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The adrenal gland is not uncommonly involved in lymphoma. It is rare, however, for adrenal lymphoma to present as Addison's disease. There are only eight reports in the English literature. This paper reports a case of adrenal lymphoma that presented with Addison's disease and hypercalcaemia.
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Cell-mediated immunity to various adrenal antigen preparations--crude extract, mitochondria and microsomes--has been investigated by means of the migration inhibition of mononuclear cells in 19 patients with established diagnosis of idiopathic Addison's disease (IAD), in 1 patient with suspected Addison's disease and in 20 controls. Adrenal antibodies were determined by immunofluorescence technique. In 13 of the IAD patients significant migration inhibition (MI) could be observed with mitochondria and in 12 patients with crude extract. In addition, MI, although less pronounced, could be detected with microsomes in 12 IAD patients. In one of the controls slight inhibition was observed with all the antigens used and in another stimulation of lymphocyte migration with crude extract could be observed. Adrenal antibodies were detected in 11 of the patients investigated. No correlation could be found between duration of the disease and humoral or cellular immune reactions to adrenal antigens.
A 65 year old woman with long-standing Addison's disease treated with oral glucocorticoid and mineralocorticoid replacement had persistently high ACTH levels, inadequate suppression of ACTH on low-dose dexamethasone, sellar enlargement, and pigmentation, and thus resembled patients alleged to develop corticotropinomas while on oral replacement for adrenal insufficiency. Since animal studies suggested that rapid rises of corticosteroids within the physiologic range can inhibit ACTH release, we administered brief infusions of cortisol every three hours with total daily dose equal to her chronic dose. Prompt suppression of ACTH and immunoreactive beta-endorphin occurred during each cortisol dose profiled, suggesting a role for ultradian cortisol fluctuations in tonic inhibition of ACTH secretion in humans, and a possible therapeutic benefit of mimicking ultradian cortisol rhythms during replacement therapy.
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