Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters











Database
Language
Publication year range
1.
Lupus ; 26(9): 917-926, 2017 Aug.
Article in English | MEDLINE | ID: mdl-27927883

ABSTRACT

Objectives The aim of this study was to assess the vitamin D status in treatment-naïve SLE patients and its association with clinical and laboratory markers of disease activity, including serum levels of IL-17 and IL-23. Methods Fifty-seven treatment-naïve SLE patients along with 42 matched controls were included. SLEDAI score was used to estimate disease activity. Serum levels of 25(OH) D, IL-17 and IL-23 were measured. Results The median level of 25(OH) D in SLE patients (40.8; 4-70 ng/ml) was significantly lower than in the controls (47; 25-93 ng/ml) ( P = 0.001). A total of 38.6% of SLE cases had 25 (OH) D levels < 30 ng/ml (hypovitaminosis D) vs. 4.8% of the controls ( P < 0.0001). Apart from thrombocytopenia, vitamin D was not associated with clinical signs of SLE. There were negative correlations between serum 25(OH) D and serum levels of IL-17, IL-23 and ANA (rho = -0.5, -0.8, -0.5, P ≤ 0.05) in SLE patients. Conclusion Hypovitaminosis D is prevalent in treatment naïve SLE patients. It contributes to ANA antibody production and is associated with high serum levels of IL-23 and IL-17; thus they may trigger the inflammatory process in SLE.


Subject(s)
Interleukin-17/blood , Interleukin-23/blood , Lupus Erythematosus, Systemic/immunology , Vitamin D Deficiency/complications , Vitamin D/blood , Adult , Antibodies, Antinuclear/blood , Biomarkers , Case-Control Studies , Cross-Sectional Studies , Egypt/epidemiology , Female , Humans , Lupus Erythematosus, Systemic/blood , Lupus Erythematosus, Systemic/complications , Lupus Erythematosus, Systemic/diagnosis , Male , Middle Aged , Prevalence , Vitamin D Deficiency/epidemiology , Vitamin D Deficiency/etiology
2.
J Physiol Biochem ; 65(3): 225-33, 2009 Sep.
Article in English | MEDLINE | ID: mdl-20119817

ABSTRACT

This study aimed to investigate whether treatments with vitamin E, L-carnitine and melatonin can protect against CCl(4) and diabetes-induced hepatic oxidative stress. Hepatic oxidative stress was performed in rats through 50% v/v carbon tetrachloride (CCl(4)) (1 ml/kg/3 days, i.p.), and through diabetes mellitus induced by streptozotocin (STZ) (40 mg/kg, i.p.). Vitamin E (100 mg/kg/day, i.p), L-carnitine (300 mg/kg/day, i.p.) and melatonin (10 mg/kg/day, i.p.) were injected for a period of 6 weeks. Thereafter, changes in serum glucose level, liver function tests, hepatic malondialdehyde (MDA) content, hepatic reduced glutathione (GSH) content, hepatic superoxide dismutase (SOD) activity, and serum total antioxidant capacity (TAC) level were evaluated. In CCl(4)-induced liver fibrosis, the efficacy order was melatonin > L-carnitine > vitamin E, while in STZ-induced diabetes, the efficacy order was vitamin E > or = melatonin > L-carnitine. In conclusion, these data indicate that low dose of melatonin is more effective than high doses of vitamin E and L-carnitine in reducing hepatic oxidative stress induced by CCl(4) and diabetes. Moreover, the potent effect of vitamin E in ameliorating diabetes can be linked not only to the antioxidant actions, but also to the superior effect in reducing diabetes-induced hyperglycaemia. Meanwhile, potency of L-carnitine was nearly the same in CCl(4) and diabetes-induced liver damage.


Subject(s)
Carbon Tetrachloride Poisoning/drug therapy , Carnitine/pharmacology , Chemical and Drug Induced Liver Injury/drug therapy , Melatonin/pharmacology , Vitamin E/pharmacology , Animals , Antioxidants/metabolism , Blood Glucose/metabolism , Carbon Tetrachloride Poisoning/complications , Carbon Tetrachloride Poisoning/metabolism , Chemical and Drug Induced Liver Injury/etiology , Chemical and Drug Induced Liver Injury/metabolism , Diabetes Mellitus, Experimental/metabolism , Glutathione/metabolism , Male , Malondialdehyde/metabolism , Oxidative Stress/drug effects , Rats , Rats, Wistar , Superoxide Dismutase/metabolism
SELECTION OF CITATIONS
SEARCH DETAIL