Nitric Oxide Synthesis in Meningococcal Meningitis

Jelle J. Visser; Rob J. P. M. Scholten; Klaas Hoekman

doi:10.7326/0003-4819-120-4-199402150-00023

Letters |15 February 1994

Nitric Oxide Synthesis in Meningococcal Meningitis

Jelle J. Visser, PhD; Rob J. P. M. Scholten, MD; Klaas Hoekman, MD

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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.

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Letters |15 February 1994

Nitric Oxide Synthesis in Meningococcal Meningitis

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Letters |15 February 1994

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