Although the pulmonary artery is involved in many cases of Takayasu arteritis, few cases have been reported in which the pulmonary artery was initially involved. Two such cases are reported here. Both of these cases had been initially diagnosed as chronic pulmonary embolism. The importance of considering Takayasu arteritis in cases of chronic pulmonary arterial obstruction of unknown cause is emphasized. Bronchial-pulmonary artery communication and coronary-bronchial artery communication in Takayasu arteritis are also discussed.
Coronary-to-pulmonary artery shunts via the bronchial artery (CA-BA-PA shunts) were observed in 16 of 2,922 consecutive patients who underwent selective coronary cineangiography. Underlying diseases included Takayasu arteritis (n = 8), chronic pulmonary inflammatory diseases (n = 4), pulmonary thromboembolism (n = 2), pulmonary artery tumor (n = 1), and tetralogy of Fallot with pulmonary atresia (n = 1). Ventilation-perfusion scans were available in 15 of the 16 patients. Mismatched defects were identified in 11 patients, and matched defects were identified in four. Bronchial-to-pulmonary artery shunts were detected on selective bronchial angiograms and/or thoracic aortograms in 13 patients. Feeding arteries of the CA-BA-PA shunts included left atrial branches (n = 13), right sinus node branches (n = 7), left sinus node branches (n = 2), right conal branch (n = 1), left conal branch (n = 1), and posterolateral branches (n = 2). These coronary branches seemed to serve as collateral vessels from a coronary arterial system with a higher pressure to a pulmonary arterial system with a lower pressure in conditions of decreased pulmonary flow or in cases of chronic pulmonary inflammatory disease. The importance of the coronary artery along with other superior thoracic collateral networks in contributing to the development of shunts to the pulmonary artery is underscored.
Adult T-cell leukemia (ATL) is one of the most difficult diseases to treat because of severe underlying immune deficiency and metabolic disturbance. Interferon has potent antiviral, antiproliferative, and immunomodulating properties, and therefore, this may be a good agent to treat such immune deficient patients with peripheral T-cell leukemia. During a period from April 1984 to August 1985, six patients were treated with interferon-beta (IFN-beta), and interferon-gamma (IFN-gamma) was given to five patients. Three patients achieved partial remission by IFN-beta administration with a response duration of 1, 1.5, and 12 months respectively, whereas one complete remission and two partial responses were experienced by IFN-gamma treatment with 4, 4, and 2 months of response. Side effects of IFN-beta were similar to those of IFN-gamma including fever, chills, fatigue, mild hematologic depression, and transient hepatic enzyme abnormalities. These promising results warrant further well-designed clinical trials including combination with other agents or modalities of treatment.
A high plasma PTX3 level in elderly hypertensive patients, particularly in those with a high 24-hour BP level, could be a significant predictor of cognitive impairment. A high PTX3 level may be a marker of frailty in elderly hypertensive patients.
We examined the associations of circulating levels of pentraxin 3 (PTX3), monocyte chemoattractant protein-1 (MCP-1), and some other inflammatory mediators with cardiorenal syndrome. In advanced chronic kidney disease (CKD) patients (estimated glomerular filtration rate <30 mL/min/1.73 m 2 ), the values of area under the curve of PTX3, tumor necrosis factor a, and high-sensitivity C-reactive protein for the detection of the association of cardiovascular disease (CVD) were 0.664, 0.507, and 0.318, respectively. In contrast, serum levels of MCP-1 were significantly higher in CKD patients than in control subjects independently of association with CVD. AbstractBoth pentraxin 3 (PTX3) and monocyte chemoattractant protein-1 (MCP-1) are mediators of inflammation. They also appear to play critical roles in vascular endothelial dysfunction but their associations with cardiorenal syndrome remain largely unknown. The objective of this study was to examine their associations with cardiorenal syndrome. Circulating levels of PTX3, MCP-1, and some other biomarkers were evaluated in 134 patients with chronic kidney disease (CKD) and/or cardiovascular disease (CVD) and 55 age-and gender-matched subjects without CKD or CVD. Levels of PTX3, high-sensitivity C-reactive protein (hsCRP), and tumor necrosis factor a (TNFa) were significantly higher in CKD patients with CVD than in those without CVD. In advanced CKD patients (estimated glomerular filtration rate <30 mL/min/1.73 m 2 ), the values of area under the curve of PTX3, TNFa, and hsCRP for the detection of the association of CVD were 0.664, 0.507, and 0.318, respectively. In contrast, serum levels of MCP-1 were significantly higher in CKD patients than in control subjects independently of association with CVD. PTX3, hsCRP, and TNFa, but not MCP-1 could predict the presence of CVD as a complication associated with CKD. Additionally, PTX3 might be a more sensitive marker for the association of CVD than hsCRP and TNFa in patients with advanced CKD.
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