Anemia normochromic

Blood count abnormalities (e.g., normocytic, normochromic anemia, relative lymphocytosis, neutrophilia, eosinophilia)... 

RH is a 7-year-old girl who presents to her pediatrician with a 1 -week history of runny nose and fever. Her mom has noted a lot of bruising on her lower exytremities. Physical examination reveals splenomegaly, multiple petechiae, and pallor. A complete blood count reveals a normochromic, normocytic anemia with a hemoglobin of 6 g/dL (60 g/L,... 

The anemia is usually normochromic and normocytic. Approximately 50% of children present with platelet counts of less than 50 x 1 03/pL (50 x 1 09/L). The WBC count may be normal, decreased, or high. About 20% of patients have WBC counts over 1 00 x 1 03/pL (100 x 109/L), which places them at risk for leukostasis. 

The major clinical features of hemolysis include anemia, jaundice, splenomegaly, and cholelithiasis. Anemia is normochromic in most cases. Macrocytosis and polychromatophilia are seen in patients with marked reticulocytosis. Red... 

Laboratory abnormalities that may be seen include normocytic, normochromic anemia thrombocytosis or thrombocytopenia leukopenia elevated erythrocyte sedimentation rate and C-reactive protein positive... 

Hemolytic anemias tend to be normocytic and normochromic and to have increased levels of reticulocytes, lactic dehydrogenase, and indirect bilirubin. 

The patient s white blood cell count may be normal or only slightly elevated. Nonspecific findings include anemia (normocytic, normochromic), thrombocytopenia, an elevated erythrocyte sedimentation rate or C-reactive protein, and altered urinary analysis (proteinuria/microscopic hematuria). 

The diagnosis (definite or possible endocarditis) according to the 1992 Duke s criteria (see Mandell et al., 2000) is based on blood cultures and echocardiography, the patient s history and findings upon physical examination. This diagnosis should always be considered in patients presenting with fever of unknown origin, especially when they also have a heart murmur and/or normocytic, normochromic anemia. 

Normochromic normocytic anemia is the most common hematological side effect of amphotericin B administration thrombocytopenia and leukopenia are much less common. Infusion of the drug into a peripheral vein usually causes phlebitis or thrombophlebitis. Nausea, vomiting, and anorexia are a persistent problem for some patients. 

L A. Nephrotoxicity is the most common and most serious toxicity associated with amphotericin B administration. This is manifested by azotemia (elevated serum blood urea nitrogen and creatinine), and by renal tubular acidosis, which results in the wasting of potassium and magnesium in the urine (leading to hypokalemia and hypomagnesemia, requiring oral or intravenous replacement therapy). Normochromic normocytic anemia is also seen with long-term amphotericin B administration. Elevation of hver enzymes is not associated with the use of amphotericin B. 

The anemia of hyperthyroidism is usually normochromic and caused by increased red blood cell turnover. The anemia of hypothyroidism may be normochromic, hyperchromic, or hypochromic and may be due to decreased production rate, decreased iron absorption, decreased folic acid absorption, or to autoimmune pernicious anemia. LDH, lactic dehydrogenase AST, aspartate aminotransferase. 

Leuprolide acetate has been reported to cause normochromic normocytic anemia in patients with benign prostatic hyperplasia (37). The anemia is usually transient, and the hemoglobin returns to baseline 6 months after stopping androgen suppression. There is a single case report of more serious red cell aplasia in a patient receiving gonadorelin, with resolution after treatment was withdrawn (38). 

Amphotericin B is the only polyene antibiotic given parenterally. When the intravenous route is contemplated, amphotericin B is dispersed fresh, as discussed, and infused slowly. Amphotericin B should not be administered rapidly because this causes cardiac toxicity. Heparin (1000 units) is often added to the infusion suspension to avert the risk of thrombophlebitis. Amphotericin B can also precipitate normocytic or normochromic anemia, leukopenia, and thrombocytopenia. 

A normochromic, normocytic, usually mild anemia develops regularly during therapy with DAMB. The erythropoietin response to anemia appears to be blunted during DAMB therapy, and survival of erythrocytes may be reduced by toxic effects of amphotericin on the cell membrane (86). 

Enalapril-induced anemia has been reported in hemodialysis patients and in kidney transplant recipients. The anemia is usually normocytic, normochromic, and non-regenerative. Deficient bone-marrow eiythropoiesis has occasionally been described. The anemia is reversible after withdrawal. Although the hypothesized mechanism of a reduction in erythropoietin blood concentrations by enalapril is controversial, in a prospective controlled study enalapril increased recombinant human erythropoietin requirements to maintain hemoglobin concentrations (5). 

A 62-year-old woman with rheumatoid arthritis developed swelling and pain of both knees. Aurothiomalate was given in a test dose of 12.5 mg, followed the next day by a dose of 25 mg, and then 50 mg twice weekly (total cumulative dose 137.5 mg). She had a leukocjde count of 2.2 X 10 /1, a normochromic anemia, and a normal platelet count. Her hver enzyme activities were raised. Aurothiomalate was withdrawn and about 6 weeks later her liver function tests returned to normal and her white cell count rose to 6.9 x 10 /1. 

Dose-dependent and reversible normochromic normo-cjrtic anemia was consistently noted within several days after starting interleukin-6, and required blood transfusion at the highest dose (3). Hemodilution was considered as the primary mechanism. 

The adverse effects of mycophenolate mofetil in children have been reviewed retrospectively in 24 renal transplant patients (mean age 14 years) switched from azathioprine to mycophenolate mofetil a mean of 4.8 years after transplantation (42). The mean dose of mycophenolate mofetil was 560 mg/m. After a mean of 9.6 months, 13 had to discontinue treatment because of adverse effects, namely severe and partially reversible anemia (10 patients, of whom three required transfusions), neutropenia n — 1), and diarrhea n — 2). The anemia was normocytic and normochromic in nine patients, and such a high incidence of severe anemia was unexpected from the available adult data. Although patients who discontinued treatment had a lower pretreatment-calculated creatinine clearance, this was not significant and probably not the major cause of anemia. The author speculated that the anemia resulted from a disproportionately high unbound plasma concentration of mycophenolate mofetil, due to reduced protein binding and impaired renal clearance. 

A 31-year-old woman developed diffuse musculoskeletal pain. She had been taking calcium and dihydrota-chysterol up to 4 mg/day for 6 months for hypoparathyroidism after subtotal thyroid resection. She had severe hypercalcemia (4.1 mmol/1), no detectable intact parathyroid hormone, renal insufficiency (serum creatinine 486 pmol/l), and a normochromic anemia (6.6 g/dl). Rehydration and forced diuresis initially improved renal function and reduced the serum calcium concentration, but the calcium concentration after 4 weeks was still 3.0 mmol/1 and it did not normalize until she was given a single intravenous dose of pamidronate 15 mg. 

Anemia has been noted in pahents with Balkan nephropathy in early studies [18] and described as normocyhc and normochromic or mildly hypochromic [88]. It has been suggested that anemia occurs earlier in the course of the disease progression than is the case in other renal diseases and that it precedes azotemia [88, 106]. However, recent studies have failed to substanh-ate this claim [98,107]. Also, there is no evidence that anemia in Balkan nephropathy differs from anemia accompanying other renal diseases in either features [107] or rate of deteiiorahon in the progression of renal failure [108]. Nevertheless, anemia in Balkan nephropathy patients treated with hemodialysis is more severe than in patients with other renal diseases [108]. 

The deficiency syndrome is characterized by sore throat, hyperemia, edema of the pharyngeal and oral mucous membranes, cheilosis, angular stomatitis, glossitis (magenta tongue), seborrheic dermatitis, and normochromic, normocytic anemia associated with pure red blood cell aplasia of the bone marrow. However, some of these symptoms, such as glossitis and dermatitis, when encountered in the field may have resulted firom other complicating deficiencies. 

Suboptimal erythropoiesis can be classified by changes in the size of RBCs noted on examination of the peripheral blood. Because the excretory and endocrine functions of the kidney usually mirror each other, renal dysfunction can lead to anemia by reduction in EPO production, resulting in a normochromic, normocytic pattern. Other causes of insufficient erythropoiesis include replacement of bone marrow by fibrosis, solid tumors, or leukemia, as well as defects in erythroid maturation. Relative deficiencies in the cofactors required for heme-RBC synthesis such as iron, folate, and vitamin B may also be important contributors. Structurally, RBC macrocytosis denotes defects in the maturation of the nucleus, whereas microcytosis is indicative of cytoplasmic defects (reduced hemoglobin synthesis). (A detailed description regarding the pathogenesis and treatment of anemic disorders is found in Chap. 99.)... 

Hemolytic anemia results in decreased survival time of RBCs secondary to destruction in the spleen or circulation. Hemolytic anemias are normocytic and normochromic, with increased levels of reticulocytes, lactate dehydrogenase, and indirect bilirubin. Treatment is directed towards correcting or controlling the underlying pathology. 

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