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

一位三十歲女性因頭痛就診，於兩個月前被診斷為甲狀腺機能亢進，斷斷續續接受治療，並無週期性癱瘓病史。理學檢查發現瀰漫性甲狀腺腫大，高血壓：血壓值達150/90亳米汞柱，心博加速120/min，及兩手顫抖，並未出現兩側近端肢體無力的症狀；門診時甲狀腺機能檢驗發現機能亢進。給予抗甲狀腺藥物methimazol。及乙型交成神經抑制劑Propranolol治療後，因持續高血壓也給予diltizam來控制血壓，六週後病患的甲狀腺機能檢驗恢復正常，但頭痛及高血壓仍然持續，因此作血液生化檢．驗發覺低血鉀（K（上標+） = 2.9 mEq/L），由於高血壓合併低血鉀，因此懷疑醛固酮aldosterone分泌過多引起次發性高血壓。收集病患臥床八小時及立姿或站姿兩小時後血液中腎激素Plasma renin activity和醛固酮，發現醛固酮（303pg /mL）上昇合併腎激素（<0.1mg/mL/hr）降低，再藉由59（subscript NP） 核醫腎上腺皮質造影及核磁同振攝影發現右側腎上腺腫瘤，診斷為原發性醛固酮瘤引起次發性高血壓。患者接受右側腎上腺手術切除後，繼續接受methimazole的治療來維持正常的甲狀腺機能，經過半年的追蹤不再出現低血鉀合併高血壓的情形，也不再有持續頭痛的症狀。推論低血鉀合併高血壓為腎上腺醛固酮瘤引起。甲狀腺機能亢進合併週期性癱瘓或醛固酮分泌過多皆可引發低血鉀合併高血壓，甲狀腺機能正常復，高血壓及低血鉀應可恢復。此一病患的高血壓及低血鉀為腎上腺醛固酮瘤分泌過多所引起。

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.