches when suitable ABO-identical donors were not found. The aim of this study was to evaluate the relationship between anti-ABO antibody (Ab) production and the outcomes of lung transplantation with ABO-mismatched living donor lungs. We reviewed 28 patients (28 recipients with 55 donors) who underwent LDLLT between October 1998 and March 2004. In this patient population, 13 patients (46.4%) received minor ABO-mismatched transplants. Anti-A or B-IgG or IgM antibodies (Abs) in the serum and red cell elutes were examined. All 28 patients are alive and well at a mean observation period of 28.0 months (ranging from 5 to 70 months). Anti-A or B-IgG or IgM Abs were detected in 5 out of 13 minor ABO-mismatched patients (38.5%) after transplantation, but only one of them showed evidence of severe hemolytic anemia due to donor-derived antibodies. The titer of that patient's Abs was higher than that of the other recipients. Anti-ABO antibody production and anemia were not associated with gender, age, relationship between donors and recipients, and HLA matching. We conclude that LDLLT across ABO mismatches is an acceptable treatment for end-stage lung disease.
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PMID:Relationship between anti-ABO antibody production and hemolytic anemia after minor ABO-mismatched living-donor lobar lung transplantation. 1584 24

Maternal-fetal ABO incompatibility is a common hematological problem affecting the newborn. In general, hemolysis is minimal and the clinical course is relatively benign, rarely causing the escalating levels of hyperbilirubinemia and significant anemia commonly associated with Rh hemolytic disease of the newborn (HDN). The incidence of HDN ranges from one in 150 births to 1:3000 births, depending on the degree of anemia and level of serum bilirubin. The etiology of ABO hemolytic disease of the newborn (ABO-HDN) is complex because anti-A and anti-B antibodies are composed mainly of IgM. Since only IgG antibodies cross the placenta, those pregnant women with high levels of IgG anti-A,B, anti-A, or anti-B with an ABO incompatible fetus will be the ones to give birth to an infant with ABO-HDN. We describe a case of a B/Rh positive term newborn born to an O/Rh negative African-American mother demonstrating aggressive hemolysis and a robust response of the bone marrow. This case was successfully managed with phototherapy and simple RBC transfusion without the need for exchange transfusion.
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PMID:Severe hemolytic disease of the newborn in a group B African-American infant delivered by a group O mother. 1668 19

While immune hemolysis due to donor isohemagglutinin (IH) production often complicates minor ABO incompatible peripheral blood hematopoietic stem cell transplantation (PBSCT), it is not known if this occurs with umbilical cord blood transplantation (UCBT). We compared IH production and hemolysis following minor ABO allogeneic PBSCT and UCBT. We reviewed 24 ABO minor incompatible allogeneic PBSCTs and 14 ABO minor incompatible UCBTs. Patients were evaluated for donor-derived IH by reverse ABO grouping. Evaluation of hemolysis was based on clinical and laboratory findings of anemia associated with increased RBC transfusion need, concomitant with the appearance of donor-derived IH. Of the 24 ABO minor incompatible allogeneic PBSCTs, 15 produced donor-derived IH from 6 to 88 days following transplantation, with seven of 15 patients exhibiting clinically evident hemolysis. There was no significant difference in days to leukocyte engraftment or infused CD34 cells in patients with or without donor-derived IH. None of the 14 patients receiving ABO incompatible UCBTs showed evidence of donor-derived IH following transplantation with a median follow-up of 60 days. We conclude that donor IHs are not produced in patients undergoing minor ABO incompatible UCBTs suggesting fundamental immunologic differences between allogeneic PBSCT and UCBT.
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PMID:Lack of isohemagglutinin production following minor ABO incompatible unrelated HLA mismatched umbilical cord blood transplantation. 1675 85


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