Abstract
Autoimmmune hypophysitis (AH) is due to an immune-mediated inflammation of the pituitary gland. The tissue damage proceeds through different stages: the initial pituitary enlargement, secondary to infiltration and oedema, can evolve to remission for spontaneous or pharmacological resolution of the inflammation, or evolve to progressive diffuse destruction with gland atrophy for fibrotic replacement, thus leading to various degrees of pituitary dysfunction.
The autoimmune process against the pituitary gland is made evident by the appearance of circulating anti-pituitary autoantibodies (APAs), mainly detected by indirect immunofluorescence on cryostatic sections of human or primate pituitary. Among the target autoantigens recognized by APA are alpha-enolase, gamma-enolase, and the pituitary gland-specific factors (PGSFs) 1a and 1b. However, the low diagnostic sensitivity and specificity of APA for AH strongly limits the clinical use of this marker.
Despite its low incidence, AH should be considered in the differential diagnosis of non-secreting space-occupying lesions of sella turcica, to avoid misdiagnosis that may lead to an aggressive surgery approach, as endocrine dysfunction and the compressive effect may be transient.
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La Torre, D., Falorni, A., Bocci, E.B., Gerli, R. (2008). Autoimmune Hypophysitis. In: Shoenfeld, Y., Cervera, R., Gershwin, M.E. (eds) Diagnostic Criteria in Autoimmune Diseases. Humana Press. https://doi.org/10.1007/978-1-60327-285-8_48
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DOI: https://doi.org/10.1007/978-1-60327-285-8_48
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