Psoriasis is an autoimmune and inflammatory skin disease. Psoriatic patients express higher levels of plasma homocysteine (Hcy) concentration and pro-inflammatory mediators than healthy people; this is frequently associated with vitamin D deficiency. The aim of this clinical study was to investigate the effects of high doses of vitamin D supplementation on the parameters of Hcy metabolism and cytokines in sera of psoriatic patients. This prospective study was conducted on 40 psoriatic patients who had the vitamin D deficiency. All patients received vitamin D 5000 IU/day for three months. Clinical and biochemical measurements were taken at baseline and at follow up (3 months). The results showed that the severity of clinical features, measured by the psoriasis area severity index (PASI) score, were considerably improved in patients after vitamin D supplementation. After vitamin D supplementation, most of the patients (n = 25 or 62.5%) had mild clinical form (p < 0.001). After twelve weeks of intervention period, there were significant increases in vitamin D and B12 serum levels in comparison to the levels that had been measured at the beginning of the study (56.77 ± 14.66 nmol/L and 301.08 ± 95.02 pg/mL vs. 103.85 ± 32.20 nmol/L and 362.81 ± 118.56 pg/mL, respectively; p < 0.001). Moreover, serum levels of Hcy and folate were significantly lower at the end of the study in comparison with the initial levels (12.45 ± 1.92 µmol/L and 8.01 ± 3.88 mg/mL vs. 10.38 ± 1.66 µmol/L and 6.27 ± 2.60 mg/mL, respectively). High doses of vitamin D supplementation led to a significant decrease in pro-inflammatory cytokines (IFN-ɤ, TNF-α, IL-1β, IL-6, IL-8, and IL-17) and high-sensitivity C-reactive protein (hsCRP), whereas the production of anti-inflammatory cytokines (IL-10, IL-5) was up-regulated. In conclusion, supplementation with high doses of vitamin D could be one of the possible preventive and therapeutic measures to reduce systemic inflammation in psoriatic patients.
Two dose levels of a tick-borne encephalitis virus were injected into normal and sublethally X-irradiated (450 r) mice. Radiation exposure resulted in marked changes in all parameters observed: (1) duration of sickness was prolonged so that irradiated mice also survived longer, although they were considerably less resistant to the lethal effect of injected virus suspensions; (2) antiviral antibodies were absent in blood of irradiated mice until the latest phase of sickness, when they occurred in a few animals only; (3) histological changes in the brains of irradiated animals showed absence of cellular reactivity and of other features of classical encephalitic process and were characterized by a diffuse encephalopathic picture. Slight appearance of microfocal inflammatory lesions was observed only in the late stages of the disease, or at the time of spontaneous death. The full classical picture of meningoencephalitis, which occurred in nonirradiated groups of animals, was never found in X-irradiated mice. Since it is, therefore, very probable that the observed changes were induced by immunosuppressive effects of X-rays, we assume that the development of the classical picture of encephalitis is a result of immunologic reaction of the host to the virus in the central nervous system.
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