Hypokalemic myopathy in a patient with gluten-sensitive enteropathy and dermatitis herpetiformis Duhring: A case report

The case of a 22-year-old patient with symptomatic hypokalemia caused by rhabdomyolysis is presented as a rarely reported complication of gluten-sensitive enteropathy (GSE) and dermatitis herpetiformis Duhring. The patient's myopathy ceased on potassium supplementation and her other complaints resolved while on gluten-free diet.Recovery was otherwise uneventful with a rapid decline in serum CPK level. At the time of her last follow-up a few months later, she was free of symptoms and CPK remained stable. Patients with GSE may present with hypokalemia in association with diarrhea and emesis, and if potassium loss is rapid, rhabdomyolysis may occur.

Involvement of heat shock proteins in gluten-sensitive enteropathy

Gluten-sensitive enteropathy,also known as coeliac disease(CD),is an autoimmune disorder occurring in genetically susceptible individuals that damages the small intestine and interferes with the absorption of other nutrients.As it is triggered by dietary gluten and related prolamins present in wheat,rye and barley,the accepted treatment for CD is a strict gluten-free diet.However,a complete exclusion of gluten-containing cereals from the diet is often difficult,and new therapeutic strategies are urgently needed.A class of proteins that have already emerged as drug targets for other autoimmune diseases are the heat shock proteins(HSPs),which are highly conserved stress-induced chaperones that protect cells against harmful extracellular factors.HSPs are expressed in several tissues,including the gastrointestinal tract,and their levels are significantly increased under stress circumstances.HSPs exert immunomodulatory effects,and also play a crucial role in the maintenance of epithelial cell structure and function,as they are responsible for adequate protein folding,influence the degradation of proteins and cell repair processes after damage,and modulate cell signalling,cell proliferation and apoptosis.The present review discusses the involvement of HSPs in the pathophysiology of CD.Furthermore,HSPs may represent a useful therapeutic target for the treatment of CD due to the cytoprotective,immunomodulatory,and anti-apoptotic effects in the intestinal mucosal barrier.

Clinical manifestations,diagnosis and long-term prognosis of adult autoimmune enteropathy:Experience from Peking Union Medical College Hospital

BACKGROUND Autoimmune enteropathy(AIE)is a rare disease whose diagnosis and long-term prognosis remain challenging,especially for adult AIE patients.AIM To improve overall understanding of this disease’s diagnosis and prognosis.METHODS We retrospectively analyzed the clinical,endoscopic and histopathological characteristics and prognoses of 16 adult AIE patients in our tertiary medical center between 2011 and 2023,whose diagnosis was based on the 2007 diagnostic criteria.RESULTS Diarrhea in AIE patients was characterized by secretory diarrhea.The common endoscopic manifestations were edema,villous blunting and mucosal hyperemia in the duodenum and ileum.Villous blunting(100%),deep crypt lymphocytic infiltration(67%),apoptotic bodies(50%),and mild intraepithelial lymphocytosis(69%)were observed in the duodenal biopsies.Moreover,there were other remarkable abnormalities,including reduced or absent goblet cells(duodenum 94%,ileum 62%),reduced or absent Paneth cells(duodenum 94%,ileum 69%)and neutrophil infiltration(duodenum 100%,ileum 69%).Our patients also fulfilled the 2018 diagnostic criteria but did not match the 2022 diagnostic criteria due to undetectable anti-enterocyte antibodies.All patients received glucocorticoid therapy as the initial medication,of which 14/16 patients achieved a clinical response in 5(IQR:3-20)days.Immunosuppressants were administered to 9 patients with indications of steroid dependence(6/9),steroid refractory status(2/9),or intensified maintenance medication(1/9).During the median of 20.5 months of followup,2 patients died from multiple organ failure,and 1 was diagnosed with non-Hodgkin’s lymphoma.The cumulative relapse-free survival rates were 62.5%,55.6%and 37.0%at 6 months,12 months and 48 months,respectively.CONCLUSION Certain histopathological findings,including a decrease or disappearance of goblet and Paneth cells in intestinal biopsies,might be potential diagnostic criteria for adult AIE.The long-term prognosis is still unsatisfactory despite corticosteroid and immunosuppressant medications,which highlights the need for early diagnosis and novel medications.

Pathogenesis of chronic enteropathy associated with the SLCO2A1 gene:Hypotheses and conundrums

Chronic enteropathy associated with the SLCO2A1 gene(CEAS)is a complex gastroenterological condition characterized by multiple ulcers in the small intestine with chronic bleeding and protein loss.This review explores the potential mechanisms underlying the pathogenesis of CEAS,focusing on the role of SLCO2A1-encoded prostaglandin transporter OATP2A1 and its impact on prostaglandin E2(PGE2)levels.Studies have suggested that elevated PGE2 levels contribute to mucosal damage,inflammation,and disruption of the intestinal barrier.The effects of PGE2 on macrophage activation and Maxi-Cl channel functionality,as well as its interaction with nonsteroidal anti-inflammatory drugs play crucial roles in the progression of CEAS.Understanding the balance between its protective and pro-inflammatory effects and the complex interactions within the gastrointestinal tract can shed light on potential therapeutic targets for CEAS and guide the development of novel,targeted therapies.

Autoantibodies related to ataxia and other central nervous system manifestations of gluten enteropathy

Gluten ataxia and other central nervous system disorders could be linked to gluten enteropathy and related autoantibodies.In this narrative review,we focus on the various neuro-logical manifestations in patients with gluten sensitivity/celiac disease,immunological and autoimmune mechanisms of ataxia in connection to gluten sensitivity and the autoantibodies that could be used as a biomarker for diagnosing and following.We focused on the anti-gliadin antibodies,antibodies to different isoforms of tissue transglutaminase(TG)(anti-TG2,3,and 6 antibodies),anti-glycine receptor antibodies,anti-glutamine acid decarboxylase antibodies,anti-deamidated gliadin peptides antibodies,etc.Most studies found a higher prevalence of these antibodies in patients with gluten sensitivity and neurological dysfunction,presented as different neurological disorders.We also discuss the role of a gluten-free diet on the clinical improvement of patients and also on imaging of these disorders.

Eosinophilic enteritis requiring differentiation from chronic enteropathy associated with SLCO2A1 gene:A case report

BACKGROUND Eosinophilic gastrointestinal disease(EGID)is a disorder characterized by infiltration of eosinophils causing mucosal damage and dysfunction of the gastrointestinal tract.The endoscopic findings of eosinophilic enteritis(EoN),an EGID variant,are nonspecific and occasionally difficult to diagnose.In contrast,chronic enteropathy associated with SLCO2A1(CEAS)is a chronic persistent small intestinal disorder characterized by endoscopic findings such as multiple oblique and circular ulcers.CASE SUMMARY We report the case of a 10-year-old boy who had suffered abdominal pain and fatigue for the preceding 6 mo.He was referred to our institute for investigation of suspected gastrointestinal bleeding because of severe anemia with hypoproteinemia and positive fecal human hemoglobin.The upper and lower gastrointestinal endoscopic findings were normal;however,double-balloon small bowel endoscopy showed multiple oblique and circular ulcers with discrete margins and mild constriction of the intestinal lumen in the ileum.The findings were highly consistent with CEAS,but urine prostaglandin metabolites were within normal limits,and no previously reported mutations in the SLCO2A1 gene were identified.Histological evaluation demonstrated moderate to severe eosinophilic infiltration localized to the small intestine suggesting a diagnosis of EoN.Clinical remission was maintained with montelukast and a partial elemental diet,but emergent surgery for bowel obstruction due to small intestinal stenosis was performed two years after the initial treatment.CONCLUSION EoN should be considered in the differential diagnosis of CEAS-like small intestinal ulcerative lesions and normal urinary prostaglandin metabolite levels.

清热利湿方联合美沙拉嗪治疗湿热内蕴证糖尿病肠病临床疗效观察

目的探讨清热利湿方治疗糖尿病肠病疗效及对患者生活质量的影响。方法将48例湿热内蕴证糖尿病肠病患者按随机数字表法分观察组和对照组,每组24例;两组均口服美沙拉嗪肠溶片,观察组加予清热利湿方日2次口服治疗,统计肠炎疾病量表(inflammatory bowel disease questionnaire,IBDQ)评分及相关症状体征。结果观察组与对照组IBDQ评分各分项得分治疗后均高于治疗前,但观察组分数增加较为明显,且观察组在全身症状、肠道症状、情感功能、社会功能、总分等方面得分增加均高于对照组,在全身症状改善方面尤为显著。两组在生活质量量表(the MOS item short from health survey,SF-36)量表中生理机能(physical functioning,PF)、生理职能(role physical,RP)、活力(vitality,VT)、精神健康(mental health,MH)、整体健康(general health,GH)等方面治疗前与治疗后差异有统计学意义(均P<0.05)。观察组总有效率91.67%(22/24),两组间疗效比较差异有统计学意义(P<0.05)。两组病例均耐受良好,未见明显不良反应,1年内复发率观察组低于对照组(均P<0.05)。结论清热利湿方可以有效清热利湿,改善患者病情,是针对糖尿病肠病的一种有效治疗方案,可以提高湿热内蕴证糖尿病肠病患者的治疗有效率,明显提高患者的生活质量,值得临床进一步研究及推广。

慢性日本血吸虫性结直肠癌的临床病理特征分析

目的探讨慢性日本血吸虫性结直肠癌的临床病理特征。方法选取2017年1月至2022年12月广德市人民医院与皖南医学院附属弋矶山医院收治的176例慢性日本血吸虫性结直肠癌患者作为观察组,以同期收治的1245例单纯性结直肠癌患者作为对照组。收集两组患者的性别、年龄及病理资料,采用t检验及χ^(2)检验分析慢性日本血吸虫性结直肠癌的临床病理特征。结果观察组患者中男性占68.75%、患病年龄(68.46±10.524)岁,明显高于对照组的58.8%及(63.46±11.281)岁,差异均具有统计学意义(P<0.05);观察组患者的肿瘤细胞低分化、T3~T4期、TNM分期为Ⅲ~Ⅳ期的占比分别为18.2%、83.0%、46.6%,明显高于对照组的12.2%,75.7%,38.0%,差异均具有统计学意义(P<0.05)。结论慢性日本血吸虫性结直肠癌患者的男性比例及年龄较高,TNM分期更高,预后不良。

Fontan循环的新时代——远期淋巴系统并发症研究进展

全腔静脉-肺动脉连接术(Fontan姑息手术)挽救了大量单心室结构患儿的生命。然而,术后远期淋巴系统并发症严重影响着患者的预后。现回顾既往相关文献,总结Fontan术后患者淋巴系统并发症的自然病程、病理生理、临床表现、诊断和治疗管理。

Experience of primary intestinal lymphangiectasia in adults: Twelve case series from a tertiary referral hospital

BACKGROUND While primary intestinal lymphangiectasia(PIL)is considered a rare condition,there have been several reported cases in adults.Nevertheless,the absence of clear guidance from diagnosis to treatment and prognosis poses challenges for both physicians and patients.AIM To enhance understanding by investigating clinical presentation,diagnosis,treatment,complications,and prognoses in adult PIL cases.METHODS We enrolled adult patients diagnosed with PIL between March 2016 and September 2021.The primary outcome involved examining the diagnosis and treatment process of these patients.The secondary outcomes included identifying complications(infections,thromboembolism)and assessing prognoses(frequency of hospitalization and mortality)during the follow-up period.RESULTS Among the 12 included patients,peripheral edema(100%)and diarrhea(75%)were the main presenting complaints.Laboratory tests showed that all the pati-ents exhibited symptoms of hypoalbuminemia and hypogammaglobulinemia.Radiologically,the predominant findings were edema of the small intestine(67%)and ascites(58%).The typical endoscopic finding with a snowflake appearance was observed in 75%of patients.Among the 12 patients,two responded positive-ly to octreotide and sirolimus,and eight who could undergo maintenance therapy discontinued subsequently.Complications due to PIL led to infection in half of the patients,thromboembolism in three patients,and one death.CONCLUSION PIL can be diagnosed in adults across various age groups,with different severity and treatment responses among patients,leading to diverse complications and prognoses.Consequently,tailored treatments will be necessary.We anticipate that our findings will contribute to the management of PIL,an etiology of protein-losing enteropathy.

肠道移植物抗宿主病中医辨识与实践

[目的]总结钦丹萍教授运用中医药治疗肠道移植物抗宿主病的经验。[方法]通过跟师临证,收集、整理医案,从疾病认识、证候变迁、临证化裁方面总结钦丹萍教授临床治疗肠道移植物抗宿主病的学术特色,并附医案加以佐证。[结果]钦丹萍教授认为,接受移植的患者机体为本体,移植的异基因造血干细胞为客体,肠道移植物抗宿主病以脾虚为本,移植后客体入里化生湿、热、寒、瘀、毒而为标,正邪相争,作用于肠道而为病,病机为本虚标实。治疗方面强调标本兼治,针对本虚,以健脾益气为基本原则;针对标实,重在化解湿热寒瘀毒,以使正邪相容而疾病得安。所举医案分别为胃肠急性移植物抗宿主病和肠道慢性移植物抗宿主病,分别治以健脾清化、和中止泻与平调寒热、健脾止泻,收效甚佳。[结论]钦丹萍教授以本体客体相容为目标,以“扶正化邪”为核心治疗肠道移植物抗宿主病,在改善患者临床症状及缓解肠道黏膜炎症方面疗效显著,值得进一步探索学习。

Portal hypertensive enteropathy

Portal hypertensive enteropathy(PHE) is a condition that describes the pathologic changes and mucosal abnormalities observed in the small intestine of patients with portal hypertension. This entity is being increasingly recognized and better understood over the past decade due to increased accessibility of the small intestine made possible by the introduction of video capsule endoscopy and deep enteroscopy. Though challenged by its diverse endoscopic appearance, multiple scoring systems have been proposed to classify the endoscopic presentationand grade its severity. Endoscopic findings can be broadly categorized into vascular and non-vascular lesions with many subtypes of both categories. Clinical manifestations of PHE can range from asymptomatic incidental findings to fatal gastrointestinal hemorrhage. Classic endoscopic findings in the setting of portal hypertension may lead to a prompt diagnosis. Occasionally histopathology and cross sectional imaging like computed tomography or magnetic resonance imaging may be helpful in establishing a diagnosis. Management of overt bleeding requires multidisciplinary approach involving hepatologists, endoscopists, surgeons, and interventional radiologists. Adequate resuscitation, reduction of portal pressure, and endoscopic therapeutic intervention remain the main principles of the initial treatment. This article reviews the existing evidence on PHE with emphasis on its classification, diagnosis, clinical manifestations, endoscopic appearance, pathological findings, and clinical management. A new schematic management of ectopic variceal bleed is also proposed.

Significance of endothelial dysfunction in the pathogenesis of early and delayed radiation enteropathy

This review summarizes the current state of knowledge regarding the role of endothelial dysfunction in the pathogenesis of early and delayed intestinal radiation toxicity and discusses various endothelial-oriented interventions aimed at reducing the risk of radiation enteropathy. Studies published in the biomedical literature during the past four decades and cited in PubMed, as well as clinical and laboratory data from our own research program are reviewed. The risk of injury to normal tissues limits the cancer cure rates that can be achieved with radiation therapy. During treatment of abdominal and pelvic tumors, the intestine is frequently a major close-limiting factor. Microvascular injury is a prominent feature of both early （inflammatory）, as well as delayed （fibroproliferative） radiation injuries in the intestine and in many other normal tissues. Evidence from our and other laboratories suggests that endothelial dysfunction, notably a deficiency of endothelial thrombomodulin, plays a key role in the pathogenesis of these radiation responses. Deficient levels of thrombomodulin cause loss of vascular thromboresistance, excessive activation of cellular thrombin receptors by thrombin, and insufficient activation of protein C, a plasma protein with anticoagulant, anti-inflammatory, and cytoprotective properties. These changes are presumed to be critically involved in many aspects of early intestinal radiation toxicity and may sustain the fibroproliferative processes that lead to delayed intestinal dysfunction, fibrosis, and clinical complications. In conclusion, injury of vascular endothelium is important in the pathogenesis of the intestinal radiation response. Endothelial-oriented interventions are appealing strategies to prevent or treat normal tissue toxicity associated with radiation treatment of cancer.

Mucosal healing effect of mesalazine granules in naproxen-induced small bowel enteropathy

AIM:To investigate the effect of mesalazine granules on small intestinal injury induced by naproxen using capsule endoscopy (CE).METHODS:This was a single center,non-randomized,open-label,uncontrolled pilot study,using the PillCam SB CE system with RAPID 5 software.The Lewis Index Score (LIS) for small bowel injury was investigated to evaluate the severity of mucosal injury.Arthropathy patients with at least one month history of daily naproxen use of 1000 mg and proton pump inhibitor co-therapy were screened.Patients with a minimum LIS of 135 were eligible to enter the 4-wk treatment phase of the study.During this treatment period,3 × 1000 mg/d mesalazine granules were added to ongoing therapies of 1000 mg/d naproxen and 20 mg/d omeprazole.At the end of the 4-wk combined treatment period,a second small bowel CE was performed to re-evaluate the enteropathy according to the LIS results.The primary objective of this study was to assess the mucosal changes after 4 wk of mesalazine treatment.RESULTS:A total of 18 patients (16 females),ranging in age from 46 to 78 years (mean age 60.3 years) were screened,all had been taking 1000 mg/d naproxen for at least one month.Eight patients were excluded from the mesalazine therapeutic phase of the study for the following reasons:the screening CE showed normal small bowel mucosa or only insignificant damages (LIS < 135) in five patients,the screening esophagogastroduodenoscopy revealed gastric ulcer in one patient,capsule technical failure and incomplete CE due to poor small bowel cleanliness in two patients.Ten patients (9 female,mean age 56.2 years) whose initial LIS reached mild and moderate-to-severe enteropathy grades (between 135 and 790 and ≥ 790) entered the 4-wk therapeutic phase and a repeat CE was performed.When comparing the change in LIS from baseline to end of treatment in all patients,a marked decrease was seen (mean LIS:1236.4 ± 821.9 vs 925.2 ± 543.4,P=0.271).Moreover,a significant difference between pre-and post-treatment mean total LIS was detected in 7 patients who had moderate-tosevere enteropathy gradings at the inclusion CE (mean LIS:1615 ± 672vs 1064 ± 424,P=0.033).CONCLUSION:According to the small bowel CE evaluation mesalazine granules significantly attenuated mucosal injuries in patients with moderate-to-severe enteropathies induced by naproxen.

Late post liver transplant protein losing enteropathy: Rare complication of incisional hernia

Development of oedema and hypoproteinaemia in a liver transplant recipient may be the first signs of graft dysfunction and should prompt a full assessment. We report the novel case of a patient who, years after liver transplantation developed a functional blind loop in an incisional hernia, which manifested as oedema and hypoproteinaemia secondary to protein losing enteropathy. After numerous investigations, the diagnosis was made by flurodeoxyglucose positron emmision tomography (FDG-PET) imaging. Surgical repair of the incisional hernia was followed several months later by resolution of the protein loss, and confirmed at a post operative FDG-PET scan at one year.

Long-term prognosis in patients with severe late radiation enteropathy:A prospective cohort study

AIM: To assess persistent symptoms and mortality in a cohort of patients with severe (grade 3-4) radiation enteropathy,59 patients were followed up after 15-18 years. METHODS: Fifty-nine patients were prospectively enrolled by twelve surgical departments. Primary malignant disease,radiation therapy and surgical management were recorded at inclusion. The cause of death or persistence of symptoms was examined in public death records or by interview of survivors. RESULTS: Thirty-nine patients had received radiation therapy for gynaecological cancers,twelve for urological cancers,four for gastrointestinal cancers and four for other malignancies. Forty-five patients (76%) required surgical intervention. Complications occurred in 11 (25%) operated patients. Forty-seven patients had died at the time of follow-up,seven (12%) died as a direct result of radiation enteropathy,while radiation enteropathy contributed to death in an additional seven patients. Four of the twelve surviving patients suffered from chronic debilitating symptoms of radiation enteropathy,while three had moderate symptoms. CONCLUSION: Patients with severe delayed radiation enteropathy have a high risk of persistence of symptoms after surgery. At least one in ten patients dies from radiation-induced bowel injury.

Protein-loosing enteropathy associated with rotavirus infection in an infant

Rotavirus is an acute enteric pathogen in infants and children. We reported a rare case of a 6-mo-old infant with protein-loosing enteropathy (PLE) caused by rotavirus gastroenteritis, and evaluated the immunological profile in peripheral blood lymphocytes. Laboratory examinations showed lymphopenia, hypoproteinemia, hypoalbuminemia, hypogammaglobulinemia, and elevation of alpha-1-antitrypsin (α1-AT) clearance. Lymphocytes subpopulation study revealed the reversal of CD4+/CD8+ ratio with the selective decrease of CD4- positive lymphocytes. Moreover, the excessive increase of T cells producing IFN-gamma (IFN-γ) was found, which plays an important role in the protection against viral infection. The primary or secondary activation of immune system by rotavirus may influence structural integrity and vascular permeability, which may play a triggering role in protein-loosing enteropathy.

Fibrinogen deficiency suppresses the development of early and delayed radiation enteropathy

To determine the mechanistic role of fibrinogen, a key regulator of inflammation and fibrosis, in early and delayed radiation enteropathy. METHODSFibrinogen wild-type (Fib+/+), fibrinogen heterozygous (Fib+/-), and fibrinogen knockout (Fib-/-) mice were exposed to localized intestinal irradiation and assessed for early and delayed structural changes in the intestinal tissue. A 5-cm segment of ileum of mice was exteriorized and exposed to 18.5 Gy of x-irradiation. Intestinal tissue injury was assessed by quantitative histology, morphometry, and immunohistochemistry at 2 wk and 26 wk after radiation. Plasma fibrinogen level was measured by enzyme-linked immunosorbent assay. RESULTSThere was no difference between sham-irradiated Fib+/+ and Fib+/- mice in terms of fibrinogen concentration in plasma and intestinal tissue, intestinal histology, morphometry, intestinal smooth muscle cell proliferation, and neutrophil infiltration. Therefore, Fib+/- mice were used as littermate controls. Unlike sham-irradiated Fib+/+ and Fib+/- mice, no fibrinogen was detected in the plasma and intestinal tissue of sham-irradiated Fib-/- mice. Moreover, fibrinogen level was not elevated after irradiation in the intestinal tissue of Fib-/- mice, while significant increase in intestinal fibrinogen level was noticed in irradiated Fib+/+ and Fib+/- mice. Importantly, irradiated Fib-/- mice exhibited substantially less overall intestinal structural injury (RIS, P = 0.000002), intestinal wall thickness (P = 0.003), intestinal serosal thickness (P = 0.009), collagen deposition (P = 0.01), TGF-β immunoreactivity (P = 0.03), intestinal smooth muscle proliferation (P = 0.046), neutrophil infiltration (P = 0.01), and intestinal mucosal injury (P = 0.0003), compared to irradiated Fib+/+ and Fib+/- mice at both 2 wk and 26 wk. CONCLUSIONThese data demonstrate that fibrinogen deficiency directly attenuates development of early and delayed radiation enteropathy. Fibrinogen could be a novel target in treating intestinal damage.

Gluten sensitive enteropathy in patients with iron deficiency anemia of unknown origin

AIM: To determine the prevalence of gluten sensitive enteropathy (GSE) in a large group of patients with iron deficiency anemia (IDA) of obscure origin. METHODS: In this cross-sectional study, patients with IDA of obscure origin were screened for GSE. Anti- endomysial antibody (EMA) and tissue transglutamin- ase antibody (tTG) levels were evaluated and duodenal biopsies were taken and scored according to the Marsh classification. The diagnosis of GSE was based on a positive serological test and abnormal duodenal histol- ogy. Gluten free diet (GFD) was advised for all the GSE patients. RESULTS: Of the 4120 IDA patients referred to our Hematology departments, 206 (95 male) patients were found to have IDA of obscure origin. Thirty out of 206 patients (14.6%) had GSE. The mean age of GSE pa- tients was 34.6 ± 17.03 (range 10-72 years). The female to male ratio was 1.3:1. Sixteen patients had Marsh 3,12 had Marsh 2, and 2 had Marsh 1 lesions. The sever- ity of anemia was in parallel with the severity of duode- nal lesions. Twenty-two GSE patients (73.3%) had no gastrointestinal symptoms. Fourteen GSE patients who adhered to GFD without receiving iron supplementation agreed to undergo follow up visits. After 6 mo of GFD, their mean hemoglobin levels (Hb) increased from 9.9 ± 1.6 to 12.8 ± 1.0 g/dL (P < 0.01). Interestingly, in 6 out of 14 patients who had Marsh 1/2 lesions (e.g. no villous atrophy) on duodenal biopsy, mean Hb increased from 11.0 ± 1.1 to 13.1 ± 1.0 g/dL (P < 0.01) while they did not receive any iron supplementation. CONCLUSION: There is a high prevalence (e.g. 14.6%) of GSE in patients with IDA of obscure origin. Gluten free diet can improve anemia in GSE patients who have mild duodenal lesions without villous atrophy.

A unique case of collagenous colitis presenting as protein-losing enteropathy successfully treated with prednisolone

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.