Airway inflammation during stable and acutely exacerbated chronic obstructive pulmonary disease.

The aim of this study was to clarify the mechanism of increased airway inflammation during an acute exacerbation. A total of 68 chronic obstructive pulmonary disease patients in a stable phase were enrolled and followed-up for 2-3 yrs. Inflammatory cells were analysed, and interleukin (IL)-8, neutrophil elastase, eotaxin, tryptase and RANTES (regulated on activation, normal T-cell expressed and secreted) were measured in sputum, both in a stable phase and during acute exacerbation. Out of 68 patients, 30 (unstable group) developed an acute exacerbation and expectorated adequate sputum during exacerbation. Thirty-two patients (stable group) did not develop any exacerbation for 2-3 yrs. The number of neutrophils, lymphocytes and eosinophils, and the levels of IL-8, eosinophil cationic protein (ECP), eotaxin and tryptase in sputum obtained from patients in both groups during the stable phase were significantly higher than those from healthy nonsmokers. There were no significant differences in cell analysis and biomarkers between the two groups, but patients in the unstable group showed more severe airflow limitation. In the unstable group, total cells, lymphocytes, neutrophils and eosinophils, and IL-8, neutrophil elastase, ECP and RANTES levels were significantly increased during an exacerbation from values in a stable phase. These findings suggest that exacerbation of chronic obstructive pulmonary disease may associate with additional increases in airway inflammation mediated by neutrophils, lymphocytes, eosinophils, interleukin-8 and RANTES.

Massive pericardial effusion in an adult case of congenital hypothyroidism due to a sublingual thyroid.

Acquired hypothyroidism is known to cause cardiac tamponade. However, pericardial effusion in cretinism in adulthood has rarely been reported. A 27-year-old dwarfish woman suffering from congestive heart failure was diagnosed with congenital hypothyroidism due to the presence of a sublingual thyroid. The patient had never received thyroid therapy until the time of diagnosis at age 27. Despite the existence of massive pericardial effusion, the patient had hypertension. Her metabolic abnormality responded dramatically to L-thyroxin. Pericardial effusion disappeared one year after the initiation of medical treatment.