78 year old Alcoholic With Anaemia

An 78 year old man presented with fatigue and breathlessness. Examination showed pallor. There was no icretus, clubbing, lymphadenopathy or hepatomegaly. There was mild splenomegaly. There was no history of haemoptysis, malena or haematochesia.

An haemogram was performed that showed a haemoglobin was 8g/dL with an MCV of 101fl. The leucocyte count was 4.5 x 109/L and the platelet count was 265 x 109/L. The differential leucocyte count was neutrophils 58% lymphocytes 32%, monocytes 6% and eosinophils 4%. The Reticulocyte count was normal. 

Anaemia in alcoholics is multifactorial. The causes of Anaemia include

  1. Direct toxic effect of alcohol: Most alcoholics have macrocytosis in the range of 100-110fl. Macrocytosis is seen before anaemia develops. Anaemia reverses after a few months of abstaining from alcohol.
  2. Iron deficiency from gastrointestinal blood loss from varices and alcoholic gastritis may presents with hypochromic microcytic anaemeia. The transferrin saturation and serum ferritin are low. Alcohol and alcohol associated disease affect MCV, transferrin saturation and serum ferritin making interpretation of test difficult.
    • Microcytosis may not be seen in alcoholics with iron deficiency. A study showed 48% of the patients with chronic liver disease and iron deficiency diagnosed by absence of bone marrow iron had an MCV more than 100fl (J Intern Med. 1998 Mar;243(3):233-41).
    • Alcohol effects transferrin saturation. Transferrin levels may be decrease because of infection or inflammation. In a study of transferrin saturation in cirrhotics a transferrin saturation of <12% was of value in diagnosing iron deficiency. But transferrin saturation did not add to the value of ferritin in diagnosis.
    • Ferritin is an acute phase reactant and can be increase in chronic liver disease. A study has suggested different cutoffs be used in patients with chronic liver disease. Iron deficiency should be diagnosed with a ferritin ≤50 μg/L. Values >400 μg/L were associated with a low probability of iron deficiency (Annals of Gastroenterology (2017) 30, 1-9).
    • sTrasnferrin receptors levels is a iron deficiency (sensitivity 91.6%, specificity 84.6%) in patients with chronic liver disease provided that hemolysis and recent blood loss have been excluded (Clin Lab Haematol. 1999 Apr;21(2):93-7)
  3. Folate and Cobalamine deficiency: Folate and cobalamin deficiency causes macrocytosis and should be suspected in patients with MCV greater than 110fl, those with decreased platelet and/or leucocyte counts and when peripheral smear shows hypersegmantation of neutrophils.
  4. Hypersplenism: Hypersplenism causes anaemia and pancytopenia. The spleen is enlarged but there is no correlation between the degree of anaemia and size of the spleen. Unlike patients with folate or cobalamin deficiency the MCV patient with hypersplenism do not have an markedly (>110fl) increased MCV.
  5. Anaemia of chronic disease: Anaemia of chronic disease may be seen in alcoholics because concurrent infection or inflammation.
  6. Haemolytic anaemia with spur cells: Patients with severe hepatocellular disease develop spur cells that result in haemolytic anaemia. This may be associated with increased jaundice and/or deteriorating liver function. Appearance of spur cells may be related to continued alcohol abuse in the presence of severe chronic liver disease. Transfused blood cells also become acanthocytic and are haemolysed. Abstinence from alcohol can eliminate/reduce spur cells. Spur cell anaemia has been cured by liver transplant.


The patient has a serum iron of 24 µg/dL the total iron binding capacity of 202µg/dL and a  transferrin saturation of 11.9%. The serum ferritin was 30 µg/L. The B 12 and folic acid levels were normal. The serum albumin was 3.2g/dL. The AST, ALT, prothrombin time and bilirubin were normal.

The patients was diagnosed to have iron deficiency. An upper gastrointestinal endoscopy showed gastro-oesophageal varices. Colonoscopy did nor show any cause of bleeding. A diagnosis of iron deficiency anaemia was made, iron supplementation given and varices banded.


Plummer-Vinson Syndrome/Paterson Kelly Syndrome

In 1912 Plummer described dysphagia and spasm of the upper oesophagus without anatomical stenosis in patients with longstanding iron deficiency. In 1919, Vinson, Paterson and Kelly independently described patients with similar findings. The triad of iron deficiency anaemia, dysphagia and oesophageal webs has been called Plummer-Vinson syndrome or Paterson-Kelly syndrome (depending in the side of Atlantic you reside) after these physicians. It is a rare disease possibly related to iron deficiency and is also known as sideropenic dysphagia.

Etiology and Pathogenesis

Etiology of Plummer –Vinson syndrome is not known, iron deficiency is the most likely cause but malnutrition and genetic predisposition may contribute. Plummer-Vinson syndrome has been associated with coeliac disease, thyroiditis and rheumatoid arthritis raising the possibility of autoimmunity playing a role in Plummer-Vinson syndrome.

The oesophagus of patients with Plummer –Vinson syndrome shows webs at the junction of the hypopharynx and oesophagus, usually extends backwards from the anterior wall. The webs may take a cuff shape and the opening may be reduced to a pinhole. Oesophageal stricture may be seen. Histologically the webs are made of normal oesophageal epithelium, sometimes with chronic inflammation.

Clinical Manifestations

Plummer –Vinson syndrome is a mainly affects women in the fourth to the seventh decade of life but has been described in other age groups. The patients present with gradual onset of dysphagia, initially for solids. Examination reveals evidence of iron deficiency including pallor, koilonachia, glossitis and cheilosis. Splenomegaly and thyroid enlargement may occur.


The webs are best demonstrated videofluoroscopically by a barum swallow. Endoscopically they appear as 2-3mm smooth grey thin extension of normal mucosa usually with an eccentric lumen. Endoscopy can rupture the webs and the scope should be introduced under direct vision. Laboratory investigations show hypochromic microcytic anaemia, low transferrin saturation and low serum ferritin characteristic of iron deficiency.


The iron deficiency should be treated. Dysphagia may be treated by dilatation or endoscopic disruption using a biopsy forceps. The prognosis is good. Patinets with Plummer –Vinson syndrome are predisposed to carcinoma of pharynx and oesophagus and a close follow up of patients is needed.