A retrospective analysis of 853 patients with cancer of the mouth, pharynx, and larynx operated on over a 30-year period was performed. Four hundred fifty-seven of them had a radical neck dissection (RND) at some point. Five hundred ninety patients had no clinically positive nodes (N-o) necks at the time of primary treatment; 99 of these had elective neck dissection, whereas 95 others had a delayed RND when nodes became clinically involved. Twenty-three percent of all N-o patients had microscopically involved nodes and less than half of these were among those patients selected for elective RND. Furthermore, 58% of those patients who had elective RND did not have positive nodes. Comparative analysis of elective RND, delayed therapeutic RND after clinical appearance of nodes, and composite operations for patients with N1-N3 disease indicates little difference in disease-free survival when the nodes in the elective RND were positive microscopically for tumors (56%, 49% and 47% respectively). It thus seems that elective RND offers no real advantage over a careful watchful waiting approach in most patients.

No abstract

We addressed the role of thiamin, a cofactor for several enzymes involved in glucose metabolism, in the glucose metabolic response to endotoxin. Characterized by hyperglycemia, increased hepatic glucose production exceeding elevated rates of whole-body glucose utilization, this response is mediated by hormones and cytokines and is dependent on the immune and nutritional status of the host. We hypothesized that a thiamin-deficient state would impair the metabolic response to endotoxin. Rats were fed a thiamin-deficient or control diet for 6 wk before in vivo assessment of glucose kinetics. In control rats, Escherichia coli endotoxin increased the rate of glucose appearance (+76%), disappearance (+70%), and metabolic clearance (+50%). Thiamin deficiency resulted in increased plasma glucose (18%) and lactate (3- to 4-fold) as well as in a 30% decrease in insulin and an increase in glucagon (2.6-fold) and corticosterone (3.6-fold). Thiamin deficiency inhibited the endotoxin-induced hyperglycemia and the rise in hepatic glucose production, glucose utilization, and metabolic clearance rate.