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A case of leukemic pleural infiltration in atypical chronic myeloid leukemia.

Kim HW, Lee SS, Ryu MH, Lee JL, Chang HM, Kim TW, Chi HS, Kim WK, Lee JS, Kang YK - J. Korean Med. Sci. (2006)

Bottom Line: Based on bone marrow examination, chromosome analysis and polymerase chain reaction he was diagnosed with Philadelphia chromosome negative, BCR/ABL gene rearrangement negative CML.Following 3 months of treatment with gemcitabine for pancreatic cancer, he developed bilateral pleural effusions.All stages of granulocytes and a few blasts were present in both the pleural fluid and a peripheral blood smear.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, University of Ulsan College of Medicine, Seoul, Korea.

ABSTRACT
Pleural effusion in chronic myeloid leukemia (CML) is poorly understood and rarely reported in the literature. When the pleural effusion is caused by leukemic pleural infiltration, the differential white blood cell count of the effusion is identical to that of the peripheral blood, and the fluid cytology reveals leukemic blasts. We report here a case of bilateral pleural involvement of atypical CML in an 83-yr old male diagnosed with pancreatic cancer with abdominal wall metastasis and incidental peripheral leukocytosis. Based on bone marrow examination, chromosome analysis and polymerase chain reaction he was diagnosed with Philadelphia chromosome negative, BCR/ABL gene rearrangement negative CML. Following 3 months of treatment with gemcitabine for pancreatic cancer, he developed bilateral pleural effusions. All stages of granulocytes and a few blasts were present in both the pleural fluid and a peripheral blood smear. After treatment with hydroxyurea and pleurodesis, the pleural effusion resolved.

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Radiograph of the chest revealing bilateral pleural effusion.
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Figure 3: Radiograph of the chest revealing bilateral pleural effusion.

Mentions: After 3 months of treatment with gemcitabine, the patient experienced progressive dyspnea and fatigue, as well as being tachypneic (30/min) and pale. Pulmonary examination revealed decreased bilateral breathing sounds and chest radiograph showed bilateral pleural effusion (Fig. 3). Right thoracentesis was performed and 1,400 mL of serous fluid was aspirated. Analysis of the pleural fluid showed glucose 109 mg/dL, protein 2.2 g/dL (serum protein 4.6 g/dL), albumin 1.1 g/dL (serum albumin 2.0 g/dL), LDH 386 IU/L (serum LDH 1,064 IU/L, reference range 120-250 IU/L), adenosine deaminase 23U/L, hematocrit 6.0%, WBC count 2,390 /µL (neutrophil 51%, lymphocyte 19%, histiocyte 9%, band form 6%, promyelocyte 3%, myelocyte 5%, metamyelocyte 5%, normoblast 3/100 WBC, blast 2%) (Fig. 4). Hematologic findings of the peripheral blood were Hb 8.7 g/dL, WBC 150×109/L (neutrophil 62%, lymphocyte 7%, monocyte 5%, promyelocyte 2%, myelocyte 18%, metamyelocyte 5%, blast 0%, normoblast 1/100 WBC), platelet 109×109/L. The ratio of erythrocytes to nucleated cells in the effusion was 8 as compared to a ratio of 18 in the blood, suggesting that the nucleated cells in the effusion were not solely due to bleeding into the pleural cavity. The pleural fluid was negative for Gram stain and acid fast bacilli. The patient was diagnosed with CML complicated with pleural effusion. Bilateral chest drainage catheters were inserted to control the pleural effusion. The patient was retreated with hydroxyurea and allopurinol, and the amount of pleural fluid decreased in accord with the decrease in the WBC count of peripheral blood. Due to loculated pleural effusion, however, the effusion did not completely resolve. At this point, a right chest tube was substituted for the right chest drainage catheter. Pleurodesis was performed for the right pleural effusion, thus relieving dyspnea of the patient. Two months after the appearance of the pleural involvement, the patient died due to hypercarbic respiratory failure. Until that time, however, no peripheral blood blast crisis was detected.


A case of leukemic pleural infiltration in atypical chronic myeloid leukemia.

Kim HW, Lee SS, Ryu MH, Lee JL, Chang HM, Kim TW, Chi HS, Kim WK, Lee JS, Kang YK - J. Korean Med. Sci. (2006)

Radiograph of the chest revealing bilateral pleural effusion.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2722009&req=5

Figure 3: Radiograph of the chest revealing bilateral pleural effusion.
Mentions: After 3 months of treatment with gemcitabine, the patient experienced progressive dyspnea and fatigue, as well as being tachypneic (30/min) and pale. Pulmonary examination revealed decreased bilateral breathing sounds and chest radiograph showed bilateral pleural effusion (Fig. 3). Right thoracentesis was performed and 1,400 mL of serous fluid was aspirated. Analysis of the pleural fluid showed glucose 109 mg/dL, protein 2.2 g/dL (serum protein 4.6 g/dL), albumin 1.1 g/dL (serum albumin 2.0 g/dL), LDH 386 IU/L (serum LDH 1,064 IU/L, reference range 120-250 IU/L), adenosine deaminase 23U/L, hematocrit 6.0%, WBC count 2,390 /µL (neutrophil 51%, lymphocyte 19%, histiocyte 9%, band form 6%, promyelocyte 3%, myelocyte 5%, metamyelocyte 5%, normoblast 3/100 WBC, blast 2%) (Fig. 4). Hematologic findings of the peripheral blood were Hb 8.7 g/dL, WBC 150×109/L (neutrophil 62%, lymphocyte 7%, monocyte 5%, promyelocyte 2%, myelocyte 18%, metamyelocyte 5%, blast 0%, normoblast 1/100 WBC), platelet 109×109/L. The ratio of erythrocytes to nucleated cells in the effusion was 8 as compared to a ratio of 18 in the blood, suggesting that the nucleated cells in the effusion were not solely due to bleeding into the pleural cavity. The pleural fluid was negative for Gram stain and acid fast bacilli. The patient was diagnosed with CML complicated with pleural effusion. Bilateral chest drainage catheters were inserted to control the pleural effusion. The patient was retreated with hydroxyurea and allopurinol, and the amount of pleural fluid decreased in accord with the decrease in the WBC count of peripheral blood. Due to loculated pleural effusion, however, the effusion did not completely resolve. At this point, a right chest tube was substituted for the right chest drainage catheter. Pleurodesis was performed for the right pleural effusion, thus relieving dyspnea of the patient. Two months after the appearance of the pleural involvement, the patient died due to hypercarbic respiratory failure. Until that time, however, no peripheral blood blast crisis was detected.

Bottom Line: Based on bone marrow examination, chromosome analysis and polymerase chain reaction he was diagnosed with Philadelphia chromosome negative, BCR/ABL gene rearrangement negative CML.Following 3 months of treatment with gemcitabine for pancreatic cancer, he developed bilateral pleural effusions.All stages of granulocytes and a few blasts were present in both the pleural fluid and a peripheral blood smear.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, University of Ulsan College of Medicine, Seoul, Korea.

ABSTRACT
Pleural effusion in chronic myeloid leukemia (CML) is poorly understood and rarely reported in the literature. When the pleural effusion is caused by leukemic pleural infiltration, the differential white blood cell count of the effusion is identical to that of the peripheral blood, and the fluid cytology reveals leukemic blasts. We report here a case of bilateral pleural involvement of atypical CML in an 83-yr old male diagnosed with pancreatic cancer with abdominal wall metastasis and incidental peripheral leukocytosis. Based on bone marrow examination, chromosome analysis and polymerase chain reaction he was diagnosed with Philadelphia chromosome negative, BCR/ABL gene rearrangement negative CML. Following 3 months of treatment with gemcitabine for pancreatic cancer, he developed bilateral pleural effusions. All stages of granulocytes and a few blasts were present in both the pleural fluid and a peripheral blood smear. After treatment with hydroxyurea and pleurodesis, the pleural effusion resolved.

Show MeSH
Related in: MedlinePlus