A Case of Persistent Anemia and Alcohol Abuse

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


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

In This Article

Summary and The Case

Background: A 56-year-old male with a history of excess alcohol consumption for over 10 years and type 2 diabetes mellitus (diagnosed 14 years previously) presented to the accident and emergency department with severe anemia and a 1-day history of nausea and 'coffee ground' vomiting. He had been admitted to hospital on several occasions in the previous 18 months, primarily because of anemia, and had received 30 units of transfused blood during this period. Previous extensive investigations included six esophagogastroduodenoscopies and a colonoscopy, a barium follow-through study, and a radionucleotide Meckel's scan. The prior working diagnosis was anemia secondary to blood loss.
Investigations: Laboratory investigations (full blood count [including reticulocytes], microscopic blood film examination, hematinics, liver function tests with direct and indirect bilirubin measurement, prothrombin time, and lactate dehydrogenase level), transjugular liver biopsy and bone-marrow biopsy.
Diagnosis: Alcohol-related anemia caused by acute hemolysis, sideroblastic anemia and cirrhosis.
Management: Correction of anemia by blood transfusion (6 units), and prevention of recurrence by strict abstinence from alcohol.

A 56-year-old male was admitted to hospital via the accident and emergency department with a 1-day history of nausea and 'coffee ground' vomiting. In the previous 18 months the patient had undergone extensive investigations for anemia that had included six esophagogastroduodenoscopies and a colonoscopy. A barium follow-through study (which demonstrated Meckel's diverticulum) and a normal radioisotope Meckel's scan had also been performed. The working diagnosis was anemia secondary to blood loss and, because no notable source of bleeding was identified in the upper gastrointestinal tract or colon, a capsule endoscopy was planned to look for a cause of bleeding in the small intestine. The patient had been admitted to hospital on several occasions during this 18-month period and had received 30 units of transfused blood. His medical history included colonic polyps (cleared during three colonoscopies in a 5-year period before the onset of anemia) and diet-controlled type 2 diabetes mellitus, which had been diagnosed 14 years previously when it had also been noted that his alcohol intake was high. At the time of his current admission, the patient stated that his alcohol intake during the past 2 years had been 1 unit a day.

Examination revealed a fully conscious and lucid individual who seemed to be well nourished and who had a normal BMI. The patient's breath smelt of alcohol, however, and recent high levels of alcohol consumption were confirmed with a measured blood alcohol level of 286 mg per 100 ml blood. Icterus, conjunctival pallor, bruising and multiple spider nevi were present. The patient's blood pressure was 110/50 mmHg with no postural drop and his pulse was 90 beats/min in sinus rhythm. The results of a chest examination were unremarkable. No organomegaly was palpable in the abdomen and the results of a rectal examination were normal.

A full blood count confirmed the presence of anemia; the patient had a hemoglobin level of 66 g/l (normal 130–165 g/l), mild macrocytosis (mean corpuscular volume <101 fl) and thrombocytopenia (66 × 109 platelets/l blood). A blood film was taken from the patient and was found to be markedly abnormal owing to the presence of spherocytes, acanthocytes and stomatocytes (Figure 1). Hematinics were normal, but the results of liver function tests were abnormal ( Table 1 ). Splenomegaly was excluded by ultrasound examination of the abdomen; however, the texture of the liver appeared coarse. A sudden rise in the patients' serum bilirubin concentration to 148 µmol/l (8.7 mg/dl) on the third day after admission combined with the presence of microspherocytosis (Figure 1) raised the possibility of hemolysis. This diagnosis was supported by the finding of an increased unconjugated bilirubin level (from approximately 20–30% in the patient to a peak of 74%), an elevated lactate dehydrogenase level of 557 U/l (normal values), and a low haptoglobin level of 50 µmol/l (500 mg/dl) (normal values).

Blood film from the case patient. Spherocytes (spherical erythrocytes lacking the normal area of central pallor), acanthocytes (erythrocytes with irregularly spaced projections) and stomatocytes (erythrocytes with an oval or rectangular area of central pallor) and microspherocytosis can be seen. Spherocytes are typically found in patients with hemolytic anemia, whereas acanthocytes and stomatocytes can be present in patients with liver disease. The neutrophil present shows vacuolation characteristic of acute alcohol ingestion (May-Giemsa stain, original magnification × 1,000).

Further examination of the patient's blood indices revealed a marked increase in both the percentage of reticulocytes and the absolute reticulocyte count ( Table 2 ). A direct Coombs test was negative and the fasting serum lipid profile was normal. All these results suggested that hemolysis might have been contributing substantially to the anemia. The results of hemoglobin and bilirubin measurements in the patient recorded during the previous 18 months were then reviewed and revealed similar episodes of a rapidly falling hemoglobin level with a sudden increase in serum bilirubin concentration. These and other serially recorded laboratory indices are shown in Figure 2.

Laboratory variables for the 18 months preceding the current admission of the case patient. The patient's ferritin level was initially low, which might have reflected chronic blood loss and/or poor dietary intake. A steady increase in the ferritin level thereafter to >225 pmol/l (>100 ng/ml) reflects the replenishment of iron stores by the multiple blood transfusions received by the patient. The arrows indicate examples where a sudden fall in hemoglobin concentration is mirrored by a rise in bilirubin, reflecting bouts of hemolysis.

Underlying liver disease was diagnosed from a transjugular liver biopsy sample, which revealed micronodular cirrhosis with low-grade steatohepatitis. Bone-marrow aspiration was also undertaken and showed mild erythroid hyperplasia (30% of cells were erythroblasts), in keeping with a bone-marrow response to blood loss. A Perl's iron stain of the bone marrow revealed the conspicuous presence of ringed sideroblasts and no evidence of iron deficiency (Figure 3). Both the liver pathology and the sideroblastic bone-marrow changes were consistent with a high alcohol intake.

Histological image of a bone-marrow aspirate from the case patient that demonstrates the presence of ringed sideroblasts. Abnormal accumulation of hemosiderin in the mitochondria surrounding the nucleus can be seen (Perl's iron stain, original magnification × 1,000).

The patient's admission was complicated by another unwitnessed hematemesis after vomiting; no obvious melena was present but a stool sample gave a positive fecal occult blood test. A repeat esophagogastroduodenoscopy (that revealed mild portal gastropathy) and a radioactively labeled red blood cell scan (to identify intraluminal aggregations of labeled blood cells that would suggest gastrointestinal hemorrhage) were undertaken. Neither investigation revealed substantive intestinal blood loss. The patient was transfused with a total of 6 units of blood during his 10-day admission. A subsequent pre-arranged capsule endoscopy performed shortly after the patient was discharged revealed no abnormalities. The patient completely abstained from alcohol for a 6-month follow-up period as an outpatient and his hemoglobin level was maintained at over 100 g/l for the first time in 2 years. After 6 months the patient traveled abroad and was no longer seen in the clinic.

The anemia in this case was prompted by an acute alcohol binge of a patient with a history of chronic alcohol consumption, and could be attributed to acute hemolysis, sideroblastic anemia and cirrhosis.


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