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<article article-type="research-article" dtd-version="1.0" xml:lang="ko" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id journal-id-type="publisher-id">KJM</journal-id>
<journal-title-group>
<journal-title>The Korean Journal of Medicine</journal-title><abbrev-journal-title>Korean J Med</abbrev-journal-title></journal-title-group>
<issn pub-type="ppub">1738-9364</issn>
<issn pub-type="epub"></issn>
<publisher>
<publisher-name>The Korean Journal of Medicine</publisher-name></publisher></journal-meta>
<article-meta>
<article-id pub-id-type="doi">10.3904/kjm.2012.82.4.393</article-id>
<article-id pub-id-type="publisher-id">kjm-82-4-393-1</article-id>
<article-categories>
<subj-group>
<subject>특집</subject><subject>내분비 질환에 의한 이차 고혈압의 진단과 치료</subject>
</subj-group>
<subj-group xml:lang="en">
<subject>Special Review</subject>
</subj-group>
</article-categories>

<title-group>
<article-title>내분비 고혈압의 개요</article-title>
<trans-title-group>
<trans-title xml:lang="en">The Overview of Endocrine Hypertension</trans-title>
</trans-title-group>
</title-group>

<contrib-group>
<contrib contrib-type="author">
<name-alternatives>
<name name-style="western" xml:lang="en"><surname>Lee</surname><given-names>Hyejin</given-names></name>
<name name-style="eastern" xml:lang="ko"><surname>이</surname><given-names>혜진</given-names></name>
</name-alternatives>
<xref ref-type="corresp" rid="c1-kjm-82-4-393-1"/>
</contrib>

<aff-alternatives id="af1-kjm-82-4-393-1">
<aff xml:lang="en">Division of Endocrinology and Metabolism, Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, <country>Korea</country></aff>
<aff xml:lang="ko">이화여자대학교 의학전문대학원 내분비내과학교실</aff>
</aff-alternatives>
</contrib-group>

<author-notes>
<corresp id="c1-kjm-82-4-393-1" xml:lang="en">Correspondence to Hyejin Lee, M.D., Ph.D. &#x02003; Department of Internal Medicine, Ewha Womans University Medical Center, 1071 Anyangcheon-ro, Yangcheon-gu, Seoul 158-710, Korea &#x02003; Tel: +82-2-2650-2846, Fax: +82-2-2061-5235, E-mail: <email>hyejinlee@ewha.ac.kr</email></corresp>
</author-notes>

<pub-date pub-type="ppub">
<day>1</day>
<month>4</month>
<year>2012</year></pub-date>

<pub-date pub-type="epub">
<day>1</day>
<month>4</month>
<year>2012</year></pub-date>

<volume>82</volume>
<issue>4</issue>
<fpage>393</fpage>
<lpage>395</lpage>
<permissions>
<copyright-statement xml:lang="en">Copyright &#x024d2; 2012 The Korean Association of Internal Medicine</copyright-statement>
<copyright-year>2012</copyright-year>
<license xml:lang="en">
<license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/">http://creativecommons.org/licenses/by-nc/3.0/</ext-link>) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions>

<trans-abstract xml:lang="en"><p>The prevalence of hypertension is approximately 30&#x0025;. Hypertension is a major risk factor for stroke, ischemic heart disease and cardiac failure. In most, hypertension is essential or idiopathic, but a subgroup of approximately 15&#x0025; has secondary hypertension. Endocrine hypertension is one of the common causes of secondary hypertension and is characterized by hormonal derangements. There are at least 14 endocrine disorders for which hypertension may be the initial clinical presentation. An accurate diagnosis of endocrine hypertension provides the clinician with a unique treatment opportunity. Therefore understanding about the appropriate diagnosis and management is very important. (Korean J Med 2012;82:393-395)</p></trans-abstract>

<kwd-group xml:lang="ko">
<kwd>내분비 고혈압</kwd>
<kwd>이차성 고혈압</kwd>
</kwd-group>
<kwd-group xml:lang="en">
<kwd>Endocrine hypertension</kwd>
<kwd>Secondary hypertension</kwd>
</kwd-group></article-meta></front>



<body>
<p>고혈압은 약 30&#x0025;의 유병률을 보이며, 뇌졸중, 허혈심장병, 심부전 등의 주된 위험인자이다[<xref ref-type="bibr" rid="b1-kjm-82-4-393-1">1</xref>,<xref ref-type="bibr" rid="b2-kjm-82-4-393-1">2</xref>]. 고혈압의 대부분은 본태성 고혈압이지만 약 15&#x0025; 정도는 이차성 고혈압이며, 내분비 고혈압은 이차성 고혈압의 흔한 원인 중 하나로 호르몬 이상에 의한 고혈압을 의미한다(<xref rid="t1-kjm-82-4-393-1" ref-type="table">Table 1</xref>) [<xref ref-type="bibr" rid="b3-kjm-82-4-393-1">3</xref>,<xref ref-type="bibr" rid="b4-kjm-82-4-393-1">4</xref>]. 내분비 고혈압은 이전에 정상 혈압이었던 환자에서 새로 진단되는 경우, 기존에 잘 조절되던 고혈압이 잘 조절되지 않는 경우, 혈압조절이 불안정한 경우 등의 다양한 양상으로 나타날 수 있다. 내분비 고혈압은 본태성 고혈압과는 다르게 갑자기 발생하거나, 혈압이 매우 높고, 고혈압의 가족력이 없는 경우가 많다.</p>
<p>내분비 고혈압의 흔한 원인으로는 일차 알도스테론증, 갈색세포종, 쿠싱증후군을 들 수 있다. 일차 알도스테론증은 이전에는 고혈압의 드문 원인으로 여겨졌으며, 특징적인 저칼륨혈증이 있는 경우에만 고려되는 질환이었다. 그러나 선별 검사로 혈장 알도스테론/혈장 레닌 활성도의 비를 사용하면서 전체 고혈압의 약 10&#x0025;가 일차 알도스테론증에 의한 것으로 평가되었다[<xref ref-type="bibr" rid="b5-kjm-82-4-393-1">5</xref>,<xref ref-type="bibr" rid="b6-kjm-82-4-393-1">6</xref>]. 또한 대부분의 일차 알도스테론증 환자는 정상 혈중 칼륨농도를 보이며, 일부(9-37&#x0025;) 환자만이 저칼륨혈증을 보이고 있음이 밝혀졌다[<xref ref-type="bibr" rid="b6-kjm-82-4-393-1">6</xref>]. 갈색세포종의 유병률은 정확하게 알려져 있지 않으며, 고혈압 환자의 약 0.05-0.2&#x0025;를 차지하는 것으로 보고되었으나, 실제로는 더 높을 것으로 예상되며, Mayo Clinic의 연구에서는 약 50&#x0025;의 갈색세포종이 부검에서 발견되었다[<xref ref-type="bibr" rid="b7-kjm-82-4-393-1">7</xref>]. 갈색세포종을 가진 환자 중 약 13&#x0025;는 정상 혈압소견을 보이며, 48&#x0025;에서 발작성 고혈압을 29&#x0025;에서는 지속성 고혈압을 보인다[<xref ref-type="bibr" rid="b8-kjm-82-4-393-1">8</xref>]. 쿠싱증후군은 고혈압 환자의 0.1&#x0025; 미만을 차지하지만, 쿠싱증후군 환자의 약 80&#x0025;에서 고혈압을 보인다. 고혈압의 유병률은 코티솔 과다의 정도나 원인과 관련되어 있으며, 코티솔 과다의 기간과도 밀접하게 관련되어 있다. 쿠싱증후군에서 나타나는 고혈압은 일중 변동에 변화를 일으켜, 혈압의 정상적인 야간 저하가 소실되는 경우가 많다[<xref ref-type="bibr" rid="b9-kjm-82-4-393-1">9</xref>]. 쿠싱증후군 환자는 일반인보다 심혈관계 질환의 위험이 4-5배 증가되어 있는데, 고혈압이 이런 심혈관계 질환의 위험을 올리는데 있어 중요한 역할을 하는 것으로 보인다.</p>
<p>그 외의 내분비 고혈압의 원인으로는 선천성 부신피질증식증, 말단비대증, 갑상선항진증, 갑상선저하증 등이 있다[<xref ref-type="bibr" rid="b10-kjm-82-4-393-1">10</xref>-<xref ref-type="bibr" rid="b13-kjm-82-4-393-1">13</xref>] (<xref rid="t2-kjm-82-4-393-1" ref-type="table">Table 2</xref>). CYP11B1 (CYP, cytochrome P450) 결핍은선천성 부신피질증식증의 8-16&#x0025;를 차지하며, CYP11B1 결핍의 60-70&#x0025;에서 고혈압을 동반하는데 이는 증가된 11-데옥시코르티코스테론에 의한다[<xref ref-type="bibr" rid="b14-kjm-82-4-393-1">14</xref>]. CYP17 결핍은 선천성 부신피질증식증의 드문 형태로 사춘기에 고혈압, 저칼륨혈증 및 성선 기능 저하증으로 주로 나타난다. 대부분의 환자는 고혈압을 동반하지만 10-15&#x0025;는 정상 혈압을 보인다[<xref ref-type="bibr" rid="b15-kjm-82-4-393-1">15</xref>]. 말단비대증 환자의 약 30&#x0025;에서 고혈압을 포함한 심혈관계 질환이 발생한다. 말단비대증 환자의 사망률은 일반인에 비하여 30&#x0025; 가량 증가되어 있으며, 이 중 60&#x0025;가 심혈관계 질환에 기인한다[<xref ref-type="bibr" rid="b16-kjm-82-4-393-1">16</xref>]. 갑상선중독증 환자의 20-30&#x0025;에서 고혈압이 발견되며, 주로 수축기 고혈압으로 나타난다. 갑상선 호르몬은 혈관저항 감소로 인한 혈액량 증가를 유발하며, 심박동의 증가, 심장 구축률의 증가 등으로 수축기 혈압의 상승을 가져온다.</p>
<p>이차성 고혈압은 난치성 고혈압으로 발현되는 경우가 많은데, 이때는 내분비 고혈압을 반드시 고려해야 한다. 내분비 고혈압은 상대적으로 빈도가 높은 질환을 중심으로 접근해야 하며, 이에 대한 선별검사는 <xref ref-type="table" rid="t3-kjm-82-4-393-1">표 3</xref>과 같다. 철저한 병력청취와 신체검진, 적절한 실험실 검사를 통하여 내분비 고혈압을 조기에 발견하는 것은 적절한 고혈압 약물치료 및 수술적 치료를 통하여 고혈압을 완치시키고 심혈관계 질환의 이환율과 사망률을 감소시킬 수 있을 것이다.</p>

</body>



<back>



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<sec sec-type="display-objects" xml:lang="en">
		<title>Tables</title>

<table-wrap id="t1-kjm-82-4-393-1" position="float">
<label>Table 1.</label>
<caption><p>Secondary forms of hypertension [<xref ref-type="bibr" rid="b4-kjm-82-4-393-1">4</xref>]</p></caption>
<table rules="groups" frame="hsides">
<tbody>
	<tr>
		<td align="left" valign="top">Endocrine disorders</td>
	</tr>
	<tr>
		<td align="left" valign="top">Renal disease</td>
	</tr>
	<tr>
		<td align="left" valign="top">Neurological disorders</td>
	</tr>
	<tr>
		<td align="left" valign="top">Acute stress</td>
	</tr>
	<tr>
		<td align="left" valign="top">Drug-induced hypertension</td>
	</tr>
	<tr>
		<td align="left" valign="top">Miscellaneous</td>
	</tr>
</tbody>
</table>
</table-wrap>

<table-wrap id="t2-kjm-82-4-393-1" position="float">
<label>Table 2.</label>
<caption><p>Endocrine causes of hypertension [<xref ref-type="bibr" rid="b13-kjm-82-4-393-1">13</xref>]</p></caption>
<table rules="groups" frame="hsides">
<tbody>
	<tr>
		<td align="left">Adrenal-dependent causes</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Pheochromocytoma</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Primary aldosteronism</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Hyperdeoxycorticosteronism</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;&#x02003;Congenital adrenal hyperplasia</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;&#x02003;&#x02003;11&#x003B2;-hydroxylase deficiency</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;&#x02003;&#x02003;17&#x003B1;- hydroxylase deficiency</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;&#x02003;Deoxycorticosterone-producing tumor</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;&#x02003;Primary cortisol resistance</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Cushing&#x02019;s syndrome</td>
	</tr>
	<tr>
		<td align="left" valign="top">Apparent mineralocorticoid excess (AME)/11&#x003B2;-HSD deficiency</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Genetic</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;&#x02003;Type 1 AME</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Acquired</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;&#x02003;Licorice or carbenoxolone ingestion (type 1 AME)</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;&#x02003;Cushing&#x02019;s syndrome (type 2 AME)</td>
	</tr>
	<tr>
		<td align="left" valign="top">Thyroid-dependent causes</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Hypothyroidism</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Hyperthyroidism</td>
	</tr>
	<tr>
		<td align="left" valign="top">Parathyroid-dependent causes</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Hyperparathyroidism</td>
	</tr>
	<tr>
		<td align="left" valign="top">Pituitary-dependent causes</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Acromegaly</td>
	</tr>
	<tr>
		<td align="left" valign="top">&#x02003;Cushing&#x02019;s syndrome</td>
	</tr>
</tbody>
</table>
<table-wrap-foot>
	<fn id="tfn1-kjm-82-4-393-1"><label></label><p>HSD, hydroxysteroid deydrogenase.</p></fn>
</table-wrap-foot>
</table-wrap>

<table-wrap id="t3-kjm-82-4-393-1" position="float">
<label>Table 3.</label>
<caption><p>A schematic diagnostic algorithm in the assessment of different origins of endocrine hypertension [<xref ref-type="bibr" rid="b1-kjm-82-4-393-1">1</xref>]</p></caption>
<table rules="groups" frame="hsides">
<thead>
	<tr>
		<th align="left" valign="middle">Endocrine hypertension</th>
		<th align="left" valign="middle">Screening tests</th>
		<th align="left" valign="middle">Confirmatory tests</th>
	</tr>
</thead>
<tbody>
	<tr>
		<td align="left">Primary aldosteronism</td>
		<td align="left" valign="top">ARR</td>
		<td align="left" valign="top">Any one of four test</td>
	</tr>
	<tr>
		<td align="center"></td>
		<td align="center"></td>
		<td align="left" valign="top">&#x02003;1) FST</td>
	</tr>
	<tr>
		<td align="center"></td>
		<td align="center"></td>
		<td align="left" valign="top">&#x02003;2) SST</td>
	</tr>
	<tr>
		<td align="center"></td>
		<td align="center"></td>
		<td align="left" valign="top">&#x02003;3) OLT</td>
	</tr>
	<tr>
		<td align="center"></td>
		<td align="center"></td>
		<td align="left" valign="top">&#x02003;4) CCT</td>
	</tr>
	<tr>
		<td align="left">Pheochromocytoma</td>
		<td align="left" valign="top">Plasma/urine metanephrines</td>
		<td align="left" valign="top">Clonidine suppression test</td>
	</tr>
	<tr>
		<td align="center"></td>
		<td align="center"></td>
		<td align="left" valign="top">Adrenal CT</td>
	</tr>
	<tr>
		<td align="center"></td>
		<td align="center"></td>
		<td align="left" valign="top">I<sup>123</sup> MIBG</td>
	</tr>
	<tr>
		<td align="left">Cushing&#x02019;s syndrome</td>
		<td align="left" valign="top">Any one of four test</td>
		<td align="left" valign="top">Dexamethasone-CRH test</td>
	</tr>
	<tr>
		<td align="center"></td>
		<td align="left" valign="top">&#x02003;1) UFC-at least two measurements</td>
		<td align="left" valign="top">Midnight serum cortisol</td>
	</tr>
	<tr>
		<td align="center"></td>
		<td align="left" valign="top">&#x02003;2) Late night salivary cortisol-two measurements</td>
		<td align="left" valign="top">Adrenal CT/pituitary MRI</td>
	</tr>
	<tr>
		<td align="center"></td>
		<td align="left" valign="top">&#x02003;3) 1 mg DST</td>
		<td align="center"></td>
	</tr>
	<tr>
		<td align="center"></td>
		<td align="left" valign="top">&#x02003;4) Longer low-dose DST (2 mg/day for 48 hr)</td>
		<td align="center"></td>
	</tr>
</tbody>
</table>
<table-wrap-foot>
	<fn id="tfn2-kjm-82-4-393-1"><label></label><p>ARR, aldosterone/renin ratio; FST, fludrocortisone suppression test; SST, saline suppression test; OLT, oral sodium loading test; CCT, captopril challenge test; CT, computed tomography; I<sup>123</sup> MIBG, I123-labeled metaiodobenzylguanidine scintigraphy; UFC, urinary free cortisol; DST, overnight dexamethasone suppression test; CRH, corticotrophin-releasing hormone; MRI, magnetic resonance imaging.</p></fn>
</table-wrap-foot>
</table-wrap>

</sec>
</back></article>