LETTER
Nitric Oxide Synthesis in Meningococcal Meningitis
Jelle J. Visser, PhD;
Rob J. P. M. Scholten, MD; and
Klaas Hoekman, MD
15 February 1994 | Volume 120 Issue 4 | Pages 345-346
TO THE EDITOR:
Clinical meningitis arises largely from the inflammatory response to bacteria invading the cerebrospinal fluid. Because nitric oxide, an endogenous mediator with vasodilator, neurotransmitter, and cytotoxic activities may be involved [1], we measured cerebrospinal fluid levels of nitrate and nitrite, the stable degradation products of nitric oxide, in 94 patients with meningococcal meningitis and in 44 patients with noninflammatory neurologic disease.
Controls had mean cerebrospinal fluid nitrate levels of 6.3 µmol/L (range, 2.3 to 17.3 µmol/L) and nitrite levels of 0.5 µmol/L (range, 0.4 to 1.7 µmol/L). Compared with controls, patients with meningitis had a mean nitrate level of 18.4 µmol/L (range, 3.1 to 150.7 µmol/L) and a mean nitrite level of 25.8 µmol/L (range, 0.2 to 330.2 µmol/L) (P < 0.001, Mann-Whitney test). Because Neisseria meningitidis is not known to form nitrate or nitrite, these increases must have resulted from increased endogenous production through the only known metabolic route for their formation in body tissues, namely degradation of nitric oxide [2]. Our findings show that nitric oxide synthesis is induced in cells within the central nervous system compartment in response to bacterial invasion.
The pathophysiologic significance of the local increase in nitric oxide remains to be elucidated. High levels of nitric oxide are known to be toxic to endothelial cells and neurons [3, 4]; consequently, local increases in nitric oxide may play a role in the microvascular damage and the neurologic sequelae of meningitis. If so, treatment with specific inhibitors of inducible nitric oxide synthesis might be beneficial in patients with bacterial meningitis.
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Author and Article Information
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Free University Hospital; 1007 MB Amsterdam; The Netherlands
1. Moncada S, Palmer RM, Higgs EA. Nitric oxide: Physiology, pathophysiology, and pharmacology. Pharmacol Rev. 1991; 43:109-42.
2. Marletta MA, Yoon PS, Iyengar R, Leaf CD, Wishnok JS. Macrophage oxidation of L-arginine to nitrite and nitrate: nitric oxide is an intermediate. Biochemistry. 1988; 21:8706-11.
3. Nathan C. Nitric oxide as a secretory product of mammalian cells. FASEB J. 1992; 6:3051-64.
4. Dawson TM, Dawson VL, Snyder SH. A novel neuronal messenger molecule in the brain: the free radical, nitric oxide. Ann Neurol. 1992; 32:297-311.
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