A Case of Persistent Anemia and Alcohol Abuse

Gemma Lewis; Matthew P Wise; Christopher Poynton; Andrew Godkin

Disclosures

Nat Clin Pract Gastroenterol Hepatol. 2007;4(9):521-526. 

In This Article

Discussion of Diagnosis

Anemia is defined as a reduction in blood hemoglobin concentration (and hence also a reduced hematocrit), to <135 g/l in adult males and <115 g/l in adult females. The main causes of acquired anemia can be divided into loss of blood (hemolysis or hemorrhage) or inadequate bone-marrow function (e.g. ineffective erythropoiesis, sideroblastic changes, hematinic deficiency, chronic inflammation or malignancy). A simple, pragmatic algorithm that can be used for the investigation of anemia in alcoholics is shown in Figure 4. It is important to remember that alcohol can complicate the interpretation of the results of certain common laboratory tests that are used to investigate the causes of anemia. For example, although the mean corpuscular volume is increased by recognized causes that include vitamin B12 deficiency or folic acid deficiency, it is also raised by high alcohol intake alone. In addition, the ferritin level is raised by inflammation of the liver (as seen after high alcohol intake), which can mask the decrease in ferritin that occurs with iron deficiency.

An algorithm giving a straightforward approach to the investigation of anemia in alcoholics. Abbreviations: AST, aspartate transaminase; EGD, esophagogastroduodenoscopy; LDH, lactate dehydrogenase.

The etiology of anemia in alcoholics is complex and often multifactorial, causes include a combination of poor nutrition, chronic inflammation, blood loss, liver dysfunction and ineffective erythropoiesis.[1] Effective erythropoiesis can be indicated by the reticulocyte count.[2] It is important to be aware of both the absolute number of reticulocytes and the percentage of reticulocytes, as marked anemia can misleadingly increase the relative percentage. Thus, if the lifespan of the red blood cells is short, the percentage of reticulocytes will seem to be higher than the absolute numbers would suggest (reflecting the reduced number of mature red blood cells). Clearly, sequential reticulocyte counting is useful for obtaining information on the lifespan of RBCs in these situations.

The accurate assessment of anemia in alcoholics requires identification of the relative contributions of the direct toxic effects of alcohol and poor nutrition on the synthesis, function and survival of red blood cells, and of the role of underlying chronic disease such as cirrhosis or chronic sepsis. The presence or absence of chronic liver disease can be obvious from the patient's medical history and examination, but a liver biopsy sample is often useful for typing and staging of disease. Confirmation of chronic liver disease can then prompt the search for other factors that might be contributing to anemia. These contributing factors include abnormalities of red blood cells (e.g. target cells, spur cells) associated with perturbations in lipid metabolism, hemolysis, anemia of chronic disease, acute or chronic blood loss from varices and/or gastropathy (which is often exacerbated by coexistent coagulopathy and hypersplenism).

Alcohol can be directly toxic to the bone marrow, as suggested by pre-erythroblast vacuolation or sideroblastic changes. Alcoholism and the debilitating factors with which it is often associated (e.g. chronic sepsis and poor nutrition) frequently causes marked anemia even if liver disease is absent (e.g. sideroblastic anemia, megaloblastic anemia and the anemia of chronic inflammation). Thus, a proportion of alcoholics have both reduced erythrocyte production in the bone marrow and accompanying reduced red blood cell survival time. Studies have shown that bone-marrow biopsy samples from alcoholics are abnormal in the majority of cases: approximately two-thirds reveal megaloblastic and/or sideroblastic changes and fewer than a fifth are suggestive of any underlying iron deficiency.[3,4] If doubt remains about the diagnosis after an initial careful inspection of the peripheral blood film, a bone-marrow aspirate can provide useful information and, equally importantly, exclude more-sinister causes of the anemia (e.g. malignancy or other blood dyscrasias).

Some diagnoses are pertinent to both excess alcohol intake and liver disease, for example the marked hemolysis of spur cell anemia that can be seen in patients with jaundice and severe alcoholic cirrhosis[5] and the mild hemolysis found with steatosis, hypertriglyceridemia and acute alcohol ingestion (Zieve syndrome).[6] The hemolytic crises prompted by alcoholic binges are poorly understood. The case described here exhibited features similar to those of Zieve syndrome, even though his serum triglyceride levels were normal; these features might, therefore, have reflected the effect of alcohol directly on the erythrocyte.[7]

The present case demonstrates the often complex mechanism of anemia in alcoholics. The etiology included both reduced red blood survival and reduced red blood cell production (e.g. bone-marrow dysfunction) and hence the anemia was the end result of more than one process. Table 3 summarizes some of the different pathological processes that can contribute to anemia in alcoholics, with or without accompanying chronic liver disease.

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