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Hypocortisolemia in Graves Hyperthyroidism
Affiliation:1. Epilepsy Center, University Hospital Freiburg, Germany;2. Department of Stereotactic and Functional Neurosurgery, University Hospital Freiburg, Germany;3. Department of Neurosurgery, University Hospital Freiburg, Germany;5. Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, NC, USA;2. Center for Patient Care and Outcomes Research, Medical College of Wisconsin, Milwaukee, WI, USA;3. Medical Social Sciences, Northwestern University, Chicago, IL, USA;4. TRICARE Management Activity, Department of Defense—Health Affairs, Falls Church, VA, USA;11. Qualitas Advising, Wauwatosa, WI, USA;123. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University, Baltimore, MD, USA;1. Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan;2. Department of Healthcare Administration, Nagoya University Graduate School of Medicine, Nagoya, Japan;3. Department of Obstetrics and Gynecology, Wakayama Medical University, Wakayama, Japan
Abstract:ObjectiveTo assess the risk of concomitant adrenal sufficiency in 2 patients with Graves thyrotoxicosis.MethodsWe present the clinical course and laboratory findings of 2 patients with hyperthyroidism associated with low basal serum cortisol and briefly review the literature with regard to possible mechanisms of hypocortisolemia in thyrotoxic states.ResultsTwo women aged 37 and 43 years with longstanding Graves disease presented with hyperthyroidism secondary to nonadherence to prescribed antithyroid medications. Both women also had symptoms suggestive of adrenal insufficiency including nausea, vomiting, and diffuse abdominal pain in Patient 1 and fatigue and hypotension in Patient 2. In both patients, physical examination findings were consistent with hyperthyroidism. Laboratory results of Patient 1 included the following: thyrotropin, < 0.002 mIU/L; free thyroxine, > 6 μg/dL; and total triiodothyronine, 539 ng/dL. Laboratory results of Patient 2 included the following: thyrotropin, < 0.002 mIU/L; free thyroxine, > 6 μg/dL; and total triiodothyronine, 539 ng/dL. Morning basal cortisol levels were 0.9 μg/dL in Patient 1 and 0.6 pg/dL in Patient 2. Because of the low basal serum cortisol levels, the patients underwent a high-dose (250 mcg) cosyntropin-stimulation test; however, both patients had adequate cortisol response. At 60 minutes, serum cortisol concentration was 31.4 μg/dL in Patient 1 and 25.5 pg/dL in Patient 2. After adequately treating the hyperthyroidism, basal cortisol levels in both patients returned to the reference range.ConclusionSymptomatic hypocortisolemia may be present in severe hyperthyroidism, and it resolves with adequate treatment of the hyperthyroidism. (Endocr Pract. 2009;15:220-224)
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