A 30-year-old woman is evaluated for a 3-month history of progressive fatigue, decreased appetite, and 10-lb (4.5-kg) weight loss. The patient has type 1 diabetes mellitus and has noticed decreased insulin requirements over this time. She has no other medical conditions and does not use tobacco, alcohol, or illicit drugs. Physical examination shows a generalized increase in pigmentation of the skin, especially involving the palmar creases. Measurement of serum cortisol before and after administration of exogenous adrenocorticotropic hormone (ACTH) shows no difference in the levels. Which of the following changes in serum laboratory values is most likely present in this patient?

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11ec160b_3aae_8625_9249_e910066805ec_MD0001_00 This patient's fatigue and weight loss are likely due to primary adrenal insufficiency (Addison disease). Type 1 diabetes mellitus is caused by autoimmune destruction of pancreatic beta cells and is associated with an increased risk of other autoimmune endocrinopathies. Autoimmune adrenalitis is the most common cause of primary adrenal insufficiency and results from autoantibodies against all 3 zones of the adrenal cortex. Because the main defect is in the adrenal gland, exogenous ACTH administration does not increase cortisol levels. Decreased negative feedback of cortisol on the pituitary gland increases release of ACTH and melanocyte-stimulating hormone, resulting in hyperpigmentation. Patients with diabetes often have reduced insulin requirements due to decreased appetite, weight loss, and increased insulin sensitivity (glucocorticoids decrease insulin sensitivity). Hypoaldosteronism in primary adrenal insufficiency leads to decreased Na⁺ reabsorption and decreased urinary excretion of K⁺ and H⁺. Decreased H⁺ excretion causes a nonanion gap metabolic acidosis with low plasma HCO₃^-. This leads to compensatory Cl^- retention to maintain electrical neutrality of the extracellular fluid. The hypotension induced by lack of aldosterone stimulates vasopressin release, increasing free water reabsorption and further exacerbating hyponatremia. As a result, patients with primary adrenal insufficiency present with hyponatremia, hyperkalemia, hyperchloremia, and nonanion gap metabolic acidosis. (Choice A) Mineralocorticoid excess (ie, primary hyperaldosteronism) leads to Na⁺ retention, urinary loss of K⁺ and H⁺, and metabolic alkalosis (ie, increased plasma HCO₃^-). However, significant hypernatremia is avoided due to aldosterone escape. (Choice C) Thiazide diuretics block Na⁺/Cl^- reabsorption in the distal tubule. This allows more Na⁺ to reach the collecting tubule, enhancing K⁺ and H⁺ excretion. Findings include hyponatremia, hypokalemia, and metabolic alkalosis. (Choice D) Isolated hyperkalemia is usually due to excess dietary potassium intake or cell lysis (eg, hemolysis, rhabdomyolysis). Hyperkalemia can also be caused by decreased shift of K⁺ into the cells due to insulin deficiency or occasionally by beta 2 antagonists (eg, metoprolol). (Choice E) Normal serum sodium in the setting of hypokalemia and hyperchloremic metabolic acidosis suggests distal hypokalemic or proximal renal tubular acidosis. Educational objective: Patients with type 1 diabetes mellitus are at increased risk for other autoimmune endocrinopathies, including primary adrenal insufficiency (Addison disease). Electrolyte abnormalities in primary adrenal insufficiency include hyponatremia, hyperkalemia, hyperchloremia, and nonanion gap metabolic acidosis. __________ References: Diagnosis and classification of Addison's disease (autoimmune adrenalitis). (http://www.ncbi.nlm.nih.gov/pubmed/24424183)

A 30-Year-Old Woman Is Evaluated for a 3-Month History of Progressive