ABSTRACT
Tuberculosis is highly prevalent worldwide, accounting for nearly two million deaths annually. Vitamin D influences the immune response to tuberculosis, and vitamin D deficiency has been associated with increased tuberculosis risk in different populations [Bedoya and Ronnenberg, 2009]. The aim of this study has been to determine the possibility of an association between tuberculosis and low serum vitamin D concentration in young male patientsand to monitor the changes in vitamin D levels after TB treatment. Twenty five [25] Patients aged 20-40 with newly diagnosed TB were enrolled in this study. They were divided into eleven [11] cases on first line TB treatment for 2-3 months and fourteen [14] cases before starting TB treatment. Twenty five [25] age and sex matched healthy volunteers were enrolled as controls. For all groups body mass index [BMI] was calculated. Also serum calcium [Ca[+]], 25-hydroxyvitamin D [25-OHD] and 1-25-hydroxyvitamin D [1-25-OHD] levels were measured and compared. There was significant difference between groups as regard BMI, serum Ca, 25-OHD and1-25- OHD [p<0.0001 for all groups]. In the TB group both25-OHD and1-25-OHD were lower in patients who were under TB treatment compared to patients who didn't received treatment [p<0.001]. Low serum vitamin D concentrations may be a consequence of TB disease. The possibility that low serum 25-OHD and1-25-[OH] [2] D concentrations may predispose to tuberculosis infection cannot, be excluded. Antituberculous treatment has been shown to reduce serum 25-OHD and1-25- [OH] [2] vitD, which may increase the risk of vitamin D deficiency
Subject(s)
Humans , Male , Vitamin D/blood , Male , Antitubercular AgentsABSTRACT
Background: macrophage migration inhibitory factor [MIF] has a regulator role of host responses to infection and stress. It is now emerging as a key integrator of the immunoneuroendocrine interface and has capacity to counter-regulate the effects of glucocorticoids on immune cells. Functional promoter polymorphisms of the human A4IF gene single-nucleotide polymorphism [SNP] at position 173 *G/C altered level of MIF gene transcription and contribute to increase susceptibility for early onset, severity and poor outcome of Atopic Dermatitis [AD]
Objective: to evaluate values of human MIF gene single nucleotide polymorphism [SNP], immunohistochemically study of MIF expression in biopsies from the skin lesions [as it mirrors serum MIF levels] versus serum cortisol levels and their relation to different degrees of severity in early onset AD
Patients and Method: this study was carried out on twenty four Participants. Fourteen with AD, 11 females and 3 males, their ages ranged from 3-12ys with mean+/- sd [7.6+/-3.03] [group l]. Ten healthy participant's age and sex matched were taken as controls, their ages ranged from 4-llys with mean+/-sd [6.15+1.53] [group2].Group 1 after that were subdivided for immunohistochemically staining into group A and Group B. They were selected from dermatology outpatient clinic at Al-Zahraa University Hospital after taking informed consent from their parents, and they were subjected to full history, clinical and dermatological examinations; measuring CEC, ESR, morning serum cortisol levels; Genetic study for human MIF gene single-nucleotide polymorphism [SNP] [MIF-173*G/C], and immunohistochemically study of MIF expression in skin biopsies
Results: five out of Fourteen patients were moderate AD [Objective SCORAD index]. They had been associated with SNP of human MIF at 173 *C [35.71%]. There was strong and moderate positive expressions of MIF in skin biopsies from moderate AD patients with SNP, while mild or no expressions of MlF in mild AD skin lesions by immunohistochemically staining. No significant difference in morning serum cortisol in group1 and 2; mean +/- SD was [10.67+/-3.73], [12.34+/-3.58], and also between cases with MIF gene SNP [group B] and without [group A], mean +/- SD was [11.64+/-2.68]. [10.13+/-4.26] respectively p>0.05
Concision: potent association was found between human MIF gene [SNP], Tissue expression of MIF and severity of AD. Anti MIF antibodies can be used in management of different forms of AD. Higher doses of steroid therapy may be required in some cases to antagonize elevated MIF level and possibility of subclinical hypo function of adrenal gland