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      An Interleukin-6-Producing Cardiac Myxoma Associated with Mediastinal Lymphadenopathy


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          We report our experience with a patient whose mediastinal lymphadenopathy resolved after resection of a cardiac myxoma that secreted interleukin-6 (IL-6). The patient was a 68-year-old female who complained of nocturnal chest discomfort related to congestive heart failure. An echocardiogram demonstrated a large left atrial mass. A computed tomogram showed not only the left atrial mass but multiple enlarged mediastinal lymph nodes. The serum IL-6 level was markedly elevated at 13.7 pg/ml. After resection of the cardiac myxoma, serum IL-6 returned to the normal range. A repeat computed tomogram showed no mediastinal lymphadenopathy. We believe that overproduction of IL-6 by the cardiac myxoma was the cause of the mediastinal lymphadenopathy.

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          Most cited references 3

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          Cardiac myxomas.

           K Reynen (1995)
          Although cardiac myxomas are histologically benign, they may be lethal because of their strategic position. They can mimic not only every cardiac disease but also infective, immunologic, and malignant processes. Myxomas must therefore be included in the differential diagnosis of valvular heart disease, cardiac insufficiency, cardiomegaly, bacterial endocarditis, disturbances of ventricular and supraventricular rhythm, syncope, and systemic or pulmonary embolism. The symptoms depend on the size, mobility, and location of the tumor. Echocardiography, including the transesophageal approach, is the most important means of diagnosis; CT and MRI may also be helpful. Coronary arteriography in patients over 40 years of age is generally required to rule out concomitant coronary artery disease. Surgical removal of the tumor should be performed as soon as possible; the long-term prognosis is excellent, and recurrences are rare. In follow-up examinations as well, echocardiography is essential.
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            Interleukin-6 secreted from human myxoma reduces murine viral myocarditis

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              Suboptimal Clinical Response to Anti-tumor Necrosis Factor alpha (TNFa) Antibody Therapy in a Patient with Severe Rheumatoid Arthritis and Lymphadenopathy: CASE REPORT


                Author and article information

                S. Karger AG
                April 2000
                19 April 2000
                : 92
                : 4
                : 275-277
                aCardiovascular Hospital of Central Japan, Hokkitsu-mura, bSecond Department of Internal Medicine, and cDepartment of Laboratory Medicine, Gunma University School of Medicine, Maebashi, Japan
                6986 Cardiology 1999;92:275–277
                © 2000 S. Karger AG, Basel

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                Figures: 2, References: 11, Pages: 3
                Case Report


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