Vitamin D and Autoimmune Diseases

Vitamin D has many and profound effects on the immune system. Vitamin D deficiency is known to be related to the development of autoimmune diseases. In particular, vitamin D deficiency is related to the development and the severity of rheumatoid arthritis (RA). RA develops in patients with vitamin D deficiency, and the activity of the disease is related to vitamin D deficiency. Vitamin D deficiency is also related to the development of systemic lupus erythematosus (SLE). SLE develops in patients with vitamin D deficiency, and the activity of the disease is also greater in patients with vitamin D deficiency. Vitamin D deficiency is also related to the development and the severity of multiple sclerosis. Vitamin D should be administered to patients with multiple sclerosis, and this seems to mitigate the symptoms of the disease and to prevent disease progression. Vitamin D deficiency is also observed in patients with inflammatory bowel disease and may be related to disease severity. Low vitamin D levels have also been observed in patients with autoimmune Hashimoto’s thyroiditis. Low vitamin D levels have been observed in patients with systemic sclerosis, especially in the diffuse form of the disease. Optimal vitamin D levels appear to be required for normal immune function and for the prevention and treatment of autoimmune diseases

Endocrine Manifestations of Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease affecting all organ systems. It affects primarily female patients in the reproductive age. The disease has a variable course from very mild to severe and may be fatal. It is characterized by exacerbations of disease activity called flares. Estrogens seem to be involved in SLE pathogenesis as they have multiple immunomodulating properties. In SLE the autoimmune process affects the neuroendocrine axis. Stress modulates disease expression in lupus patients. The disease affects the endocrine system. Hypothyroidism occurs in SLE patients in a higher rate than that of the general population. Hyperthyroidism is also observed in SLE, however, in the rate expected for the general population. Hashimoto’s thyroiditis is observed in SLE in a higher rate than that of the general population. Hyperparathyroidism is also observed in SLE, primary and secondary in the context of renal insufficiency due to lupus nephritis. Addison’s disease is rare in SLE. Cushing’s disease due to an adrenal adenoma has been observed, but it is rare. Ovarian function may be compromised in SLE, due to autoimmune oophoritis or drug toxicity. The recognition of endocrine disease in SLE is important as it may guide proper management and symptom amelioration

Novel Therapeutic Interventions in Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease. It is characterized by a variable clinical course ranging from mild to fatal disease. It can affect the kidneys. The aim of treatment in SLE is the prevention of flares and the prevention of accumulation of damage to the main organs affected as well as the prevention of drug side effects. The cornerstone of SLE treatment is hydroxychloroquine. Corticosteroids are used both as induction treatment in disease flares as well as in small doses as maintenance treatment. Immunosuppressants, such as azathioprine, methotrexate and mycophenolate mofetil are used as steroid sparing agents. Calcineurin inhibitors, namely tacrolimus and cyclosporin A may also be used as immunosuppressants and steroid sparing agents. Pulse methylprednisolone, along with mycophenolate mofetil and cyclophosphamide are used as induction treatment in lupus nephritis. Rituximab, an anti-CD20 biologic agent may be used in non-renal SLE. In patients insufficiently controlled with hydroxychloroquine, low dose prednisone and/or immunosuppressive agents, belimumab may be used with beneficial effects in non-renal disease and lupus nephritis

Thyroid Cancer: From Genes to Treatment—Recent Developments

Thyroid cancer carries a good prognosis in most cases and is treated by thyroidectomy, radioiodine administration thereafter, thyroxine treatment. Although, most cases of thyroid cancer are curable, if thyroid cancer loses the ability to concentrate iodine and thus becomes refractory to radioiodine, and if thyroid cancer becomes a progressive disease, the need for targeted treatment becomes necessary. Research in the area of the biology of thyroid cancer and in particular the discovery of somatic genetic mutations involved in the pathophysiology of thyroid cancer as well as research in the treatment of other cancer types with tyrosine kinase inhibitors have led to the application of tyrosine kinase and angiogenetic factor inhibitors in the treatment of thyroid cancer. The application of tyrosine kinase inhibitors in other tumor types led to the discovery that they target the thyroid. Thus, tyrosine kinase inhibitors entered the field of radioactive iodine refractory and advanced thyroid cancer treatment. Multi-kinase and angiogenetic factor inhibitors have provided a novel method that targets thyroid tumors and have revolutionized the treatment of radioiodine refractory and advanced thyroid cancer

Sarcopenia in patients with diabetes mellitus.

IntroductionDiseases such as diabetes mellitus may be associated with adverse changes in body composition. Sarcopenia is characterized by a progressive and generalized loss of skeletal muscle mass and functionality.AimTo investigate the relationship between type 2 diabetes mellitus (T2DM) and sarcopenia.Materials and methodsIn a retrospective, non-randomized study, 35 T2DM patients, aged 20-80 years, were assessed for sarcopenia prevalence compared to controls (n=16). Appendicular skeletal mass (ASM) (kg) was measured, and sarcopenia was defined as SMI ResultsIncidence of sarcopenia was significantly higher in T2DM patients vs. controls (27% vs. 20%, p=0.01) and elderly vs. young participants (40% vs. 12%, pConclusionsA moderate prevalence of sarcopenia in patients with type 2 diabetes mellitus was observed, which appeared to increase significantly in older men. Finally, incidence of T2DM displayed decreased physical performance in both genders

Oxytocin and cholecystokinin secretion in women with colectomy

BACKGROUND: Cholecystokinin (CCK) concentrations in plasma have been shown to be significantly higher in colectomised subjects compared to healthy controls. This has been ascribed to reduced inhibition of CCK release from colon. In an earlier study CCK in all but one woman who was colectomised, induced release of oxytocin, a peptide present throughout the gastrointestinal (GI) tract. The aim of this study was thus to examine if colectomised women had a different oxytocin response to CCK compared to healthy controls. METHODS: Eleven women, mean age 34.4 ± 2.3 years, who had undergone colectomy because of ulcerative colitis or constipation were studied. Eleven age-matched healthy women served as controls. All subjects were fasted overnight and given 0.2 μg/kg body weight of CCK-8 i.v. in the morning. Samples were taken ten minutes and immediately before the injection, and 10, 20, 30, 45, 60, 90 and 120 min afterwards. Plasma was collected for measurement of CCK and oxytocin concentrations. RESULTS: The basal oxytocin and CCK concentrations in plasma were similar in the two groups. Intravenous injection of CCK increased the release of oxytocin from 1.31 ± 0.12 and 1.64 ± 0.19 pmol/l to 2.82 ± 0.35 and 3.26 ± 0.50 pmol/l in controls and colectomised women, respectively (p < 0.001). Given the short half-life of CCK-8 in plasma, the increased concentration following injection could not be demonstrated in the controls. On the other hand, in colectomised women, an increase of CCK in plasma was observed for up to 20 minutes after the injection, concentrations increasing from 1.00 ± 0.21 to a maximum of 1.81 ± 0.26 pmol/l (p < 0.002). CONCLUSION: CCK stimulates the release of oxytocin in women. There is no difference in plasma concentrations between colectomised and controls. However, colectomy seems to reduce the metabolic clearance of CCK. The hyperCCKemia in patients who had undergone colectomy is consequently not only dependent on CCK release, but may also depend on reduced clearance

Pharmacometabolomics of Response to Sertraline and to Placebo in Major Depressive Disorder - Possible Role for Methoxyindole Pathway

10.1371/journal.pone.0068283PLoS ONE87-POLN