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مواضيع متنوعة أخرى

الانزيمات
Comparison of Etiologies of Anemia in Adults and Children
المؤلف:
Hoffman, R., Benz, E. J., Silberstein, L. E., Heslop, H., Weitz, J., & Salama, M. E.
المصدر:
Hematology : Basic Principles and Practice
الجزء والصفحة:
8th E , P466-468
2026-03-04
29
As already noted, the designation that anemia is present relies on com parison of the patient’s hemoglobin or hematocrit with an age- and sex-appropriate normal range (see Table 1). Although many types of anemia may occur across the age spectrum, certain types tend to be identified more commonly in either adults or children, and some are primarily identified in neonates. In children, the most common causes of anemia are related to nutritional deficiency or to a primary hematologic process, either hereditary or acquired. In contrast, the most common causes of anemia in adults are iron deficiency caused by blood loss or anemia caused by systemic illness, such as renal failure, inflammatory conditions, or malignancy (Table 2).
Table1. Normal Red Blood Cell Values
Table2. Comparison of the More Common Causes of Anemia in Children and Adult
Anemia in Children
Hypoproliferative anemia in children may be associated with either acquired or congenital etiologies. Acquired cases are most commonly caused by nutritional deficiency but also include those caused by acquired aplastic anemia, transient erythroblastopenia of childhood (TEC), the anemia of acute inflammation, and marrow replacement caused by malignancy. Congenital causes include Diamond-Blackfan anemia and other rare syndromes, including refractory sideroblastic anemia and the congenital dyserythropoietic anemias. Iron deficiency may occur in children because of a diet that is rich in cow’s milk to the exclusion of other iron-containing foods. This is particularly common during the first 2 years of life. The anemia may be quite severe and may be associated with a mean corpuscular volume (MCV) of 50 to 65 fL. Acquired aplastic anemia, as opposed to pure RBC aplasia, is associated with bicytopenia or pancytopenia. TEC is an acquired disorder that generally occurs during the first 3 years of life in otherwise healthy children, although it can be seen in children from 6 months to 10 years old. It is thought to have a viral or immunologic cause and resolves without specific intervention. The anemia of acute inflammation may be encountered in children who are hospitalized and is generally transient, resolving when the underlying condition has improved. Leukemia may result in BM replacement and is usually associated with abnormalities in other cell lineages in addition to RBCs.
Hemolytic anemia in children is most commonly associated with inherited disorders of hemoglobin or the RBC membrane. However, acquired causes such as autoimmune hemolytic anemia and micro angiopathic hemolytic anemia, particularly Shiga toxin–associated hemolytic uremic syndrome (HUS), also occur. In older children, many etiologies of hemolytic anemia overlap with those considered in adults, and a similar diagnostic algorithm may be appropriate. However, in newborns, jaundice as an indicator of the inherited causes of hemolytic anemia must be distinguished from more pronounced cases of the physiologic hyperbilirubinemia that occurs during the perinatal period. After true hemolysis has been identified in an infant, the differential diagnosis is relatively limited (Fig. 1). Immune mediated hemolysis may result from ABO, Rh, or minor blood group incompatibility. Other causes include metabolic disorders and dis orders of the RBC membrane, and some forms of α-thalassemia. Of note, however, is the fact that hemoglobinopathies, such as sickle cell disease and β-thalassemia, are silent during the newborn period and only become manifest at 4 to 6 months of age when the fetal-to adult hemoglobin transition has been completed. Newborn screening programs in the United States may provide salient information in this regard on the presence or absence of a hemoglobinopathy. Alternatively, ethnic background and family history may be helpful in suspecting the appropriate diagnosis.
Fig1. APPROACH TO THE DIFFERENTIAL DIAGNOSIS OF ANEMIA IN A NEWBORN. G6PD, Glucose-6-phosphate dehydrogenase; MCV, mean corpuscular volume.
Anemia in Adults
Hypoproliferative anemia in adults is relatively common. If acute blood loss is excluded, hypoproliferative causes are the most common entities associated with anemia in adults. These are iron deficiency, inflammation (anemia of chronic disease), and renal disease (Fig. 2). The megaloblastic anemias that represent maturation abnormalities, including folate and vitamin B12 deficiency, are often categorized along with the hypoproliferative anemias because they present with a low reticulocyte count as well. Myelosuppressive drugs and toxins such as ethanol can also be associated with hypoproliferative anemia. Pure RBC aplasia may be associated with other diseases (thymoma) or viral infection (parvovirus B19) or be idiopathic. Finally, MDS may present with hypoproliferative anemia, as may an infiltrative process such as metastatic malignancies, myelofibrosis, or acute leukemia. The distinction between the various causes of anemia is facilitated by historical factors, physical findings, and concomitant laboratory abnormalities in conjunction with review of the MCV and RBC distribution width (RDW) along with the peripheral blood smear. In the setting of a low reticulocyte count, MCV values below 70 fL are most commonly associated with iron-deficiency anemia, and those above 120 fL are most commonly associated with folate or vitamin B12 deficiency. The differential diagnosis broadens for MCV values that fall just outside of the normal range. For example, in the setting of a low reticulocyte count, MCV values in the range from 75 to 80 fL may be associated with iron-deficiency anemia, the anemia of inflammation, and endocrine causes of anemia. MCV values between 100 and 110 fL may be associated with folate or vitamin B12 deficiency, aplastic anemia, MDS, liver disease, and immune hemolytic anemias.
Fig2. APPROACH TO THE DIFFERENTIAL DIAGNOSES OF ANEMIA IN ADULTS AND CHILDREN. G6PD, Glucose-6-phosphate dehydrogenase; MCV, mean corpuscular volume; PNH, paroxysmal nocturnal hemoglobinuria; RDW, red blood cell distribution width.
Hemolytic anemia in adults is less common than hypoproliferative anemia, and the differential diagnosis is broad. Congenital causes associated with mild to moderate hemolysis may be clinically silent until detected later in life. This is particularly the case for milder cases of β-thalassemia intermedia, sickle cell (SC) disease and sickle-β+-thalassemia, and hereditary spherocytosis. Additionally, the most common RBC enzymopathy (which is also one of the most common human enzyme defect deficiencies), G6PD deficiency, does not present until individuals encounter oxidant stress either because of infection or drugs such as sulfonamides and antimalarials. Acquired hemolytic anemias include autoimmune hemolytic anemia, which is often associated with hematologic malignancies or rheumatologic disorders, and the microangiopathic hemolytic anemias, including disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), and HUS. Distinction of the various causes of hemolytic anemia is also facilitated by the associated historical features, physical findings, and laboratory abnormalities of the clinical presentation. For these disorders, review of the peripheral blood smear may be particularly revealing as to the etiology.
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