Addison's disease

Addison's disease is an uncommon endocrine condition manifested by a variety of nonspecific symptoms, such as malaise, anorexia and nausea. Symptoms usually do not occur until most of the adrenal gland has been destroyed. Autoimmune disease has surpassed tuberculosis as the primary cause of Addison's disease. Nevertheless, tuberculosis still accounts for a significant proportion of cases. The rapid adrenocorticotropic hormone (ACTH) stimulation test is useful for identifying adrenal insufficiency. Maintenance therapy consists of hydrocortisone and fludrocortisone.     

Tuberculous Addison's disease

Addison's disease is a possible diagnosis in any patient who presents with weakness, weight loss, hyperpigmentation, hyponatremia, and hypotension. Laboratory findings, including depressed levels of cortisol and aldosterone, help to confirm the diagnosis. Computed tomography may reveal adrenal calcification and abnormal-sized adrenal glands. In most cases, autoimmune destruction of the adrenal cortex is the cause of Addison's disease; however, as in the patient described here, tuberculosis is a possible cause.     

Addison's Disease with Renal Microangiopathy and Renal Failure (a New Syndrome)

A syndrome comprising Addison's disease, renal microangiopathyand renal failure is described in two patients. The renal lesionsmanifested despite corticosteroid replacement therapy and werecharacterized by glomerular damage and thrombo-microangiopathicchanges in afferent arterioles and intralobular arteries. Bothpatients died as a result of their renal disease.     

Thyrotoxicosis in a patient with Addison's disease

We report the case of a patient who suffered recurrent episodes of hypoadrenal crisis, despite conventional replacement therapy for Addison's disease. She was found to have hyperthyroidism and after this was treated, she had no further relapse. Thyrotoxicosis should be considered when patients taking replacement therapy for Addison's disease present in hypoadrenal crisis.     

HL-A antigens in idiopathic Addison's disease.

The frequencies of 36 HL-A antigens of the SD-1, SD-2 and SD-3 locus have been determined in 20 patients with idiopathic Addison's disease and compared with those of 450 controls. No significantly different HL-A antigen frequencies could be observed in both groups. These findings are in contradiction to data reported by a Copenhagen group. Possible mechanisms which might have led to this discrepancy are discussed.     

Reversible cardiomyopathy in a child with Addison's disease

An 11-year-old boy in acute adrenal crisis was subsequently diagnosed with Addison's disease and presumably had an unrecognized preceding chronic adrenal insufficiency. His adrenal insufficiency and hypovolemic shock were promptly diagnosed and treated in the emergency room. However, 24 h later, signs of congestive heart failure developed and an echocardiogram revealed cardiomyopathy. He responded to i.v. dopamine and his cardiomyopathy resolved over some days. Acute adrenal insufficiency and actual ventricular dysfunction had not been described in humans until last year; this is the second reported case of cardiomyopathy in a patient with acute adrenal insufficiency.     

Primary adrenocortical insufficiency (Addison's disease).

In the United States the etiology of most cases of adrenal gland atrophy or destruction is unknown. Autoimmune processes may be responsible. With rare exceptions, all three zones of the adrenal cortex are destroyed and there is reduced glucocorticoid, mineralocorticoid and androgen secretion. Although the deficiency of glucocorticoid is probably the most severe threat to life, treatment is available to correct all the deficiencies. Patient education and preparedness can prevent serious complications.