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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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(A) Smear of marrow aspirate showing increased numbers of granulocytes at all stages of development and blasts (Wright-Giemsa stain, ×400). (B) Smear of marrow aspirate showing hypogranular myelocytes (arrow) (Wright-Giemsa stain, ×1,000).
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Figure 1: (A) Smear of marrow aspirate showing increased numbers of granulocytes at all stages of development and blasts (Wright-Giemsa stain, ×400). (B) Smear of marrow aspirate showing hypogranular myelocytes (arrow) (Wright-Giemsa stain, ×1,000).

Mentions: On physical examination, the patient's liver and spleen were not palpable. A tender and firm mass, measuring 1×2 cm, was noted on the periumbilical abdominal wall. Hematologic findings were Hb 10.6 g/dL, WBC 71×109/L (neutrophil 58%, lymphocyte 7%, monocyte 13%, eosinophil 3%, promyelocyte 2%, myelocyte 10%, metamyelocyte 4%, blast 1%, normoblast 1/100 WBC), and platelet 192×109/L. Pathologic examination showed that his palpable abdominal wall mass was a metastatic adenocarcinoma that differed from the previous non small cell lung cancer. Immunohistochemically, the tumor cells were positive for cytokeratin 7 (CK7) and negative for thyroid transcription factor 1 (TTF-1) and cytokeratin 20 (CK20), whereas his non small cell lung cancer cells had been positive for TTF-1 and CK7 and negative for CK20. Bone marrow examination showed hypercellular marrow (cellularity 90%) containing cells at all stages of granulocytic hyperplasia and 0.6% blasts. There were some hypogranular myelocytes, indicating dysgranulopoiesis (Fig. 1). Polymerase chain reaction for BCR/ABL fusion gene was negative. The leukocyte alkaline phosphatase (LAP) activity score was 13 (reference range 30-130). Computed tomography of the abdomen showed a solid mass in the tail of the pancreas with attachment to the spleen and invasion of the spleen and splenic artery by the mass, leading to splenic infarction (Fig. 2). Based on these results, he was diagnosed with atypical CML. He was treated with gefitinib 250 mg/day for metastatic pancreatic cancer and hydroxyurea 1,500 mg/day plus allopurinol for atypical CML. Treatment with hydroxyurea was interrupted intermittently when WBC count of the peripheral blood decreased to 10×109/L or less. Beginning in November 2004, he was treated with gemcitabine for pancreatic cancer, interrupted periodically because of infectious diarrhea, acute renal failure due to use of aminoglycoside antibiotics and skin rash. At that time, treatment with hydroxyurea was stopped due to thrombocytopenia.


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)

(A) Smear of marrow aspirate showing increased numbers of granulocytes at all stages of development and blasts (Wright-Giemsa stain, ×400). (B) Smear of marrow aspirate showing hypogranular myelocytes (arrow) (Wright-Giemsa stain, ×1,000).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: (A) Smear of marrow aspirate showing increased numbers of granulocytes at all stages of development and blasts (Wright-Giemsa stain, ×400). (B) Smear of marrow aspirate showing hypogranular myelocytes (arrow) (Wright-Giemsa stain, ×1,000).
Mentions: On physical examination, the patient's liver and spleen were not palpable. A tender and firm mass, measuring 1×2 cm, was noted on the periumbilical abdominal wall. Hematologic findings were Hb 10.6 g/dL, WBC 71×109/L (neutrophil 58%, lymphocyte 7%, monocyte 13%, eosinophil 3%, promyelocyte 2%, myelocyte 10%, metamyelocyte 4%, blast 1%, normoblast 1/100 WBC), and platelet 192×109/L. Pathologic examination showed that his palpable abdominal wall mass was a metastatic adenocarcinoma that differed from the previous non small cell lung cancer. Immunohistochemically, the tumor cells were positive for cytokeratin 7 (CK7) and negative for thyroid transcription factor 1 (TTF-1) and cytokeratin 20 (CK20), whereas his non small cell lung cancer cells had been positive for TTF-1 and CK7 and negative for CK20. Bone marrow examination showed hypercellular marrow (cellularity 90%) containing cells at all stages of granulocytic hyperplasia and 0.6% blasts. There were some hypogranular myelocytes, indicating dysgranulopoiesis (Fig. 1). Polymerase chain reaction for BCR/ABL fusion gene was negative. The leukocyte alkaline phosphatase (LAP) activity score was 13 (reference range 30-130). Computed tomography of the abdomen showed a solid mass in the tail of the pancreas with attachment to the spleen and invasion of the spleen and splenic artery by the mass, leading to splenic infarction (Fig. 2). Based on these results, he was diagnosed with atypical CML. He was treated with gefitinib 250 mg/day for metastatic pancreatic cancer and hydroxyurea 1,500 mg/day plus allopurinol for atypical CML. Treatment with hydroxyurea was interrupted intermittently when WBC count of the peripheral blood decreased to 10×109/L or less. Beginning in November 2004, he was treated with gemcitabine for pancreatic cancer, interrupted periodically because of infectious diarrhea, acute renal failure due to use of aminoglycoside antibiotics and skin rash. At that time, treatment with hydroxyurea was stopped due to thrombocytopenia.

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