Adult form of Leigh's disease in a patient with Addison's disease and Hashimoto's disease.
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Myocardial involvement in Addison's disease has been described previously. A 36-year-old man presented with cardiomyopathy and was found to have Addison's disease. The patient's myocardial function improved after steroid therapy for Addison's disease. This is the only case report of reversible cardiomyopathy associated with Addison's disease in an adult patient.
Sixteen cases of newly diagnosed Addison disease were studied by CT scan. An initial diagnosis was performed according to the clinical data of each patient, and a second diagnosis after examining the abdominal CT scan. According to the second diagnosis there were six patients with primary adrenal failure of probable autoimmune origin, six tuberculosis, two metastatic, one undetermined and one hemorrhagic. The second diagnosis coincided with the first one in 10 cases (62.5%), but was different in six cases (37.5%). Information obtained by CT scan modified the therapeutic attitude in 4 cases (25%). The main morphologic patterns of adrenal glands in CT scan (atrophy, calcification and enlargement) are commented as well as the importance of CT scan in the study of the more common etiologies of Addison's disease (tuberculosis, autoimmune, neoplastic metastasis and hemorrhage). It is concluded that the information obtained by CT scan is important in the etiological diagnosis of Addison disease and it is advised to perform it in all newly diagnosed cases.
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Modern adrenal function studies can facilitate both diagnosis and management in patients with chronic adrenal insufficiency. These tests are readily available at commercial laboratories and can be conveniently carried out in the physician's office during working hours. As use of these adrenal function studies becomes more common, patients with chronic adrenal insufficiency can expect to have a great improvement in quality of life.
A 32 year old woman with untreated primary adenocortical insufficiency presented with prominent depressive symptoms. Upon treatment with physiological doses of glucocorticoids she developed a self-limiting acute manic illness. We suggest that up-regulation of hippocampal glucocorticoid receptors as a consequence of prolonged hypocortisolaemia resulted in increased cerebral sensitivity to exogenous corticosteroids, which are known to precipitate manic symptoms in some normal individuals when given in supraphysiological doses.
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