PubMed · 15446120
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L R SATALINE, C POWELL, G HAMWI. 1963. HYPERCALCEMIA.. https://pubmed.ncbi.nlm.nih.gov/15446120/
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Thomas Addison first described, 150 years ago, a clinical syndrome characterized by salt-wasting and skin hyperpigmentation, associated with a destruction of the adrenal gland. Even today, over a century after Addison's report, primary adrenal insufficiency can present as a life-threatening condition, since it frequently goes unrecognized in its early stages. In the 1850s, tuberculous adrenalitis was present in the majority of patients, but nowadays, autoimmune Addison's disease is the most common cause of primary adrenal insufficiency. In the present report, we show the prevalence of different etiologies, clinical manifestations and laboratorial findings, including the adrenal cortex autoantibody, and 21-hydroxylase antibody in a Brazilian series of patients with primary adrenal insufficiency followed at Divisão de Endocrinologia da Universidade Federal de São Paulo (UNIFESP) and at Faculdade de Medicina de Ribeirão Preto-USP (FMRP-USP).
Primary adrenal insufficiency is a rare pediatric condition, which can be presented as chronic or acute forms, especially during stress. The clinical features are unspecific and include weakness, nausea and vomiting, abdominal pain and diarrhea, arterial hypotension, hypoglycemia and dehydration. The etiology can be acquired such as infectious, hemorrhagic and drug-induced disorders, or be dependent on a genetic origin, such as congenital adrenal hyperplasia, Addisons disease, congenital adrenal hypoplasia, adrenoleucodystrophy, or deposit disorders of the adrenal gland. The familial history, presence of consanguinity, adjacent diseases and associate factors, should be considered to confirm the diagnosis. Laboratory investigation includes cortisol, ACTH and the determination of the steroidogenic precursors. The ACTH stimulation test is performed in intermediate conditions. Adrenal auto-antibodies quantitation and molecular studies can be helpful to confirm specific diseases. A substitutive glucocorticoid and mineralocorticoid therapy should be started as soon as the diagnosis is confirmed. The treatment aimed to control the symptoms with the smaller dose that can allow an adequate growth and pubertal development.
Synthetic corticosteroids have variable glucocorticoid and mineralocorticoid potencies. Depending on their galenic form they can be administered either by intravenous, oral, intraarticular, intramuscular, inhalative or topic route. A local application is preferable over a systemic administration to avoid side effects. An initially high dose should always be tapered to the lowest possible effective dose. Among the side effects some have substantial clinical implications: Osteoporosis (to be treated during any long-term steroid application with calcium, vitamin D and eventually bis-phosphonates), immunodeficiency and a risk for often atypical infections, diabetes mellitus and psychiatric disorders such a depression and psychosis. A long-term glucocorticoid treatment can lead to a permanent adrenal insufficiency (M. Addison), which must be recognized and properly managed.