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.
Part of the book: Vitamin D Deficiency
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.
Part of the book: Lupus
Autoimmune Hashimoto’s thyroiditis is an organ specific autoimmune disorder. It affects the thyroid gland and it is characterized by the presence of antibodies to thyroid proteins, namely, thyroid peroxidase, TPOab and thyroglobulin, Tgab and thyroid tissue invasion by lymphocytes. The presence of Hashimoto’s thyroiditis may be associated with normal thyroid function or hypothyroidism. In many cases of Hashimoto’s thyroiditis with normal thyroid function may progress to subclinical hypothyroidism or overt hypothyroidism. Risk factors for the development of Hashimoto’s thyroiditis are genetic and environmental. Genetic factors are HLA-DR4, CD40, CTLA-4 and PTP-N22 and genetic factors related to thyroglobulin gene and TSH receptor gene. Environmental factors include the presence of iodine excess in the environment, infectious agents such as hepatitis C virus and the SARS-CoV-2 virus, smoking, alcohol, selenium deficiency, drugs such as amiodarone, interferon-a, highly active antiretroviral therapy and immune checkpoint inhibitors. Female sex is also a risk factor for Hashimoto’s thyroiditis. The disease runs a variable course. Presently there are experimental efforts to pause or reverse the autoimmune process which leads to Hashimoto’s thyroiditis and may progress to the destruction of the thyroid gland. Hypothyroidism is treated by the administration of thyroxine usually for life.
Part of the book: Hypothyroidism