甲狀腺機能亢進合併原發性醛固酮症引起之次發性高血壓

Secondary Hypertension in a Patient with Hyperthyroidism and Primary Aldosteronism

陳春森(Chung-Sen Chen)

《台灣醫學》 8卷5期 (2004/09) Pp. 648-651

https://doi.org/10.6320/FJM.2004.8(5).05

摘要

Abstract: A 30-year-old woman presented with headache and hypertension. She had a history of hyperthyroidism for 2 months. Physical examination showed diffuse goiter, palpitation, and fine hands tremor; thyroid function test revealed hyperthyroidism. After treatment with methimazole and propranolol, hypertension and headache were still persisted. Diltizam was given for further blood pressure control. Laboratory data revealed euthyroidism and hypokalemia (2.9 mEq/dL) after treatment. On account of hypertension and hypokalemia, secondary hypertension caused by hyperaldosteronism was suspected. Samples were collected for PRA (plasma renin activity) and aldosterone when patient was recumbent and after 2 hour of standing or walking. Investigation revealed elevated aldosterone level (303pg/mL) and reduced PRA(＜0.lng/mL/hr). 59(subscript NP) adrenal scintigraphy and MRI scan showed a tumor in the right adrenal gland. Aldosterone-producing adenoma of the adrenal gland was diagnosed, and right adrenalectomy was performed. At six month follow-up examination, the patient's blood pressure and potassium level (4.2 mEq/dL) were normal. Euthyroid state was kept by treatment with methimazole. It meant hypertension and hypokalemia was induced by aldosterone-producing adenoma. Hypokalemia with hypertension might be a manifestation of either hyperthyroidism with periodic paralysis or hyperaldosteronism or both. These findings indicate that hyperaldosteronism played a major role in the development of hypokalemia and hypertension, while hyperthyroidism with periodic paralysis might induce the similar condition and apparently increased the patients vulnerability to hypokalemia and hypertension.

關鍵字

腎上腺醛固酮瘤 ； 甲狀腺機能亢進 ； 次發性高血壓 ； 低血鉀

並列摘要

Abstract: A 30-year-old woman presented with headache and hypertension. She had a history of hyperthyroidism for 2 months. Physical examination showed diffuse goiter, palpitation, and fine hands tremor; thyroid function test revealed hyperthyroidism. After treatment with methimazole and propranolol, hypertension and headache were still persisted. Diltizam was given for further blood pressure control. Laboratory data revealed euthyroidism and hypokalemia (2.9 mEq/dL) after treatment. On account of hypertension and hypokalemia, secondary hypertension caused by hyperaldosteronism was suspected. Samples were collected for PRA (plasma renin activity) and aldosterone when patient was recumbent and after 2 hour of standing or walking. Investigation revealed elevated aldosterone level (303pg/mL) and reduced PRA(＜0.lng/mL/hr). 59(subscript NP) adrenal scintigraphy and MRI scan showed a tumor in the right adrenal gland. Aldosterone-producing adenoma of the adrenal gland was diagnosed, and right adrenalectomy was performed. At six month follow-up examination, the patient's blood pressure and potassium level (4.2 mEq/dL) were normal. Euthyroid state was kept by treatment with methimazole. It meant hypertension and hypokalemia was induced by aldosterone-producing adenoma. Hypokalemia with hypertension might be a manifestation of either hyperthyroidism with periodic paralysis or hyperaldosteronism or both. These findings indicate that hyperaldosteronism played a major role in the development of hypokalemia and hypertension, while hyperthyroidism with periodic paralysis might induce the similar condition and apparently increased the patients vulnerability to hypokalemia and hypertension.

並列關鍵字

primary aldosteronism ； hyperthyroidism ； hypokalemia ； secondary hypertension