Should curative surgery be attempted in patients with cancer of the main stem bronchus?

Among tumors of the lung, main stem bronchial cancer offers a particularly unfavorable prognosis, probably because of its rapid extension to the segmental bronchi, trachea, and extrapulmonary structures. However, analysis of data gathered by the End Results Group indicates that survival among those patients with main stem bronchial cancer whose tumor was resected was virtually the same as that of patients with resectable lung cancer of other sites. From these data it is impossible to assess what role, if any, the resection itself played, and a randomized trial would be necessary to determine whether resection improves the probability of patient survival. On the other hand, it is not now advisable to deny resection to patients with operable main stem bronchial tumors (except oat cell tumors) on the basis of the available nonexperimental evidence alone.     

Activation of the alternate complement pathway in Staph. aureus infective endocarditis and its relationship to thrombocytopenia, coagulation abnormalities, and acute glomerulonephritis

Twenty-four patients with infective endocarditis (IE) are described, fourteen with Staph. aureus and ten with other organisms. Despite the acute nature of the infection, ten of the fourteen with Staph. aureus IE were hypocomplementaemic; six of these ten had normal levels of C4 associated with low C3 levels, suggesting activation of the alternate complement pathway. Factor B (C3PA) was also low in three of these six cases. In the ten patients with non-Staph. IE, three had hypocomplementaemia with low levels of C4, C3, and Factor B, probably due to C1 (classical pathway) activation with feedback activation of the alternate pathway. In addition, thrombocytopenia was noted in nine of the twenty-four patients and was associated with hypocomplementaemia; the degree of renal insufficiency noted in these patients also correlated with hypocomplementaemia. In Staph. aureus IE thrombocytopenia and hypocomplementaemia, occurring early in the course of the disease, may be due to a non-immune interaction of Staph. cell wall products (Protein A) with immunoglobulin, complement components, and thrombocytes.