Dr. Panagiotis Athanassiou graduated from the University of Thessaloniki in 1982 where he obtained his MD. He specialized in Rheumatology in 1991. He also graduated from Law School, University of Athens (1991) and obtained his Ph.D. from the Medical School, University of Athens (1999). He was given a fellowship that lasted for two years (1992-1994) from the Hellenic Society for Rheumatology for specialization in autoimmune rheumatic diseases.
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
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.
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