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A case of comorbid myxoma and chronic lymphocytic leukemia: not just a coincidence?

Laird-Fick H, Tiwari A, Narayanan S, Qin Y, Vodnala D, Bhutani M - Case Rep Oncol Med (2014)

Bottom Line: Biopsy confirmed B cell CLL/small lymphocytic lymphoma.Conclusions.Possibilities include chronic inflammation, vascular endothelial growth factor A, shared genetic mutations, changes in posttranslational regulation, or alterations in other cellular signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Michigan State University College of Human Medicine, 788 Service Road Suite B301, East Lansing, MI 48824, USA.

ABSTRACT
Background. It is unclear why cardiac myxomas develop. We describe a case of comorbid myxoma and chronic lymphocytic leukemia (CLL) to offer insights into the tumor's pathophysiology. Case. A 56-year-old female with recurrent venous thromboembolism developed embolic stroke. Transesophageal echocardiogram showed a 1.7 × 1 cm sessile left atrial mass at the interatrial septum. Histopathology revealed myxoma with a B cell lymphocytic infiltrate suggestive of a low grade lymphoproliferative disorder. Bone marrow biopsy and flow cytometry of blood and the cardiac infiltrate supported the diagnosis of atypical CLL. She was followed clinically in the absence of symptoms, organ infiltration, or cytopenia. After eighteen months, she developed cervical and axillary lymphadenopathy. Biopsy confirmed B cell CLL/small lymphocytic lymphoma. She elected to undergo chemotherapy with fludarabine, cyclophosphamide, and rituximab, with clinical remission. Conclusions. The coexistence of two neoplastic processes may be coincidental, but the cumulative likelihood is estimated at 0.002 per billion people per year. A shared pathogenic mechanism is more likely. Possibilities include chronic inflammation, vascular endothelial growth factor A, shared genetic mutations, changes in posttranslational regulation, or alterations in other cellular signaling pathways. Additional studies could expand our current understanding of the molecular biology of both myxomas and CLL.

No MeSH data available.


Related in: MedlinePlus

H&E stain. H&E stained slide demonstrating atrial myxoma tissue (A) and B cell lymphoma (*) and a 40x image (top left corner) showing B cell lymphocytic infiltrates into atrial myxoma.
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fig1: H&E stain. H&E stained slide demonstrating atrial myxoma tissue (A) and B cell lymphoma (*) and a 40x image (top left corner) showing B cell lymphocytic infiltrates into atrial myxoma.

Mentions: A 56-year-old Caucasian female with a history of recurrent venous thromboembolism developed embolic stroke of the left pons and left occipital cortex while hospitalized with sepsis, pyelonephritis, and nephrolithiasis. Transesophageal echocardiogram showed a 1.7 × 1 cm sessile left atrial mass attached to the interatrial septum suggestive of myxoma, thrombus, or other tumor. The mass persisted at six weeks despite anticoagulation and antibiotic therapy. She therefore underwent surgical resection. Histopathological examination revealed myxoma with a B-cell lymphocytic infiltrate suggestive of a low grade lymphoproliferative disorder (Figure 1).


A case of comorbid myxoma and chronic lymphocytic leukemia: not just a coincidence?

Laird-Fick H, Tiwari A, Narayanan S, Qin Y, Vodnala D, Bhutani M - Case Rep Oncol Med (2014)

H&E stain. H&E stained slide demonstrating atrial myxoma tissue (A) and B cell lymphoma (*) and a 40x image (top left corner) showing B cell lymphocytic infiltrates into atrial myxoma.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4020543&req=5

fig1: H&E stain. H&E stained slide demonstrating atrial myxoma tissue (A) and B cell lymphoma (*) and a 40x image (top left corner) showing B cell lymphocytic infiltrates into atrial myxoma.
Mentions: A 56-year-old Caucasian female with a history of recurrent venous thromboembolism developed embolic stroke of the left pons and left occipital cortex while hospitalized with sepsis, pyelonephritis, and nephrolithiasis. Transesophageal echocardiogram showed a 1.7 × 1 cm sessile left atrial mass attached to the interatrial septum suggestive of myxoma, thrombus, or other tumor. The mass persisted at six weeks despite anticoagulation and antibiotic therapy. She therefore underwent surgical resection. Histopathological examination revealed myxoma with a B-cell lymphocytic infiltrate suggestive of a low grade lymphoproliferative disorder (Figure 1).

Bottom Line: Biopsy confirmed B cell CLL/small lymphocytic lymphoma.Conclusions.Possibilities include chronic inflammation, vascular endothelial growth factor A, shared genetic mutations, changes in posttranslational regulation, or alterations in other cellular signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Michigan State University College of Human Medicine, 788 Service Road Suite B301, East Lansing, MI 48824, USA.

ABSTRACT
Background. It is unclear why cardiac myxomas develop. We describe a case of comorbid myxoma and chronic lymphocytic leukemia (CLL) to offer insights into the tumor's pathophysiology. Case. A 56-year-old female with recurrent venous thromboembolism developed embolic stroke. Transesophageal echocardiogram showed a 1.7 × 1 cm sessile left atrial mass at the interatrial septum. Histopathology revealed myxoma with a B cell lymphocytic infiltrate suggestive of a low grade lymphoproliferative disorder. Bone marrow biopsy and flow cytometry of blood and the cardiac infiltrate supported the diagnosis of atypical CLL. She was followed clinically in the absence of symptoms, organ infiltration, or cytopenia. After eighteen months, she developed cervical and axillary lymphadenopathy. Biopsy confirmed B cell CLL/small lymphocytic lymphoma. She elected to undergo chemotherapy with fludarabine, cyclophosphamide, and rituximab, with clinical remission. Conclusions. The coexistence of two neoplastic processes may be coincidental, but the cumulative likelihood is estimated at 0.002 per billion people per year. A shared pathogenic mechanism is more likely. Possibilities include chronic inflammation, vascular endothelial growth factor A, shared genetic mutations, changes in posttranslational regulation, or alterations in other cellular signaling pathways. Additional studies could expand our current understanding of the molecular biology of both myxomas and CLL.

No MeSH data available.


Related in: MedlinePlus