Relative hypoparathyroidism induced by interferon treatment in a hemodialysis patient

Muray, S; Mp, Marco; Carrera, Iván; Craver, Lourdes; Fernàndez, Elvira

doi:10.5414/cnp64163

Cited by 1 publication

(1 citation statement)

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“…While much less common, other syndromes have also been observed in patients treated with IFNα, including (but not limited to) hypoparathyroidism [89, 90], celiac disease [91–93], myasthenia gravis [94, 95], Guillain-Barré syndrome [94], polymyositis [94], acute and chronic demyelinating polyneuropathy [94], psoriasis [96], vitiligo [97], both psoriasis and vitiligo [98], porphyria cutanea tarda [99], autoimmune hemolysis [100, 101], myositis and polymyositis [102], sarcoidosis [103] and retinal hemorrhage [104].…”

Section: Ifnα In Other Autoimmune Disordersmentioning

confidence: 99%

Interferon alpha: The key trigger of type 1 diabetes

Lombardi

Tsomos

Hammerstad

et al. 2018

Journal of Autoimmunity

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IFNα is a cytokine essential to a vast array of immunologic processes. Its induction early in the innate immune response provides a priming mechanism that orchestrates numerous subsequent pathways in innate and adaptive immunity. Despite its beneficial effects in viral infections IFNα has been reported to be associated with several autoimmune diseases including autoimmune thyroid disease, systemic lupus erythematosus, rheumatoid arthritis, primary biliary cholangitis, and recently emerged as a major cytokine that triggers Type 1 Diabetes. In this review, we dissect the role of IFNα in T1D, focusing on the potential pathophysiological mechanisms involved. Evidence from human and mouse studies indicates that IFNα plays a key role in enhancing islet expression of HLA-I in patients with T1D, thereby increasing autoantigen presentation and beta cell activation of autoreactive cytotoxic CD8 T-lymphocytes. The binding of IFNα to its receptor induces the secretion of chemokines, attracting monocytes, T lymphocytes, and NK cells to the infected tissue triggering autoimmunity in susceptible individuals. Furthermore, IFNα impairs insulin production through the induction of endoplasmic reticulum stress as well as by impairing mitochondrial function. Due to its central role in the early phases of beta cell death, targeting IFNα and its pathways in genetically predisposed individuals may represent a potential novel therapeutic strategy in the very early stages of T1D.

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