Article Text

  1. A. J. Mehr1,
  2. B. M. Paulus1,
  3. K. T. Weber1
  1. 1The University of Tennessee Health Science Center, Memphis, TN.


Purpose Different genes (eg, tumor suppressor genes) are involved in endocrine gland tumorigenesis, which is described clinically as an association between multiple endocrine neoplasia 1 and 2. It is also possible to acquire, over time, multiple endocrine abnormalities with autonomous (tertiary) function in response to a single endocrine disorder. Herein we describe a patient with aldosteronism, hyperthyroidism, and acromegaly.

Methods and Results A 72-year-old African American male presented to the ER with progressive dyspnea on exertion and at rest with orthopnea and bilateral lower extremity edema of several days' duration. Vital signs: blood pressure 170/98 mm Hg; irregularly irregular heart rate with a pulse deficit of 20 bpm; respiratory rate 20/min without arterial hypoxemia; and afebrile. His physical examination revealed rapid atrial fibrillation and decompensated congestive heart failure (CHF) with expanded intra- and extravascular volumes. He also was noted to have coarse facial features and large hands and feet, without thyromegaly. Abdominal CT revealed a 1.2 cm left adrenal gland nodule consistent with adrenal adenoma. Serum aldosterone was 28 (normal 1-16 ng/dL), plasma renin activity < 0.15 (normal 1-10 ng/mL/h), TSH 0.11 (normal 0.34-5.6 μIU/mL), T3 114 (normal 87-178 ng/dL), T4 9.2 (normal 4.1-10.9 μg/dL, T3RU 41 (normal 32-48%), and GH 1.7 (normal 0.0-1.0 ng/mL. Collectively, these clinical and laboratory findings were interpreted to suggest the patient who had aldosteronism, hyperthyroidism with atrial fibrillation, and acromegaly. Rate control of his atrial fibrillation was achieved with β-adrenergic receptor antagonist, and his hypertension and CHF were managed with spironolactone, an aldosterone receptor antagonist, and an angiotensin-converting enzyme inhibitor. He remains stable at follow-up visits several months after hospital discharge.

Conclusions A mutation on chromosome 11 is a potential origin of the clinical presentation in our patient due to the different range of syndromes reportedly associated with heterogenous mutations at different sites of this chromosome. An acquired variant, however, cannot be discounted, which may have begun as hyperpituitarism with excessive ACTH and TSH provocation, leading to autonomous function of adrenal and thyroid glands.

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