Subject(s)
Glomerulonephritis/diagnosis , Posterior Leukoencephalopathy Syndrome/diagnosis , Streptococcal Infections/complications , Acute Disease , Child , Glomerulonephritis/etiology , Headache/etiology , Humans , Male , Posterior Leukoencephalopathy Syndrome/etiology , Tomography, X-Ray Computed , Vomiting/etiologySubject(s)
Hemagglutination Tests , Weil Disease/diagnosis , Adolescent , Anti-Bacterial Agents/therapeutic use , Denmark , Diagnosis, Differential , Fever/etiology , Hemagglutination Tests/methods , Humans , Italy , Male , Travel , Treatment Outcome , Weil Disease/blood , Weil Disease/complications , Weil Disease/drug therapy , Weil Disease/immunologyABSTRACT
BACKGROUND & AIMS: We investigated whether improving 25-hydroxyvitamin D status in young type 1A diabetic patients reduces reactivity of peripheral blood mononuclear cells against islet autoantigens and associates with beta-cell functional changes. METHODS: Eight patients with 25-hydroxyvitamin D deficiency (<20 ng/ml), out of 15 consecutive young type 1A diabetic subjects received 25-hydroxyvitamin D3 to achieve and maintain levels above 50 ng/ml for up to one year. Peripheral blood mononuclear cell reactivity (Interferon-γ spots) against beta-cell autoantigens (glutamic acid decarboxylase 65-kD isoform, proinsulin and tyrosine phosphatase-like protein IA-2) and C-peptide during mixed meal were assessed before and after 25-hydroxyvitamin D3 replenishment. RESULTS: Target 25-hydroxyvitamin D blood levels were safely reached and maintained. Peripheral blood mononuclear cell reactivity against glutamic acid decarboxylase 65-kD isoform (3.8 ± 4.0 vs. 45 ± 16) and proinsulin (3.5 ± 3.2 vs. 75 ± 51) decreased significantly (p < 0.001 and p < 0.02) upon 25-hydroxyvitamin D3 replenishment, which was correlated with 25-hydroxyvitamin D concentrations. C-peptide values remained stable after one year of treatment. CONCLUSIONS: Safely restored and maintained 25-hydroxyvitamin D levels associated with reduced peripheral blood mononuclear cell reactivity against beta-cell autoantigens with no significant decrease of beta-cell function in this cohort of patients.
