Primary aldosteronism

Oral sodiumloading test

病人接受連續三天共218 mmol之鈉鹽(約合12.8公克氯化鈉)之高鈉飲食18

，在第三天到第四天間收集二十四小時小便測量尿液中的醛固酮、鈉離子及肌酸酐(creatinine)。為確認體內鈉鹽是足夠的，小便中之鈉離子應超過每天200 mmol，而尿液醛固酮超過每天33.3 nmol(約合12 μg)即可診斷

Intravenous saline infusion test

overnight空腹的情況下，兩公升生理食鹽水以超過四小時之流速靜脈輸注於側躺之病人，完成輸注時，抽血檢查病人之血清醛固酮濃度；若血清醛固酮濃度超過10 ng/dL，則可診斷為原發性高醛固酮症；介於5~10 ng/dL則可能為雙側腎上腺增生；而正常人小於5 ng/dL。

Fludrocortisone suppression test

Fludrocortisone acetate每六小時0.1mg共四天，同時照三餐每餐給予氯化鈉鹽片2公克。在第四天抽血檢查病人之血清醛固酮濃度，若高於6 ng/dL則可診斷原發性高醛固酮症。

Captopril test

在採檢血清醛固酮濃度及血清張力素活性前一 ~ 二小時單次口服captopril 25 ~ 50 mg，在正常情形下血清醛固酮濃度受captopril抑制會下降超過30%；但原發性高醛固酮症患者則否，且其血清張力素活性仍持續受到抑制。

Posture change test

病人前一晚維持臥姿睡眠，隔天抽晨血後，持續站姿2~4小時再抽第二次血，比較兩次之血清醛固酮濃度，若第二次高於第一次50%以上則為陽性反應；大部分雙側腎上腺增生呈陽性反應，但醛固酮分泌腺瘤及醣皮質醇可矯正型皮質醛酮症其第二次血清醛固酮濃度不會上升，反而下降或不變，故姿勢變化檢查為陰性。

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Gout

A case of gouty arthritis with tophi was admitted for operation. He accepted febuxostat as treatment in 榮總. The goal of therapy in an acute gout attack is prompt and safe termination of pain and disability. NSAID is the first-line therapy for most patients with acute gout if no contraindication. Usually, the duration of NSAID therapy is about 1 week. After clinical signs have completely resolved, NSAID may be stoped. However, due to inpaired renal function, both Colchicine and NSAID may be contraindicated. In this circumstance, glucocorticoids may be tried(IV, oral, or intraarticular according to clinical condition) if no contraindiation (such as infection). Besides, antihyperuricemic therapy is recommend in patients with a history of gout who have frequent and disabling attacks of gouty arthritis, clinical or radiographic signs of chronic gouty joint disease, tophi, unexplained renal insufficiency, recurrent nephrolithiasis, or urinary uric acid excretion >1100 mg/day. His Uric Acid is 5.0. Antihyperuricemic therapy should be adjusted to a dose to keep serum urate <6 mg/dL.  Allopurinol and febuxostat may be prescribed, but the dose should adjusted according to renal function. In the mean time, please control underline disease as your experience. If necessary, you may consult rheumatologist for further evaluation and suggestion.

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基本

For patient with DM history, sugar monitor is indicated. In addition to underline disease control, history taking is the first priority, including medication history. Basic LAB data may provide further information for our treatment. Also, nutrition support could not be neglected.

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Subclinical hypothyroidism

For patients with subclinical hypothyroidism and TSH concentrations ≥10 mU/L, we suggest treatment with thyroid hormone (T4).

For non-older patients with TSH concentrations between 4.5 and 10 mU/L who have symptoms of hypothyroidism, we also suggest treatment with T4.

For older patients (over age 70 years) with subclinical hypothyroidism and TSH between 4.5 and 8 mU/L, we suggest "not" treating.

We recommend initiating T4 replacement in women with subclinical hypothyroidism (TSH values >2.5 mU/L) who are pregnant.

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Subclinical hyperthyroidism with multiple nodular goiter

Multinodular goiters was noted in our hospital in Sep. She did not compalined of any discomfort. Although operation and RAI will reduce the size of goiter and relieve symptoms, these treatment should be discussed with the patient first.

Autonomously functioning thyroid adenomas and multinodular goiters are the most common causes of endogenous subclinical hyperthyroidism. The LAB may be normal on retesting weeks or months later, so that intervention should not be considered unless persistently low TSH is noted.

Overt hyperthyroidism is associated with increased bone resorption, low bone density, and an increase in fracture. Patients with subclinical hyperthyroidism also have an increased risk of atrial fibrillation and have more subtle cardiac findings(increases in heart rate, cardiac contractility, and left ventricular mass). In patients at high risk for skeletal or cardiac complications, if the serum TSH <0.1 mU/L, we treat the underlying cause of subclinical hyperthyroidism. If the serum TSH is 0.1 to 0.5 mU/L, we suggest treatment if there is underlying cardiovascular disease or if the bone density is low or the radionuclide scan shows one or more focal areas of increased uptake. For patient with low risk for cardiac or skeletal complications with TSH <0.1 mU/L, we suggest treatment if the radionuclide scan shows one or more focal areas of increased uptake.

Thyroid echo was just preformed on 9/17. Microsomal Ab and TSHR Ab was negative then. There was no FNA data and it was not performed before(according to family statement). Thus, you may arranged aspiration cytology this time and recheck thyroid function later. However, the patient's will of invasive evaluation is not high. Please discusse with her and her family first.

Besides, Amiodarone may also cause mild Hyperthyroidism (3% to 10%). ARB may exaggerate CKD and induce hyperkalemia. Please evalute these drugs. You may also check ACTH and Cortisol, renin activity and aldosterone for hyperkalemia evalulation. Nephrologist may be consulted  if necessary.

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Hyperlupedemia

In patients with mild to moderate hypertriglyceridemia (150 to 500 mg/dL), the main indication for therapy is reduction of cardiovascular (CV) risk. Lifestyle changes are a central part of managing such patients. Pharmacologic therapy with statin therapy for CV risk reduction has been best proven.  Benefit from lowering the cholesterol with statins in patients without clinical evidence of CVD has also been demonstrated. Besides, glucocorticoids may cause peripheral insulin resistance, hyperinsulinemia, and increased VLDL synthesis.

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Suspected adrenal insufficency

Adrenal insufficiency is likely if the serum cortisol level is below 15 during critical condition or < 3 at 8:00 AM. Critically ill patients with established hypoadrenalism should be treated with hydrocortisone if no cintraindication. Ideally, a corticotropin test should be performed for diagnosis. If adrenal insufficiency is confirmed and ACTH levels are normal or high, further evaluation for mineralocorticoid deficiency should be performed (check PRA and aldosterone).

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