副腎皮質ホルモン(ふくじんひしつホルモン、Corticosteroid)は、副腎皮質より産生されるホルモンの総称である。炎症の制御、炭水化物の代謝、タンパク質の異化、血液の電解質のレベル、免疫反応など広範囲の生理学系に深く関わっている。ストレス、侵襲などさまざまな影響によって分泌され、医薬品としても使用される。
男性ホルモンは男女問わず副腎皮質からも分泌されるが、副腎皮質ホルモンに含めないことが多い。
副腎皮質ホルモンは以下の二種に大別される。
- 糖質コルチコイド:炭水化物、脂肪、およびタンパク代謝を制御し、リン脂質の生成を防ぐことによって抗炎症剤としても働いたり、好酸球の活動を抑制するなど様々な作用を持つ。
- 鉱質コルチコイド:主に腎臓でナトリウム貯留を促進させ、電解質と水分を制御する働きを持つ。
それぞれコルチゾール、アルドステロンが代表的なホルモンである。
目次
- 1 生化学
- 2 生理学
- 3 健康と副腎皮質ホルモン
- 3.1 合成薬
- 3.2 副腎皮質ホルモン値の増減に関わる因子
- 4 体内で合成される副腎皮質ホルモン
- 5 関連項目
生化学
生合成
副腎皮質ホルモンは、副腎皮質内でコレステロールから合成される。ほとんどのステロイドの反応がシトクロムP450ファミリーの酵素によって促進される。酵素は、ミトコンドリアの中に位置し、補助因子としてアドレノドキシンを必要とする(21-ヒドロキシラーゼと17α-ヒドロキシラーゼを除く)。
アルドステロンとコルチコステロンはその生合成経路の最初の部分を共有しており、アルドステロンシンターゼによってアルドステロンに、11β-ヒドロキシラーゼによってコルチコステロンが生成される。これらの酵素はほとんど同じで、11β-ヒドロキシル化反応と18-ヒドロキシ化反応の機能を共有している。
アルドステロンシンターゼは、18-酸化を行うこともできる。アルドステロンシンターゼは副腎皮質の球状帯に存在する。また、11β-ヒドロキシラーゼは束状帯と網状帯に存在している。
生理学
分泌・調節
副腎皮質ホルモンは下垂体からの副腎皮質刺激ホルモン(ACTH)により分泌・調節されている。調節の経路は、視床下部から副腎皮質刺激ホルモン放出ホルモン(CRH)が分泌され、下垂体から副腎皮質刺激ホルモン(ACTH)が分泌され、副腎で副腎皮質ホルモンが分泌されるといった順序である。
健康と副腎皮質ホルモン
合成薬
副腎皮質ホルモンと同等の効果がある合成薬は、脳腫瘍から皮膚病までさまざまな病気の治療に使用されている。デキサメサゾンとその誘導体は、ほぼ純粋な糖質コルチコイドで、一方プレドニゾンとその誘導体は、糖質コルチコイドとしての作用と鉱質コルチコイドとしての少しの作用とを持つ。フルドロコルチゾン(フロリネフ®)は、合成された鉱質コルチコイドである。ヒドロコルチゾン(コルチゾール)は代替療法、例えば、副腎機能障害 (en:Adrenal insufficiency) と先天性副腎過形成症 (en:CAH) の治療に使われる。
合成された糖質コルチコイドは、関節痛または関節炎、側頭動脈炎、皮膚炎、アレルギー反応、喘息、肝炎、全身性紅斑性狼瘡、炎症性腸疾患(潰瘍性大腸炎とクローン病)、眼疾患(ブドウ膜炎)、サルコイドーシスの治療、そして、慢性原発性副腎皮質機能低下症、副腎機能障害など糖質コルチコイドの欠乏症の治療にも使われる。また、副腎皮質ホルモンは、嘔吐の抑制剤としてしばしば5-HT3受容体拮抗型制吐剤(例えば、オンダンセトロン)と組み合わせて使われる。
糖質コルチコイド(コルチゾール)過剰でクッシング症候群が発現し、コルチゾール低下とACTH過剰でアジソン病(副腎低形成)が発現する。鉱質コルチコイドの副作用は、高血圧、低カリウム血症、高ナトリウム血症であり、これらは、足のむくみや代謝性アルカローシス、結合組織薄弱の原因になる。
臨床実験では、副腎皮質ホルモンが目の障害である中心性網脈絡膜症;en:CSR(または、中心性漿液性脈絡網膜症;CSC)を引き起こすことが分かっている。
副腎皮質ホルモン値の増減に関わる因子
アジソン病(慢性副腎皮質機能低下症)。下垂体の副腎皮質刺激ホルモン(ACTH)の分泌不全による。コルチゾール、デヒドロエピアンドロステロン(DHEA)、デヒドロエピアンドロステロンサルフェート(DHEA-S)の分泌が低下する。
先天性副腎低形成(原発性副腎低形成)。X連鎖性(DAX-1異常症)、常染色体性(SF-1異常症)、IMAge症候群、ACTH不応症、Triple A症候群(Allgrove症候群)に分類される。
下垂体機能低下症。下垂体前葉ホルモンであるACTH、TSH、GH、LH、FSH、プロラクチンの一つ以上の分泌が低下した状態である。ACTHのみの欠損をACTH単独欠損症と呼ぶ。
副腎酵素欠損症(ステロイドホルモンを生産するための酵素が先天的に欠損する)・先天性副腎過形成症。リポイド過形成症(Protein(StAR)蛋白の異常とコレステロール側鎖切断酵素に欠損)、21-水酸化酵素欠損症、11β-水酸化酵素欠損症、17α-水酸化酵素欠損症、3β-ヒドロキシステロイドデヒドロゲナーゼ欠損症、21水酸化酵素と17α-水酸化酵素の複合欠損(P450オキシドレダクターゼ欠損により発現)がある。
副腎酵素欠損症には、18-水酸化酵素欠損症、P450オキシドレダクターゼ欠損症、3β-水酸化ステロイド脱水素酵素欠損症、18-ヒドロキシラーゼ欠損症、18-ヒドロキシステロイドデヒドロゲナーゼ欠損症がある。
クッシング病。副腎が原因のものがACTH非依存性クッシング症候群(副腎性クッシング症候群)、ACTHが過剰に分泌されコルチゾールが増加するものがACTH依存性クッシング症候群と呼ばれる。さらにが下垂体の原因(下垂体腫瘍)によるACTH過剰分泌がクッシング病、下垂体以外に原因のあるものが異所性ACTH症候群と呼ばれる。
偽性低アルドステロン症。I型、II型、III型がある。
原発性アルドステロン症。
グルココルチコイド抵抗症。グルココルチコイド受容体遺伝子の変異により起こる。
体内で合成される副腎皮質ホルモン
- アルドステロン
- コルチゾン
- コルチゾール
- デスオキシコルチコステロン
関連項目
- クッシング症候群
- ステロイド
- ステロイドホルモン
- ステロイド剤の適応疾患
- ステロイドの略語一覧
- 副腎髄質ホルモン
- 蜂刺され
- ヒドロコルチゾン
- ステロイド系抗炎症薬
- ステロイド外用薬
- 性ホルモン
- アンドロゲン
- テストステロン
- デヒドロエピアンドロステロン(DHEA)
- エストロゲン
- エストラジオール
- エストリオール
- エストロン
- ゲスターゲン
- プロゲステロン
- コレステロール
- 性染色体
- 下垂体
- 視床下部
- 副腎皮質刺激ホルモン
- 内分泌学
薬理学:医薬品の分類 |
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消化器/代謝(A) |
- 胃酸中和剤
- 制吐薬
- 瀉下薬
- 止瀉薬/止痢薬
- 抗肥満薬
- 血糖降下薬
- ビタミン
- ミネラル
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血液、血液生成器官(B) |
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循環器系(C) |
- 心臓療法/狭心症治療薬
- 高血圧治療薬
- 利尿薬
- 血管拡張薬
- 交感神経β受容体遮断薬
- カルシウム拮抗剤
- レニン-アンジオテンシン系
- ACE阻害薬
- アンジオテンシンII受容体拮抗薬
- レニン阻害薬
- 脂質降下薬
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皮膚(D) |
- 皮膚軟化剤
- 瘢痕形成剤
- 鎮痒薬
- 乾癬治療薬
- 他の皮膚薬
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泌尿生殖器系(G) |
- ホルモン避妊薬
- 排卵誘発治療
- SERM
- 性ホルモン
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内分泌器(H) |
- 視床下部脳下垂体ホルモン
- 副腎皮質ホルモン
- 性ホルモン
- 甲状腺ホルモン/抗甲状腺薬
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感染(J、P、QI) |
- 抗菌薬
- 抗真菌薬
- 抗ウイルス薬
- 抗寄生虫薬
- 外部寄生虫駆除剤
- 静注用免疫グロブリン
- ワクチン
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悪性腫瘍(L01-L02) |
- 抗がん剤
- 代謝拮抗薬
- 抗腫瘍性アルキル化薬
- 紡錘体毒
- 抗悪性腫瘍薬
- トポイソメラーゼ阻害薬
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免疫系(L03-L04) |
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筋肉、骨、関節(M) |
- アナボリックステロイド
- 抗炎症薬
- 抗リウマチ
- 副腎皮質ホルモン
- 筋弛緩剤
- ビスホスホネート
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脳、神経(N) |
- 鎮痛剤
- 麻酔剤
- 食欲低下薬
- ADHD治療
- 中毒医学
- 抗てんかん薬
- アルツハイマー治療
- 抗うつ薬
- 片頭痛治療
- 抗パーキンソン病薬
- 抗精神病薬
- 抗不安薬
- 抑制剤
- エンタクトゲン
- エンセオジェン
- 陶酔薬
- 幻覚剤
- 催眠薬/鎮静薬
- 気分安定薬
- 神経保護
- スマートドラッグ
- 神経毒
- 食欲促進
- セレニック
- 精神刺激薬
- 覚醒促進物質
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呼吸器(R) |
- 鬱血除去薬
- 気管支拡張薬
- 鎮咳去痰薬
- 抗ヒスタミン薬
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感覚器(S) |
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その他ATC(V) |
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内分泌器:ホルモン(ペプチドホルモン、ステロイドホルモン) |
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視床下部 - 脳下垂体 |
視床下部
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GnRH - TRH - ドーパミン - CRH - GHRH - ソマトスタチン - ORX - MCH - MRH - MIH
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脳下垂体後葉
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バソプレッシン - OXT
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脳下垂体中葉
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MSH(インテルメジン)
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脳下垂体前葉
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αサブユニット糖タンパク質ホルモン(FSH - LH - TSH) - GH - PRL - POMC(ACTH - エンドルフィン - リポトロピン)
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副腎 |
副腎髄質
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副腎髄質ホルモン(アドレナリン - ノルアドレナリン - ドーパミン)
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副腎皮質
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副腎皮質ホルモン(アルドステロン - コルチゾール - DHEA)
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甲状腺 |
甲状腺
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甲状腺ホルモン(T3 - T4 - カルシトニン)
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副甲状腺
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PTH
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生殖腺 |
精巣
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テストステロン - AMH - インヒビン
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卵巣
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エストラジオール - プロゲステロン - インヒビン/アクチビン - リラキシン(妊娠時)
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その他の内分泌器 |
膵臓
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グルカゴン - インスリン - ソマトスタチン
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松果体
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メラトニン
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内分泌器でない器官 |
胎盤:hCG - HPL - エストロゲン - プロゲステロン - 腎臓:レニン - EPO - カルシトリオール - プロスタグランジン - 心臓:ANP - BNP - ET - 胃:ガストリン - グレリン - 十二指腸:CCK - GIP - セクレチン - モチリン - VIP - 回腸:エンテログルカゴン - 脂肪組織:レプチン - アディポネクチン - レジスチン - 胸腺:サイモシン - サイモポイエチン - サイムリン - STF - THF - 肝臓:IGFs(IGF-1 - IGF-2) - 耳下腺:バロチン - 末梢神経系:CGRP - P物質
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誘導タンパク質 |
NGF - BDNF - NT-3
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副腎皮質ホルモン |
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アルドステロン - コルチゾン - コルチゾール - デスオキシコルチコステロン - デヒドロエピアンドロステロン - コルチコステロン
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ステロイド |
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前駆体 |
スクアレン · ラノステロール
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一般 |
コレステロール · プレグネノロン · 17-ヒドロキシプレグネノロン · DHEA · アンドロステンジオン · アンドロスタンジオール
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性ホルモン |
エストロゲン
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エストラジオール · エストリオール · エストロン
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アンドロゲン
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テストステロン · デヒドロテストステロン · アンドロステロン
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プロゲストーゲン
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プロゲステロン · 17-ヒドロキシプロゲステロン · プロゲスチン
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副腎皮質ホルモン |
糖質コルチコイド
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コルチゾール · プレドニゾン · コルチコステロン · コルチゾン · プロゲステロン
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鉱質コルチコイド
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アルドステロン
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フィトステロール |
スチグマステロール · ブラシカステロール
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エルゴステロール |
エルゴステロール · エルゴカルシフェロール
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主要な生体物質:炭水化物(アルコール、糖タンパク質、配糖体) · 脂質(エイコサノイド · 脂肪酸/脂肪酸の代謝中間体 · リン脂質 · スフィンゴ脂質 · ステロイド) · 核酸(核酸塩基 · ヌクレオチド代謝中間体) · タンパク質(タンパク質を構成するアミノ酸/アミノ酸の代謝中間体) · テトラピロール · ヘムの代謝中間体 |
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This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (January 2010) |
Corticosteroids are a class of chemicals that includes the steroid hormones that are produced in the adrenal cortex of vertebrates as well as the synthetic analogues of these hormones. Corticosteroids are involved in a wide range of physiological processes, including stress response, immune response, and regulation of inflammation, carbohydrate metabolism, protein catabolism, blood electrolyte levels, and behavior.
- Glucocorticoids such as cortisol control carbohydrate, fat and protein metabolism, and are anti-inflammatory by preventing phospholipid release, decreasing eosinophil action and a number of other mechanisms.[1]
- Mineralocorticoids such as aldosterone control electrolyte and water levels, mainly by promoting sodium retention in the kidney.
Some common natural hormones are corticosterone (C
21H
30O
4), cortisone (C
21H
28O
5, 17-hydroxy-11-dehydrocorticosterone) and aldosterone.
Contents
- 1 Medical uses
- 2 Side effects
- 3 Biosynthesis
- 4 Classification
- 4.1 Chemical structure
- 4.1.1 Group A — Hydrocortisone type
- 4.1.2 Group B — Acetonides (and related substances)
- 4.1.3 Group C — Betamethasone type
- 4.1.4 Group D — Esters
- 4.1.4.1 Group D1 — Halogenated (less labile)
- 4.1.4.2 Group D2 — Labile prodrug esters
- 4.2 Route of administration
- 4.2.1 Topical steroids
- 4.2.2 Inhaled steroids
- 4.2.3 Oral forms
- 4.2.4 Systemic forms
- 5 History
- 6 See also
- 7 References
Medical uses
Synthetic pharmaceutical drugs with corticosteroid-like effects are used in a variety of conditions, ranging from brain tumors to skin diseases. Dexamethasone and its derivatives are almost pure glucocorticoids, while prednisone and its derivatives have some mineralocorticoid action in addition to the glucocorticoid effect. Fludrocortisone (Florinef) is a synthetic mineralocorticoid. Hydrocortisone (cortisol) is available for replacement therapy, e.g. in adrenal insufficiency and congenital adrenal hyperplasia.
Synthetic glucocorticoids are used in the treatment of joint pain or inflammation (arthritis), temporal arteritis, dermatitis, allergic reactions, asthma, hepatitis, systemic lupus erythematosus, inflammatory bowel disease (ulcerative colitis and Crohn's disease), sarcoidosis and for glucocorticoid replacement in Addison's disease or other forms of adrenal insufficiency.[2] Topical formulations are also available for the skin, eyes (uveitis), lungs (asthma), nose (rhinitis), and bowels. Corticosteroids are also used supportively to prevent nausea, often in combination with 5-HT3 antagonists (e.g. ondansetron).
Typical undesired effects of glucocorticoids present quite uniformly as drug-induced Cushing's syndrome. Typical mineralocorticoid side-effects are hypertension (abnormally high blood pressure), hypokalemia (low potassium levels in the blood), hypernatremia (high sodium levels in the blood) without causing peripheral edema, metabolic alkalosis and connective tissue weakness.[3] There may also be impaired wound healing or ulcer formation because of the immunosuppressive effects.
Clinical and experimental evidence indicates that corticosteroids can cause permanent eye damage by inducing central serous retinopathy (CSR, also known as central serous chorioretinopathy, CSC). A variety of steroid medications, from anti-allergy nasal sprays (Nasonex, Flonase) to topical skin creams, to eye drops (Tobradex), to prednisone have been implicated in the development of CSR.[4][5]
Corticosteroids have been widely used in treating people with traumatic brain injury.[6] A systematic review identified 20 randomised controlled trials and included 12,303 participants, then compared patients who received corticosteroids with patients who received no treatment. The authors recommended people with traumatic head injury should not be routinely treated with corticosteroids.[7]
Side effects
Lower arm of a 47-year-old female showing skin damage due to topical steroid use
Use of corticosteroids has numerous side-effects, some of which may be severe:
- Neuropsychiatric: steroid psychosis,[8] and anxiety,[9] depression. Therapeutic doses may cause a feeling of artificial well-being ("steroid euphoria").[10] The neuropsychiatric effects are partly mediated by sensitization of the body to the actions of adrenaline. Therapeutically, the bulk of corticosteroid dose is given in the morning to mimic the body's diurnal rhythm; if given at night, the feeling of being energized will interfere with sleep. An extensive review is provided by Flores and Gumina.[11]
- Cardiovascular: Corticosteroids can cause sodium retention through a direct action on the kidney, in a manner analogous to the mineralocorticoid aldosterone. This can result in fluid retention and hypertension.
- Metabolic: Corticosteroids cause a movement of body fat to the face and torso, resulting respectively in "moon face" and "buffalo hump". and away from the limbs. Due to the diversion of amino-acids to glucose, they are considered anti-anabolic, and long term therapy can cause muscle wasting[12]
- Endocrine: By increasing the production of glucose from amino-acid breakdown and opposing the action of insulin, corticosteroids can cause hyperglycemia,[13] insulin resistance and diabetes mellitus.[14]
- Skeletal: Steroid-induced osteoporosis may be a side-effect of long-term corticosteroid use. Use of inhaled corticosteroids among children with asthma may result in decreased height.[15]
- Gastro-intestinal: While cases of colitis have been reported, corticosteroids are therapeutically employed when the colitis has an auto-immune nature, e.g. ulcerative colitis and Crohn's disease. While the evidence for corticosteroids causing peptic ulceration is relatively poor except for high doses taken for over a month,[16] the majority of doctors as of 2010[update] still believe this is the case, and would consider protective prophylactic measures.[17]
- Eyes: chronic use may predispose to cataract and retinopathy.
- Vulnerability to infection: By suppressing immune reactions (which is one of the main reasons for their use in allergies), steroids may cause infections to flare up, notably candidiasis.[18]
- Pregnancy: Corticosteroids have a low but significant teratogenic effect, causing a few birth defects per 1,000 pregnant women treated. Corticosteroids are therefore contraindicated in pregnancy.[19]
- Habituation: Topical steroid addiction (TSA) has been reported in long-term users of topical steroids (users who applied topical steroids to their skin over a period of weeks, months, or years).[20][21] TSA is characterised by uncontrollable, spreading dermatitis and worsening skin inflammation which requires a stronger topical steroid to get the same result as the first prescription. When topical steroid medication is lost, the skin experiences redness, burning, itching, hot skin, swelling, and/or oozing for a length of time. This is also called 'red skin syndrome' or 'topical steroid withdrawal'(TSW). After the withdrawal period is over the atopic dermatitis can cease or is less severe than it was before.[22]
Corticosteroids were voted Allergen of the Year in 2005 by the American Contact Dermatitis Society.[23]
Biosynthesis
Corticosteroid biosynthetic pathway in rat
The corticosteroids are synthesized from cholesterol within the adrenal cortex. Most steroidogenic reactions are catalysed by enzymes of the cytochrome P450 family. They are located within the mitochondria and require adrenodoxin as a cofactor (except 21-hydroxylase and 17α-hydroxylase).
Aldosterone and corticosterone share the first part of their biosynthetic pathway. The last part is mediated either by the aldosterone synthase (for aldosterone) or by the 11β-hydroxylase (for corticosterone). These enzymes are nearly identical (they share 11β-hydroxylation and 18-hydroxylation functions), but aldosterone synthase is also able to perform an 18-oxidation. Moreover, aldosterone synthase is found within the zona glomerulosa at the outer edge of the adrenal cortex; 11β-hydroxylase is found in the zona fasciculata and zona glomerulosa.
Classification
Chemical structure
In general, corticosteroids are grouped into four classes, based on chemical structure. Allergic reactions to one member of a class typically indicate an intolerance of all members of the class. This is known as the "Coopman classification",[24] after S. Coopman, who defined this classification in 1989.[25]
The highlighted steroids are often used in the screening of allergies to topical steroids.[26]
Group A — Hydrocortisone type
Hydrocortisone, hydrocortisone acetate, cortisone acetate, tixocortol pivalate, prednisolone, methylprednisolone, and prednisone (Short- to medium-acting glucocorticoids).
Group B — Acetonides (and related substances)
Triamcinolone acetonide, triamcinolone alcohol, mometasone, amcinonide, budesonide, desonide, fluocinonide, fluocinolone acetonide, and halcinonide.
Group C — Betamethasone type
Betamethasone, betamethasone sodium phosphate, dexamethasone, dexamethasone sodium phosphate, and fluocortolone.
Group D — Esters
Group D1 — Halogenated (less labile)
Hydrocortisone-17-valerate, halometasone, alclometasone dipropionate, betamethasone valerate, betamethasone dipropionate, prednicarbate, clobetasone-17-butyrate, clobetasol-17-propionate, fluocortolone caproate, fluocortolone pivalate, and fluprednidene acetate.
Group D2 — Labile prodrug esters
Hydrocortisone-17-butyrate, hydrocortisone-17-aceponate, hydrocortisone-17-buteprate, ciclesonide and prednicarbate.
Route of administration
Topical steroids
Main article: Topical steroid
For use topically on the skin, eye, and mucous membranes.
Topical corticosteroids are divided in potency classes I to IV,
Inhaled steroids
for use to treat the nasal mucosa, sinuses, bronchii, and lungs.[27] This group includes:
- Flunisolide[28]
- Fluticasone furoate
- Fluticasone propionate[28]
- Triamcinolone acetonide[28]
- Beclomethasone dipropionate[28]
- Budesonide[28]
There is also a combination preparation containing fluticasone propionate and salmeterol xinafoate (a long-acting bronchodilator).[28] It is approved for children over 12 years old.
Oral forms
Such as prednisone and prednisolone.[29]
Systemic forms
Available in injectables for intravenous and parenteral routes.[29]
History
First known use was in 1944.[30] Tadeusz Reichstein together with Edward Calvin Kendall and Philip Showalter Hench were awarded the Nobel Prize for Physiology and Medicine in 1950 for their work on hormones of the adrenal cortex, which culminated in the isolation of cortisone.[31]
Corticosteroids have been used as drug treatment for some time. Lewis Sarett of Merck & Co. was the first to synthesize cortisone, using a complicated 36-step process that started with deoxycholic acid, which was extracted from ox bile.[32] The low efficiency of converting deoxycholic acid into cortisone led to a cost of US $200 per gram. Russell Marker, at Syntex, discovered a much cheaper and more convenient starting material, diosgenin from wild Mexican yams. His conversion of diosgenin into progesterone by a four-step process now known as Marker degradation was an important step in mass production of all steroidal hormones, including cortisone and chemicals used in hormonal contraception.[33] In 1952, D.H. Peterson and H.C. Murray of Upjohn developed a process that used Rhizopus mold to oxidize progesterone into a compound that was readily converted to cortisone.[34] The ability to cheaply synthesize large quantities of cortisone from the diosgenin in yams resulted in a rapid drop in price to US $6 per gram, falling to $0.46 per gram by 1980. Percy Julian's research also aided progress in the field.[35] The exact nature of cortisone's anti-inflammatory action remained a mystery for years after, however, until the leukocyte adhesion cascade and the role of phospholipase A2 in the production of prostaglandins and leukotrienes was fully understood in the early 1980s.
See also
- Vitiligo
- Steroids (general term)
- Fluorometholone
- List of steroid abbreviations
References
- ^ Joseph P. Edardes. "Steroids and Warfarin Therapy". Coumarin Anticoagulant Research Progress. Nova Publishers, 2008. p. 18.
- ^ Higashi AS, Zhu S, Stafford RS, Alexander GC (Dec 2011). "National trends in outpatient asthma treatment, 1997-2009". Journal of General Internal Medicine 26 (12): 1465–1470. doi:10.1007/s11606-011-1796-4. PMID 21769507.
- ^ Werner R (2005). A massage therapist's guide to Pathology (3rd ed.). Pennsylvania: Lippincott Williams & Wilkins.
- ^ Carvalho-Recchia, CA; Yannuzzi, LA; Negrão, S; Spaide, RF; Freund, KB; Rodriguez-Coleman, H; Lenharo, M; Iida, T (2002). "Corticosteroids and central serous chorioretinopathy". Ophthalmology 109 (10): 1834–7. doi:10.1016/S0161-6420(02)01117-X. PMID 12359603.
- ^ "The New York Times :: A Breathing Technique Offers Help for People With Asthma". buteykola.com. Retrieved 2012-11-30.
- ^ Alderson P, Roberts I. "Plain Language Summary". Corticosteroids for acute traumatic brain injury. The Cochrane Collaboration. p. 2.
- ^ Alderson, P.; Roberts, I. (2005). Alderson, Phil, ed. "Corticosteroids for acute traumatic brain injury". Cochrane Database Syst Rev (1): CD000196. doi:10.1002/14651858.CD000196.pub2. PMID 15674869.
- ^ Hall, Richard. "Psychiatric Adverse Drug Reactions: Steroid Psychosis". Director of Research Monarch Health Corporation Marblehead, Massachusetts.
- ^ Korte SM (2001). "Corticosteroids in relation to fear, anxiety and psychopathology". Neurosci Biobehav Rev 25 (2): 117–42. doi:10.1016/S0149-7634(01)00002-1. PMID 11323078.
- ^ C R Swinburn, J M Wakefield, S P Newman, and P W Jones Evidence of prednisolone induced mood change ('steroid euphoria') in patients with chronic obstructive airways disease" Br J Clin Pharmacol 1988 December; 26(6) 709–713. URL:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1386585/
- ^ Benjamin H. Flores and Heather Kenna Gumina. The Neuropsychiatric Sequelae of Steroid Treatment. URL:http://www.dianafoundation.com/articles/df_04_article_01_steroids_pg01.html
- ^ Per-Olof Hasselgren, Nima Alamdari, Zaira Aversa, Patricia Gonnella, Ira J Smith, and Steven Tizio. CORTICOSTEROIDS AND MUSCLE WASTING ROLE OF TRANSCRIPTION FACTORS, NUCLEAR COFACTORS, AND HYPERACETYLATION. Curr Opin Clin Nutr Metab Care. 2010 July; 13(4): 423–428. URL:http://ncbi.nlm.nih.gov/pmc/PMC2911625
- ^ Donihi AC, Raval D, Saul M, Korytkowski MT, DeVita MA (2006). "Prevalence and predictors of corticosteroid-related hyperglycemia in hospitalized patients". Endocr Pract 12 (4): 358–62. doi:10.4158/ep.12.4.358. PMID 16901792.
- ^ Blackburn D, Hux J, Mamdani M (2007). "Quantification of the risk of corticosteroid-induced diabetes mellitus among the elderly". Journal of General Internal Medicine 17 (9): 1525–1497. doi:10.1046/j.1525-1497.2002.10649.x.
- ^ Zhang, L; Prietsch, SO; Ducharme, FM (Jul 17, 2014). "Inhaled corticosteroids in children with persistent asthma: effects on growth.". The Cochrane database of systematic reviews 7: CD009471. doi:10.1002/14651858.CD009471.pub2. PMID 25030198.
- ^ Pecora PG, Kaplan B (1996). "Corticosteroids and ulcers: is there an association?". Ann Pharmacother 30 (7–8): 870–2. doi:10.1177/106002809603000729. PMID 8826575.
- ^ Martínek J, Hlavova K, Zavada F; et al. (June 2010). ""A surviving myth" —corticosteroids are still considered ulcerogenic by a majority of physicians". Scand J Gastroenterol 45 (10): 1156–61. doi:10.3109/00365521.2010.497935. PMID 20569095.
- ^ Fukushima, C.; Matsuse, H.; Tomari, S.; Obase, Y.; Miyazaki, Y.; Shimoda, T.; Kohno, S. (2003). "Oral candidiasis associated with inhaled corticosteroid use: Comparison of fluticasone and beclomethasone". Annals of Allergy, Asthma & Immunology 90 (6): 646–651. doi:10.1016/S1081-1206(10)61870-4. PMID 12839324.
- ^ Shepard, TH.; Brent, RL.; Friedman, JM.; Jones, KL.; Miller, RK.; Moore, CA.; Polifka, JE. (April 2002). "Update on new developments in the study of human teratogens". Teratology 65 (4): 153–61. doi:10.1002/tera.10032. PMID 11948561.
- ^ Nnoruka, Edith; Daramola, Olaniyi; Ike, Samuel (2007). "Misuse and abuse of topical steroids: implications.". Expert Review of Dermatology 2 (1): 31–40. doi:10.1586/17469872.2.1.31. Retrieved 2014-12-18.
- ^ Sanjay, Rathi; D'Souza, Paschal (2012). "Rational and ethical use of topical corticosteroids based on safety and efficacy.". Indian Journal of Dermatology 57 (4): 251–259. doi:10.4103/0019-5154.97655.
- ^ Fukaya, M; Sato, K; Sato, M; Kimata, H; Fujisawa, S; Dozono, H; Yoshizawa, J; Minaguchi, S (2014). "Topical steroid addiction in atopic dermatitis.". Drug, healthcare and patient safety 6: 131–8. doi:10.2147/dhps.s69201. PMID 25378953.
- ^ "Contact Allergen of the Year: Corticosteroids: Introduction". Medscape.com. 2005-06-13. Retrieved 2012-11-30.
- ^ Rietschel, Robert L. (2007). Fisher's Contact Dermatitis, 6/e. Hamilton, Ont: BC Decker Inc. p. 256. ISBN 1-55009-378-9.
- ^ Coopman S, Degreef H, Dooms-Goossens A (July 1989). "Identification of cross-reaction patterns in allergic contact dermatitis from topical corticosteroids". Br. J. Dermatol. 121 (1): 27–34. doi:10.1111/j.1365-2133.1989.tb01396.x. PMID 2757954.
- ^ Wolverton, SE (2001). Comprehensive Dermatologic Drug Therapy. WB Saunders. p. 562.
- ^ "Asthma Steroids: Inhaled Steroids, Side Effects, Benefits, and More". Webmd.com. Retrieved 2012-11-30.
- ^ a b c d e f Frieden, Thomas R. (March 2004). "Inhaled Corticosteroids — Long-Term Control Asthma medicine" (PDF). New York City Asthma Initiative.
- ^ a b "Systemic steroids (corticosteroids). DermNet NZ". . DermNet NZ. 2012-05-19. Retrieved 2012-11-30.
- ^ Webster. "First therapeutic use of Corticosteroid". Retrieved 30 July 2012.
- ^ http://nobelprize.org/nobel_prizes/medicine/laureates/1950/kendall-lecture.pdf
- ^ Sarett, Lewis H. (1947). "Process of Treating Pregnene Compounds", U. S. Patent 2,462,133
- ^ Marker, Russell E.; Wagner, R. B.; Ulshafer, Paul R.; Wittbecker, Emerson L.; Goldsmith, Dale P. J.; Ruof, Clarence H. (1947). "Steroidal Sapogenins". J. Am. Chem. Soc. 69 (9): 2167–2230. doi:10.1021/ja01201a032. PMID 20262743.
- ^ Peterson D.H., Murray, H.C. (1952). "Microbiological Oxygenation of Steroids at Carbon 11". J. Am. Chem. Soc. 74 (7): 1871–2. doi:10.1021/ja01127a531.
- ^ Julian, Percy L., Cole, John Wayne, Meyer, Edwin W., and Karpel, William J. (1956) "Preparation of Cortisone". U. S. Patent 2,752,339
Endogenous steroids (and metabolic intermediates)
|
|
Precursors |
- Cholesterol
- 22R-Hydroxycholesterol
- 20α,22R-Dihydroxycholesterol
|
|
Corticosteroids |
Glucocorticoids
|
- Corticosterone
- Cortisol
- Cortisone
- DHC
- Deoxycortisol
- Deoxycorticosterone
- 17-Hydroxypregnenolone
- 17-Hydroxyprogesterone
- Pregnenolone
- Progesterone
- THB
|
|
Mineralocorticoids
|
- Aldosterone
- Corticosterone
- Cortisol
- Deoxycortisol
- Deoxycorticosterone
- 5α-Dihydroaldosterone
- 16α,18-Dihydroxy-11-deoxycorticosterone
- 18-Hydroxy-11-deoxycorticosterone
- 18-Hydroxycorticosterone
- 18-Hydroxydeoxycorticosterone
|
|
|
Sex steroids |
Androgens
|
- 3α-Androstanediol
- Δ5-Androstenediol
- Δ4-Androstenedione
- Androsterone
- DHEA
- DHEA sulfate
- Dihydrotestosterone
- Epiandrosterone
- Epitestosterone
- 16α-Hydroxyandrostenedione
- 16α-Hydroxy-DHEA
- 16α-Hydroxy-DHEA sulfate
- Testosterone
|
|
Estrogens
|
- 27-Hydroxycholesterol
- 3α-Androstanediol
- 3β-Androstanediol
- Δ4-Androstenedione
- Δ5-Androstenediol
- DHEA
- DHEA sulfate
- 7-Oxo-DHEA
- 7α-Hydroxy-DHEA
- 16α-Hydroxy-DHEA
- 7β-Hydroxyepiandrosterone
- Estetrol
- Estradiol
- Estrone
- Estriol
- 2-Hydroxyestrone
- 16-Hydroxyestrone
|
|
Progestogens
|
- Progesterone
- 17α-Hydroxyprogesterone
- 20α-Dihydroprogesterone
- 5α-Dihydroprogesterone
- Deoxycorticosterone
- 5α-DHDOC
|
|
|
Neurosteroids |
- Allopregnanolone
- 3α-Androstanediol
- 3α-Dihydroprogesterone
- 3β-Dihydroprogesterone
- Androstenol
- Androsterone
- Cholesterol
- Corticosterone
- DHC
- DHDOC
- DHEA
- DHEA sulfate
- 5α-Dihydroprogesterone
- 5β-Dihydroprogesterone
- Deoxycorticosterone
- Epipregnanolone
- Estradiol
- Etiocholanolone
- 17-Hydroxypregnenolone
- 17-Hydroxyprogesterone
- Isopregnanolone
- Pregnanolone
- Pregnenolone
- Pregnenolone sulfate
- Progesterone
- THB
- THDOC
- Pheromones: 3α-Androstenol
- 3β-Androstenol
- Androstadienol
- Androstadienone
- Androstenone
- Androsterone
- Estratetraenol
|
|
Others |
- Vitamin D: 7-Dehydrocholesterol
- Calcidiol/Calcifediol
- Calcitriol
- Cholecalciferol
|
|
Corticosteroid signaling
|
|
Glucocorticoid signaling
|
|
Receptor
(ligands) |
GR
|
Agonists
|
|
|
Mixed (SEGRAs)
|
- Dagrocorat
- Fosdagrocorat
- Mapracorat
|
|
Antagonists
|
- 3α-Hydroxytibolone
- 3β-Hydroxytibolone
- Aglepristone
- Asoprisnil
- C108297
- C113176
- CORT-108297
- Cyproterone acetate
- Guggulsterone
- Ketoconazole
- Lilopristone
- LLY-2707
- Miconazole
- Mifepristone
- Onapristone
- Org 34850
- Pregnenolone 16α-carbonitrile
- Spironolactone
- Telapristone
- Tibolone
- Toripristone
- Ulipristal acetate
|
|
|
|
Enzyme |
Modulators
|
- See here instead (modulators of 20,22-desmolase, 17α-hydroxylase/17,20-lyase, 3β-HSD, 11β-HSD, 21-hydroxylase, 11β-hydroxylase, and 18-hydroxylase).
|
|
|
Others |
Precursors/prohormones
|
- Cholesterol
- 22R-Hydroxycholesterol
- 20α,22R-Dihydroxycholesterol
- Pregnenolone
- Pregnenolone sulfate
- 17-Hydroxypregnenolone
- Progesterone
- 17-Hydroxyprogesterone
- 11-Deoxycorticosterone
|
|
Indirect
|
- ACTH (corticotropin)
- CRH
- DHEA
- DHEA sulfate
- Plasma proteins (albumin, transcortin)
- Vasopressin
|
|
|
See also: Androgenics • Estrogenics • Mineralocorticoids • Progestogenics
|
|
Mineralocorticoid signaling
|
|
Receptor
(ligands) |
MR
|
Agonists
|
- 11-Deoxycorticosterone (desoxycortone)
- 11-Deoxycortisol (cortodoxone)
- 16α,18-Dihydroxy-11-deoxycorticosterone
- 17-Hydroxyaldosterone
- 18-Hydroxy-11-deoxycorticosterone
- 19-Norprogesterone
- Aldosterone
- Corticosterone
- Desoxycortone acetate
- Desoxycortone enanthate
- Desoxycortone glucoside
- Desoxycortone pivalate
- Hydrocortisone (cortisol)
- Fludrocortisone
- Fludrocortisone acetate
- Mometasone furoate
- Prednisolone
- Prednisone
|
|
Antagonists
|
- 3α-Hydroxytibolone
- 3β-Hydroxytibolone
- 6β-Hydroxy-7α-thiomethylspironolactone
- 7α-Thiomethylspironolactone
- 17-Hydroxyprogesterone
- Benidipine
- Canrenoate potassium (potassium canrenoate)
- Canrenoic acid
- Canrenone
- Dicirenone
- Drospirenone
- Eplerenone
- Finerenone
- Gestodene
- Guggulsterone
- Mespirenone
- Mexrenoate potassium
- Mexrenoic acid
- Mexrenone
- Oxprenoic acid
- Oxprenoate potassium (RU-28318)
- Pregnenolone
- Progesterone
- Prorenoate potassium
- Prorenoic acid (prorenoate)
- Prorenone
- RU-26752
- Spirorenone
- Spironolactone
- Spiroxasone
- Tibolone
|
|
|
|
Enzyme |
Modulators
|
- See here instead (modulators of 20,22-desmolase, 17α-hydroxylase/17,20-lyase, 3β-HSD, 11β-HSD, 21-hydroxylase, 11β-hydroxylase, and 18-hydroxylase).
|
|
|
Others |
Precursors/prohormones
|
- Cholesterol
- 22R-Hydroxycholesterol
- 20α,22R-Dihydroxycholesterol
- Pregnenolone
- Pregnenolone sulfate
- 17-Hydroxypregnenolone
- Progesterone
- 17-Hydroxyprogesterone
- 11-Deoxycorticosterone
- 18-Hydroxydeoxycorticosterone
- Corticosterone
- 18-Hydroxycorticosterone
|
|
Indirect
|
- ACTH (corticotropin)
- CRH
- Plasma proteins (albumin, transcortin)
- Vasopressin
|
|
|
See also: Androgenics • Estrogenics • Glucocorticoids • Progestogenics
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Authority control |
- LCCN: sh85001012
- NDL: 00563657
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