今日の臨床サポート

薬剤性腸炎(含む 偽膜性腸炎、NSAIDs腸炎、薬剤起因性collagenous colitis等)

著者: 林繁和 医療法人和合会 和合病院

監修: 上村直実 国立国際医療研究センター 国府台病院

著者校正済:2021/09/15
現在監修レビュー中
患者向け説明資料

概要・推奨   

  1. 下痢、血便、腹痛など腸炎を疑う場合はもちろん軽度の下痢の場合でも、薬剤性腸炎を念頭に置いて本トピックを参照していただきたい。
  1. 薬剤性腸炎を起こしうる薬剤を熟知していただくことにより、重症に至る前に対処できます。
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:
林繁和 : 特に申告事項無し[2021年]
監修:上村直実 : 未申告[2021年]

改訂のポイント:
  1. 定期レビューを行い、抗腫瘍薬による腸炎のうち、従来の細胞傷害性抗腫瘍薬とは発症機序の異なる免疫チェックポイント阻害薬による腸炎を加筆した。

病態・疫学・診察

疾患情報(疫学・病態)  
  1. 薬剤性腸炎とは、文字通り薬剤によって誘発される腸炎のことであり、下痢、腹痛などの症状を来す疾患である。
  1. 薬剤性腸炎といえば、かつては抗菌薬投与後に起こる抗菌薬起因性腸炎が大半を占めていたが、これには偽膜性腸炎と出血性腸炎(非偽膜性)がある。
  1. 偽膜性腸炎の大部分はClostridium difficile(CD)の異常増殖により発症し、今日でも院内感染が問題になるなどしばしばみられるが、出血性腸炎は1980年代前半をピークに今日では激減した[1][2]
  1. そのほかに腸炎を引き起こす薬剤として非ステロイド系抗炎症薬(NSAIDs)、金製剤、抗腫瘍薬、経口避妊薬、大腸検査前処置の下剤、漢方薬(山梔子)、ステロイド薬、免疫抑制薬、ランソプラゾール(タケプロン)、オルメサルタンなどが知られている。
  1. NSAIDs腸炎[3]は高齢化に伴う使用頻度の増加と、小腸・大腸内視鏡や小腸カプセル内視鏡(capsule endoscopy以下CE)の普及に伴って近年多数の報告がみられる。小腸CEを用いた検討としてはボランティアにジクロフェナク(ボルタレン)を服用させ、68%に小腸潰瘍を認めた報告[4]や、リウマチで3カ月以上NSAIDsを服用している患者で16例中13例に小腸にびらんないし潰瘍を認めたという報告[5]、3カ月以上NSAIDs内服の関節炎患者の71%に小腸粘膜障害を認め、コントロール群の10%に対し有意に高率であった報告[6]などがある。なお、小腸CEは比較的侵襲の少ない検査であり、ボランティアや健常者における治験も比較的行いやすいが、保険診療においては「上部消化内視鏡検査および大腸内視鏡検査で出血の原因が不明の場合」という制限がある。
  1. 病理組織学的特徴から診断されるcollagenous colitisのなかに、NSAIDsやランソプラゾールなどの薬剤が関与する例が近年多数報告されている(薬剤起因性collagenous colitis[7])。
  1. 抗腫瘍薬のうち細胞傷害性薬による腸炎では消化管粘膜の直接障害の結果みられる下痢症状は投与量や投与方法にもよるが、フルオロウラシル系抗腫瘍薬で60%を超えるとの報告もある。しかし血便を伴うような重症例の報告[8]は、使用頻度の増加の割には増えていない。
  1. 近年開発された免疫チェックポイント阻害薬(immune checkpoint inhibitor 以下ICI、抗PD-1抗体ニボルマブ(オプジーボ)や抗CTLA-4抗体イピリムマブ(ヤーボイ)など)による腸炎はさまざまな臓器で報告されている免疫関連の副作用の一つであり、腸管免疫システムのバランスが崩れることにより発症する。その頻度はニボルマブ投与の5.52%、イピリムマブ投与の5.8~12.9%、両者併用で28.6%と報告されている[9]
  1. 金製剤による腸炎はリウマチの治療薬として強力な内服薬や生物学的製剤が出現して金製剤の使用頻度が低下したこともあり、筆者の報告[10]以後は報告されていない。
  1. 経口避妊薬[11]、大腸検査前処置の下剤で発症する虚血性大腸炎[12]はよく知られている。
  1. 腸間膜静脈硬化症は、かつては原因不明とされていたが、近年漢方薬の原料の1つ、山梔子を服用していた症例が、多数報告されている。山梔子に含まれるゲニポシドは回盲部、特に盲腸で腸内細菌のβグルコシダーゼにより加水分解されてゲニピンとなり、これがアミノ酸やタンパク質などと反応すると青色を呈する。これが大腸の着色および腸間膜静脈の線維化・石灰化を起こすと考えられている[13]
  1. オルメサルタン関連スプルー様腸疾患は2012年米国で降圧剤オルメサルタンが関与したと思われる吸収不良症候群22例を解析、報告された新しい疑念である。わが国でも最近報告が散見されている[14][15]
問診・診察のポイント  
  1. 薬剤投与歴を聴取する。前医で投与され、薬剤を持参していない場合には前医に薬剤名、投与期間を問い合わせる。抗菌薬の場合は投与経路(経口か非経口)を知ることも重要である。

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文献 

著者: Laurence Maiden, Bjarni Thjodleifsson, Asgeir Theodors, Juan Gonzalez, Ingvar Bjarnason
雑誌名: Gastroenterology. 2005 May;128(5):1172-8.
Abstract/Text BACKGROUND & AIMS: Conventional acidic nonsteroidal anti-inflammatory drugs frequently cause small bowel inflammation. Diagnosis is largely based on assay of surrogate markers of inflammation in stool, such as fecal calprotectin. However, stool markers are not widely available and the precise nature of this inflammation is uncertain. We used wireless capsule enteroscopy to quantitate and assess the nature of the small bowel damage caused by nonsteroidal anti-inflammatory drugs when taken on a short-term basis.
METHODS: Forty healthy volunteers underwent a baseline capsule enteroscopy and fecal calprotectin test. After taking diclofenac slow-release 75 mg twice a day (with omeprazole 20 mg twice a day for gastroprotection) for a total of 14 days, both investigations were repeated.
RESULTS: After drug treatment, 30 subjects (75%) had increased repeat fecal calprotectin concentrations above the upper limit of normal. Capsule enteroscopy showed new pathology in 27 subjects (68%). The commonest lesions were mucosal breaks, seen in 16 (40%), which were seen to be bleeding in 2 (5%); reddened folds in 14 (35%); petechiae or red spots in 13 (33%); denuded mucosa in 8 (20%); and blood in the lumen without a visualized source in 3 (8%). Fifteen of the 27 subjects had more than one lesion concurrently.
CONCLUSIONS: This study provides both biochemical and direct evidence of macroscopic injury to the small intestine in 68%-75% of volunteers resulting from 2 weeks' ingestion of slow-release diclofenac.

PMID 15887101  Gastroenterology. 2005 May;128(5):1172-8.
著者: Satoshi Sugimori, Toshio Watanabe, Masahiko Tabuchi, Natsuhiko Kameda, Hirohisa Machida, Hirotoshi Okazaki, Tetsuya Tanigawa, Hirokazu Yamagami, Masatsugu Shiba, Kenji Watanabe, Kazunari Tominaga, Yasuhiro Fujiwara, Nobuhide Oshitani, Tatsuya Koike, Kazuhide Higuchi, Tetsuo Arakawa
雑誌名: Digestion. 2008;78(4):208-13. doi: 10.1159/000190403. Epub 2009 Jan 13.
Abstract/Text BACKGROUND AND AIM: The medical treatment of rheumatoid arthritis (RA) includes nonsteroidal anti-inflammatory drugs (NSAIDs), low-dose corticosteroids, and disease-modifying antirheumatic drugs (DMARDs). We evaluated the incidence of small bowel injury in RA patients who were taking anti-RA drugs with or without concomitant NSAIDs by capsule endoscopy.
METHODS: A total of 28 RA patients who took low-dose corticosteroids and/or DMARDs for more than 1 year were enrolled.
RESULTS: The incidence of red spots did not differ between the 2 groups: 14 of 16 patients (87.5%) in the NSAID group and 11 of 12 patients (91.7%) in the non-NSAID group. In contrast, the incidence of mucosal breaks was significantly higher in the NSAID group than in the non-NSAID group: mucosal breaks were detected in 13 of 16 patients (81.3%) and 4 of 12 patients (33.3%) in the NSAID and non-NSAID groups, respectively. In the NSAID group, mucosal breaks developed in users of preferential cyclooxygenase-2 inhibitors at a frequency similar to that in users of traditional NSAIDs.
CONCLUSION: Patients taking anti-RA drugs may have an increased frequency of small bowel injury regardless of NSAID use, and NSAID use may be associated with an increased incidence of severe small bowel injury.

PMID 19142000  Digestion. 2008;78(4):208-13. doi: 10.1159/000190403. E・・・
著者: David Y Graham, Antone R Opekun, Field F Willingham, Waqar A Qureshi
雑誌名: Clin Gastroenterol Hepatol. 2005 Jan;3(1):55-9.
Abstract/Text BACKGROUND & AIMS: Patients who regularly take nonsteroidal anti-inflammatory drugs (NSAIDs) have an increased risk for small-intestinal mucosal ulceration and bleeding, which may present as anemia of undetermined gastrointestinal origin or protein loss. The prevalence and severity of small-intestinal lesions remains unclear. Our aim was to assess the frequency of NSAID-induced small-bowel injury among chronic NSAID users.
METHODS: Ambulatory patients with various types of arthritides who took NSAIDs daily (>3 mo duration) or took either acetaminophen alone or nothing were enrolled in the study. All patients fasted overnight and underwent wireless video capsule endoscopy. Two investigators, blind to therapy, reviewed each video beginning after the pylorus. Lesions were scored as normal, red spots, small erosions, large erosions, or ulcers. An ulcer was defined as a larger lesion with apparent depth and a definite rim.
RESULTS: Forty-one patients, 36 men and 5 women, ages ranging from 22 to 66 years (mean age, 49.8 y) were analyzed including 21 chronic NSAID users and 20 control patients. Small-bowel injury was seen in 71% of NSAID users compared with 10% of controls (P < .001). Injury was mild (few or no erosions, absence of large erosions/ulcers) in 10 NSAID users compared with 2 controls. Five NSAID users had major (>4 erosions or large ulcers/ulcers) damage compared with none in the control group. There were no complications or problems with the capsule endoscopy procedure.
CONCLUSIONS: Endoscopically evident small-intestinal mucosal injury is very common among chronic NSAID users. The role of endoscopically evident injury in unexplained iron-deficiency anemia and hypoalbuminemia among chronic NSAID users remains undetermined.

PMID 15645405  Clin Gastroenterol Hepatol. 2005 Jan;3(1):55-9.
著者: Christoph Högenauer, Cord Langner, Eckhard Beubler, Irmgard T Lippe, Rudolf Schicho, Gregor Gorkiewicz, Robert Krause, Nikolas Gerstgrasser, Guenter J Krejs, Thomas A Hinterleitner
雑誌名: N Engl J Med. 2006 Dec 7;355(23):2418-26. doi: 10.1056/NEJMoa054765.
Abstract/Text BACKGROUND: Antibiotic-associated hemorrhagic colitis is a distinct form of antibiotic-associated colitis in which Clostridium difficile is absent. Although the cause is not known, previous reports have suggested a role of Klebsiella oxytoca.
METHODS: We studied 22 consecutive patients who had suspected antibiotic-associated colitis and who were negative for C. difficile. Patients underwent diagnostic colonoscopy, and among those who received a diagnosis of antibiotic-associated hemorrhagic colitis, stool samples were cultured for K. oxytoca. We isolated K. oxytoca strains and tested them for cytotoxin production using a tissue-culture assay. In addition, we also cultured stool samples obtained from 385 healthy subjects for K. oxytoca. An in vivo animal model for antibiotic-associated hemorrhagic colitis was established with the use of Sprague-Dawley rats.
RESULTS: Of the 22 patients, 6 had findings on colonoscopy that were consistent with the diagnosis of antibiotic-associated hemorrhagic colitis, and 5 of these 6 patients had positive cultures for K. oxytoca. No other common enteric pathogens were found in the five patients. Before the onset of colitis, all five were receiving penicillins, and two were also taking nonsteroidal antiinflammatory drugs (NSAIDs). All isolated K. oxytoca strains produced cytotoxin. K. oxytoca was found in 1.6% of the healthy subjects. In the animal model, K. oxytoca was found only in the colon of rats that received amoxicillin-clavulanate in addition to being inoculated with K. oxytoca. In these rats, infection with K. oxytoca induced a right-sided hemorrhagic colitis that was not observed in uninfected animals that received amoxicillin-clavulanate, indomethacin (an NSAID), or both.
CONCLUSIONS: Our fulfillment of Koch's postulates for cytotoxin-producing K. oxytoca suggests that it is the causative organism in at least some cases of antibiotic-associated hemorrhagic colitis. Infection with K. oxytoca should be considered in patients with antibiotic-associated colitis who are negative for C. difficile.

Copyright 2006 Massachusetts Medical Society.
PMID 17151365  N Engl J Med. 2006 Dec 7;355(23):2418-26. doi: 10.1056/・・・
著者: Junji Umeno, Takayuki Matsumoto, Shotaro Nakamura, Yukihiko Jo, Shinichiro Yada, Katsuya Hirakawa, Ryuji Yoshimura, Hajime Yamagata, Tetsuji Kudo, Atsushi Hirano, Masaki Gushima, Takashi Yao, Yutaka Nakashima, Mitsuo Iida
雑誌名: Gastrointest Endosc. 2008 Jun;67(7):1185-91. doi: 10.1016/j.gie.2008.02.013.
Abstract/Text BACKGROUND: Although some cases of collagenous colitis have been induced by lansoprazole (LPZ), the clinicopathologic features of LPZ-associated collagenous colitis have not been elucidated.
OBJECTIVE: To elucidate the clinical, endoscopic, and histopathologic features of LPZ-associated collagenous colitis.
DESIGN: Retrospective case study.
PATIENTS: The subjects were 13 patients with collagenous colitis diagnosed during a period from 2002 to 2007.
MAIN OUTCOME MEASUREMENTS: The colonoscopic and histopathologic findings were compared retrospectively between 9 cases of LPZ use (LPZ group) and 4 cases without the use of LPZ (non-LPZ group).
RESULTS: A colonoscopy revealed a linear mucosal defect more frequently in the LPZ group (7 of 9 cases [78%]) than in the non-LPZ group (0 of 4 cases [0%], P = .02). Friable mucosa was also noted in 4 patients (44%) in the LPZ group but none in the non-LPZ group. The colonoscopic finding in the non-LPZ group was either normal mucosa or nonspecific minimal abnormalities, whereas patients in the LPZ group had either a linear mucosal defect, mucosal bleeding, or both (P = .001). On histologic examination, the subepithelial collagen band was thicker in patients in the LPZ group than in those in the non-LPZ group (median 45 vs 26.3 mum). All patients in the LPZ group recovered from diarrhea after discontinuance of LPZ.
LIMITATION: A small number of patients.
CONCLUSIONS: Linear mucosal defects and friable mucosa may be characteristic colonoscopic findings in cases of LPZ-associated collagenous colitis.

PMID 18513560  Gastrointest Endosc. 2008 Jun;67(7):1185-91. doi: 10.10・・・
著者: R Kiesslich, A Hoffman, M Goetz, S Biesterfeld, M Vieth, P R Galle, M F Neurath
雑誌名: Gut. 2006 Apr;55(4):591-2. doi: 10.1136/gut.2005.084970.
Abstract/Text
PMID 16531549  Gut. 2006 Apr;55(4):591-2. doi: 10.1136/gut.2005.084970・・・
著者: A Zambelli, V Villanacci, E Buscarini, G Bassotti, L Albarello
雑誌名: Endoscopy. 2008 Jul;40(7):606-8. doi: 10.1055/s-2008-1077376.
Abstract/Text Confocal laser endomicroscopy (CLE) was carried out in seven patients with chronic watery diarrhea (three men; age range 68 - 84 years) to find the correspondence between CLE and histological findings in collagenous colitis. On the basis of the CLE images, two to five biopsies were performed in various segments of the colon. The endoscopic and histological diagnoses of collagenous colitis were made blindly. The quality of the CLE images was quantified from 0 (the endoscopist could not visualize the corresponding histologic equivalent) to 3 (the endoscopist could identify >or= 80 % of the corresponding histologic equivalent). Four out of seven patients had histological findings of collagenous colitis. Correspondence between histology and CLE images yielded the following scores: 3 for epithelial architecture, 3 for goblet cells, 3 for vessels, and 2 for inflammatory infiltrate. In collagenous colitis patients, CLE identified a well-defined "shell" around the crypts, corresponding to the increase in the thickness of the subepithelial collagenous plate evidenced by histology. CLE appears to be a promising means of identifying typical collagenous colitis features.

PMID 18609454  Endoscopy. 2008 Jul;40(7):606-8. doi: 10.1055/s-2008-10・・・
著者: Mark W Hull, Paul L Beck
雑誌名: Can Fam Physician. 2004 Nov;50:1536-40, 1543-5.
Abstract/Text OBJECTIVE: To review the basic microbiology, pathogenesis of disease, and diagnosis of the nosocomial pathogen Clostridium difficile and to examine therapies recommended by the Canadian Task Force on Preventive Health Care. QUALITY OF EVIDENCE MEDLINE: was searched using MeSH headings. Controlled trials for therapy were sought, but case-control studies and observational reviews were included.
MAIN MESSAGE: Clostridium difficile causes approximately 20% of cases of diarrhea associated with antibiotics, including clindamycin and the second- and third-generation cephalosporins. Diarrhea is usually mild, but can be severe; extreme cases develop toxic megacolon. Diagnosis is dependent on demonstrating presence of clostridial toxin in stool specimens or of pseudomembranes through sigmoidoscopy. First-line therapy for C. difficile diarrhea is restricted to metronidazole. Second-line therapy for treatment failure is vancomycin. For relapse, a second course of metronidazole is recommended; tapering courses of vancomycin and probiotics are used for multiple recurrences.
CONCLUSION: Clostridium difficile is an important nosocomial pathogen requiring prudent use of antibiotics and strict infection-control policies to prevent large health care costs.

PMID 15597970  Can Fam Physician. 2004 Nov;50:1536-40, 1543-5.
著者: I Tonna, P D Welsby
雑誌名: Postgrad Med J. 2005 Jun;81(956):367-9. doi: 10.1136/pgmj.2004.028480.
Abstract/Text This paper reviews the pathogenesis and management of Clostridium difficile diarrhoea, in particular the management of recurrent episodes.

PMID 15937201  Postgrad Med J. 2005 Jun;81(956):367-9. doi: 10.1136/pg・・・
著者: Israel Lowy, Deborah C Molrine, Brett A Leav, Barbra M Blair, Roger Baxter, Dale N Gerding, Geoffrey Nichol, William D Thomas, Mark Leney, Susan Sloan, Catherine A Hay, Donna M Ambrosino
雑誌名: N Engl J Med. 2010 Jan 21;362(3):197-205. doi: 10.1056/NEJMoa0907635.
Abstract/Text BACKGROUND: New therapies are needed to manage the increasing incidence, severity, and high rate of recurrence of Clostridium difficile infection.
METHODS: We performed a randomized, double-blind, placebo-controlled study of two neutralizing, fully human monoclonal antibodies against C. difficile toxins A (CDA1) and B (CDB1). The antibodies were administered together as a single infusion, each at a dose of 10 mg per kilogram of body weight, in patients with symptomatic C. difficile infection who were receiving either metronidazole or vancomycin. The primary outcome was laboratory-documented recurrence of infection during the 84 days after the administration of monoclonal antibodies or placebo.
RESULTS: Among the 200 patients who were enrolled (101 in the antibody group and 99 in the placebo group), the rate of recurrence of C. difficile infection was lower among patients treated with monoclonal antibodies (7% vs. 25%; 95% confidence interval, 7 to 29; P<0.001). The recurrence rates among patients with the epidemic BI/NAP1/027 strain were 8% for the antibody group and 32% for the placebo group (P=0.06); among patients with more than one previous episode of C. difficile infection, recurrence rates were 7% and 38%, respectively (P=0.006). The mean duration of the initial hospitalization for inpatients did not differ significantly between the antibody and placebo groups (9.5 and 9.4 days, respectively). At least one serious adverse event was reported by 18 patients in the antibody group and by 28 patients in the placebo group (P=0.09).
CONCLUSIONS: The addition of monoclonal antibodies against C. difficile toxins to antibiotic agents significantly reduced the recurrence of C. difficile infection. (ClinicalTrials.gov number, NCT00350298.)

2010 Massachusetts Medical Society
PMID 20089970  N Engl J Med. 2010 Jan 21;362(3):197-205. doi: 10.1056/・・・
著者: A Abdo, J Raboud, H J Freeman, P Zetler, J Tilley, H Chaun, J S Whittaker, J Amar, L Halparin, R Enns
雑誌名: Am J Gastroenterol. 2002 May;97(5):1164-8. doi: 10.1111/j.1572-0241.2002.05688.x.
Abstract/Text OBJECTIVES: Collagenous colitis (CC) is an uncommon form of inflammatory bowel disease. The response to typical medical therapies (antimotility agents, 5-aminosalicylic acid [5-ASA], and corticosteroids) is variable. We aimed to determine if there are clinical or histological variables that can predict response to medical therapy.
METHODS: All cases of CC were identified in three tertiary care medical centers. All charts of included patients were reviewed and clinical variables (age, gender, duration of symptoms, frequency of bowel movements, and the use of nonsteroidal anti-inflammatory drugs [NSAIDs]) were recorded. Available histology slides were reviewed by one GI pathologist. Intraepithelial inflammation, epithelial loss or detachment, inflammation in the lamina propria, presence of eosinophilia, crypt inflammation, Paneth's cell metaplasia, and collagen layer thickness were recorded. Depending on their response to therapy, patients were divided into three groups: 1) spontaneous recovery or response to antidiarrheal agents alone, 2) response to 5-ASA agents, and 3) response to corticosteroids after failure of antidiarrheal agents and 5-ASA.
RESULTS: Ninety-four patients with CC were identified. Of these, 62 patients were included. The median age was 58 (range = 20-85), and 88% were female. Among the histological parameters only the degree of inflammation in the lamina propria significantly differed between the three response groups (p = 0.007). Patients who required corticosteroids had greater inflammation. Among the clinical parameters age at presentation and use of NSAIDs significantly differed between groups. In the antidiarrheal group, patients tended to be more elderly, and in the corticosteroid group, more patients were on NSAIDs.
CONCLUSIONS: 1) The degree of lamina propria inflammation can be used as a histological predictor to guide treatment in patients with CC. 2) Patients who responded to antidiarrheal agents or had spontaneous remissions were significantly older than those patients requiring 5-ASA compounds or corticosteroids. 3) Patients who were taking NSAIDs were more likely to require corticosteroid therapy, presumably reflecting more severe disease.

PMID 12014722  Am J Gastroenterol. 2002 May;97(5):1164-8. doi: 10.1111・・・
著者: Soichi Sano, Keiko Yamagami, Ayako Tanaka, Minako Nishio, Tomoyuki Nakamura, Yuki Kubo, Takeshi Inoue, Wataru Ueda, Kiyotaka Okawa, Katsunobu Yoshioka
雑誌名: World J Gastroenterol. 2008 Oct 21;14(39):6083-6.
Abstract/Text A 76-year-old woman with a 5-mo history of recurrent diarrhea and generalized edema was admitted to our hospital. Colonoscopy revealed edematous mucosa, and histopathological examination was compatible with collagenous colitis. Protein leakage from the colon, particularly in the ascending portion, was identified on 99mTc-human serum albumin scintigraphy. Collagenous colitis associated with protein-losing enteropathy (PLE) without small bowel disease was diagnosed. Prednisolone treatment ameliorated diarrhea and hypoproteinemia. Collagenous colitis should be included in the differential diagnosis of chronic diarrhea with hypoproteinemia for appropriate management.

PMID 18932290  World J Gastroenterol. 2008 Oct 21;14(39):6083-6.

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