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  Vol. 125 No. 1, January 1990 TABLE OF CONTENTS
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  PAPERS READ BEFORE THE NINTH ANNUAL MEETING OF THE SURGICAL INFECTION SOCIETY, DENVER, COLO, APRIL 13 TO APRIL 14, 1989-PAR T II
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Elevated Tumor Necrosis Factor{alpha} Production Concomitant to Elevated Prostaglandin E2 Production by Trauma Patients' Monocytes

Thomas K. Takayama, MD; Carol Miller, PhD; Gyongyi Szabo, MD

Arch Surg. 1990;125(1):29-35.


Abstract

• The level of tumor necrosis factor{alpha} (TNF{alpha}), a monokine implicated in mediating septic shock, is elevated in the blood of some patients with sepsis. Monocytes from 11 trauma patients and 11 burn patients were suboptimally stimulated with interferon gamma and muramyl dipeptide, an analogue of bacterial wall products. The patients with sepsis showed significantly greater total TNF{alpha} levels (secreted in combination with cell-associated) 3 days before septic episodes, as compared with normal controls (32.38 to 2231.76 ng/106 monocytes per milliliter, median = 121.03 ng/106 monocytes per milliliter; normal control: 0.00 to 18.20 ng/106 monocytes per milliliter, median = 5.93 ng/106 monocytes per milliliter). Increases in patients' total monocyte TNF{alpha} levels greater than 30 ng/106 monocytes per milliliter correlated with septic episodes. In patients with sepsis, the total monocyte TNFlevels were increased despite a concomitant increase in their prostaglandin E2 levels in both stimulated (interferon gamma plus muramyl dipeptide) and unstimulated in vitro assays (9 patients: stimulated prostaglandin E2 range, 30.1 to 123.6 ng/106 monocytes per milliliter). Massively elevated monocyte TNF{alpha} and prostaglandin E2 production occurred simultaneously in patients with sepsis.

(Arch Surg. 1990;125:29-35)



Author Affiliations

From the Departments of Surgery (Drs Takayama, Miller, and Szabo) and Molecular Genetics and Microbiology (Drs Miller and Szabo), University of Massachusetts Medical Center, Worcester.


Footnotes

Accepted for publication September 11, 1989.

Read before the Ninth Annual Meeting of the Surgical Infection Society, Denver, Colo, April 13, 1989.

Reprint requests to Division of Research, Department of Surgery, University of Massachusetts Medical Center, 55 Lake Ave N, Worcester, MA 01655 (Dr Miller).



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