Coexistence of primary aldosteronism and Hashimoto’s thyroiditis

A 36-year-old woman was admitted to our hospital to determine the reasons for arterial hypertension she had suffered for 6 years and which was resistant to standard antihypertensive therapy. Hypertension was accompanied by muscle weakness, acral paresthesias, polyuria and polydipsia, observed irrespective of the time of the day. In view of significant hypokalemia (2.8 mmol/l) with kaliuresis 112 mEq/l (reference range: 25–100 mmol/l) and hyperglycemia (6.8 mmol/l), primary aldosteronism was suspected and investigated. Supine plasma renin activity was 0.02 ng/ml/h, (reference range: 0.3–2.8 ng/ml/h), while supine plasma aldosterone was 648 pg/ml (normal values: 30–150 pg/ml). After standing for 4 h, plasma renin activity and plasma aldosterone levels increased only slightly to 0.03 ng/ml/h and 687 ng/dl, respectively. Provocative tests, the saline infusion test (2 l during 4 h) and the fludrocortisone with salt loading test revealed unsuppressed plasma aldosterone levels (389 and 426 ng/dl, respectively; normal values in both these tests <5.0 ng/dl). Computed tomography examination demonstrated a minimally enhancing hypodense mass (16 mm in diameter) in the left adrenal gland. A 1 mg dexamethasone suppression test significantly decreased plasma cortisol levels (to 0.6 μg/dl). Urinary-free cortisol, plasma dehydroepiandrosterone sulfate as well as diurnal urinary excretion of metanephrines were also normal. Because of contraindications (allergy to contrast dye), bilateral adrenal vein sampling was not performed. Owing to the presence of concomitant weight gain, depressive symptoms and cold intolerance, we also investigated thyroid function and autoimmunity. Increased plasma TSH levels (23.2 mIU/l, reference range: 0.4–4.5) and reduced plasma levels of free thyroxine (8.8 pmol/l, reference range: 12.0–22.0) and free triiodothyronine (2.6 pmol/l, reference range: 2.8–6.0) supported the presence of hypothyroidism. In turn, very high titers of both thyroid peroxidase antibodies (3,200 U/ml, normal values <32) and thyroglobulin antibodies (3,400 U/ml, normal values <100), diffused thyroid hypoechogenecity on sonography as well as extensive lymphocytic infiltration and numerous Askanazy cells on fine needle aspiration biopsy all were compatible with Hashimoto’s thyroiditis. Cultures of human peripheral blood monocytes and lymphocytes,¹ performed as described previously [7, 8], showed increased monocyte release of TNF-α (3,870 pg/ml, reference range: 580–860), interleukin-1β (440 pg/ml, reference range: 51–79), interleukin-6 (30.2 ng/ml, reference range: 4.3–8.7) and monocyte chemoattractant protein (36.4 ng/ml, reference range: 10.1–14.5), as well as increased lymphocyte release of TNF-α (810 pg/ml reference range: 145–225), interferon-γ (180 ng/ml reference range: 21–45) and interleukin-2 (10.1 ng/ml reference range: 1,4–4.4). To normalize thyroid function, the patient required levothyroxine supplementation at the daily dose of 125 μg. Three months later after pretreatment with spironolactone, the patient underwent laparoscopic left adrenalectomy. Interestingly, after the following 4 months, the patient noticed weight loss despite increased appetite, hyperactivity, heat intolerance, irritability and tachycardia. TSH levels were found suppressed (0.002 mU/l), while free thyroxine and free triiodothyronine were found increased (24.2 and 7.4 pmol/l, respectively). Thyroid peroxidase antibodies and thyroglobulin antibodies (345 and 420 U/ml) were only moderately elevated, and thyroid hypoechogenecity was much less expressed than seven months earlier. Only after reducing the daily dose of levothyroxine to 50 μg, all his clinical symptoms resolved and thyroid function returned to normal. Post-surgery monocyte release of TNF-α (1,020 pg/ml), interleukin-1β (89 pg/ml), interleukin-6 (9.8 ng/ml) and monocyte chemoattractant protein (16.1 ng/ml) as well as lymphocyte release of TNF-α (285 pg/ml), interferon-γ (59 ng/ml) and interleukin-2 (5.1 ng/ml) was only slightly elevated and much lower than observed after spironolactone pretreatment (monocyte release of TNF-α—2,780 pg/ml, interleukin-1β—245 pg/ml, interleukin-6–28.3 ng/ml and monocyte chemoattractant protein—27.2 ng/ml; lymphocyte release of TNF-α—630 pg/ml, interferon-γ—172 ng/ml and interleukin-2–8.8 ng/ml).