Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year-old postpartum woman was admitted to our hospital because of progressive anemia, malaise, night sweating, headache and low grade fever which began 9 days after delivery (day 0). She had normocytic hypochromic anemia accompanied with marked decrease in reticulocytes. In addition, a temporary decrease in platelets and white blood cells especially neutrophils were observed. Bone marrow smears showed an apparent decrease in erythroid cells and the presence of giant proerythroblasts (1.2%) as well as hemophagocytes (1.2%). IgM and IgG antibody against human parvovirus B19 (HPV) was detected on day 22 of the disease although negative results were obtained on day 3. The presence of the virus in the blood on admission was confirmed by dot-blot analysis. Thus, this case was diagnosed as acute pure red cell aplasia and hemophagocytic syndrome caused by HPV infection. This patient had been given iron for iron deficiency anemia before delivery and the iron deficiency was still present after the episode of the present disease although the iron metabolism data was perturbed during the disease. These findings suggest that HPV could cause acute pure red cell aplasia not only in patients with hemolytic anemia but also in patients with iron deficiency anemia or after acute bleeding. Furthermore it is suggested that pancytopenia often observed on HPV infection could be at least partly caused by hemophagocytic syndrome.
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PMID:[Postpartum parvovirus B19-associated acute pure red cell aplasia and hemophagocytic syndrome]. 756 95

Human parvovirus B19 (HPVB19) infects and replicates in erythroid progenitor cells. Its specific cytotoxic effect on these cells results in aplastic crises in patients with congenital hemolytic anemias. Aplastic crisis due to HPVB19 infection in a healthy girl revealed occult iron deficiency anemia. The condition is characterized by a high serum iron level in the aplastic phase and rapid recovery after administration of iron. Temporary HPVB19-induced red blood cell aplasia could occur in patients with other anemias, particularly those with non-inherited form of hemolysis.
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PMID:Human parvovirus B19-induced aplastic crisis in iron deficiency anemia. 794 15

A 38-year-old female was referred to Takaoka City Hospital for treatment of common-cold-like symptom and an episode of transient unconsciousness. Physical examination on admission revealed severe anemia and an ejection heart murmur. Complete blood count revealed microcytic hypochromic anemia (Hb 4.1 g/dl), leukocytopenia (2.600/microliters), thrombocytopenia (7.1 x 10(4)/microliters) and reticulocytopenia (17,000/microliters). The bone marrow cellularity was within normal limits. Cells in the erythroid series were decreased to 5% of total bone marrow nucleated cells with maturation arrest at the level of proerythroblasts. Giant proerythroblasts were observed in 0.2% of marrow nucleated cells. No stainable iron was seen. Both anti-parvovirus B19 IgM antibody and IgG antibody were positive in the serum and parvovirus B19 DNA was detected in the bone marrow cells by polymerase chain reaction. From these results, iron deficiency anemia complicated with pure red cell aplasia secondary to parvovirus B19-induced infection was diagnosed. The anemia gradually improved with administration of sodium ferrous citrate one month after admission. Parvovirus B19 has been reported to cause an aplastic crisis in the patients who has a rapid red cell turn over such as hemolytic anemia or acute blood loss. This report suggested that severe aplastic crisis is also induced in patients with iron deficiency anemia by parvovirus B19-induced infection and warns that careful observation is necessary for the follow up of patients with iron deficiency anemia.
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PMID:[Parvovirus B19-induced aplastic crisis in a patient with iron deficiency anemia]. 806 19

A 35-year-old female was referred to our hospital for fever and anemia. Physical examination was unremarkable. Complete blood count revealed microcytic hypochromic anemia and reticulocytopenia. The bone marrow cellularity was normal. Some giant pronormoblasts were seen but other erythroid cells were absent. No stainable iron was seen. Parvovirus B19 (PVB19) DNA was detectable by polymerase chain reaction. Anti-PVB19 IgM-antibody was also positive in the serum on admission. Antibodies against rubella, measles, mumps, EB virus and HBs were negative and HBs antigen was also negative. Thus the diagnosis of iron deficiency anemia complicated with pure red cell aplasia secondary to PVB19 infection was made. The PVB19 DNA was still positive on days 6 and 11, suggesting that PVB19 virus persists as long as 3 weeks after the onset of PVB19 infection. However, the erythroid cells had recovered by day 6 after admission suggesting that the development of IgM antibody successfully protected the erythroid cells from infection by the residual PVB19. Hence, careful observation for PVB19 DNA and the antibody may be necessary if immunodeficient patients developed anemia of unknown etiology.
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PMID:[Transient pure red cell aplasia in an adult with acute parvovirus B19 infection: observation of PVB19 DNA by polymerase chain reaction, viral antibody and erythroid cells in the bone marrow]. 851 Mar 37

Anemia in children after renal transplantation is more common than previously appreciated. Multiple factors appear to play roles in the development of post-transplant anemia, the most common of which is absolute and/or functional iron deficiency anemia. Most experts recommend that iron limited anemias in transplant patients should be diagnosed using the same criteria as for chronic renal failure patients. Serum erythropoietin (EPO) levels are expected to normalize after a successful renal transplantation with a normal kidney function, yet both EPO deficiency and resistance have been reported. While no large controlled trials comparing the effect of different immunosuppressive agents on erythropoiesis after transplantation have been performed, generalized bone marrow suppression attributable to azathioprine (AZA), mycophenolate mofetil (MMF), tacrolimus, antithymocyte preparations has been reported. Pure red cell aplasia (PRCA) occurs rarely after transplantation and is characterized by the selective suppression of erythroid cells in the bone marrow. PRCA has been reported with the use of AZA, MMF, tacrolimus, angiotensin converting enzyme inhibitors (ACEI), but not with cyclosporine (CSA) use. Post-transplant hemolytic uremic syndrome has been reported with orthoclone anti T-cell antibody (OKT3), CSA and tacrolimus therapy. Viral infections including cytomegalovirus, Epstein-Barr virus and human parvovirus B19 have been reported to cause generalized marrow suppression. Management of severe anemia associated with immunosuppressive drugs generally requires lowering the dose, drug substitution or, when possible, discontinuation of the drug. Because this topic has been incompletely studied, our recommendation as to the best immunosuppressive protocol after renal transplantation remains largely dependent on the clinical response of the individual patient.
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PMID:Anemia in children after transplantation: etiology and the effect of immunosuppressive therapy on erythropoiesis. 1289 2

Although most persons with parvovirus B19 infection are asymptomatic or have mild, nonspecific, cold-like symptoms, several clinical conditions have been linked to the virus. Parvovirus B19 usually infects children and causes the classic "slapped-cheek" rash of erythema infectiosum (fifth disease). The virus is highly infectious and spreads mainly through respiratory droplets. By the time the rash appears, the virus is no longer infectious. The virus also may cause acute or persistent arthropathy and papular, purpuric eruptions on the hands and feet ("gloves and socks" syndrome) in adults. Parvovirus B19 infection can trigger an acute cessation of red blood cell production, causing transient aplastic crisis, chronic red cell aplasia, hydrops fetalis, or congenital anemia. This is even more likely in patients with illnesses that have already shortened the lifespan of erythrocytes (e.g., iron deficiency anemia, human immunodeficiency virus, sickle cell disease, thalassemia, spherocytosis). A clinical diagnosis can be made without laboratory confirmation if erythema infectiosum is present. If laboratory confirmation is needed, serum immunoglobulin M testing is recommended for immunocompetent patients; viral DNA testing is recommended for patients in aplastic crisis and for those who are immunocompromised. Treatment is usually supportive, although some patients may require transfusions or intravenous immune globulin therapy. Most patients recover completely.
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PMID:Clinical presentations of parvovirus B19 infection. 1730 69

We describe a young woman with profound anemia whose serum iron studies were incongruous with what we expected from iron deficiency anemia. Her high serum iron was not fully explainable until we examined the patient and noticed a large black tattoo on her left flank area. Apparently iron oxide in the ink used for the tattoo was absorbed transcutaneously and led to high serum iron in the face of the other data, which suggested iron deficiency. She was slow in mobilizing her serum iron for erythropoiesis and we discovered that there was a concurrent acute B19 parvovirus infection, which impeded utilization of the iron for red blood cell production. We believe that this case report reinforces the imperative to always do a careful physical examination with any patient who has anemia, and also illustrates the potential toxicity of tattoo ink. The impairment of utilization of the serum iron because of the patient's acute B19 parvovirus infection demonstrates the many consequences of infection induced aplastic anemia.
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PMID:The girl with the iron tattoo. 2307 30