Peripheral primitive neuroectodermal tumor of the chest wall of a 69-year-old man.

We report a case of peripheral primitive neuroectodermal tumor (pPNET), which belongs to the pPNET/Ewing's sarcoma family, arising in the chest wall of a 69-year-old man. He had high levels of serum neuron-specific enolase and pro-gastrin-releasing peptide, which are believed to be useful diagnostic blood markers for small cell lung carcinoma (SCLC). Microscopically, the tumor was composed of solid nests and sheets of monotous, primitive, small round cells with a few rosettes, making it difficult to distinguish from SCLC. Immunohistochemically, the tumor cells showed intense cell membranous immunoreactivity for MIC2 protein (CD99). EWS/FLI-1 chimeric mRNA that originated from the characteristic t(11;22)(q24;q12) chromosomal translocation was detected by RT-PCR and nucleotide sequence analysis. These results confirmed the diagnostic validity of the present tumor being a pPNET, thus raising the possibility that in the past, pPNETs which have arisen in the chest have been mistakenly diagnosed as SCLC.

Secondary pulmonary alveolar proteinosis associated with myelodysplastic syndrome.

A 47-year-old man, who had been diagnosed as myelodysplastic syndrome (MDS), complained of a severe cough and a high-grade fever. Chest CT disclosed scattered small nodules and ground-glass opacities with interlobular septal thickening in both lung fields and a mass lesion in the right lower lobe. Pathological findings of the ground-glass opacities and the mass lesion obtained by video-assisted thoracoscopic surgery revealed the accumulation of eosinophilic amorphous material in the alveoli and confirmed the diagnosis of pulmonary alveolar proteinosis (PAP). Autoantibodies against granulocyte-macrophage colony-stimulating factor (GM-CSF) in sera were below sensitivity, while the GM-CSF level was elevated in bronchoalveolar lavage fluid. He was diagnosed as secondary PAP associated with MDS.

Elevated levels of serum macrophage migration inhibitory factor in patients with pulmonary tuberculosis.

Macrophage migration inhibitory factor (MIF) was originally described as a T-cell-derived cytokine that inhibits the random migration of macrophages and promotes the delayed-type hypersensitivity reaction. MIF plays an important role in the regulation of the Th1/Th2 balance in inflammatory response. This study investigated serum levels of circulating MIF in patients with pulmonary tuberculosis. The levels of MIF in sera were measured by enzyme-linked immunosorbent assay in 34 patients with pulmonary tuberculosis (16 males and 18 females) and 30 healthy controls (15 males and 15 females). The mean levels of circulating MIF values were significantly higher in those with pulmonary tuberculosis (19.84 +/- 11.27 ng/ml; P < 0.0001) than in the healthy controls (4.38 +/- 1.34 ng/ml). Circulating MIF values significantly correlated with circulating interferon-gamma values (r = 0.537, P < 0.0001). Thus, MIF may play an important role in immune responses to human infection with Mycobacterium tuberculosis.