今日の臨床サポート

下垂体機能低下症

著者: 西山 充 高知大学医学部附属病院 内分泌代謝・腎臓内科

監修: 平田結喜緒 公益財団法人 兵庫県予防医学協会 健康ライフプラザ

著者校正/監修レビュー済:2020/03/26
参考ガイドライン:
  1. 日本内分泌学会雑誌95(suppl),2019:間脳下垂体機能障害の診断と治療の手引き(平成30年度改訂)
患者向け説明資料

概要・推奨   

  1. ACTH分泌不全:通常ヒドロコルチゾン1520mg/日を朝・夕2回に分けて補充する(推奨度1。感染症、発熱、外傷などのストレス時は23倍に増量する。
  1. TSH分泌不全:通常少量(12.5μg25μg/日)より開始し、24週間ごとに徐々に増量、甲状腺ホルモン値がFT4基準範囲上限、FT3基準範囲となるよう用量調整する(推奨度2ACTH分泌不全合併する場合は、ヒドロコルチゾン補充開始57日後に開始する。
  1. GH分泌不全:小児に対しては早期からGH注射を開始し、最終身長の正常化を目標とする。成人に対しては、重症GH欠損であることをGHRP2試験で確認のうえ、比較的少量からGHの自己注射を開始し、血中IGF-I値を目安として維持量を決定する(推奨度2
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参考文献:[1][2]
閲覧にはご契
薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
西山 充 : 特に申告事項無し[2021年]
監修:平田結喜緒 : 特に申告事項無し[2021年]

改訂のポイント:
  1. 最近のガイドライン(間脳下垂体機能障害の診断と治療の手引き)などを参考にして内容の改訂を行った。

病態・疫学・診察

疾患情報(疫学・病態)  
  1. 下垂体機能低下症とは、下垂体前葉ホルモン(ACTH, TSH, GH, LH, FSH, PRL)が部分的ないし完全に欠損した病態である。下垂体後葉ホルモン(主としてバソプレシン)の欠乏は、中枢性尿崩症(参照: 尿崩症 )として別に扱われる。
  1. すべての下垂体前葉ホルモンが欠乏した汎下垂体前葉機能低下症と、複数のホルモンが種々の程度に欠乏した部分型下垂体前葉機能低下症、1種類のホルモンのみ欠損した下垂体ホルモン単独欠損症に分類される。
  1. 基礎疾患として、腫瘍、炎症、分娩時大出血(シーハン症候群)、外科手術・薬剤服用などによる続発性、原因の不明な特発性、および遺伝子異常に起因する家族性がある。基礎疾患として多いのは腫瘍性病変(下垂体腺腫、胚細胞腫瘍、頭蓋咽頭腫など)であり、下垂体機能低下症の原因の半数を占める。
  1. どの下垂体ホルモン分泌がどの程度障害されているかを内分泌試験などで把握したうえで、必要に応じて対応する末梢ホルモンの補充療法を行う。
  1. 生命維持のために補充が必要なホルモンは、コルチゾールとサイロキシン(T4)である。また、代謝改善やQOL維持のため成長ホルモン(GH)(参照: 成長ホルモン分泌不全症 )と性ホルモンの補充が行われる。妊孕性の回復を期待する場合は、ゴナドトロピンの補充を行う。基礎疾患に対する治療も併せて行う。
  1. 以上の一連の流れについては、下垂体機能低下症:初診のアルゴリズム(図アルゴリズム)に図示してあるので参照されたい。
  1. 下垂体前葉機能低下症(ゴナドトロピン分泌低下症、副腎皮質刺激ホルモン(ACTH)分泌低下症、甲状腺刺激ホルモン(TSH)分泌低下症、成長ホルモン(GH)分泌不全症、プロラクチン(PRL)分泌低下症)は指定難病であり、中等症および重症などの場合は申請し認定されると、保険料の自己負担分の一部が公費負担として助成される。(平成27年1月施行)
  1. 難病法に基づく医療費助成制度
病歴・診察のポイント  
  1. 欠乏するホルモンの種類により多彩な症状を呈する。

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文献 

著者: Maria Fleseriu, Ibrahim A Hashim, Niki Karavitaki, Shlomo Melmed, M Hassan Murad, Roberto Salvatori, Mary H Samuels
雑誌名: J Clin Endocrinol Metab. 2016 Nov;101(11):3888-3921. doi: 10.1210/jc.2016-2118. Epub 2016 Oct 13.
Abstract/Text OBJECTIVE: To formulate clinical practice guidelines for hormonal replacement in hypopituitarism in adults.
PARTICIPANTS: The participants include an Endocrine Society-appointed Task Force of six experts, a methodologist, and a medical writer. The American Association for Clinical Chemistry, the Pituitary Society, and the European Society of Endocrinology co-sponsored this guideline.
EVIDENCE: The Task Force developed this evidence-based guideline using the Grading of Recommendations, Assessment, Development, and Evaluation system to describe the strength of recommendations and the quality of evidence. The Task Force commissioned two systematic reviews and used the best available evidence from other published systematic reviews and individual studies.
CONSENSUS PROCESS: One group meeting, several conference calls, and e-mail communications enabled consensus. Committees and members of the Endocrine Society, the American Association for Clinical Chemistry, the Pituitary Society, and the European Society of Endocrinology reviewed and commented on preliminary drafts of these guidelines.
CONCLUSIONS: Using an evidence-based approach, this guideline addresses important clinical issues regarding the evaluation and management of hypopituitarism in adults, including appropriate biochemical assessments, specific therapeutic decisions to decrease the risk of co-morbidities due to hormonal over-replacement or under-replacement, and managing hypopituitarism during pregnancy, pituitary surgery, and other types of surgeries.

PMID 27736313  J Clin Endocrinol Metab. 2016 Nov;101(11):3888-3921. do・・・
著者: N V Esteban, T Loughlin, A L Yergey, J K Zawadzki, J D Booth, J C Winterer, D L Loriaux
雑誌名: J Clin Endocrinol Metab. 1991 Jan;72(1):39-45. doi: 10.1210/jcem-72-1-39.
Abstract/Text Growth retardation as well as the development of Cushingoid features in adrenally insufficient patients treated with the currently accepted replacement dose of cortisol (33-41 mumol/day.m2; 12-15 mg/m2.day) prompted us to reevaluate the cortisol production rate (FPR) in normal subjects and patients with Cushing's syndrome, using a recently developed thermospray liquid chromatography-mass spectrometry method. The stable isotope [9,12,12-2H3]cortisol was infused continuously for 31 h at about 5% of the anticipated FPR. Blood samples were obtained at 20-min intervals for 24 h, spun, and pooled in 4-h groups. Tracer dilution in plasma was determined by liquid chromatography/mass spectrometry. The method was validated with controlled infusions in 6 patients with adrenal insufficiency. Results from 12 normal volunteers revealed a FPR of 27.3 +/- 7.5 mumol/day (9.9 +/- 2.7 mg/day) or 15.7 mumol/day.m2; 5.7 mg/m2. day). A previously unreported circadian variation in FPR was observed. Patients with Cushing's syndrome demonstrated unequivocal elevation of FPR and cortisol concentration correlated during each sample period in normal volunteers, indicating that cortisol secretion, rather than metabolism, is mainly responsible for changes in plasma cortisol. Our data suggest that the FPR in normal subjects may be lower than previously believed.

PMID 1986026  J Clin Endocrinol Metab. 1991 Jan;72(1):39-45. doi: 10.・・・
著者: Ragnhildur Bergthorsdottir, Maria Leonsson-Zachrisson, Anders Odén, Gudmundur Johannsson
雑誌名: J Clin Endocrinol Metab. 2006 Dec;91(12):4849-53. doi: 10.1210/jc.2006-0076. Epub 2006 Sep 12.
Abstract/Text BACKGROUND: The survival rate of patients with primary adrenal insufficiency (Addison's disease) undergoing currently accepted replacement therapy is not known, although well-informed patients are considered to have a normal survival rate. In this study, we evaluated the mortality of patients with Addison's disease in Sweden.
METHODS: A population-based, retrospective, observational study was performed, using the National Swedish Hospital and Cause of Death Registers, covering the period from 1987-2001. After a diagnosis of Addison's disease, each patient was followed until the end of follow-up or death. Mortality was compared with that of the Swedish background population.
FINDINGS: We identified 1675 patients (995 women and 680 men) diagnosed with primary adrenal insufficiency. The average follow-up from initial diagnosis was 6.5 yr. Five hundred seven patients died during the study period compared with an expected 199. The risk ratio for all-cause mortality was 2.19 (confidence interval 1.91-2.51) for men and 2.86 (confidence interval 2.54-3.20) for women. The excess mortality in both men and women was attributed to cardiovascular, malignant, and infectious diseases. Concomitant diabetes mellitus was observed in 12% of the patients, but only contributed to the increased mortality to a minor extent.
INTERPRETATION: Compared with the background population, we observed that the risk ratio for death was more than 2-fold higher in patients with Addison's disease. Cardiovascular, malignant, and infectious diseases were responsible for the higher mortality rate.

PMID 16968806  J Clin Endocrinol Metab. 2006 Dec;91(12):4849-53. doi: ・・・
著者: M Sherlock, R C Reulen, A Aragon Alonso, J Ayuk, R N Clayton, M C Sheppard, M M Hawkins, A S Bates, P M Stewart
雑誌名: J Clin Endocrinol Metab. 2009 Nov;94(11):4216-23. doi: 10.1210/jc.2009-1097. Epub 2009 Oct 6.
Abstract/Text CONTEXT: A number of retrospective studies report that patients with acromegaly have increased morbidity and premature mortality, with standardized mortality ratios (SMR) of 1.3-3. Many patients with acromegaly develop hypopituitarism as a result of the pituitary adenoma itself or therapies such as surgery and radiotherapy. Pituitary radiotherapy and hypopituitarism have also been associated with an increased SMR.
METHODS: Using the West MIDLANDS: Acromegaly database (n = 501; 275 female), we assessed the influence of prior radiotherapy and hypopituitarism (and replacement therapy) on mortality in patients with acromegaly. Median duration of follow-up was 14.0 yr (interquartile range, 7.9-21 yr).
RESULTS: All-cause mortality was elevated [SMR, 1.7 (1.4, 2.0); P < 0.001]. On external analysis, prior radiotherapy, ACTH, and gonadotropin deficiency were associated with an elevated SMR [radiotherapy SMR, 2.1 (1.7-2.6); P = 0.006; ACTH deficiency SMR, 2.5 (1.9-3.2); P < 0.0005; and gonadotropin deficiency SMR, 2.1 (1.6-2.7); P = 0.037]. On internal analysis, the relative risk (RR) of mortality was increased in the radiotherapy [RR, 1.8 (1.2-2.8); P = 0.008] and ACTH-deficiency groups [RR, 1.7 (1.2-2.5); P = 0.004], but not in the gonadotropin- or TSH-deficiency groups. In the ACTH-deficient group, increased replacement doses of hydrocortisone greater than 25 mg/d were associated with increased mortality compared to lower doses.
CONCLUSIONS: Radiotherapy and ACTH deficiency are significantly associated with increased mortality in patients with acromegaly. In ACTH-deficient patients, a daily dose of more than 25 mg hydrocortisone is associated with increased mortality compared to lower doses. These results have important implications for the treatment of patients with acromegaly and also raise issues as to the optimum hydrocortisone treatment regimens for ACTH-deficient patients.

PMID 19808848  J Clin Endocrinol Metab. 2009 Nov;94(11):4216-23. doi: ・・・
著者: V Kyriazopoulou, O Parparousi, A G Vagenakis
雑誌名: J Clin Endocrinol Metab. 1984 Dec;59(6):1204-6. doi: 10.1210/jcem-59-6-1204.
Abstract/Text Rifampicin induced profound alterations in cortisol metabolism when administered to three patients with primary adrenal failure receiving adequate corticosteroid replacement therapy. In one patient, adrenal crisis was precipitated after the institution of rifampicin therapy for treatment of coexistent tuberculosis and in another, profound asthenia, decrease in blood pressure, hyperkalemia, and hyponatremia developed during the hydrocortisol kinetic study. The clinical symptoms subsided and the electrolyte abnormalities were corrected approximately 7 days after rifampicin withdrawal. The half-life of hydrocortisol and the area under the curve were decreased by 35% and 23%, respectively, whereas the systemic clearance was increased by 35% during rifampicin administration. It appears, that the effectiveness of glucocorticoids and mineralocorticoids were greatly impaired by rifampicin administration due to induction of liver steroid-metabolizing enzymes. It is strongly recommended that in patients with compromised adrenal function, treatment with rifampicin must be accompanied by doubling or tripling the dose of adrenal steroids to maintain adequate steroid replacement therapy.

PMID 6490796  J Clin Endocrinol Metab. 1984 Dec;59(6):1204-6. doi: 10・・・
著者: Marc Slawik, Björn Klawitter, Edith Meiser, Marcus Schories, Oliver Zwermann, Katrin Borm, Martin Peper, Beate Lubrich, Martin J Hug, Markus Nauck, Manfred Olschewski, Felix Beuschlein, Martin Reincke
雑誌名: J Clin Endocrinol Metab. 2007 Nov;92(11):4115-22. doi: 10.1210/jc.2007-0297. Epub 2007 Aug 21.
Abstract/Text BACKGROUND: Dosage of T(4) in central hypothyroidism is primarily guided by the free serum T(4) level (fT4). However, the optimum fT4 range is ill defined, and subtle hypothyroidism might be missed using this approach.
OBJECTIVES: Our aim was to investigate the effects of a body weight (bw)-adapted T(4) treatment, alone or in combination with T(3), on metabolism, well-being, and cognitive function in comparison to a regimen leading to normal fT4.
DESIGN: This was a placebo-controlled trial (double-blind, crossover).
PATIENTS: A total of 29 patients (age 52 +/- 2 yr; females/males, 8/21) with hypopituitarism, including TSH deficiency, participated in the study.
INTERVENTIONS: Three regimens were compared (5 wk each): "EMPIRICAL-T4," empirical T(4) dosage (1 +/- 0.05 microg/kg bw) leading to normal fT4; BW-ADAPTED-T4 (1.6 microg/kg bw T(4)); and "BW-ADAPTED-T3T4," bw-adapted combination of T(3) and T(4) (ratio of 1:10).
RESULTS: BW-ADAPTED-T4 administration increased mean fT4 concentrations to the upper limit of the normal range (peak levels). Compared with EMPIRICAL-T4, BW-ADAPTED-T4 treatment resulted in a lower body mass index (BMI) (29.0 +/- 0.7 vs. 29.5 +/- 0.7 kg/m(2); P < 0.03), lower total cholesterol (198 +/- 9 vs. 226 +/- 7 mg/dl; P < 0.01), and lower low-density lipoprotein (LDL) cholesterol (116 +/- 5 vs. 135 +/- 7 mg/dl; P < 0.01). BW-ADAPTED-T3T4 treatment was associated with additional beneficial effects on ankle reflex time and working memory but resulted in supraphysiological free serum T(3) (fT(3)) levels.
LIMITATIONS: Long-term side effects may have been missed.
CONCLUSIONS: Using a dose of 1.6 microg/kg bw improved markers commonly associated with central hypothyroidism. This suggests that T(4) dosage based on bw and aiming at fT4 in the upper reference range is superior to titration of T(4) aiming at middle normal fT4 concentrations in those patients.

PMID 17711927  J Clin Endocrinol Metab. 2007 Nov;92(11):4115-22. doi: ・・・
著者: Stefanie Hahner, Bruno Allolio
雑誌名: Best Pract Res Clin Endocrinol Metab. 2009 Apr;23(2):167-79. doi: 10.1016/j.beem.2008.09.009.
Abstract/Text Replacement therapy in adrenal insufficiency comprises treatment with glucocorticoids, mineralocorticoids and adrenal androgen precursors. Initiation of hormone replacement therapy in newly diagnosed adrenal insufficiency leads to rapid and impressive improvements. However, despite the use of established replacement concepts, well-being is often not fully restored in patients with adrenal insufficiency, and life expectancy may even be reduced. This has led to a reconsideration of current replacement strategies. Several studies demonstrate that addition of dehydroepiandrosterone (DHEA) to the treatment regimen may lead to further improvement of general well-being and also sexual function. However, long-term trials with DHEA are still lacking, and DHEA alone is not able to restore subjective health status to normal. Further innovations comprise the development of delayed-release glucocorticoid preparations that better allow mimicking of circadian cortisol secretion and may have the potential to significantly improve the treatment of patients with adrenal insufficiency. However, future studies have to prove the clinical importance of physiological cortisol day profiles. To date, no relevant risk factors for susceptibility to adrenal crisis are known, and patient education is key for a successful prevention strategy. In our experience the well-educated patient often guides the physician not familiar with this disease.

PMID 19500761  Best Pract Res Clin Endocrinol Metab. 2009 Apr;23(2):16・・・
著者: Andrew R Hoffman, Beverly M K Biller, David Cook, Joyce Baptista, Bernard L Silverman, Le Dao, Kenneth M Attie, Paul Fielder, Thomas Maneatis, Barbara Lippe, Genentech Adult Growth Hormone Deficiency Study Group
雑誌名: J Clin Endocrinol Metab. 2005 Dec;90(12):6431-40. doi: 10.1210/jc.2005-0928. Epub 2005 Sep 13.
Abstract/Text CONTEXT: Treatment of adult GH deficiency (AGHD) with daily injections of GH results in decreased adipose mass, increased lean body mass (LBM), increased bone mineral density, and improved quality of life.
OBJECTIVE: This study seeks to determine whether a depot preparation of GH given every 14 d would lead to comparable decreases in trunk adipose tissue as daily GH.
DESIGN: This open-label, randomized study compares subjects receiving depot GH, daily GH, or no therapy.
SETTING: The study was performed at 23 university or local referral endocrine centers.
PATIENTS OR OTHER PARTICIPANTS: One hundred thirty-five adults with AGHD syndrome participated in the study.
INTERVENTION: Subjects were randomized to receive depot GH (n = 51), daily GH (n = 53), or no treatment (n = 31) for 32 wk. The dose of GH was titrated so that IGF-I was less than or equal to +2 SD of the age-adjusted normal range.
MAIN OUTCOME MEASURE: Trunk adipose tissue was the main outcome measure as measured by dual energy x-ray absorptiometry.
RESULTS: The percentage of the trunk region that is fat increased by 0.4 in the no treatment group, but decreased by 3.2 (P = 0.001 vs. untreated) in the GH depot group and by 2.5 (P < 0.004 vs. untreated) in the daily GH group. Visceral adipose tissue area decreased by 9.1% in the GH depot group and by 6.8% in the daily GH group. LBM and high-density lipoprotein increased in both treatment groups. Side effect profiles were similar. Three subjects receiving GH experienced serious episodes of adrenal insufficiency.
CONCLUSIONS: GH diminishes trunk and visceral adipose tissue and increases LBM in AGHD. A depot form of GH that is administered every 14 d is as safe and effective as daily GH injections.

PMID 16159930  J Clin Endocrinol Metab. 2005 Dec;90(12):6431-40. doi: ・・・
著者: Ken K Y Ho, 2007 GH Deficiency Consensus Workshop Participants
雑誌名: Eur J Endocrinol. 2007 Dec;157(6):695-700. doi: 10.1530/EJE-07-0631.
Abstract/Text OBJECTIVE: The GH Research Society held a Consensus Workshop in Sydney, Australia, 2007 to incorporate the important advances in the management of GH deficiency (GHD) in adults, which have taken place since the inaugural 1997 Consensus Workshop.
METHOD: Two commissioned review papers, previously published Consensus Statements of the Society and key questions were circulated before the Workshop, which comprised a rigorous structure of review with breakout discussion groups. A writing group transcribed the summary group reports for drafting in a plenary forum on the last day. All participants were sent a polished draft for additional comments and gave signed approval to the final revision.
CONCLUSION: Testing for GHD should be extended from hypothalamic-pituitary disease and cranial irradiation to include traumatic brain injury. Testing may indicate isolated GHD; however, idiopathic isolated GHD occurring de novo in the adult is not a recognized entity. The insulin tolerance test, combined administration of GHRH with arginine or growth hormone-releasing peptide, and glucagon are validated GH stimulation tests in the adult. A low IGF-I is a reliable diagnostic indicator of GHD in the presence of hypopituitarism, but a normal IGF-I does not rule out GHD. GH status should be reevaluated in the transition age for continued treatment to complete somatic development. Interaction of GH with other axes may influence thyroid, glucocorticoid, and sex hormone requirements. Response should be assessed clinically by monitoring biochemistry, body composition, and quality of life. There is no evidence that GH replacement increases the risk of tumor recurrence or de novo malignancy.

PMID 18057375  Eur J Endocrinol. 2007 Dec;157(6):695-700. doi: 10.1530・・・
著者: P J Snyder, H Peachey, J A Berlin, P Hannoush, G Haddad, A Dlewati, J Santanna, L Loh, D A Lenrow, J H Holmes, S C Kapoor, L E Atkinson, B L Strom
雑誌名: J Clin Endocrinol Metab. 2000 Aug;85(8):2670-7. doi: 10.1210/jcem.85.8.6731.
Abstract/Text Treatment of hypogonadal men with testosterone has been shown to ameliorate the effects of testosterone deficiency on bone, muscle, erythropoiesis, and the prostate. Most previous studies, however, have employed somewhat pharmacological doses of testosterone esters, which could result in exaggerated effects, and/or have been of relatively short duration or employed previously treated men, which could result in dampened effects. The goal of this study was to determine the magnitude and time course of the effects of physiological testosterone replacement for 3 yr on bone density, muscle mass and strength, erythropoiesis, prostate volume, energy, sexual function, and lipids in previously untreated hypogonadal men. We selected 18 men who were hypogonadal (mean serum testosterone +/- SD, 78 +/- 77 ng/dL; 2.7 +/- 2.7 nmol/L) due to organic disease and had never previously been treated for hypogonadism. We treated them with testosterone transdermally for 3 yr. Sixteen men completed 12 months of the protocol, and 14 men completed 36 months. The mean serum testosterone concentration reached the normal range by 3 months of treatment and remained there for the duration of treatment. Bone mineral density of the lumbar spine (L2-L4) increased by 7.7 +/- 7.6% (P < 0.001), and that of the femoral trochanter increased by 4.0 +/- 5.4% (P = 0.02); both reached maximum values by 24 months. Fat-free mass increased 3.1 kg (P = 0.004), and fat-free mass of the arms and legs individually increased, principally within the first 6 months. The decrease in fat mass was not statistically significant. Strength of knee flexion and extension did not change. Hematocrit increased dramatically, from mildly anemic (38.0 +/- 3.0%) to midnormal (43.1 +/- 4.0%; P = 0.002) within 3 months, and remained at that level for the duration of treatment. Prostate volume also increased dramatically, from subnormal (12.0 +/- 6.0 mL) before treatment to normal (22.4 +/- 8.4 mL; P = 0.004), principally during the first 6 months. Self-reported sense of energy (49 +/- 19% to 66 +/- 24%; P = 0.01) and sexual function (24 +/- 20% to 66 +/- 24%; P < 0.001) also increased, principally within the first 3 months. Lipids did not change. We conclude from this study that replacing testosterone in hypogonadal men increases bone mineral density of the spine and hip, fat-free mass, prostate volume, erythropoiesis, energy, and sexual function. The full effect of testosterone on bone mineral density took 24 months, but the full effects on the other tissues took only 3-6 months. These results provide the basis for monitoring the magnitude and the time course of the effects of testosterone replacement in hypogonadal men.

PMID 10946864  J Clin Endocrinol Metab. 2000 Aug;85(8):2670-7. doi: 10・・・

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