Pathology

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Approximately 65 to 75% of cases of primary hyper-aldosteronism are caused by a solitary aldosterone-secreting adrenal adenoma. These adenomas are usually small (< 2 cm in diameter), encapsulated tumors of the adrenal cortex. On gross examination, the adenomas appear bright golden yellow in color;

on histologic examination, lipid-laden cortical cells are seen. In previous decades, the radiologic diagnosis of aldosterone-secreting adenomas was difficult because of the relatively small size of these tumors, but the introduction of high-resolution focused CT (3 mm sections) has facilitated the identification of aldosteronomas (Figure 8-3). The small size of aldosterone-secreting adenomas also makes them ideal tumors for resection via laparoscopic adrenalectomy.4-7

Twenty-five to 30% of cases of primary hyperaldosteronism are caused by bilateral adrenal hyper-plasia (also called idiopathic hyperaldosteronism). This condition is usually characterized by areas of macro- or micronodules interspersed throughout both adrenal glands. Patients with bilateral adrenal hyperplasia rarely improve in hypertension or biochemical abnormalities following surgery, unless both adrenal glands are removed, and are best managed with medical treatment, whereas patients with adenomas are best treated with surgical resection. Thus, the accurate differentiation between unilateral and bilateral disease is a crucial step in the

Figure 8-2. A 50-year-old woman with chronic severe hypertension and hypokalemia. Workup showed a serum aldosterone level of 20, a renin activity level of 0.4, and a ratio of 50. A thin-cut computed tomographic scan showed a homogeneous 1.5 cm left adrenal tumor in the posterior limb (arrow) and a normal right adrenal gland. A, She underwent a laparoscopic left adrenalectomy. Pathology showed a 1.5 cm adrenal cortical adenoma and micronodules with clear fasci-cular-type cells consistent with cortical hyperplasia. B, Her hypertension improved after the operation with no need for medication.

Figure 8-2. A 50-year-old woman with chronic severe hypertension and hypokalemia. Workup showed a serum aldosterone level of 20, a renin activity level of 0.4, and a ratio of 50. A thin-cut computed tomographic scan showed a homogeneous 1.5 cm left adrenal tumor in the posterior limb (arrow) and a normal right adrenal gland. A, She underwent a laparoscopic left adrenalectomy. Pathology showed a 1.5 cm adrenal cortical adenoma and micronodules with clear fasci-cular-type cells consistent with cortical hyperplasia. B, Her hypertension improved after the operation with no need for medication.

selection of treatment modalities for patients with primary hyperaldosteronism.1'2,8

Other rarer causes of primary hyperaldosteronism include glucocorticoid-responsive hyperaldostero-nism, primary unilateral adrenal hyperplasia, and adrenal cortical carcinoma. Glucocorticoid-responsive hyperaldosteronism is an uncommon familial condition in which adrenocorticotropic hormone (ACTH) stimulation results in the hypersecretion of aldos-terone because of a specific genomic mutation that places the ACTH-responsive promoter before the aldosterone synthase. Administration of exogenous glucocorticoids suppresses ACTH and thus suppresses the hypersecretion of aldosterone.

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