adrenocortical atrophy ICD-10: E27.3
Frau, 68 J., langdauernde Steroidmedikation wegen chronischer Polyarthritis.
Autopsiepräparat
- Architektur der Nebennierenrinde insgesamt erhalten, aber undeutlich,
vor allem Zona fasciculata nicht
mehr klar in Kolonnen angeordnet
- Rinde insgesamt verschmälert
- Kapsel verbreitert
Pathogenese:
- Inadäquate, zu schwache Stimulation durch ACTH
- Steroidmedikation: Exogene Suppression der Stimulation der Nebennierenrinde
durch CRH-ACTH: Reversible Nebennierenrindenatrophie (reversible Nebennierenrindeninsuffizienz)
- Selten: Immunologische Zerstörung der Nebennierenrinde: Zytotoxische
Adrenalitis oder Tuberkulose: Irreversible Nebennierenrindenatrophie
(irreversible Nebennierenrindeninsuffizienz: Morbus Addison)
68-year-old female was under long-term therapy with corticosteroids because of rheumatoid
arthritis (specimen from autopsy).
- The overall architecture of the adrenal gland is maintained. However, the cortex is markedly narrowed and the capsule (Kapsel) is more prominent.
- Over wide sections, the zona glomerulosa predominates in the cortex and the zona fasciculata (Zona fasciculata)
and reticularis are not readily distinguished.
Pathogenesis: A primary and secondary form of adrenocortical insufficiency is distinguished.
Primary chronic adrenocortical insufficiency (Addison disease) may be caused by autoimmune adrenalitis, infections (tuberculosis), metastatic neoplasms
and genetic disorders.
Secondary adrenocortical insufficiency is most frequently caused by long-term corticosteroid administration, which leads to a hypothalamic-pituitary
suppression and thus, inadequate
ACTH production. After discontinuation of treatment, this type of adrenocortical insufficiency is reversible. In addition, neoplasms or inflammatory
processes of hypothalamus and pituitary gland will also cause secondary insufficiency.