High‐dose vitamin C therapy for symptomatic deficiency in a patient with myasthenia gravis and Crohn's disease

Author(s):  
Jill Murphree ◽  
Diana Wells Mulherin ◽  
Colleen Morton ◽  
Dawn Adams

2019 ◽  
Vol 156 (6) ◽  
pp. S-33
Author(s):  
Jessica de Bruyn ◽  
Peter Bossuyt ◽  
Marc Ferrante ◽  
Rachel West ◽  
Gerard Dijkstra ◽  
...  


2016 ◽  
Vol 62 (2) ◽  
pp. 448-455 ◽  
Author(s):  
Neeraj Narula ◽  
Mohan Cooray ◽  
Rebecca Anglin ◽  
Zack Muqtadir ◽  
Alisha Narula ◽  
...  


Author(s):  
Jessica R. de Bruyn ◽  
Peter Bossuyt ◽  
Marc Ferrante ◽  
Rachel L. West ◽  
Gerard Dijkstra ◽  
...  


Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1083
Author(s):  
Mia Bendix ◽  
Anders Dige ◽  
Søren Peter Jørgensen ◽  
Jens Frederik Dahlerup ◽  
Bo Martin Bibby ◽  
...  

Background: Seven weeks of high-dose vitamin D treatment decreases intestinal IL17A and IFN-γ mRNA expression in active Crohn’s disease (CD). In this follow-up study, we investigated whether seven-week vitamin D treatment affected the infliximab response in the following 45 weeks compared to placebo. Methods: CD patients (n = 40) were initially randomised into four groups: infliximab + vitamin-D; infliximab + placebo-vitamin-D; placebo-infliximab + vitamin-D; and placebo-infliximab + placebo-vitamin-D. Infliximab (5 mg/kg) or placebo-infliximab was administered at weeks 0, 2 and 6. Vitamin D (5 mg bolus followed by 0.5 mg/day for 7 weeks) or placebo-vitamin D was handed out. After the 7-week vitamin D period, all patients received infliximab during follow-up. Results are reported for Group D+ (infliximab + vitamin-D and placebo-infliximab + vitamin-D) and Group D- (infliximab + placebo-vitamin-D and placebo-infliximab + placebo-vitamin-D). Results: Group D- patients had greater needs for infliximab dose escalation during follow-up compared to group D+ (p = 0.05). Group D+ had lower median calprotectin levels week 15 (p = 0.02) and week 23 (p = 0.04) compared to group D-. Throughout follow-up, group D+ had 2.2 times (95% CI: 1.1–4.3) (p = 0.02) lower median CRP levels compared with group D-. Conclusions: Seven weeks high-dose vitamin D treatment reduces the need for later infliximab dose-escalation and reduces inflammatory markers. EudraCT no. 2013-000971-34.



Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3699
Author(s):  
Mia Bendix ◽  
Anders Dige ◽  
Søren Peter Jørgensen ◽  
Jens Frederik Dahlerup ◽  
Bo Martin Bibby ◽  
...  

Background: Vitamin D treatment may reduce Crohn’s disease (CD) activity by modulating the mucosal immune function. We investigated if high-dose vitamin D +/− infliximab modulated the mucosal cytokine expression in active CD. Methods: Forty CD patients were randomized into: infliximab + vitamin D; infliximab + placebo-vitamin D; placebo-infliximab + vitamin D or placebo-infliximab + placebo-vitamin D. Infliximab (5 mg/kg) and placebo-infliximab were administered at weeks 0, 2 and 6. Oral vitamin D was administered as bolus 200,000 international units (IU) per week 0 followed by 20,000 IU/day for 7 weeks or placebo. Endoscopy with biopsies was performed at weeks 0 and 7 where endoscopic activity was measured and mucosal mRNA cytokine expression was examined. C-reactive protein (CRP), fecal calprotectin and Harvey-Bradshaw Index (HBI) were measured at weeks 0, 2 and 6. Results: High-dose vitamin D treatment alone and combined with infliximab decreased the IL17A, IFNγ and IL10 expression. High-dose vitamin D alone did not significantly decrease the disease activity, CRP or calprotectin. Combined infliximab and vitamin D treatment was not clinically significantly superior to monotherapy with infliximab. Conclusions: High-dose vitamin D as monotherapy and combined with infliximab decreases IL17A, IFNγ and IL-10 expression in mucosa within treatment groups. This did not induce a statistically significant decreased disease activity. EudraCT no.2013-000971-34.





2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ning Zhang ◽  
Wei Zhao ◽  
Zhen-Jie Hu ◽  
Sheng-Mei Ge ◽  
Yan Huo ◽  
...  

AbstractSepsis survivors present long-term cognitive deficits. The present study was to investigate the effect of early administration of high-dose vitamin C on cognitive function in septic rats and explore its possible cerebral protective mechanism. Rat sepsis models were established by cecal ligation and puncture (CLP). Ten days after surgery, the Morris water maze test was performed to evaluate the behavior and cognitive function. Histopathologic changes in the hippocampus were evaluated by nissl staining. The inflammatory cytokines, activities of antioxidant enzymes (superoxide dismutase or SOD) and oxidative products (malondialdehyde or MDA) in the serum and hippocampus were tested 24 h after surgery. The activity of matrix metalloproteinase-9 (MMP-9) and expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1(HO-1) in the hippocampus were measured 24 h after surgery. Compared with the sham group in the Morris water maze test, the escape latency of sepsis rats was significantly (P = 0.001) prolonged in the navigation test, whereas the frequency to cross the platform and the time spent in the target quadrant were significantly (P = 0.003) reduced. High-dose vitamin C significantly decreased the escape latency (P = 0.01), but increased the time spent in the target quadrant (P = 0.04) and the frequency to cross the platform (P = 0.19). In the CLP+ saline group, the pyramidal neurons were reduced and distributed sparsely and disorderly, the levels of inflammatory cytokines of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 in the serum and hippocampus were significantly increased (P = 0.000), the blood brain barrier (BBB) permeability in the hippocampus was significantly (P = 0.000) increased, the activities of SOD in the serum and hippocampus were significantly (P = 0.000 and P = 0.03, respectively) diminished while the levels of MDA in the serum and hippocampus were significantly (P = 0.007) increased. High-dose vitamin C mitigated hippocampus histopathologic changes, reduced systemic inflammation and neuroinflammation, attenuated BBB disruption, inhibited oxidative stress in brain tissue, and up-regulated the expression of nuclear and total Nrf2 and HO-1. High-dose vitamin C significantly (P < 0.05) decreased the levels of tumor necrosis factor- (TNF)-α, interleukin-6 (IL-6), MDA in the serum and hippocampus, and the activity of MMP-9 in the hippocampus, but significantly (P < 0.05) increased the levels of SOD, the anti-inflammatory cytokine (IL-10) in the serum and hippocampus, and nuclear and total Nrf2, and HO-1 in the hippocampus. In conclusion, high-dose vitamin C can improve cognition impairment in septic rats, and the possible protective mechanism may be related to inhibition of inflammatory factors, alleviation of oxidative stress, and activation of the Nrf2/HO-1 pathway.



Redox Biology ◽  
2021 ◽  
Vol 43 ◽  
pp. 101980
Author(s):  
Andree G. Pearson ◽  
Juliet M. Pullar ◽  
John Cook ◽  
Emma S. Spencer ◽  
Margreet CM. Vissers ◽  
...  


2012 ◽  
Vol 64 (4) ◽  
pp. 367-371 ◽  
Author(s):  
Khalid K. Abdul-Razzak ◽  
Karem H. Alzoubi ◽  
Salah A. Abdo ◽  
Wael M. Hananeh


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