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Anemia

Anemia (American English) or anaemia (Commonwealth English), which literally means "without blood," is a deficiency of red blood cells and/or hemoglobin. This results in a reduced ability of blood to transfer oxygen to the tissues, and this causes hypoxia; since all human cells depend on oxygen for survival, varying degrees of anemia can have a wide range of clinical consequences. Hemoglobin (the oxygen-carrying protein in the red blood cells) has to be present to ensure adequate oxygenation of all body tissues and organs. more...

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The three main classes of anemia include excessive blood loss (acutely such as a hemorrhage or chronically through low-volume loss), excessive red blood cell destruction (hemolysis) or deficient red blood cell production. In menstruating women, dietary iron deficiency is a common cause of deficient red blood cell production.

Anemia is the most common disorder of the blood. There are several kinds of anemia, produced by a variety of underlying causes. Anemia can be classified in a variety of ways, based on the morphology of RBCs, underlying etiologic mechanisms, discernible clinical spectra, to mention a few.

Different clinicians approach anemia in different ways; two major approaches of classifying anemias include the "kinetic" approach which involves evaluating production, destruction and loss, and the "morphologic" approach which groups anemia by red blood cell size. (Schier) The morphologic approach uses as its starting point a quickly available and cheap lab test as its starting point (the MCV--see below). On the other hand, focusing early on the question of production (e.g., via the reticulocyte count) may allow the clinician to more rapidly expose cases where multiple causes of anemia may coexist. Regardless of one's philosophy about the classification of anemia, however, methodical clinical evaluation should yield equally good results.

Signs and symptoms

Anemia goes undetected in many people, and symptoms can be vague. Most commonly, people with anemia report a feeling of weakness or fatigue. People with more severe anemia sometimes report shortness of breath. Very severe anemia prompts the body to compensate by markedly increasing cardiac output, leading to palpitations and sweatiness; this process can lead to heart failure in elderly people.

Pallor (pale skin and mucosal linings) is only notable in cases of severe anemia, and is therefore not a reliable sign.

Diagnosis

The only way to definitively diagnose most cases of anemia is with a blood test. Generally, clinicians order a full blood count. Apart from reporting the number of red blood cells and the hemoglobin level, the automatic counters also measure the size of the red blood cells by flow cytometry, which is an important tool in distinguishing between the causes of anemia. A visual examination of a blood smear can also be helpful in some cases, and is sometimes a necessity in regions of the world where automated analysis is less accessible.

In modern counters, 4 parameters (RBC Count, hemoglobin concentration, MCV and RDW) are measured, allowing others (hematocrit, mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration) to be calculated, and compared to values adjusted for age and sex. For males, the hemoglobin level that is suggestive of anemia is usually less than 13.0 g/dl, and for females, it is 12.0 g/dl.

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Anemia and COPD
From CHEST, 10/1/05 by Luca Mascitelli

To the Editor:

John and colleagues reported in a recent issue of CHEST (March 2005) (1) a relatively high frequency of anemia in patients with COPD. However, they did not mention whether the studied population was in treatment with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 (AT1) receptor blockers.

Several observations suggested that an intact and activated renin-angiotensin system may be an important determinant of erythropoiesis, (2,3) including a variety of clinical conditions such as hypertension, chronic renal insufficiency, heart failure, and COPD. (4) Consequently, the assumption of ACE inhibitors and AT1 receptor blockers has been shown to reduce hemoglobin concentrations both in healthy subjects (5) and in those with pathologic conditions. (4,6-8 Thus, therapy with ACE inhibitors and AT1 receptor blockers might have been a confounder in this study.

REFERENCES

(1) John M, Hoernig S, Doehner W, et al. Anemia and inflammation in COPD. Chest 2005; 127:825-829

(2) Mrug M, Stoppa T, Julian BA, et al. Angiotensin II stimulates proliferation of normal early erythroid progenitors. J Clin Invest 1997; 100:2310-2314

(3) Cole J, Ertoy D, Lin H, et al. Lack of angiotensin II-facilitated erythropoiesis causes anemia in angiotensin converting enzyme-deficient mice. J Clin Invest 2000; 106:1391-1398

(4) Marathias KP, Agroyannis B, Mavromoustakos T, et al. Hematocrit-lowering effect following inactivation of renin-angiotensin system with angiotensin converting enzyme inhibitors and angiotensin receptor blockers. Curr Top Med Chem 2004; 4:483-486

(5) Griffing GT, Melby JC. Enalapril (MK-421) and the white cell count and haematocrit [letter]. Lancet 1982; 1:1361

(6) Gaston RS, Julian BA, Diethelm AG, Curtis JJ. Effects of enalapril on erythrocytosis after renal transplantation. Ann Intern Med 1991; 115:954-955

(7) Plata R, Cornejo A, Arratia C, et al. Angiotensin-converting-enzyme inhibition therapy in altitude polycythaemia: a prospective randomised trial. Lancet 2002; 359:663-666

(8) Ishani A, Weinhandl E, Zhao Z, et al. Angiotensin-converting-enzyme inhibitor as a risk factor for the development of anemia, and the impact of incident anemia on mortality in patients with left ventricular dysfunction. J Am Coll Cardiol 2005; 45:391-399

Luca Mascitelli, MD

Comando Brigata Alpina "Julia"

Udine, Italy

Francesca Pezzetta, MD

Ospedale di San Vito al Tagliamento

San Vito al Tagliamento, Italy

Correspondence to: Luca Mascitelli, MD, Comando Brigata alpina "Julia", Sanitary Service, Via S. Agostino 8, Udine 33100, Italy; e-mail: lumasci@libero.it

To the Editor:

The author of this comment mentioned that therapy with angiotensin-converting enzyme (ACE) inhibitors might be a confounder in interpreting the results of our study. (1) In this patient population, 23 patients of the nonanemic group (88 patients) were treated with ACE inhibitors or angiotensin type-1 (AT1) receptor blockers. In the anemic group (13 patients), 3 patients received cotherapy with ACE inhibitors or receptor blockers. The [chi square] test revealed no difference in the occurrence of ACE inhibitor therapy between both groups (p = 0.813). Therefore, we conclude that the reported prevalence of anemia in COPD patients in our study is not influenced by an ACE inhibitor or AT1 receptor blocker medication. Overall, it is an interesting issue that should be taken into consideration for future studies.

REFERENCES

(1) John MS, Hoernig W, Doehner C, et al. Anemia and inflammation in chronic obstructive pulmonary disease. Chest 2005; 127:825-829

Matthias John, MD, PhD

University Hospital Charite

Berlin, Germany

Correspondence to: Matthias John, MD, PhD, Department of Pneumology, University Hospital Charite, Campus Mitte, Schumannstr. 20/21, 10098 Berlin, Germany; e-mail: matthias.john@charite.de

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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