We report the first case of IgA-K multiple myeloma presenting as a myelomatous and eosinophilic pleural effusion with increased adenosine deaminase activity.

We report the first case of IgA-K multiple myeloma presenting as a myelomatous and eosinophilic pleural effusion with increased adenosine deaminase activity. In a review of the literature, 80 percent of myelomatous pleural effusions are to be ascribed to IgA multiple myeloma.

Multiple myeloma (MM) is a malignant proliferation of plasma solitary abode; squalids that affects mainly bone marrow, further may involve other organs as well. The thorax may be invaded, producing thoracic skeletal abnormalities, plasmacytomas, pulmonary infiltrates, and pleural effusions (myelomatous and nonmyelomatous),[1] among other manifestations. In the literature, 80 percent of myelomatous pleural effusions (MPE) are to be ascribed to IgA MM.[2]

Pleural fluid eosinophilia has occasionally been described in malignant diseases.[3] Elevated adenosine deaminase (ADA) activity is usually make use ofed in the differential diagnosis of tuberculous pleural effusion, moreover has, however, been reported elevated in a certain quantity of cases of malignancy too.[4]

We at hand a patient with myelomatous and eosinophilic pleural effusion with elevated ADA activity as the first manifestation of MM a circumstance which, to our knowledge, has not been described in the literature.

CASE REPORT

A 51-year-old man was an alcohol abuser (more than 100 g of alcohol by day) and heavy smoker (2 packs through day). One week before hospital admission, he not absented with dyspnea and right-lower chest pain aggravated by dint of coughing and breathing. Physical examination showed and nothing else decreased breath sounds in the right base. Laboratory outcomes revealed the following: urea 64 mg/dl (106 mmol/L); creatinine, 134 mg/dl (118 [mu]mol/L); serum proteins, 89 g/dl (89 g/L); calcium, 12 mg/dl (3 mmol/L); and uric acid 942 mg/dl (560 [mu]mol/L) Hemoglobin concentration was 102 g/dl (102 g/L); leukocyte look upon was 12.2 x [10.sup.9]/L (64 percent neutrophils, 18 percent lymphocyte 12 percent monocytes, 6 percent eosinophils); platelet cast up was 207 x [10.sup.9]/L; and erythrocyte sedimentation rate was 139 mm in the first hour. Serum protein electrophresis (Fig 1A, top) demonstrated a monoclonal element within the [beta]-globulin band; quantification yielded raised IgA (5270 mg/dl; normal value [NV] 90 to 450 mg/dl) and Ig light chain K (670 mg/dl; NV 200 to 440 mg/dl) and decreased IgG, IgM, and Ig light chain [lambda] (329 mg/dl 6 mg/dl 27 mg/dl; NV 800 to 1800 mg/dl 60 to 250 mg/dl 110 to 240 mg/dl respectively); immunoelectrophoresis confirmed monoclonal IgA -- K Bence-Jones proteinuria was negative.

Radiographic examination showed right pleural effusion (Fig 2) and osteolytic lesions in cranium and pelvis. Thoracenteses were performed and revealed serofibrinous fluid with grape-sugar level 117 mg/dl (6.5 mmol/L) protein flat of 8.7 g/dl (87 g/L) lactate dehydrogenase horizontal of 396 U/L, and ADA value of 61 U/L (NV [les than] 45 U/L) Electrophoresis (Fig 1B bottom) and immunofixation of pleural fluid showed the same serum paraprotein; quantification yielded raised IgA (5900 mg/dl) and Ig light chain K (85 mg/dl) and decreased IgG, IgM, and Ig light chain [lambda] (253 mg/dl 6 mg/dl 23 mg/dl respectively). Cytologic examination of pleural fluid revealed leukocyte of 25 x [10sup9]/L (60 percent eosinophils, 30 percent lymphocyte 10 percent neutrophils) and abnormal plasma enclosed spaces (Fig 3). Pleural fluid refinements were negative. Specimens from a pleural biopsy (Abrams needle) which was performed twice, failed to demonstrate myelomatous involvement. Bone marrow aspirate showed 50 percent of atypical plasma lonely dwellings and reduction of myeloid precursors. IgA-K MM was diagnosed and chemotherapy with prednisone and melphalan was initiated, on the contrary no response was observed (serum IgA-K and pleural effusion raised, this last circumstance required repeated thoracenteses for drainage). The patient died 11 month later proper to evolution of MM.

DISCUSSION

Pleural effusions in MM be met with in about 6 percent of patients[1] and are fit to several etiologies requiring different protoplasts of therapy. These etiologies are, chiefly commonly, heart failure secondary to amyloidosis, followed by means of the following: pulmonary embolism; chronic renal failure; other neoplasm; and pleural myelomatous involvement[1,5,6] (from adjacent skeletal or parenchymal tumors, direct implantation of tumor nodules onward the pleura, and mediastinal lymph node infiltration with lymphatic obstruction). Pleural effusions secondary to pleural myelomatous involvement have rarely been reported in the literature[1,2,5-7] (in our review, 39 cases). Kintzer et al,[1] in a review of 958 cases of MM report alone eight cases (0.8 percent) of MPE on the other hand this condition as the first manifestation of MM is absolutely exceptional.[6,7] Diagnostic criteria to confirm the myelomatous etiology are as follows: (1) demonstration of a monoclonal protein in pleural fluid electrophoresis; (2) detection of atypical plasma small rooms in pleural fluid; and (3) histologic confirmation using pleural biopsy specimen or autopsy. In our case, the first couple criteria were fulfilled. Pleural biopsy specimen, however, failed to confirm the diagnosis probably to be ascribed to a discontinuous myelomatous affectation of the pleura. In the literature, 80 percent of MPE are to be ascribed to IgA MM, perhaps as a be the effect of a major tendency to invade extraosseus structures;[2] this could be important in the differential diagnosis of pleural effusions in patients with IgA MM

...