今日の臨床サポート

低ナトリウム血症

著者: 石川三衛 国際医療福祉大学病院 糖尿病内分泌代謝科

監修: 花房規男 東京女子医科大学 血液浄化療法科

著者校正/監修レビュー済:2021/01/13
患者向け説明資料

概要・推奨   

  1. 低ナトリウム(Na)血症は、細胞外液中のNa含量と体液量から3病型、すなわち体液量の増加を伴う低Na血症、体液量のほぼ正常な低Na血症、体液量の減少を伴う低Na血症に分けられる(推奨度1
  1. バソプレシン不適合分泌症候群(SIADH)は脱水、浮腫を認めない低Na血症である。バソプレシン(AVP)の不適切な分泌亢進に基づく水利尿不全に起因し、病初期希釈性低Na血症、経過中に代償されて体液量のほぼ正常な低Na血症となる(推奨度1
  1. 浮腫性疾患による低Na血症の頻度が最も高い。圧受容器の感受性低下を介してAVP、レニン・アルドステロン系、交感神経系が賦活されて、水利尿不全および腎におけるNaの再吸収亢進により体液量の増加をきたし希釈性低Na血症となる(推奨度1
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  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧
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:
石川三衛 : 特に申告事項無し[2021年]
監修:花房規男 : 講演料(協和キリン,ノーベルファーマ,キッセイ薬品,バイエル薬品株式会社)[2021年]

改訂のポイント:
  1. 定期レビューを行った。
  1. バソプレシン(AVP)V2受容体拮抗薬トルバプタン(サムスカ)が2020年6月SIADH治療に追加適応となった。本改訂では、SIADHのサムスカ治療について追加解説した。
  1. 浸透圧性脱髄症候群(ODS)における脳白質障害へのサイトカインの関与について追加の説明を加えた。

病態・疫学・診察

疫学情報・病態・注意事項  
  1. 低Na血症にみられる臨床徴候は、低Na血症の程度とその進行速度に依存する。血清Na値が120mmol/l以上であれば、悪心、食欲低下などの症状をみるのみであるが、血清Na値がさらに低下すると傾眠、無欲状などの軽い意識障害を認めるようになる。110mmol/lを下回ると、精神不穏やけいれんなど重篤な症状を引き起こし、不可逆的な変化に陥る危険がある。
  1. 所見では、腹部違和感、深部腱反射の減弱や病的反射の出現などを認める。さらに低Na血症が進展すると、低体温やけいれん発作などをみることがある。しかし、低Na血症が急激に進行する例では、血清Na値が120mmol/l程度でも意識障害やけいれんなどの重篤な症状を招くことがあるので留意する。
  1. 電解質測定はルーチン検査の範疇である。日常診療における低Na血症の発見はルーチン検査から見出されることが大部分で、低Na血症の臨床徴候から示唆される症例は少ないのが実情である。
  1. 入院患者の検査成績から血清Na値135mmol/l以下の症例を抽出すると、15~20%の症例で低Na血症を認める。低Na血症の病態的意義を見出すには複数回のデータを確認すること、患者の疾患背景を把握することが肝要である。
問診・診察のポイント  
  1. 低Na血症の3病型のなかで、浮腫を伴う低Na血症、脱水を伴う低Na血症が存在する。渇感、下肢のむくみ、体重の変化などを詳しく聴取する。

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文献 

著者: J C Ayus, A I Arieff
雑誌名: JAMA. 1999 Jun 23-30;281(24):2299-304.
Abstract/Text CONTEXT: Chronic hyponatremia in postmenopausal women is a common clinical problem often viewed as benign. Fluid restriction is usually the recommended therapy, largely because the extent of morbidity is unknown and because it has been postulated that intravenous (IV) sodium chloride may cause brain damage.
OBJECTIVE: To compare IV sodium chloride with fluid restriction in the treatment of postmenopausal women with chronic symptomatic hyponatremia.
DESIGN: Nonrandomized prospective study.
SETTING: Two university medical centers and affiliated community hospitals.
PATIENTS: A total of 53 postmenopausal women with chronic symptomatic hyponatremia (chronic plasma sodium <130 mmol/L in the presence of central nervous system manifestations) treated consecutively from 1988-1997 and followed up for 1 year. The mean (SD) age of the patients was 62 (11) years.
INTERVENTIONS: The therapeutic interventions were IV sodium chloride before respiratory insufficiency (n = 17), IV sodium chloride after respiratory insufficiency (n = 22), and fluid restriction only (n = 14).
MAIN OUTCOME MEASURES: Morbidity and neurological outcome at 4 months or longer as assessed by cerebral performance category (CPC) in relation to the therapy, initial plasma sodium level, and rate of correction.
RESULTS: Chronic symptomatic hyponatremia (mean [SD] sodium level 111 [12] mmol/L) was present for 5.2 [4.5] days. Death or major morbidity occurred in 44 (83%) of 53 patients, including 10 with orthopedic injury. Twelve patients had hypoxemia (PO2 = 63 [25] mm Hg) and cerebral edema. Among patients who received IV sodium chloride before respiratory insufficiency, plasma sodium levels were increased by 22 (10) mmol/L in 35 hours and patients had a CPC of 1.0 (normal or slight disability). Among patients who received IV sodium chloride after respiratory insufficiency, plasma sodium levels were increased by 30 (6) mmol/L in 41 hours and patients had a CPC of 3.0 (1.2) (severe disability). Among patients who had fluid restriction only, plasma sodium levels were increased by 3 (2) mmol/L in 41 hours and patients had a CPC of 4.6 (0.7) (4 = persistent vegetative state; 5 = death). The outcomes did not correlate with either the initial plasma sodium level (r=0.05, P>.12) or the rate of correction (r=0.31, P>.10).
CONCLUSIONS: Chronic symptomatic hyponatremia in postmenopausal women can be associated with major morbidity and mortality. Therapy with IV sodium chloride was associated with significantly better outcomes than fluid restriction.

PMID 10386554  JAMA. 1999 Jun 23-30;281(24):2299-304.
著者: Fabrice Gankam-Kengne, Alain Soupart, Roland Pochet, Jean Pierre Brion, Guy Decaux
雑誌名: J Am Soc Nephrol. 2010 Dec;21(12):2099-108. doi: 10.1681/ASN.2010050467. Epub 2010 Nov 4.
Abstract/Text Osmotic demyelination syndrome is a devastating neurologic condition that occurs after rapid correction of serum sodium in patients with hyponatremia. Pathologic features of this injury include a well-demarcated region of myelin loss, a breakdown of the blood-brain barrier, and infiltration of microglia. The semisynthetic tetracycline minocycline is protective in some animal models of central nervous system injury, including demyelination, suggesting that it may also protect against demyelination resulting from rapid correction of chronic hyponatremia. Using a rat model of osmotic demyelination syndrome, we found that treatment with minocycline significantly decreases brain demyelination, alleviates neurologic manifestations, and reduces mortality associated with rapid correction of hyponatremia. Mechanistically, minocycline decreased the permeability of the blood-brain barrier, inhibited microglial activation, decreased both the expression of IL1α and protein nitrosylation, and reduced the loss of GFAP immunoreactivity. In conclusion, minocycline modifies the course of osmotic demyelination in rats, suggesting its possible therapeutic use in the setting of inadvertent rapid correction of chronic hyponatremia in humans.

PMID 21051736  J Am Soc Nephrol. 2010 Dec;21(12):2099-108. doi: 10.168・・・
著者: Haruyuki Suzuki, Yoshihisa Sugimura, Shintaro Iwama, Hiromi Suzuki, Ozaki Nobuaki, Hiroshi Nagasaki, Hiroshi Arima, Makoto Sawada, Yutaka Oiso
雑誌名: J Am Soc Nephrol. 2010 Dec;21(12):2090-8. doi: 10.1681/ASN.2010040438. Epub 2010 Oct 28.
Abstract/Text Rapid correction of chronic hyponatremia can lead to osmotic demyelination syndrome (ODS), a severe demyelination disease. The microglia that accumulate in the demyelinative lesions may play a detrimental role in the pathogenesis of ODS by producing proinflammatory cytokines, suggesting that they may be a target for therapeutic intervention. Here, we investigated whether minocycline, a selective and potent inhibitor of microglial activation, could protect against ODS in rats. We induced hyponatremia by liquid diet feeding and dDAVP infusion. Rapid correction of the hyponatremia 7 days later resulted in neurologic impairment with severe demyelinative lesions. Activated microglia accumulated at the site of demyelination. Treatment with minocycline within 24 hours of rapid correction, however, was protective: rats exhibited minimal neurologic impairment, and survival improved. Histologic analysis showed that minocycline inhibited demyelination and suppressed the accumulation of microglia at the site of demyelination. Real-time RT-PCR and immunohistochemical analyses showed that minocycline inhibited the activity of microglia and the expression of inflammatory cytokines (e.g. IL-1β, inducible nitric-oxide synthase, and TNF-α), monocyte chemoattractant protein-1, and matrix metalloproteinase-12 in microglia. These results demonstrate that minocycline can protect against ODS by inhibiting the activation and accumulation of microglia at the site of demyelinative lesions, suggesting its possible use in clinical practice.

PMID 21030598  J Am Soc Nephrol. 2010 Dec;21(12):2090-8. doi: 10.1681/・・・
著者: T Saito, M Higashiyama, S Nagasaka, S Sasaki, T Saito, S E Ishikawa
雑誌名: Kidney Int. 2001 Oct;60(4):1266-76. doi: 10.1046/j.1523-1755.2001.00965.x.
Abstract/Text BACKGROUND: In a state of chronic arginine vasopressin (AVP) excess, the action of antidiuresis has been attenuated, resulting in some water diuresis. This state has been termed an "AVP escape" phenomenon. The present study was designed to determine what mechanisms underlie this attenuation in renal concentrating ability, which is found in chronic AVP excess, both in the presence and absence of volume expansion.
METHODS: Two groups of experimental rats were established. One group received solid chow with water ad libitum. The second group received chow, which was offered as a liquid diet. Both groups received subcutaneous administration of 1-deamino-8-D-arginine vasopressin (dDAVP) at 5 ng/h for the entire observation period of one week. Over the course of the observation period, tissue levels of aquaporin-2 (AQP-2) mRNA and protein were measured. Levels of AVP V2 receptor were monitored, both by measuring mRNA levels and by ligand-binding studies using [3H]AVP. Tissue levels of cAMP also were determined.
RESULTS: Experimental rats with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) had severe hyponatremia below 120 mmol/L, and impaired urinary concentrating ability, during the seven-day observation period. In contrast, the dDAVP-excess rats, given solid chow, maintained maximally concentrated urine and normal levels of serum sodium. The down-regulation of AVP V2 receptor function was comparable in the two groups. The maximal binding capacity (Bmax) fell to the nadir on day 2 and was thereafter suppressed at approximately 60% of control rats during the experiment. Up-regulation of AQP-2 mRNA expression was found, but this up-regulation was significantly less in the SIADH rats compared with the dDAVP-excess rats (153.5 +/- 29.8% vs. 323.7 +/- 23.8% on day 7, P < 0.05). This differential response between these two groups was affirmed by measured differences in AQP-2 protein levels, both in tissue and in urinary excretion.
CONCLUSIONS: These results indicate that the attenuated regulation of the AQP-2 gene leads to the decrease in urinary concentrating ability in the experimental SIADH rats, suffering from hypervolemic state, compared with the normonatremic rats receiving AVP. Either hypervolemia or hypotonicity may diminish the post-receptor signaling of AVP in renal collecting duct cells, under the chronic AVP excess state found in SIADH.

PMID 11576341  Kidney Int. 2001 Oct;60(4):1266-76. doi: 10.1046/j.1523・・・
著者: Takako Saito, Tomoyuki Saito, Keizo Kasono, Hiroyuki Tamemoto, Masanobu Kawakami, Sei Sasaki, San-e Ishikawa
雑誌名: Exp Physiol. 2008 Oct;93(10):1147-56. doi: 10.1113/expphysiol.2008.042663. Epub 2008 May 30.
Abstract/Text The present study was undertaken to determine whether hypotonicity regulates the aquaporin-2 (AQP-2) gene in vitro. The 5'-flanking region of the AQP-2 gene contains the tonicity-response enhancer (TonE) promoter located between -570 and -560 bp, and another distinct hypertonicity-responsive region between -6.1 and -4.3 kb of the AQP-2 gene. The 5'-flanking region of murine AQP-2 gene up to -9.5 kb was cloned into a luciferase (Luc) reporter plasmid. The constructs, which have TonE and/or the hypertonicity-responsive region, together with the murine AQP-2 gene, were co-transfected into murine IMCD(3) cells. When the cells were co-transfected with the construct containing more than 1.1 kb of the 5'-flanking region of murine AQP-2 gene (-9.5AQP2, -6.1AQP2 and -1.1AQP2) and the AQP-2 gene, 24 h exposure to 5 micromol l(-1) dibutyryl cAMP (DBcAMP) significantly increased the Luc activity by 2.3-fold in the isotonic medium (300 mosmol kg(-1)). In the hypotonic medium (225 mosmol kg(-1)), basal activity was not altered, and the response of Luc activity to 24 h exposure to 5 micromol l(-1)DBcAMP was abolished. Similar findings were obtained in isosmotic, urea-supplemented medium (estimated tonicity, 225 mosmol kg(-1)). The response of Luc activity to 5 micromol l(-1) DBcAMP in the hypotonic medium was not affected in cells either transfected with 0.36 kb of the 5'-flanking region of AQP-2 or co-transfected with -1.1AQP2 and a dominant-negative TonE binding protein (pDNTonEBP). Pre-incubation of cells with 1 micromol l(-1) SP600125, an inhibitor of c-Jun N-terminal kinase (JNK), restored the response of Luc activity to 5 micromol l(-1) DBcAMP under hypotonic conditions. These findings may indicate that hypotonicity reduces the cAMP-induced AQP-2 promoter activity mediated via TonE by activating JNK kinase.

PMID 18515471  Exp Physiol. 2008 Oct;93(10):1147-56. doi: 10.1113/expp・・・
著者: Robert W Schrier, Peter Gross, Mihai Gheorghiade, Tomas Berl, Joseph G Verbalis, Frank S Czerwiec, Cesare Orlandi, SALT Investigators
雑誌名: N Engl J Med. 2006 Nov 16;355(20):2099-112. doi: 10.1056/NEJMoa065181. Epub 2006 Nov 14.
Abstract/Text BACKGROUND: Hyponatremia (serum sodium concentration, <135 mmol per liter) is a predictor of death among patients with chronic heart failure and cirrhosis. At present, therapy for acute and chronic hyponatremia is often ineffective and poorly tolerated. We investigated whether tolvaptan, an orally active vasopressin V(2)-receptor antagonist that promotes aquaresis--excretion of electrolyte-free water--might be of benefit in hyponatremia.
METHODS: In two multicenter, randomized, double-blind, placebo-controlled trials, the efficacy of tolvaptan was evaluated in patients with euvolemic or hypervolemic hyponatremia. Patients were randomly assigned to oral placebo (223 patients) or oral tolvaptan (225) at a dose of 15 mg daily. The dose of tolvaptan was increased to 30 mg daily and then to 60 mg daily, if necessary, on the basis of serum sodium concentrations. The two primary end points for all patients were the change in the average daily area under the curve for the serum sodium concentration from baseline to day 4 and the change from baseline to day 30.
RESULTS: Serum sodium concentrations increased more in the tolvaptan group than in the placebo group during the first 4 days (P<0.001) and after the full 30 days of therapy (P<0.001). The condition of patients with mild or marked hyponatremia improved (P<0.001 for all comparisons). During the week after discontinuation of tolvaptan on day 30, hyponatremia recurred. Side effects associated with tolvaptan included increased thirst, dry mouth, and increased urination. A planned analysis that combined the two trials showed significant improvement from baseline to day 30 in the tolvaptan group according to scores on the Mental Component of the Medical Outcomes Study 12-item Short-Form General Health Survey.
CONCLUSIONS: In patients with euvolemic or hypervolemic hyponatremia, tolvaptan, an oral vasopressin V2-receptor antagonist, was effective in increasing serum sodium concentrations at day 4 and day 30. (ClinicalTrials.gov numbers, NCT00072683 [ClinicalTrials.gov] [SALT-1] and NCT00201994 [ClinicalTrials.gov] [SALT-2].).

PMID 17105757  N Engl J Med. 2006 Nov 16;355(20):2099-112. doi: 10.105・・・
著者: Toshimitsu Yatagai, Ikuyo Kusaka, Tomoatsu Nakamura, Shoichiro Nagasaka, Kazufumi Honda, Shun Ishibashi, San-e Ishikawa
雑誌名: Eur J Endocrinol. 2003 Feb;148(2):221-6.
Abstract/Text OBJECTIVE: Hyponatremia occurs not infrequently in hypopituitarism. Arginine vasopressin (AVP)-induced impaired water excretion is found in patients with hypopituitarism and experimental models of glucocorticoid deficiency.
DESIGN: The present study was undertaken to determine whether augmented release of AVP is involved in the development of hyponatremia in elderly subjects with secondary adrenal insufficiency.
METHODS: Forty patients with ACTH-deficient, secondary adrenal insufficiency were examined. They were divided into three groups according to the age at which diagnosis was ascertained (group A <20 Years, group B 20-64 Years, and group C>or=65 Years).
RESULTS: Hyponatremia was more manifest in the elderly group than in the other two groups, serum sodium (Na) levels being 124.7 mmol/l in the elderly group, a value significantly less than 141.5 and 133.5 mmol/l in groups A and B. Plasma AVP levels seemed likely to be high compared with the respective hypo-osmolality in plasma in the elderly group, as plasma AVP levels were 1.7 pmol/l despite a mean plasma osmolality of 259 mmol/kg. Such an alteration was less clear in group B and was not found in group A. Therefore, elevation of plasma AVP was apparent in the elderly patients. Hydrocortisone replacement promptly normalized serum Na levels from 125 to 142 mmol/l (P<0.01) and reduced plasma AVP levels from 1.7 to 0.9 pmol/l (P<0.05), which were comparable to the respective plasma osmolality in the elderly patients.
CONCLUSION: These results indicate that non-suppressible release of AVP is crucially involved in the impaired water excretion and hyponatremia seen in elderly patients with secondary adrenal insufficiency compared with the younger patients, and that exaggerated release of AVP becomes manifest as the subjects grow older.

PMID 12590641  Eur J Endocrinol. 2003 Feb;148(2):221-6.
著者: Ishikawa Se, T Saito, A Fukagawa, M Higashiyama, T Nakamura, I Kusaka, S Nagasaka, K Honda, T Saito
雑誌名: J Clin Endocrinol Metab. 2001 Apr;86(4):1665-71. doi: 10.1210/jcem.86.4.7426.
Abstract/Text The present study was undertaken to determine whether urinary excretion of aquaporin-2 (AQP-2) participates in the involvement of arginine vasopressin (AVP) in hyponatremia less than 130 mmol/L in 33 elderly subjects (> or =65 yr old) during the last 5-yr period. Subjects were separated into euvolemic hyponatremia groups: 13 with hypopituitarism, 8 with syndrome of inappropriate secretion of antidiuretic hormone (SIADH), 8 with mineralocorticoid-responsive hyponatremia of the elderly, and 4 with miscellaneous diseases. Approximately 40% of those with hyponatremia was derived from hypopituitarism, but severe hyponatremia was found in the patients with SIADH and mineralocorticoid-responsive hyponatremia of the elderly. Plasma AVP levels remained relatively high despite hypoosmolality and were tightly linked with exaggerated urinary excretion of AQP-2 and antidiuresis in the 3 groups of patients, except for one miscellaneous one. An acute water load test verified the impairment in water excretion, because the percent excretion of the water load was less than 42% and the minimal urinary osmolality was not sufficiently diluted. Also, plasma AVP and urinary excretion of AQP-2 were not reduced after the water load. The inappropriate secretion of AVP was evident in the patients with SIADH and hypopituitarism, and hydrocortisone replacement normalized urinary excretion of AQP-2 and renal water excretion in those with hypopituitarism. In contrast, the appropriate antidiuresis seemed to compensate loss of body fluid in the patients with mineralocorticoid-responsive hyponatremia of the elderly, who lost circulatory blood volume by 7.3% (mean). Fludrocortisone acetate increased renal sodium handling and body fluid, resulting in the reduction in AVP release and urinary excretion of AQP-2 in mineralocorticoid-responsive hyponatremia of the elderly. These findings indicate that urinary excretion of AQP-2 may be a more sensitive measure of AVP effect on renal collecting duct cells than are plasma AVP levels, and that increased urinary excretion of AQP-2 shows exaggerated AVP-induced antidiuresis in hyponatremic subjects in the elderly. In addition, mineralocorticoid-responsive hyponatremia of the elderly has to be carefully differentiated from SIADH in elderly subjects.

PMID 11297601  J Clin Endocrinol Metab. 2001 Apr;86(4):1665-71. doi: 1・・・
著者: R W Schrier, W T Abraham
雑誌名: N Engl J Med. 1999 Aug 19;341(8):577-85. doi: 10.1056/NEJM199908193410806.
Abstract/Text
PMID 10451464  N Engl J Med. 1999 Aug 19;341(8):577-85. doi: 10.1056/N・・・
著者: Christopher S D Almond, Andrew Y Shin, Elizabeth B Fortescue, Rebekah C Mannix, David Wypij, Bryce A Binstadt, Christine N Duncan, David P Olson, Ann E Salerno, Jane W Newburger, David S Greenes
雑誌名: N Engl J Med. 2005 Apr 14;352(15):1550-6. doi: 10.1056/NEJMoa043901.
Abstract/Text BACKGROUND: Hyponatremia has emerged as an important cause of race-related death and life-threatening illness among marathon runners. We studied a cohort of marathon runners to estimate the incidence of hyponatremia and to identify the principal risk factors.
METHODS: Participants in the 2002 Boston Marathon were recruited one or two days before the race. Subjects completed a survey describing demographic information and training history. After the race, runners provided a blood sample and completed a questionnaire detailing their fluid consumption and urine output during the race. Prerace and postrace weights were recorded. Multivariate regression analyses were performed to identify risk factors associated with hyponatremia.
RESULTS: Of 766 runners enrolled, 488 runners (64 percent) provided a usable blood sample at the finish line. Thirteen percent had hyponatremia (a serum sodium concentration of 135 mmol per liter or less); 0.6 percent had critical hyponatremia (120 mmol per liter or less). On univariate analyses, hyponatremia was associated with substantial weight gain, consumption of more than 3 liters of fluids during the race, consumption of fluids every mile, a racing time of >4:00 hours, female sex, and low body-mass index. On multivariate analysis, hyponatremia was associated with weight gain (odds ratio, 4.2; 95 percent confidence interval, 2.2 to 8.2), a racing time of >4:00 hours (odds ratio for the comparison with a time of <3:30 hours, 7.4; 95 percent confidence interval, 2.9 to 23.1), and body-mass-index extremes.
CONCLUSIONS: Hyponatremia occurs in a substantial fraction of nonelite marathon runners and can be severe. Considerable weight gain while running, a long racing time, and body-mass-index extremes were associated with hyponatremia, whereas female sex, composition of fluids ingested, and use of nonsteroidal antiinflammatory drugs were not.

Copyright 2005 Massachusetts Medical Society.
PMID 15829535  N Engl J Med. 2005 Apr 14;352(15):1550-6. doi: 10.1056/・・・

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