Stomatocytosis is a rare morphological condition of the red blood cells in which the normal central zone of pallor is replaced by a mouth-like or slit-like pattern. Stomatocytosis can be either hereditary or acquired in the setting of acute alcohol consumption, chronic liver disease [1]. It may be asymptomatic or lead to hemolysis presenting as anemia. We present a case of a young lady with chronic alcoholism who presented with symptomatic anemia. Alcoholism is known to cause hypophosphatemia [2], which can cause stomatocytosis. Repletion of phosphorus and abstinence of alcohol improved the patient’s anemia, improving the stomatocytosis on the peripheral smear. The use of an easily available, rapid and cheap test like peripheral smear in guiding the therapy in such a patient reflects the importance of peripheral smear and its cost-effectiveness.

A 38-year-old African-American female with history of chronic pancreatitis, cholelithiasis, diabetes mellitus and alcohol abuse presented with severe anemia and light-headedness. She was consuming about 80 grams of alcohol on a daily basis. On admission, she had hemoglobin of 5.6 g/dL, mean corpuscular volume (MCV) 90 fL (normal), iron level 92 mg/dL (normal) and ferritin 1188 ng/mL. Her vitamin B12 and folate levels were normal and reticulocyte count corrected for anemia was 1.2%. Her phosphorus was 1.0 mg/dL (critically low). Abdominal ultrasound was consistent with hepatic steatosis and distended gallbladder with possible gallstones. On peripheral smear, she had stomatocytosis (Figure 1A). Numerous RBCs were described with fish mouth appearance, lacking the typical central pallor. After three days of phosphorus repletion, the phosphorus level improved to 2.7 mg/dL and peripheral smear showed marked improvement with negligible stomatocytes (Figure 1B). Patient’s anemia improved significantly. She was counseled to abstain from alcohol use, and discharged home with adequate follow-up.

Stomatocytosis can be hereditary or acquired secondary to medications (vincristine, vinblastine, chlorpromazine, etc.), acute alcohol intoxication or chronic liver disease [1][3][4]. Our patient had hypophosphatemia due to alcohol ingestion, which further led to stomatocytosis of the blood cells. In a study by Rauchenzauner et al., 3.4% of patients with acute alcohol intoxication had hypophosphatemia [5]. This results from decreased phosphate absorption and increased urinary phosphate excretion. In addition, chronic alcoholism can induce cellular phosphate depletion [6] . A study done in 1979 by Wisloff et al. studied the peripheral blood smears in 100 alcoholic patients. They reported 15% patients manifesting marked stomatocytosis [1]. Low serum phosphorus level depletes the ATP level in RBC affecting the RBC pliability. The complex metabolic sequelae of hypophosphatemia also include 2,3-diphosphoglyceric acid depletion, a shift to the left in the oxygen dissociation curve, decreased glucose utilization, and increased lactate production, resulting in rigid and non-yielding RBCs.

In the review of recent literature, not many studies have commented on the association of hypophosphatemia with stomatocytosis. This case illustrates the presence of hypophosphatemia with chronic alcohol use and its effect on peripheral smear in the form of stomatocytosis. It also reports the prompt improvement of stomatocytosis with repletion of phosphorus. Peripheral smear is an easily available, rapid and a cheap test. The presence of a rare finding in a common scenario like chronic alcohol consumption highlights the clinical importance of peripheral smear.

This case depicts the reflection of significant laboratory value on the peripheral smear in a patient with severe hypophosphatemia in the setting of chronic alcohol consumption leading to stomatocytosis. This rare occurrence in a common clinical scenario highlights the importance of peripheral smear as a clinical tool.

1. Wislöff F, Boman D. Acquired stomatocytosis in alcoholic liver disease. Scand J Haematol 1979 Jul;23(1):43–50.   [CrossRef]   [Pubmed]    
2. Fernández López MT, García Bargo MD, Rivero Luis MT, Álvarez Vázquez P, Saenz Fernández CA, Mato Mato JA. Alcoholic ketoacidosis and reversible neurological complications due to hypophosphataemia. [Article in Spanish]. Nutr Hosp 2012 May-Jun;27(3):936–9.   [CrossRef]   [Pubmed]    
3. Alvarez-Sala Walther JL, Urbán Poza MA, Sicilia de Salamanca JJ, Fernández Mendieta F, Serrano Heranz R, Espinós Pérez D. Hematologic aspects of alcoholism. [Article in Spanish]. Med Clin (Barc) 1979 Feb 25;72(4):158–65.   [Pubmed]    
4. Wislöff F, Boman D. Haemolytic anaemia in alcohol abuse. A review of 14 cases. Acta Med Scand 1979;205(3):237–42.   [CrossRef]   [Pubmed]    
5. Rauchenzauner M, Kountchev J, Ulmer H, et al. Disturbances of electrolytes and blood chemistry in acute alcohol intoxication. Wien Klin Wochenschr 2005 Feb;117(3):83–91.   [CrossRef]   [Pubmed]    
6. Ferguson ER, Blachley JD, Carter NW, Knochel JP. Derangements of muscle composition, ion transport, and oxygen consumption in chronically alcoholic dogs. Am J Physiol 1984 May;246(5 Pt 2):F700–9.   [Pubmed]