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Year : 2016  |  Volume : 9  |  Issue : 1  |  Page : 101-103  

Leukemoid reaction in a patient with severe alcoholic hepatitis: A case report and review of literature

1 Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Medicine, University College of Medical Sciences, New Delhi, India
3 Department of Pathology, University College of Medical Sciences, New Delhi, India

Date of Web Publication22-Dec-2015

Correspondence Address:
Nikhil Gupta
Department of Medicine, University College of Medical Sciences, Dilshad Garden, New Delhi - 110 095
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-2870.167968

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Alcoholic hepatitis is a clinicopathologic syndrome that results from active alcohol consumption in a patient with or without underlying alcoholic liver disease. Leukemoid reaction has been described as an adverse prognostic factor in severe alcoholic hepatitis. We describe a case of 40-year-old male who had severe alcoholic hepatitis and on investigations was found to have leukemoid reaction. The patient improved with steroids, and hence we report this case to create awareness among physicians dealing with such cases.

Keywords: Alcoholic hepatitis, leukemoid reaction, steroids

How to cite this article:
Chabbra P, Gupta N, Malik S, Garg P. Leukemoid reaction in a patient with severe alcoholic hepatitis: A case report and review of literature . Med J DY Patil Univ 2016;9:101-3

How to cite this URL:
Chabbra P, Gupta N, Malik S, Garg P. Leukemoid reaction in a patient with severe alcoholic hepatitis: A case report and review of literature . Med J DY Patil Univ [serial online] 2016 [cited 2020 Aug 9];9:101-3. Available from:

  Introduction Top

Leukemoid reaction is characterized by total leukocyte count (TLC) >50 × 10 3 /μl of blood. [1] It is differentiated from myeloproliferative states by clinical profile, the absolute TLC (>100 × 10 3 /μl of blood unlikely in leukemoid reaction), and leukocyte alkaline phosphatase (LAP) score. Leukemoid reaction is seen in various conditions including burns, sepsis, inflammatory states associated with systemic inflammatory response syndrome such as pancreatitis, etc. It is a very rare situation in alcoholic hepatitis, and very few reports are available in literature. So we report this case of a 40-year-old male who had leukemoid reaction with severe alcoholic hepatitis and was treated with steroids, and there was decrease in the TLC also during the follow-up.

  Case Report Top

A 40-year-old male came to the emergency room with complaints of jaundice, pain abdomen, and recurrent vomiting for past 15 days. The patient was consuming alcohol in cirrhogenic doses for past 20 years (80-100 g/day whisky, C+A+G+E−) with a history of last consumption 20 days back. There was no history of upper gastrointestinal bleed (hematemesis or melena), altered sensorium, abdominal distention, or oliguria. On examination, patient was icteric and had stigmata of alcoholic liver disease in the form of bilateral parotidomegaly and dupuytren's contracture. Patient also had tachycardia and tachypnea. Per abdominal examination revealed tender hepatomegaly with a span of 21 cm in the midclavicular line with no evidence of free fluid in the abdomen. Investigations revealed a bilirubin of 13.4 mg/dl with a direct fraction of 7.4 mg/dl. TLC was 75 × 10 3 /μl of blood (N88L10M1E1) with normal platelet count and hemoglobin of 10.4 g/dl. C-reactive protein was elevated (32 mg/dl). Sonogram of the abdomen revealed hepatomegaly with increased echogenicity but no evidence of cirrhosis. Coagulogram revealed prothrombin time prolongation by 6 s with an activated partial thromboplastin times of 39 s. Maddrey's discriminatory function score was 41 with a Child-Pugh-Turcotte of 7 and Glasgow alcoholic hepatitis score of 7, and MELD was 20. So it was decided to start the patient on steroids after a septic screen and bone marrow examination to rule out any myeloproliferative state. Blood and urine cultures were sterile. There was no evidence of any collection on imaging. Bone marrow examination [Figure 1] showed myeloid to erythroid ratio of 9/1 with no evidence of any myeloproliferative state. LAP [Figure 2] score was 400. The JAK 2 mutation was tested which was negative thus ruling out myeloproliferative disorders. The patient was started on prednisolone 1 mg/kg body weight, and there was decrease in bilirubin and TLC after 1 week. Lilie's score was <0.45 at the end of 1 week, so steroids were continued for 3 more weeks followed by a taper for 2 weeks. Patient also received intravenous thiamine, antacids, and ursodeoxycholic acid. The patient improved, bilirubin came down to 2 mg/dl. TLC at the time of discharge was 20 × 10 3 /μl of blood. Currently, after 2 months of follow-up, TLC has normalized along with bilirubin, and patient is doing fine and has been advised to abstain from alcohol. Currently, the patient is off steroids and completely asymptomatic.
Figure 1: H and E, ×400 photomicrograph of bone marrow trephine biopsy showing leukemoid reaction

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Figure 2: Leukocyte alkaline phosphatase score photomicrograph showing 2 neutrophils with leukocyte alkaline phosphatase score of 3 each. Total leukocyte alkaline phosphatase score in this case was 400

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  Discussion Top

Leukemoid reaction is a very rare event in alcoholic hepatitis. [1] When it is associated with alcoholic hepatitis, it is presumed to be a poor prognostic marker. [2] The literature regarding the occurrence of leukemoid reaction in alcoholic hepatitis is very scarce and limited to few case reports only. [3],[4],[5] The pathophysiological basis for the leukemoid reaction in the setting of alcoholic hepatitis is probably as a result of the increased levels of granulocyte colony stimulating factor (G-CSF) released by the damaged hepatocytes. [6] Now, paradoxically people have recently been trying to administer G-CSF in patients with severe alcoholic hepatitis and have even demonstrated positive results also. [7],[8]

The role of steroids in alcoholic hepatitis has always been an issue of debate. Various placebo controlled randomized controlled trials have been performed with few showing a survival benefit. Now, since leukemoid reaction has been associated with poor outcome in severe alcoholic hepatitis, our patient improved with steroids. Whether leukemoid reaction should be used as a criterion for starting steroids needs further evaluation.

We conclude that high TLC in a patient with severe alcoholic hepatitis is not always sepsis related. A bone marrow examination is mandatory in patients with severe alcoholic hepatitis with TLC in the range of 40-50,000. If patients with severe alcoholic hepatitis are found to have leukemoid reaction, treatment with steroids should be considered after excluding sepsis.

  References Top

Haque AU, Aan NU. Leukemoid reaction. Unusual causes. Int J Pathol 2010;8:39-40.  Back to cited text no. 1
Argüelles-Grande C, Leon F, Matilla J, Domínguez J, Montero J. Steroidal management and serum cytokine profile of a case of alcoholic hepatitis with leukemoid reaction. Scand J Gastroenterol 2002;37:1111-3.  Back to cited text no. 2
Morales AM, Hashimoto LA, Mokhtee D. Alcoholic hepatitis with leukemoid reaction after surgery. J Gastrointest Surg 2006;10:83-5.  Back to cited text no. 3
Larvol L, Colardelle P, Callard P, Levecq H. Acute alcoholic hepatitis and leukemoid reaction. Gastroenterol Clin Biol 1993;17:972-3.  Back to cited text no. 4
Petracca E, Ramazzina E, Zennaro R. Leukemoid reaction in acute alcoholic hepatitis. Clin Ter 1988;126:249-53.  Back to cited text no. 5
Natali G, Trotta A, Colantonio D, Cascone F, Di Lauro G, Ruggieri M, et al. Leukemoid reaction in a case of severe acute alcoholic hepatitis. Minerva Med 1982;73:1497-501.  Back to cited text no. 6
Koyama Y, Imoto M, Fukuda Y, Nakano I, Hattori M, Urano F, et al. Alcoholic hepatitis with hyperleukocytosis. Jpn J Med 1991;30:473-6.  Back to cited text no. 7
Spahr L, Lambert JF, Rubbia-Brandt L, Chalandon Y, Frossard JL, Giostra E, et al. Granulocyte-colony stimulating factor induces proliferation of hepatic progenitors in alcoholic steatohepatitis: A randomized trial. Hepatology 2008;48: 221-9.  Back to cited text no. 8


  [Figure 1], [Figure 2]


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