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Problems in Family Practice the Common Anemias

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Problems in Family Practice the Common Anemias Problems in Family Practice The Common Anemias Ralph 0. Wallerstein, MD San Francisco, C alifornia Anemia is a common clinical problem requiring precise diagnosis of its Stippled cells are young cells, still con­ underlying etiology in order to provide effective therapy. Most com­ taining RNA like reticulocytes, but the mon anemias are characterized by discrete hematologic patterns. The RNA is denatured and precipitated by most useful laboratory studies in most instances are red cell indices, Wright’s stain, unlike the reticulocytes blood film, reticulocyte count, platelet count, serum iron and total whose RNA is precipitated only by supravital stain. Prominent stippling is iron binding capacity. This paper presents simple guidelines for the seen in lead poisoning or thalassemia rational use of common laboratory tests in the diagnostic assessment minor. Howell-Jolly bodies are nuclear of anem ia. remnants and are characteristic of sple- nectomized patients. Tables 3 and 4 summarize the important elements in Anemia is a common clinical find­ Laboratory Work-up of Anemia the blood films of anemic patients and ing that requires explanation. Before When history and physical examina­ their diagnostic significance. appropriate therapy can begin, its eti­ tion have not explained the anemia, The reticulocyte count is a most ology must be established. In practice the following baseline data should be useful test in the evaluation of anemia, all anemias are due to one, or some­ obtained before ordering other tests: as illustrated in Table 5. A very high times a combination of the following (1) Red cell indices, (2) A look at the reticulocyte count (50 percent or mechanisms: blood film, (3) Reticulocyte count, (4) more) means autoimmune hemolytic 1. Iron deficiency, ie, blood loss Platelet count, and (5) Serum iron and anemia when the Coombs’ test is posi­ 2. Marrow failure total iron binding capacity. tive; on very rare occasions it means a) relative — anemias of chronic Red cell indices (Table 2) are usual­ pyruvate kinase deficiency, a red cell disease ly supplied automatically if a Coulter enzyme defect associated with a nega­ b) absolute — aplastic anemia, S is used. Sometimes they make an im­ tive Coombs’ test. Moderate elevation myelofibrosis, leukemia, lym­ mediate diagnosis. MCV above 120 of the reticulocyte count (ten to 20 phoma, myeloma usually means liver disease or megalo­ percent) usually means hemolysis but c) ineffective erythropoiesis — blastic anemia. MCV above 110 strong­ occasionally indicates other underlying refractory normoblastic ane­ ly argues against anemia of chronic dis­ problems. Acute blood loss can bring mia ease or acute blood loss. MCV below the count this high and patients with 3. Hemolytic anemia 100 is not pernicious anemia, and pernicious anemia or folic acid defi­ 4. Megaloblastic anemia MCV below 80 is either iron deficien­ ciency may have counts at this level or Table 1 gives the approximate fre­ cy or thalassemia minor. MCHC above higher a week after specific therapy quency of anemias in practice. These 36 means hereditary spherocytosis, was started; their counts, however, frequencies change, of course, in a uni­ and MCHC below 32.5 usually means show an orderly rise, peak at one week versity setting and in subspecialty iron deficiency or thalassemia minor. and decline at two weeks, unlike a practice where hemolytic anemias and Inspection of the blood film should hem olytic anemia, whose counts, the anemias of leukemia, lymphoma, include a specific check for hypochro­ while fluctuating, stay high. If the re­ and myeloma are more common. mic microcytes, oval macrocytes, ticulocyte count is under five percent, spherocytes, schistocytes, target cells, the patient probably does not have hypersegmented P.M.N.’s and abnor­ hemolytic anemia. Very low counts, mal white blood cells. Spherocytes especially in absolute terms, are char­ From the Departments of Medicine and indicate hereditary spherocytosis or acteristic of aplastic anemia and perni­ mical P a th o lo g y , U n iv e rs ity o f C a lifo rn ia autoimmune hemolytic anemia. Schis­ cious anemia. ennce, San Francisco General Hospital, San Francisco, C a lifo rn ia . R eq u e sts f o r re p rin ts tocytes (contracted cells, helmet cells, The platelet count is also a useful snould be addressed to Dr. Ralph O. Walier- laboratory test in the initial workup of s'ein, 3838 California Street, Suite 707, San triangular cells) usually suggest damage Francisco, C a lif 94118. to blood vessels by fibrosis or cancer. anemia. (Table 6) A low platelet count THE JOURNAL OF FAM ILY PRACTICE, VOL. 2, NO. 3, 1975 in an anemic patient, who does not caused by iron deficiency, and finding and serum iron may even be mid.,,, have frank thrombocytopenic purpura, a low serum iron but high TIBC means ing. When a patient with p e r n S points to the marrow as the site of dis­ iron deficiency. If the serum iron is anemia is treated with vitamin B ease. In other words, this is not just not low, the patient does not have iron the serum iron plummets to very low iron deficiency or anemia of chronic deficiency; if the serum iron is low and levels and stays low for weeks, even disease, but possible leukemia, aplastic the TIBC is also low, one has learned with ample iron states. anemia, or some other malignancy. nothing because many of the anemias The Schilling test is not w orth do­ Hypersplenism may also present with of chronic disease may have a very low ing in patients with MCV below 100 moderate anemia, platelet count - of serum iron — as low as 10 meg/100 ml or in patients with elevated WBC and 70,000 and white count under 2,000. as seen in hemochromatosis, and often high reticulocyte counts or sphero­ The serum iron and total iron bind­ in megaloblastic anemias. cytes. Vitamin B, 2 level should, 0f ing capacity is worth doing early in the Some hematologic tests are fre­ course, not be done after a Schilling work-up because so many anemias are quently misapplied. The serum iron/ test. The Coombs’ test is usually not TIBC (Table 7) should not be done in worth doing with a normal reticulo­ a patient with fever or infection be­ cyte count. The osmotic fragility is Table 1. Relative Incidence of useful only in the diagnosis of heredi­ Anemia per 1,000 cause it will always be low. It should also not be done in a patient With a tary spherocytosis. It is no longer use­ high reticulocyte count because iron ful in the work-up of patients with Anem ia o f chronic disease 10 deficiency is not the patient’s problem hypochromic anemia. Hemoglobin Iron deficiency 10 Sickle cell anemia 2 Black population Pernicious anemia .4 Table 4. Abnormal Red Cells on the Blood Film Hereditary anemia .2 Leukemia .05 Abnormal Cells Possible Causes M yeloma .03 Aplastic anemia .004 Spherocytes Hereditary spherocytosis Autoimmune hemolytic anemia Acute alcoholism Table 2. Red Cell Indices Hb C disease Burns ABO incompatibility MCV Oval cells Ovalocytosis Above 120 Liver disease Megaloblastic anemia Megaloblastic anemia Myelofibrosis Refractory normoblastic anemia Above 110 NOT anemia of chronic disease, chronic blood Microangiopathic cells Thrombotic thrombocytopenic purpura loss (fragmented, helmet M etastatic cancer (stomach, pancreas, ovary) NOT pernicious anemia Below 100 cells, etc) Postcardiotomy Below 80 Iron deficiency Calcific aortic stenosis (?) Thalassemia minor Drugs (± G6PD deficiency) Hemolytic-uremic syndrome of infants MCHC Acute nephritis (rare) Above 36 Hereditary spherocytosis Malignant hypertension (rare) Uremia Below 32.5 Iron deficiency Thalassemia minor Target cells Jaundice Thalassemia Iron deficiency Table 3. Blood Film Splenectomy Hem oglobi nopath ies Look fo r: S tippling Lead poisoning Thalassemia minor Hypochromic microcytes Several severe anemias Oval macrocytes Spherocytes Spur cells Cirrhosis Schist ocytes Acanthocytosis Target cells PK deficiency Hypersegmented P.M.N.'s Howell-Jolly bodies Splenectomy Abnormal WBC Megaloblastic anemia 2 1 8 THE JOURNAL OF FAM ILY PRACTICE, VOL. 2, NO. 3,1975 electrophoresis is not worthwhile in ic anemia, such as hereditary sphero­ The anemia of cancer is sometimes patients with low platelets and white cytosis, can increase its output by six complicated by blood loss, sometimes cells or normal looking red blood cells. to ten times. it features contracted cells, schisto- Other abnormal findings have to do cytes, a sign of marrow invasion. Patterns of Common Anemias with impaired protein synthesis result1 Ineffective erythropoiesis or intra­ The most common anemias have ing in low transferrin, erythropoietin, medullary hemolysis refers to a phe­ their own hematologic patterns.1' 5 and albumin levels. The serum iron is nomenon that combines greatly in­ 1 iron deficiency anemia. This is usually also low because of impaired creased production of erythroblasts characterized by an MCHC below 32.5 reutilization of iron, that is, the reticu­ with destruction of these nucleated and MCV usually below 80, serum iron loendothelial cells do not readily re­ red cells right in the marrow, permit­ below 50, TIBC above 350, and an ab­ lease iron obtained from decaying red ting only few, and often misshapen sent marrow hemosiderin. In blood cells. Another example of the relative and poorly made red cells to reach the loss of recent onset (ie, within two to unavailability of iron is an increase in blood stream. Pernicious anemia is the four weeks) these laboratory devia­ red cell protoporphyrin in these condi­ best known example of this mecha­ tions
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