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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/02/09 23:32:46」(JST)

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活性化部分トロンボプラスチン時間(かっせいか・ぶぶん・トロンボプラスチン・じかん)とは、血液凝固能検査のひとつ。APTT(activated partial thromboplastin time)とも略される。内因系及び共通系の凝固異常を判定する検査として用いられる。

検査法

まず、被検者の静脈血を採取する。このうち血漿に部分トロンボプラスチン、カルシウムの他、カオリン、セライトまたはエラジン酸などの接触因子活性化物質を添加し、凝固時間を測定する。PTT(部分トロンボプラスチン時間)に比べ、より安定した結果を得られる。^[1]

PTTは部分トロンボプラスチン(脳抽出粗製セファリン=血小板第３因子作用物質)と適量のカルシウムを添加し、凝固時間を測定するもの。

正常ではAPTT (試薬がリン脂質＋カルシウム＋エラジン酸) 30-45秒。

一般に正常対照（ネガティブ・コントロール）と共に測定する。

活性化部分トロンボプラスチン時間の意義

APTTに関与する因子は、プレカリクレイン・HMW-キニノゲン・第XII因子・第XI因子・第IX因子・第VIII因子・第V因子・第II因子およびフィブリノーゲンである。

その他

血液凝固障害における検査所見 (表 - 話)
状態	プロトロンビン時間	活性化部分トロンボプラスチン時間	出血時間	血小板数
ビタミンK欠乏 or ワルファリン	延長	変化なしまたはやや延長	変化なし	変化なし
播種性血管内凝固症候群	延長	延長	延長	減少
ヴォン・ヴィレブランド病	変化なし	延長 or 変化なし	延長	変化なし
血友病	変化なし	延長	変化なし	変化なし
アスピリン	変化なし	変化なし	延長	変化なし
血小板減少症	変化なし	変化なし	延長	減少
急性肝不全	延長	変化なし	変化なし	変化なし
末期肝不全	延長	延長	延長	減少
尿毒症	変化なし	変化なし	延長	変化なし
無フィブリノーゲン血症	延長	延長	延長	変化なし
第Ⅴ因子欠乏	延長	延長	変化なし	変化なし
第Ⅹ因子欠乏	延長	延長	変化なし	変化なし
血小板無力症	変化なし	変化なし	延長	変化なし
ベルナール・スリエ症候群	変化なし	変化なし	延長	減少または変化なし
第ⅩⅡ因子欠乏	変化なし	延長	変化なし	変化なし
遺伝性血管浮腫	変化なし	短縮	変化なし	変化なし

血友病は内因系の第VIII因子や第IX因子に異常がある。そのためAPTTは延長するものの、プロトロンビン時間(PT)は延長しない。
同様に第Ⅷ因子に異常があるヴォン・ヴィレブランド病もAPTT延長・PT正常を示す。

脚注

[ヘルプ]

^ 野村武夫ほか、血小板-止血・凝固・線溶-,中外医学社, 1994年, p100-101

Methodology

Blue Top Vacutainer tube used for PT and PTT blood tests

Prothrombin time is typically analyzed by a medical technologist or a laboratory technician on an automated instrument at 37 °C (as a nominal approximation of normal human body temperature). The test is termed "partial" due to the absence of tissue factor from the reaction mixture.

Blood is drawn into a test tube containing oxalate or citrate, molecules which act as an anticoagulant by binding the calcium in a sample. The blood is mixed, then centrifuged to separate blood cells from plasma (as Partial thromboplastin time is most commonly measured using blood plasma).

A sample of the plasma is extracted from the test tube and placed into a measuring test tube.

Next, an excess of calcium (in a phospholipid suspension) is mixed into the plasma sample (to reverse the anticoagulant effect of the oxalate enabling the blood to clot again).

Finally, in order to activate the intrinsic pathway of coagulation, an activator (such as silica, celite, kaolin, ellagic acid) is added, and the time the sample takes to clot is measured optically. Some laboratories use a mechanical measurement, which eliminates interferences from lipemic and icteric samples.

Interpretation

The typical reference range is between 30 seconds and 50 s (depending on laboratory). Shortening of the PTT is considered to have little clinical relevance, but some research indicates that it might increase risk of thromboembolism.^[3] Normal PTT times require the presence of the following coagulation factors: I, II, V, VIII, IX, X, XI, & XII. Notably, deficiencies in factors VII or XIII will not be detected with the PTT test. Prolonged APTT may indicate:

use of heparin (or contamination of the sample)
antiphospholipid antibody (especially lupus anticoagulant, which paradoxically increases propensity to thrombosis)
coagulation factor deficiency (e.g. hemophilia)
Sepsis - coagulation factor consumption
Presence of antibodies against coagulation factors (factor inhibitors)

To distinguish the above causes, mixing tests are performed, in which the patient's plasma is mixed (initially at a 50:50 dilution) with normal plasma. If the abnormality does not disappear, the sample is said to contain an "inhibitor" (either heparin, antiphospholipid antibodies or coagulation factor specific inhibitors), while if it does disappear a factor deficiency is more likely. Deficiencies of factors VIII, IX, XI and XII and rarely von Willebrand factor (if causing a low factor VIII level) may lead to a prolonged aPTT correcting on mixing studies.

Laboratory findings in various platelet and coagulation disorders (V - T)
Condition	Prothrombin time	Partial thromboplastin time	Bleeding time	Platelet count
Vitamin K deficiency or warfarin	Prolonged	Normal or mildly prolonged	Unaffected	Unaffected
Disseminated intravascular coagulation	Prolonged	Prolonged	Prolonged	Decreased
Von Willebrand disease	Unaffected	Prolonged or unaffected	Prolonged	Unaffected
Hemophilia	Unaffected	Prolonged	Unaffected	Unaffected
Aspirin	Unaffected	Unaffected	Prolonged	Unaffected
Thrombocytopenia	Unaffected	Unaffected	Prolonged	Decreased
Liver failure, early	Prolonged	Unaffected	Unaffected	Unaffected
Liver failure, end-stage	Prolonged	Prolonged	Prolonged	Decreased
Uremia	Unaffected	Unaffected	Prolonged	Unaffected
Congenital afibrinogenemia	Prolonged	Prolonged	Prolonged	Unaffected
Factor V deficiency	Prolonged	Prolonged	Unaffected	Unaffected
Factor X deficiency as seen in amyloid purpura	Prolonged	Prolonged	Unaffected	Unaffected
Glanzmann's thrombasthenia	Unaffected	Unaffected	Prolonged	Unaffected
Bernard-Soulier syndrome	Unaffected	Unaffected	Prolonged	Decreased or unaffected
Factor XII deficiency	Unaffected	Prolonged	Unaffected	Unaffected
C1INH deficiency	Unaffected	Shortened	Unaffected	Unaffected

History

The aPTT was first described in 1953 by researchers at the University of North Carolina at Chapel Hill explaining the Carolina blue Vacutainer tube top color.^[4]

References

^ "MedlinePlus Medical Encyclopedia: Partial thromboplastin time (PTT)". Retrieved 2009-01-01.
^ "KCCT - General Practice Notebook". GP Notebook. Oxbridge Solutions Ltd. Retrieved 2010-06-08.
^ Korte, Wolfgang; Clarke, Susan; Lefkowitz, Jerry B. (January 2000). "Short activated partial thromboplastin times are related to increased thrombin generation and an increased risk for thromboembolism". American journal of clinical pathology 113 (1): 123–7. doi:10.1309/G98J-ANA9-RMNC-XLYU. PMID 10631865.
^ Langdell RD, Wagner RH, Brinkhous KM (1953). "Effect of antihemophilic factor on one-stage clotting tests; a presumptive test for hemophilia and a simple one-stage antihemophilic factor assy procedure". J. Lab. Clin. Med. 41 (4): 637–47. PMID 13045017.

UpToDate Contents

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1. 凝固検査の臨床使用 clinical use of coagulation tests
2. 出血性素因を有する成人患者へのアプローチ approach to the adult patient with a bleeding diathesis
3. 出血症状を有する小児に対するアプローチ approach to the child with bleeding symptoms
4. Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock
5. ヘパリンおよび低分子ヘパリンの治療使用 therapeutic use of heparin and low molecular weight heparin

English Journal

Hypofibrinogenemia induced by tigecycline: a potentially life-threatening coagulation disorder.

Sabanis N1, Paschou E, Gavriilaki E, Kalaitzoglou A, Vasileiou S.
Infectious diseases (London, England).Infect Dis (Lond).2015 Oct;47(10):747-50. doi: 10.3109/23744235.2015.1043942. Epub 2015 May 8.
A 74-year-old female patient with end-stage renal disease, undergoing periodic hemodialysis, was hospitalized due to infection by multidrug-resistant Acinetobacter baumannii after hip replacement surgery. She was treated with tigecycline, a glycylcycline agent. Subsequently she developed coagulation
PMID 25951751

Coagulation defects associated with massive blood transfusion: A large multicenter study.

Yang JC1, Sun Y1, Xu CX2, Dang QL3, Li L4, Xu YG5, Song YJ1, Yan H6.
Molecular medicine reports.Mol Med Rep.2015 Sep;12(3):4179-86. doi: 10.3892/mmr.2015.3971. Epub 2015 Jun 22.
The variations in the coagulation indices of patients receiving massive blood transfusion were investigated across 20 large‑scale general hospitals in China. The data of 1,601 surgical inpatients receiving massive transfusion were retrospectively collected and the trends in the platelet counts a
PMID 26095897

First living-related liver transplant to cure factor VII deficiency.

Mohan N1, Karkra S1, Jolly AS2, Vohra V2, Mohanka R2, Rastogi A2, Soin AS2.
Pediatric transplantation.Pediatr Transplant.2015 Sep;19(6):E135-8. doi: 10.1111/petr.12539. Epub 2015 Jul 8.
Congenital factor VII deficiency is an autosomal recessive serious disorder of blood coagulation with wide genotypic and phenotypic variations. The clinical presentation can vary from asymptomatic patients to patients with major bleedings in severe deficiency (factor VII <1%). Investigations show
PMID 26152797

Japanese Journal

咽頭出血を初発とした後天性血友病例

森祐輔,辻純,安里亮,神田智子,本多啓吾,牛呂幸司,渡邊佳紀
耳鼻咽喉科臨床 104(6), 455-459, 2011-06-01
… We finally diagnosed her condition as acquired hemophilia because of aberrant bleeding, prolonged coagulation time (APTT), and decreased factor VIII and inhibitor-positive factor VIII. …
NAID 10028223043

A case of atypical hemolytic uremic syndrome due to anti-factor H antibody in a patient presenting with a factor XII deficiency identified two novel mutations

MATSUKUMA Eiji,GOTOH Yoshimitsu,KUROYANAGI Yoshiyuki,YAMADA Takuji,IWASA Mitsuji,YAMAKAWA Satoshi,NAGAI Takuhito,TAKAGI Nobuaki,MAE Hiromu,IIJIMA Kenji,BRESIN Elena
Clinical and experimental nephrology 15(2), 269-274, 2011-04-01
NAID 10029005337

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