[Hemoptysis caused by bleeding into a bleb].

A man in his 40s was admitted to our hospital for hemoptysis. A chest computed tomography showed a mediastinal mass adjacent to the left side wall of the ascending aorta with infiltrative shadows of the left upper lobe. In spite of medical treatment, hemoptysis continued, and the surgery was performed. The thoracoscopic findings showed hematoma in the bullous cavity. Partial resection of the left upper lobe was performed. Histopathological findings in the resected specimen revealed a bleb that was filled with blood.

The effect of high salt concentration on detection of serum immune complexes and autoantibodies to C1q in patients with systemic lupus erythematosus.

OBJECTIVE: To compare the binding of immune complexes and anti-Clq in systemic lupus erythematosus (SLE) sera to Clq and to the purified collagen-like region of Clq (CLR) in high and physiologic NaCl concentrations. METHODS: Sera from patients with SLE were tested for binding of IgG to Clq and to CLR in physiologic (0.15 M NaCl) or high (1.0 M NaCl) salt concentration. Sera were ultracentrifuged to separate monomeric IgG and high molecular weight IgG (immune complexes), and fractions were tested for binding to C1q and to CLR in the presence of physiologic or high salt concentrations. RESULTS: Decrease in binding of immune complexes to Clq in the presence of high salt ranged from 0 to 96.8%, with a median of 48.4%. Decrease of the binding of monomeric IgG to C1q in the presence of high salt ranged from 2.2 to 74.3%, with a median of 46.2%. Binding of monomeric autoantibodies to CLR also was decreased by high salt. Nevertheless, anti-Clq measured by binding to CLR in physiologic salt correlated highly with the binding to Clq in both physiologic (r = 0.978) and high salt (r = 0.983). CONCLUSION: Clq-binding of immune complexes in SLE sera is not uniformly abrogated by high salt and binding of autoantibodies to CLR is variably reduced by high salt. Binding of IgG to Clq in high salt correlates with but is not equivalent to quantifying these autoantibodies by binding to CLR.