Plasma vitamin C concentrations in patients with cystic fibrosis: evidence of associations with lung inflammation

Abstract

Vitamin C status and possible associations with the disease process in cystic fibrosis (CP) patients were investi gated. Plasma vitamin C concentrations in patients from two different mid-European populations (Swiss, n = 62; Austrian, /j -60) taking no or low-dose vitamin C from multivitamin supplements did not differ from each oilier or from control subjects (» ~ 34). Vitamin C concentrations decreased with age (5,05 /xmol ■ L 1 • y~ '). When followed up for 12 mo, patients had the highest plasma vitamin C concentrations in February and the lowest in May and August (P < 0.01); the decrease in vitamin C was accompanied by increases in plasma malondialdehyde (P < 0.001) and tumor necrosis factor a concentrations (P < 0.01). During supplementation with vitamin E for 2 mo or /3-carotene for 12 mo vitamin C concentrations did not change. They correlated inversely with white blood cell count (r --0.36, P = 0.008), bands (r --0.36, P = 0.02), a j-acid glycoprotein (/* --0.45, P = 0.002), interleukin 6 (r = -0.46, P = 0.0006), and neutrophil elastase/a,-proteinase inhibitor complexes (r = -0.34, P ~ 0.02). In patients with vitamin C concentrations < 40 /xmol/L, all in dexes of inflammation were relatively high, whereas those with concentrations > 80 /¿mol/L (upper quartile of control subjects) showed clearly lower values. These results are consistent with the hypothesis that by scavenging oxygen free radicals vitamin C interacts with an in lì am mat ion-amplifying cycle of activation of alveolar macrophages and neutrophils, release of proinflammatory cytokines and oxygen free radicals, and inactivation of anti pro teases, Am J Clin Nutr 1997;65:1858-66.

Mega-dose Vitamin C modulates T cell functions in Balb/c mice only when administered during T cell activation

“…It exerts these effects by scavenging ROS that is produced by macrophages, destroys tissues and activates macrophages and neutrophils to progress inflammation [33,34]. It inhibits the activation of transcription factor NF-B, which plays a critical role in the production of inflammatory cytokines such as TNF-␣, IL-1, and IL-6 [35][36][37].…”

Vitamin C controls the cystic fibrosis transmembrane conductance regulator chloride channel

“…Insufficient dietary intake of vitamin C (9), environmental pollutants (9,10), and a number of inflammatory disorders of the airways are known to severely deplete the pools of vitamin C in ASL or plasma. For example, low levels of vitamin C were found in patients with bronchial asthma (6,11), cystic fibrosis (CF) (12,13), chronic obstructive pulmonary disease (14), and acute respiratory distress syndrome (15), and in smokers (16) as well as in children exposed to environmental tobacco smoke (17).…”

Nutritional status in cystic fibrosis: where to go from here?

“…In other studies, a significant positive correlation between forced vital capacity and plasma albumin concentrations was shown (5), and hypoalbuminemia at diagnosis was recognized as a marker of a severe respiratory course (6). Recent studies found inverse correlations between plasma vitamin C concentrations and different indexes of pulmonary inflammation (13) and between pulmonary function and indexes of oxidative stress (14), supporting the concept that oxidant-antioxidant imbalance affects the disease process in CF patients (15).…”