今日の臨床サポート

蛋白漏出性胃腸症

著者: 篠村恭久 川西市医師会メディカルセンター

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/監修レビュー済:2020/03/26
患者向け説明資料

概要・推奨   

  1. 腸リンパ管拡張症患者には、低脂肪食と中鎖脂肪酸(medium-chain triglyceride、 MCT)の補充が推奨される(推奨度2)。
  1. Ménétrier病患者にはH. pyloriの除菌が推奨される(推奨度2)。
  1. Ménétrier病患者にはプロトンポンプ阻害薬(PPI)による治療を試みることが推奨される(推奨度2)。
  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
  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
  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
  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
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:
篠村恭久 : 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. 定期レビューを行った(変更なし)。

病態・疫学・診察

疾患情報(疫学・病態)  
  1. 蛋白漏出性胃腸症とは、消化管内腔へ蛋白が異常に漏出し、低蛋白血症を来す症候群である。
  1. 蛋白漏出性胃腸症について、有病率などの疫学情報は明らかにされていない。
  1. 蛋白漏出性胃腸症を来す種々の疾患があり、漏出の機序には、リンパ系の異常、毛細血管の透過性亢進、胃腸粘膜上皮の異常などがある。蛋白漏出性胃腸症を来す代表的疾患に腸リンパ管拡張症やMénétrier病、Cronkhite-Canada症候群がある。
問診・診察のポイント  
  1. 浮腫は高頻度にみられる症状であり、浮腫がある場合は胸水や腹水による息切れや腹部膨満の有無を問診し、胸水や腹水の有無を診察で確認する。

これより先の閲覧には個人契約のトライアルまたはお申込みが必要です。

最新のエビデンスに基づいた二次文献データベース「今日の臨床サポート」。
常時アップデートされており、最新のエビデンスを各分野のエキスパートが豊富な図表や処方・検査例を交えて分かりやすく解説。日常臨床で遭遇するほぼ全ての症状・疾患から薬剤・検査情報まで瞬時に検索可能です。

まずは15日間無料トライアル
本サイトの知的財産権は全てエルゼビアまたはコンテンツのライセンサーに帰属します。私的利用及び別途規定されている場合を除き、本サイトの利用はいかなる許諾を与えるものでもありません。 本サイト、そのコンテンツ、製品およびサービスのご利用は、お客様ご自身の責任において行ってください。本サイトの利用に基づくいかなる損害についても、エルゼビアは一切の責任及び賠償義務を負いません。 また、本サイトの利用を以て、本サイト利用者は、本サイトの利用に基づき第三者に生じるいかなる損害についても、エルゼビアを免責することに合意したことになります。  本サイトを利用される医学・医療提供者は、独自の臨床的判断を行使するべきです。本サイト利用者の判断においてリスクを正当なものとして受け入れる用意がない限り、コンテンツにおいて提案されている検査または処置がなされるべきではありません。 医学の急速な進歩に鑑み、エルゼビアは、本サイト利用者が診断方法および投与量について、独自に検証を行うことを推奨いたします。

文献 

著者: Björn K I Meijers, Simon Schalla, Filip Eerens, Robert-J Van Suylen, Bernard Broers, Emile M Cheriex, Jan-P Smedema
雑誌名: Int J Cardiovasc Imaging. 2006 Jun-Aug;22(3-4):389-92. doi: 10.1007/s10554-005-9067-2. Epub 2006 Feb 25.
Abstract/Text Although acute pericarditis is a common and usual benign disorder, sometimes evolution to constrictive pericarditis may occur. We present a case of constrictive pericarditis late after coronary bypass grafting, complicated by right sided heart failure. Edema formation was aggravated due to protein-losing enteropathy, resulting in hypoalbuminemia. Imaging of constrictive pericarditis was done by ultrasound as well as simultaneous pressure recording of the right and left ventricle. Imaging of intestinal protein loss was possible using intravenous Technetium-99m-labelled human serum albumin.

PMID 16502021  Int J Cardiovasc Imaging. 2006 Jun-Aug;22(3-4):389-92. ・・・
著者: G H JEFFRIES, A CHAPMAN, M H SLEISENGER
雑誌名: N Engl J Med. 1964 Apr 9;270:761-6. doi: 10.1056/NEJM196404092701503.
Abstract/Text
PMID 14107315  N Engl J Med. 1964 Apr 9;270:761-6. doi: 10.1056/NEJM19・・・
著者: Kunihiko Aoyagi, Mitsuo Iida, Takayuki Matsumoto, Shotaro Sakisaka
雑誌名: Dig Dis Sci. 2005 Aug;50(8):1467-70.
Abstract/Text Intestinal lymphangiectasia (IL) is a rare disease requiring oral fat restriction. The aim of this study was to evaluate the efficacy of enteral nutrition compared to that of total parenteral nutrition (TPN). We retrospectively reviewed nine patients with IL presenting with protein-losing enteropathy. Of these, seven patients not responding to a low-fat diet were treated with elemental diet (ED), polymeric diet (PD) containing medium-chain triglycerides, or TPN. Improvement in serum total protein was observed in two of three on ED and in one of two on PD, compared with three of three on TPN. Enteric protein loss was improved in two of two on ED, one of two on PD, and two of two on TPN. Outpatients who continued to receive enteral nutrition maintained a total protein level. Enteral nutirition appears to be as effective as TPN for patients with IL, and it may provide a valid and safe alternative therapy.

PMID 16110837  Dig Dis Sci. 2005 Aug;50(8):1467-70.
著者: Y Yasunaga, Y Shinomura, S Kanayama, M Yabu, T Nakanishi, Y Miyazaki, Y Murayama, J J Bonilla-Palacios, Y Matsuzawa
雑誌名: Gut. 1994 Nov;35(11):1571-4.
Abstract/Text This study examined the effects of eradication of Helicobacter pylori (H pylori) infection on gastric mucosal morphology and acid secretion. Sixteen H pylori positive patients with enlarged gastric body folds were divided into two groups: (a) patients with moderate enlargement (fold width: 6 to 10 mm, n = 8) and (b) patients with severe enlargement (> 10 mm, n = 8). After successful treatment, gastric body fold width was reduced in both groups (p < 0.01) with an associated decrease in inflammatory infiltrates in the body mucosa (p < 0.01 and p < 0.05). Basal acid output and tetragastrin stimulated maximal acid output (mean (SEM)) in all 16 patients significantly increased from 1.1 (0.5) to 2.9 (0.9) mmol/h (p < 0.05) and from 5.4 (1.3) to 18.7 (2.3) mmol/h (p < 0.01), respectively, with a significant decrease in fasting serum gastrin concentrations, from 127.1 (16.1) to 59.6 (3.8) pg/ml (p < 0.01). The increase in acid secretion after eradication of H pylori was more noticeable in the severe group, who had shown lower acid secretion and higher serum gastrin concentrations (p < 0.05) before eradication, than the increase seen in the moderate group. The decreases in ammonia nitrogen content seen after eradication were significant in basal (from 0.91 (0.17) to 0.37 (0.08) mmol/h, p < 0.05) and stimulated gastric secretions (from 1.57 (0.19) to 0.37 (0.13) mmol/h, p < 0.01), although these changes were too small to explain the increases in basal acid output and maximal acid output. These results suggest that inflammation of the gastric body mucosa caused by H pylori infection is associated with enlarged gastric body folds and inhibition of acid secretion in H pylori positive patients with enlarged gastric body folds.

PMID 7828975  Gut. 1994 Nov;35(11):1571-4.
著者: M Stolte, C H Bätz, E Bayerdörffer, S Eidt
雑誌名: Z Gastroenterol. 1995 Apr;33(4):198-201.
Abstract/Text In an earlier study, we were able to show that giant fold gastritis is probably a special form of Helicobacter pylori-associated gastritis. Proof of this contention, however--namely regression of the giant folds following eradication of the organism--in a large number of patients was not then possible. To rectify this, Helicobacter pylori (HP) eradication treatment with omeprazole and amoxicillin was applied to 47 patients with HP gastritis and giant folds (5 patients with giant folds localized in the anterior or posterior wall, 42 patients with generalised giant folds within the corpus and fundus). The results of treatment were investigated by endoscopy and histology at the earliest 4 weeks after termination of treatment. In 40 of the 47 patients (85.1%), HP eradication treatment was successful. In 7 patients in whom treatment was unsuccessful, follow-up examinations revealed no changes in the endoscopic or histological findings. In 2 out of 3 patients in whom the endoscopic findings were unchanged despite successful HP eradication, biopsy material revealed the cause of the giant folds to be a signet ring cell carcinoma; in the remaining patient the cause of giant fold persistence was unclear. In 36 patients, the endoscopic--findings normalised completely, while in one patient there was obvious regression of the giant folds. We conclude from this study that giant fold gastritis is indeed a special form of HP gastritis, and that eradicating the organism in patients with gastric giant folds may help to distinguish between inflammatory, hyperplastic and tumorous giant folds.

PMID 7793118  Z Gastroenterol. 1995 Apr;33(4):198-201.
著者: E Bayerdörffer, M M Ritter, R Hatz, W Brooks, G Ruckdeschel, M Stolte
雑誌名: Gut. 1994 May;35(5):701-4.
Abstract/Text Hypertrophic gastropathy--that is, Ménétrier's disease--was found, in a retrospective analysis, to be associated with Helicobacter pylori in more than 90% of patients. It is proposed that hypertrophic gastropathy represents a special form of H pylori gastritis in these patients. A case is described of a 28 year old woman with Ménétrier's disease associated with proved protein loss from the stomach. Treatment with cimetidine for more than three years had little benefit when colonisation by H pylori was detected. Density of H pylori colonisation and activity of gastritis, which was also present in the first biopsy specimens taken five years ago, were more pronounced in the body than in the antrum, which is in agreement with the characteristics of H pylori gastritis found in other cases with Ménétrier's disease. A 14 day antibacterial treatment course with 750 mg amoxicillin three times a day combined with 40 mg omeprazole three times a day was started in April 1991. This resulted in eradication of H pylori and the return to normal of giant folds and the mucosal histology. Serum protein concentrations returned to normal within six weeks and remained normal at two endoscopies during a two year follow up. This case report suggests that a subgroup of the patients with Ménétrier's disease may be healed by the eradication of H pylori.

PMID 8200570  Gut. 1994 May;35(5):701-4.
著者: M Kawasaki, K Hizawa, K Aoyagi, S Nakamura, M Fujishima
雑誌名: Am J Gastroenterol. 1997 Oct;92(10):1909-12.
Abstract/Text We herein report a case of a 46-yr-old female with Ménétrièr's disease associated with Helicobacter pylori (H. pylori) infection, in whom the appearance of enlarged gastric folds and hypoproteinemia were both successfully treated by antibacterial treatment. The patient had been treated with famotidine for 3 yr under a diagnosis of Ménétrièr's disease, which caused an increase in her serum protein concentration to a level at which she suffered no clinical problems; however, the concentration never reached a normal range, and the presence of enlarged gastric folds also remained unchanged. Because H. pylori colonization was detected in the stomach and was also retrospectively recognized in the initial histologic specimens, antibacterial treatment with omeprazole, clarithromycin, and metronidazole was thus attempted. As a result of the successful eradication of H. pylori, the enlarged gastric folds returned to normal and the serum protein concentration thus increased to a normal level after the treatment. The etiology of Ménétrièr's disease remains unknown; however, the above findings suggest that H. pylori infection may in some cases cause Ménétrièr's disease and should therefore be carefully treated in any patient with this condition.

PMID 9382064  Am J Gastroenterol. 1997 Oct;92(10):1909-12.
著者: T Kaneko, T Akamatsu, A Gotoh, K Shimodaira, T Shimizu, K Kiyosawa, T Katsuyama, A Momose
雑誌名: Am J Gastroenterol. 1999 Jan;94(1):272-3. doi: 10.1111/j.1572-0241.1999.00816.x.
Abstract/Text We report here a case of Ménétrier's disease (MD) that required a prolonged period for remission after eradication therapy of Helicobacter pylori (HP). The appropriate time needed to judge the efficacy of the eradication therapy for HP infection in an MD case is discussed.

PMID 9934772  Am J Gastroenterol. 1999 Jan;94(1):272-3. doi: 10.1111/・・・
著者: D M Bradburn, N F Redwood, C W Venables, A Gunn
雑誌名: Digestion. 1992;52(3-4):204-8.
Abstract/Text Medical therapy of Ménétrier's disease is often unsatisfactory and may lead to surgical treatment. Two cases, previously unresponsive to H2 antagonists, are presented showing a marked response to omeprazole.

PMID 1459354  Digestion. 1992;52(3-4):204-8.
著者: S D Ladas, P S Tassios, H C Malamou, D P Protopapa, S A Raptis
雑誌名: Eur J Gastroenterol Hepatol. 1997 Aug;9(8):811-3.
Abstract/Text We report a patient with Ménétrier's disease presenting with extensive subcutaneous oedema, ascites and pleural effusion due to hypoalbuminaemia. Gastric secretory studies showed no free basal and stimulated acid secretion. The gastric juice contained significant amounts of albumin (0.2 g/dl) and immunoglobulin G (IgG) (1.11 mg/dl), corresponding to an estimated daily loss of 9.7 g and 45 mg, respectively. Protein-losing gastropathy was initially unsuccessfully treated with famotidine (80 mg/day) for 17 months, but a long-term (25 months) clinical remission was subsequently achieved with omeprazole (20 mg/day). We suggest that excellent clinical remission of Ménétrier's disease and the associated protein-losing gastropathy may be obtained with long-term omeprazole maintenance treatment, possibly due to Helicobacter pylori suppression.

PMID 9282281  Eur J Gastroenterol Hepatol. 1997 Aug;9(8):811-3.
著者: M Vendelboe, J Jespersen
雑誌名: Acta Med Scand. 1981;209(1-2):125-7.
Abstract/Text A man aged 46 developed Ménétrier's disease with massive hypertrophic gastritis and significantly elevated gastrointestinal protein clearance. During treatment with cimetidine the protein loss decreased markedly and the gastric mucosa normalized.

PMID 7211482  Acta Med Scand. 1981;209(1-2):125-7.
著者: J Y Kang, K F Tang, A Goh, F X Sundram, C S Seah
雑誌名: Aust N Z J Med. 1990 Oct;20(5):716-7.
Abstract/Text We describe a patient with Ménétrier's disease in whom acute administration of ranitidine reduced gastric protein loss more effectively than cimetidine or propantheline. This patient went into remission following a course of ranitidine. We reviewed the literature on remissions in Ménétrier's disease occurring without surgery. More detailed studies of various anti-secretory agents on individual patients are required to determine whether or not they are truly efficacious.

PMID 2285389  Aust N Z J Med. 1990 Oct;20(5):716-7.
著者: M Kondo, M Ikezaki, H Kato, M Masuda
雑誌名: Scand J Gastroenterol. 1978;13(7):851-6.
Abstract/Text In five cases of giant hypertrophic gastritis (Menetrier's disease) biopsied gastric mucosa was examined for fibrinolytic activity; in all cases there was marked elevation of the activity due mainly to tissue plasminogen activator. The patients were given antifibrinolytic therapy with oral tranexamic acid (trans-4-aminomethyl cyclohexane carboxylic acid; trans-AMCHA), and four of the patients showed marked improvement of their hypoproteinemia as well as their mucosal disorders. One patient, who showed moderate increase of serum protein level but no reduction of the mucosal disorder, finally received gastrectomy. It was concluded that antifibrinolytic therapy seemed to block the vicious circle of 'membrane disorders', 'increased tissue fibrinolysis', 'increased vascular permeability' and 'hypoproteinemia' in Menetrier's disease.

PMID 364627  Scand J Gastroenterol. 1978;13(7):851-6.
著者: G E Davis, M C O'Rourke, J R Metz, W V Kindig, J G Sweeney, K N Kane
雑誌名: J Clin Gastroenterol. 1991 Aug;13(4):436-41.
Abstract/Text We describe a 33-year-old man with giant hypertrophic gastropathy (Menetrier's disease), which, on operative biopsy of the stomach, showed a significant inflammatory component. The patient was treated with prednisone and quickly responded. Although a review of the literature revealed only two cases similarly treated, with equivocal results, spontaneous remission, does occur. Symptoms associated with this disease may respond to corticosteroids, which may offer effective therapy while awaiting involution of the gastropathy. Thus total gastrectomy may be avoided.

PMID 1918850  J Clin Gastroenterol. 1991 Aug;13(4):436-41.
著者: M Geist, A Fich, P Mogle
雑誌名: Am J Gastroenterol. 1992 May;87(5):648-50.
Abstract/Text A 33-yr-old man, with known peptic disease, developed giant thickening of the gastric mucosa and hypoproteinemia. Serial endoscopic and x-ray examinations of the upper gastrointestinal tract were available before and after the development of Menetrier's disease. In a 1-yr interval, erosive gastritis developed in a normal gastric mucosa, which was followed a few months later by hypoproteinemia. The patient developed the disease while being treated with histamine-2 receptor antagonists.

PMID 1595656  Am J Gastroenterol. 1992 May;87(5):648-50.
著者: H W Scott, H J Shull, D H Law, H Burko, D L Page
雑誌名: Ann Surg. 1975 May;181(5):765-77.
Abstract/Text Three patients with Menetrier's disease and protein-losing gastropathy who were studied during a 12 year period have been presented. The characteristic findings which differentiate them from patients with hypertrophic hypersecretory gastropathy, including the Zollinger-Ellison syndrome, are: 1) hypertrophy of gastric mucosa with giant rugal folds involving the fundus, cardia and body of the stomach but sparing the antrum; 2) muscosal hypertrophy consisting of gastric mjcus-secreting cells while parietal cells and chief cells are diminished in number and may be absent from many microscopic sections; 3) gastric secretion of large volume containing excess mucus, low to absent hydrochloric acid and protein concentration 5 or 6 times normal (1.7 mg/ml); 4) hypoalbuminemia and hypoglobulinemia due to loss of serum proteins fron gastric mucosa into the gastric lumen; 5) rare association with gastric ulcer. Unlike the Zollinger-Ellison syndrome none of our patients had duodenal ucler or multiple endocrine adenomatosis or a family history of these conditions. We have found no authenticated reports in the literature which document a relationship of Menetrier's disease ( as defined above) with multiple endocrine adenomatosis. Menetrier's disease with protein-losing gastropathy is a potentially lethal disorder of unknown cause with no specific treatment. Resection of the site of gastric protein losses as first done by Waugh is logical and effective. One of our three patients died in hospital before gastrectomy was done. Two others have done well for 11 months and 12 years, respectively, after total gastrectomy with Roux-en-Y esophagojejunostomy and Hunt-Lawrence jejunal pouch.

PMID 1130890  Ann Surg. 1975 May;181(5):765-77.
著者: T M Sundt, C C Compton, R A Malt
雑誌名: Ann Surg. 1988 Dec;208(6):694-701.
Abstract/Text Current conceptions of Ménétrier's disease only obliquely resemble those originally described. Bona-fide cases are so uncommon that, of 125 cases diagnosed as Ménétier's disease, hypertrophic gastritis, or protein-losing gastropathy treated at the Massachusetts General Hospital during the 26-year period of 1962-1987, only six cases merited an unequivocal anatomic diagnosis. Two other cases previously described proved on review to be nondiagnostic in one instance and Campylobacter pylori gastritis in the other. Because abnormalities in the secretion of gastric acid and in the loss of protein from the stomach may coexist, a representation of each case in semiquantitative terms can be described on triaxial coordinates. Three patients had a hypercoagulable state, one in association with gastric carcinoma. One other case of gastric carcinoma and one of esophageal carcinoma coexistant with Ménétrier's disease were identified. Administration of subcutaneous heparin during the perioperative period to patients with Ménétrier's disease is appropriate regardless of whether or not hypercoagulation or carcinoma is manifest. If treatment with anticholinergic drugs and inhibitors of gastric acid secretion fails, total gastrectomy is the best solution, because it stops protein loss, eliminates hyperchlorhydria, prevents development of gastric carcinoma, and permits anastomotic reconstruction between normal esophagus and normal small bowel.

PMID 3264139  Ann Surg. 1988 Dec;208(6):694-701.
著者: J S Burdick, E Chung, G Tanner, M Sun, J E Paciga, J Q Cheng, K Washington, J R Goldenring, R J Coffey
雑誌名: N Engl J Med. 2000 Dec 7;343(23):1697-701. doi: 10.1056/NEJM200012073432305.
Abstract/Text
PMID 11106719  N Engl J Med. 2000 Dec 7;343(23):1697-701. doi: 10.1056・・・
著者: Stephen H Settle, Kay Washington, Christopher Lind, Scott Itzkowitz, W Haley Fiske, J Steven Burdick, W Gray Jerome, Margaret Ray, Wilfred Weinstein, Robert J Coffey
雑誌名: Clin Gastroenterol Hepatol. 2005 Jul;3(7):654-9.
Abstract/Text BACKGROUND & AIMS: Ménétrier's disease is a rare premalignant hypertrophic gastropathy characterized by large rugal folds, foveolar hyperplasia with glandular atrophy, hypochlorhydria, and hypoalbuminemia. Patients with severe disease often exhibit refractory nausea and vomiting and require gastrectomy. Evidence from both mice and human beings suggests a critical role for epidermal growth factor receptor (EGFR) signaling in the pathogenesis of this disease. We previously reported significant clinical and biochemical improvement of a single patient treated for 1 month with Erbitux, a monoclonal antibody that blocks ligand binding to EGFR.
METHODS/RESULTS: We describe 2 patients who were given longer-term treatment with Erbitux as an alternative to gastrectomy. The first patient presented with nausea, hypoalbuminemia, and peripheral edema that required total parenteral nutrition (TPN) and infusions of albumin. On institution of Erbitux, there was rapid improvement in nausea and vomiting and stabilization of serum albumin with discontinuation of TPN and albumin infusions. Serum albumin remained stable during a 1-year course of Erbitux without supplemental protein. Application before and after Erbitux of the radiopaque dye ruthenium red to biopsies of the gastric oxyntic gland mucosa demonstrated prompt and persistent closure of tight junctions by electron microscopy. The second patient presented with chronic gastric bleeding that required bimonthly blood transfusions. During a 4-month course of Erbitux, his hematocrit stabilized, and transfusion requirements were eliminated.
CONCLUSIONS: The present report demonstrates the efficacy of prolonged Erbitux therapy in patients with different presentations of severe Ménétrier's disease and also provides insight into the pathophysiology of the protein-losing gastropathy.

PMID 16206497  Clin Gastroenterol Hepatol. 2005 Jul;3(7):654-9.
著者: J Takahata, K Okubo, T Komeda, T Kono, I Fukui
雑誌名: Digestion. 1972;5(3):153-61.
Abstract/Text
PMID 5059423  Digestion. 1972;5(3):153-61.
著者: D M Russell, P S Bhathal, D J St John
雑誌名: Gastroenterology. 1983 Jul;85(1):180-5.
Abstract/Text A case of Cronkhite-Canada syndrome, where there was complete remission confirmed by radiology, endoscopy, and histology, is reported. On presentation, there was generalized gastrointestinal polyposis, hypoalbuminemia, skin pigmentation, onycho-dystrophy, and alopecia. Enteral nutrition alone was administered for 10 wk, with resolution of the ectodermal features and disappearance of the polyps within 4 mo of commencement of the treatment. This report of complete remission supports the generally accepted nonneoplastic and essentially inflammatory nature of the polyps in Cronkhite-Canada syndrome. Consideration needs to be given to nutritional deficiency as a cause of the syndrome.

PMID 6406289  Gastroenterology. 1983 Jul;85(1):180-5.
著者: Rajagopal Chadalavada, D Kaine Brown, Anna N Walker, Shahriar Sedghi
雑誌名: Am J Gastroenterol. 2003 Jun;98(6):1444-6. doi: 10.1111/j.1572-0241.2003.07509.x.
Abstract/Text
PMID 12818298  Am J Gastroenterol. 2003 Jun;98(6):1444-6. doi: 10.1111・・・
著者: Kenta Okamoto, Hajime Isomoto, Saburo Shikuwa, Hitoshi Nishiyama, Masahiro Ito, Shigeru Kohno
雑誌名: Digestion. 2008;78(2-3):82-7. doi: 10.1159/000165354. Epub 2008 Oct 24.
Abstract/Text A 67-year-old man with nausea, appetite loss, frequent diarrhea and severe weight loss presented with alopecia, skin hyperpigmentation and onychodystrophy. Laboratory investigations showed mild anemia, hypoproteinemia and hypoalbuminemia. Colonoscopy identified the numerous, hyperemic and sessile polyps with mucous exudation of various sizes throughout the colorectum. The ileocecal valve was substantially swollen. Magnified chromoendoscopy revealed sparsely distributed crypt openings with widening of the preicryptal space without destruction in the affected lesions. Upper gastrointestinal endoscopy revealed multiple small, reddish, and sessile polyps in the duodenum and Helicobacter pylori-associated gastritis. Histopathological examination of the colonic polyps revealed cystic dilatation and elongation of scattered glands with epithelial hyperplasia and stromal edema and inflammatory cell infiltrates. Thus, a diagnosis of Cronkhite-Canada syndrome was made. The patient was given clarithromycin, amoxicillin and lansoprazole, resulting in negative (13)C-urea breath tests. Three months later, his clinical symptoms and edema of the legs resolved with normalization of serum total protein and albumin levels and return to his previous body. The ectodermal abnormalities were resolved 8 months later. On repeat colonoscopic examinations, there was progressive remission of the duodenal and colorectal polyposis, leaving scattered pedunculated polyps in the transverse and ascending colon and on the almost normal-appearing ileocecal valve. At the follow-up magnifying endoscopic examination 8 months later, small round or round-oval pits were densely and regularly distributed.

Copyright 2008 S. Karger AG, Basel.
PMID 18948692  Digestion. 2008;78(2-3):82-7. doi: 10.1159/000165354. E・・・

ページ上部に戻る

戻る

さらなるご利用にはご登録が必要です。

こちらよりご契約または優待日間無料トライアルお申込みをお願いします。

(※トライアルご登録は1名様につき、一度となります)


ご契約の場合はご招待された方だけのご優待特典があります。

以下の優待コードを入力いただくと、

契約期間が通常12ヵ月のところ、14ヵ月ご利用いただけます。

優待コード: (利用期限:まで)

ご契約はこちらから