Lithium
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Polyendocrinopathy in an elderly patient: case report A 67-year-old man developed polyendocrinopathy, including thyroid storm, diabetes insipidus and hyperparathyroidism, during treatment with lithium for bipolar disorder. The man started receiving lithium [dosages and route not stated] in 1996, and was hospitalised with lithium toxicity in March 2007. At that time, his wife reported that he was experiencing visual hallucinations, tremors and increased thirst for 2 days. He had interrupted lithium therapy for 1 week, and had restarted the drug at a higher dosage 3 days before admission. His lithium concentration was 2.074 mEq/L on admission. Two days later, he developed atrial fibrillation, fever, nausea and vomiting, and confusion. On examination, he was tremulous, cachectic and only oriented to person and place; his gait was widebased and unsteady. Thyroid storm was suspected. Further laboratory investigations showed a TSH level of 0.009 µU/mL and a free thyroxine (fT4) level of 2.0 ng/dL. The man was transferred to an ICU and started receiving IV fluids, propylthiouracil, esmolol, potassium iodide and hydrocortisone. He was intubated for airway protection after becoming somnolent. Soon after transfer, he became hypercalcaemic, and his intact parathyroid level was found to be elevated at 91.3 pg/mL; findings were compatible with lithium-induced parathyroid dysfunction. His lithium concentration became subtherapeutic over 7 days. His fT4 level decreased to 0.69 ng/dL on day 20, and propylthiouracil was withdrawn. It then became evident that his thyroid stimulating immunoglobulin and antithyroid peroxidase antibody levels were low. His thyroid gland was small on ultrasound, and showed decreased blood flow. Over the course of hospitalisation, his atrial fibrillation, nausea, tachycardia and psychosis resolved. However, he developed hypernatraemia and polyuria with low urine osmolality suggestive of diabetes insipidus while he was intubated. His urine osmolality remained low despite desmopressin administration, confirming nephrogenic diabetes insipidus. Treatment comprised aggressive rehydration, amiloride, hydrochlorothiazide and indometacin. He received pamidronic acid on day 14, and his serum calcium level normalised on day 16. He was discharged with normal serum sodium and calcium levels on day 33; he was slightly hypothyroid on day 50, but euthyroid on day 55. Author comment: "The temporal relationship between the reinitiation of lithium therapy and the development of thyroid storm suggests that lithium therapy was a plausible cause for the thyroiditis. This was further supported by the fact that no other precipitating cause was discovered despite an extensive workup while the patient was in the hospital." Fridman A, et al. A case of lithium-induced polyendocrinopathy including thyroid storm. Endocrinologist 20: 131-133, No. 3, Jun 2010. Available from: URL: http:// 803025719 dx.doi.org/10.1097/ten.0b013e3181dfdb14 - USA
0114-9954/10/1310-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
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