DOCSLIB.ORG

Collagenous Gastritis: a Case Report, Morphologic Evaluation, and Review Z

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Collagenous Gastritis: a Case Report, Morphologic Evaluation, and Review Z CASE REPORT Collagenous Gastritis: A Case Report, Morphologic Evaluation, and Review Z. Vesoulis, M.D., Gerard Lozanski, M.D., Pars Ravichandran, M.D., Edward Esber, M.D. Departments of Pathology (ZV, GL, PR) and Gastroenterology (EE), Summa Health Systems, Akron, Ohio dently identified by using analogous defined fea- Collagenous gastritis is rare; there are only four tures of collagenous colitis: subepithelial collagen previous case reports. Histologic features seem to more than 10 ␮ in a patchy distribution, lamina overlap with the other “collagenous enterocoliti- propria lymphoplasmacytic infiltrates, intraepithe- des”; however, pathologic criteria are not yet estab- lial lymphocytes, and surface epithelial damage. lished for the diagnosis of collagenous gastritis. We Collagenous gastritis also seems to have the same describe an additional case of ostensible collage- spectrum of associated clinical findings as collage- nous gastritis in a patient who initially presented nous colitis, including frequent coexistence of celiac with celiac sprue and subsequently developed co- sprue, watery diarrhea syndrome, and female pre- lonic manifestations of mucosal ulcerative colitis. dominance. Endoscopic biopsies of the stomach revealed depo- sition of patchy, very thick bandlike subepithelial KEY WORDS: Celiac sprue, Collagenous colitis, Col- collagen in gastric antral mucosa, focal superficial lagenous gastritis, Lymphocytic colitis, Lympho- epithelial degeneration, numerous intraepithelial cytic gastritis, Mucosal ulcerative colitis. lymphocytes, and a dense lamina propria lymphop- Mod Pathol 2000;13(5):591–596 lasmacytic infiltrate. Image analysis evaluation of gastric antral biopsies demonstrated a mean thick- Collagenous colitis, first described by Lindstrom in ness of subepithelial collagen of 27.07 ␮. Morpho- 1976 (1), is an inflammatory bowel lesion; diagnosis logic comparison was made with age-matched con- requires the clinical presentation of chronic watery trol groups of 10 patients who had normal gastric diarrhea, an endoscopically normal or “near nor- mucosal biopsies and 10 patients who had “chron- mal” mucosa and colon biopsy with subepithelial ic” gastritis, which revealed mean subepithelial col- collagen deposition, chronic inflammation, and ep- lagen measures of 1.37 ␮ and 1.19 ␮, respectively. ithelial degeneration. Collagenous colitis is proba- We compared these morphologic findings with bly an autoimmune disorder (2–6), although re- those of all previous case reports of collagenous cently other potential causes have been proposed gastritis and propose a pathologic definition based and include bacterial toxins, cytotoxins, nonsteroi- on the limited combined data. It seems that subep- dal anti-inflammatory drugs, infectious agents, and ithelial collagen is dramatically thickened in re- antibiotics (7–10). ported cases of collagenous gastritis, with a cumu- “Collagenous” sprue was originally described as a lative mean measure of 36.9 ␮. ⌱t is also apparent variant of typical sprue with villous atrophy, prom- from this and previous reports that the thickened inent subepithelial collagen deposition, and refrac- subepithelial collagen is accompanied by a chronic toriness to a gluten-free diet (11). Some degree of or chronic active gastritis and sometimes intraepi- collagen deposition in sprue may be a common and thelial lymphocytes and surface epithelial damage. relatively nonspecific finding that occurs without Recently described associations of lymphocytic gas- alteration of the typical clinical course (12). tritis, sprue, and lymphocytic colitis as well as col- Collagen deposition in gastric mucosa has rarely lagenous and lymphocytic colitis suggest a common been described; there are four case reports to date, pathogenesis that empirically may include collage- and no detailed pathologic descriptions or diagnos- nous gastritis in the same disease spectrum. We tic criteria have been elucidated (13–16). We de- propose that collagenous gastritis can be confi- scribe a case of collagenous gastritis that developed in association with celiac disease and ulcerative colitis. Careful morphometric comparison of this Copyright © 2000 by The United States and Canadian Academy of Pathology, Inc. case and control groups of normal gastric antral VOL. 13, NO. 5, P. 591, 2000 Printed in the U.S.A. biopsies and “chronic gastritis” cases illustrates the Date of acceptance: November 2, 1999. Address reprint requests to: Dr. Vesoulis, Department of Pathology, striking and overt subepithelial collagen deposition Summa Health Systems, 525 E. Market Street, Akron, OH 44304. that delineates this unusual lesion. We also review 591 and compare the clinical and pathologic features of strict emphasis on maintaining a gluten-free diet, other reported cases of collagenous gastritis and his diarrhea and hematochezia resolved. Antiglia- attempt to derive unifying features and histopatho- din and antiendomysial antibodies were negative in logic criteria that characterize this lesion. The rela- follow-up studies. tionship and frequent co-occurrence of collagenous gastritis, collagenous and lymphocytic colitis, and sprue is also examined. MATERIALS AND METHODS Five endoscopic biopsies from the stomach, 6 CASE REPORT biopsies from the small intestine, and 15 biopsies from the colon were received in 10% buffered for- A 57-year-old Caucasian man presented with a malin and processed for histologic evaluation in the hypochromic, microcytic anemia and loose stools typical manner. All sections were stained with he- for several months. He experienceda5lbweight matoxylin and eosin, and sections of the stomach loss and denied abdominal pain. His medical his- were additionally stained with Masson’s trichrome, tory was remarkable for coronary artery disease and Giemsa, and Warthin-Starry silver stains. Immu- lower extremity vascular surgery. There was no his- nohistochemical staining with a selected panel tory of food allergies, arthritis, or autoimmune dis- of antibodies, including CD3, UCHL-1(CD45ro), ease. His initial workup included an unremarkable L-26 (CD20), and ␬ and ␭, were performed on colonoscopy, but 4 months later, after persistence all biopsies. Immunostaining incorporated the of loose stools, continued weight loss, and anemia, streptavidin-biotin-peroxidase method after over- an upper gastrointestinal and small bowel series night incubation in humidity chambers at 4° C. A demonstrated small bowel dilation. Repeat esopha- microwave antigen retrieval method was used with gogastric duodenoscopy (EGD) with biopsy of the all antibodies. Slides were immersed in 200 mL of small intestine revealed a severe mucosal villous APK (Ventana Corp., Tucson, AZ) microwave buffer abnormality. Antigliadin IgG and IgA was elevated and heated in an 800 W microwave oven using a (Ͼ15 EIA units) and antiendomysial IgA was ele- high setting for 5 min. Fifty milliliters of deionized vated (Ͼ1:5). The patient was treated with a gluten- water was added to replace evaporated water from free diet; symptoms resolved, but intermittent heating, and slides were microwaved for an addi- flares of diarrhea continued. Strict adherence to a tional 5 min before automated immunostaining on gluten-free diet was considered questionable for the Ventana Nexes (Ventana Corp.). Control tissues this patient. Repeat upper endoscopy with biopsies with established reactivity were stained concomi- revealed a persistent mild villous abnormality with- tantly. Morphometric measurements of subepithe- out significant collagen deposition. The patient was lial collagen in the hematoxylin and eosin and not rechallenged with gluten. Another colonoscopy trichrome sections of the stomach were performed was performed after the patient once again pre- on the CAS 200 image analyzer (Becton-Dickinson, sented with diarrhea. Stool cultures were negative San Jose, CA). Mean measures for each gastric frag- for bacterial infection, ova, and parasites, and C. ment were determined by two independent observ- difficile toxin assays were negative. Colon biopsy ers (GL and PR) using Ocular Micrometer v.1 soft- revealed a “nonspecific” increase in the inflamma- ware (Cell Analysis Systems, Elmhurst, IL). Only tory content of the lamina propria. The patient biopsy fragments with optimal orientation were continued to have intermittent bouts of moderate used in measurements to avoid the artifactual diarrhea and eventually developed bloody diarrhea. thickening introduced by tangential sections. Each Colonoscopy performed at this time revealed of the five optimally oriented gastric tissue frag- marked erythema with granularity and ulceration of ments was measured in at least three separate areas the entire colon. Biopsies were taken from proxi- representing the thickest visually determined zones mal, transverse, and distal colon and rectum. Pe- of subepithelial collagen. Each measurement con- rinuclear antineutrophilic cytoplasmic antibody sisted of 10 independent readings in each of the (pANCA) was positive (Ͼ1:160), and cytoplasmic three selected zones. Deposition of excessive colla- antineutrophilic cytoplasmic antibody (cANCA) gen at each point of measurement was confirmed was negative (Ͻ1:20). Serum IgA was elevated at by comparison with Masson’s trichrome stain of 682 mg/dL (range, 89 to 446 mg/dl). and IgG, IgM, parallel sections. Because there is no standard for complement C3, C4, antinuclear antibody, antithy- excessive thickness of subepithelial collagen in gas- roglobulin, and antimicrosomal antibodies were tric
Load more

Recommended publications
  • Inflammatory Bowel Disease Irritable Bowel Syndrome
    Inflammatory Bowel Disease and Irritable Bowel Syndrome Similarities and Differences 2 www.ccfa.org IBD Help Center: 888.MY.GUT.PAIN 888.694.8872 Important Differences Between IBD and IBS Many diseases and conditions can affect the gastrointestinal (GI) tract, which is part of the digestive system and includes the esophagus, stomach, small intestine and large intestine. These diseases and conditions include inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). IBD Help Center: 888.MY.GUT.PAIN 888.694.8872 www.ccfa.org 3 Inflammatory bowel diseases are a group of inflammatory conditions in which the body’s own immune system attacks parts of the digestive system. Inflammatory Bowel Disease Inflammatory bowel diseases are a group of inflamma- Causes tory conditions in which the body’s own immune system attacks parts of the digestive system. The two most com- The exact cause of IBD remains unknown. Researchers mon inflammatory bowel diseases are Crohn’s disease believe that a combination of four factors lead to IBD: a (CD) and ulcerative colitis (UC). IBD affects as many as 1.4 genetic component, an environmental trigger, an imbal- million Americans, most of whom are diagnosed before ance of intestinal bacteria and an inappropriate reaction age 35. There is no cure for IBD but there are treatments to from the immune system. Immune cells normally protect reduce and control the symptoms of the disease. the body from infection, but in people with IBD, the immune system mistakes harmless substances in the CD and UC cause chronic inflammation of the GI tract. CD intestine for foreign substances and launches an attack, can affect any part of the GI tract, but frequently affects the resulting in inflammation.
    [Show full text]
  • Dyspepsia (Indigestion)
    Indigestion (dydpepsia). Indigestion information - Patient | Patient Page 1 of 5 View this article online at https://patient.info/health/dyspepsia-indigestion Dyspepsia (Indigestion) Dyspepsia (indigestion) is a term which describes pain and sometimes other symptoms which come from your upper gut (the stomach, oesophagus or duodenum). There are various causes (described below). Treatment depends on the likely cause. Understanding digestion Food passes down the gullet (oesophagus) into the stomach. The stomach makes acid which is not essential but helps to digest food. Food then passes gradually into the first part of the small intestine (the duodenum). In the duodenum and the rest of the small intestine, food mixes with chemicals called enzymes. The enzymes come from the pancreas and from cells lining the intestine. The enzymes break down (digest) the food. Digested food is then absorbed into the body from the small intestine. What is dyspepsia? Dyspepsia is a term which includes a group of symptoms that come from a problem in your upper gut. The gut (gastrointestinal tract) is the tube that starts at the mouth and ends at the anus. The upper gut includes the oesophagus, stomach and duodenum. Various conditions cause dyspepsia. The main symptom is usually pain or discomfort in the upper tummy (abdomen). In addition, other symptoms that may develop include: • Bloating. • Belching. • Quickly feeling full after eating. • Feeling sick (nausea). • Being sick (vomiting). Symptoms are often related to eating. Doctors used to include heartburn (a burning sensation felt in the lower chest area) and bitter-tasting liquid coming up into the back of the throat (sometimes called 'waterbrash') as symptoms of dyspepsia.
    [Show full text]
  • Microscopic Colitis: Collagenous Colitis and Lymphocytic Colitis
    Microscopic Colitis: Collagenous Colitis and Lymphocytic Colitis National Digestive Diseases Information Clearinghouse What is microscopic colitis? The term bowel refers to any part of the small or large intestine. The large intes- Microscopic colitis is inflammation of the tine includes the colon and the rectum, and bowel that is only visible using a microscope. together they are about 5 feet long. The Microscopic colitis is a type of inflammatory U.S. Department small intestine can be 12 to 20 feet long. bowel disease (IBD), which refers to a group of Health and Colitis means inflammation of the colon. Human Services of conditions that causes inflammation in the Microscopic colitis is inflammation of the bowel due to an excessive build-up of white colon and rectum. NATIONAL blood cells in the bowel lining. Microscopic INSTITUTES OF HEALTH colitis is less severe than other types of IBD because it does not lead to cancer and rarely What are collagenous colitis requires surgery. However, microscopic and lymphocytic colitis? colitis can cause considerable pain and Microscopic colitis has two main forms: discomfort. collagenous colitis and lymphocytic colitis. The symptoms of and treatment for both are identical. Some scientists believe the two forms may be different presentations of the same disease. Slight differences in the way intestinal tissues appear when seen with a microscope set them apart. In both forms, an increase in white blood cells can be seen within the intestinal epithelium—the layer of Stomach Liver cells that lines the intestine. Increased white blood cells are a sign of inflammation. But with collagenous colitis, the layer of collagen Colon (shaded) beneath the epithelium appears thicker than normal.
    [Show full text]
  • Abdominal Pain - Gastroesophageal Reflux Disease
    ACS/ASE Medical Student Core Curriculum Abdominal Pain - Gastroesophageal Reflux Disease ABDOMINAL PAIN - GASTROESOPHAGEAL REFLUX DISEASE Epidemiology and Pathophysiology Gastroesophageal reflux disease (GERD) is one of the most commonly encountered benign foregut disorders. Approximately 20-40% of adults in the United States experience chronic GERD symptoms, and these rates are rising rapidly. GERD is the most common gastrointestinal-related disorder that is managed in outpatient primary care clinics. GERD is defined as a condition which develops when stomach contents reflux into the esophagus causing bothersome symptoms and/or complications. Mechanical failure of the antireflux mechanism is considered the cause of GERD. Mechanical failure can be secondary to functional defects of the lower esophageal sphincter or anatomic defects that result from a hiatal or paraesophageal hernia. These defects can include widening of the diaphragmatic hiatus, disturbance of the angle of His, loss of the gastroesophageal flap valve, displacement of lower esophageal sphincter into the chest, and/or failure of the phrenoesophageal membrane. Symptoms, however, can be accentuated by a variety of factors including dietary habits, eating behaviors, obesity, pregnancy, medications, delayed gastric emptying, altered esophageal mucosal resistance, and/or impaired esophageal clearance. Signs and Symptoms Typical GERD symptoms include heartburn, regurgitation, dysphagia, excessive eructation, and epigastric pain. Patients can also present with extra-esophageal symptoms including cough, hoarse voice, sore throat, and/or globus. GERD can present with a wide spectrum of disease severity ranging from mild, intermittent symptoms to severe, daily symptoms with associated esophageal and/or airway damage. For example, severe GERD can contribute to shortness of breath, worsening asthma, and/or recurrent aspiration pneumonia.
    [Show full text]
  • Practical Approach to Microscopic Colitis and Inflammatory Bowel Disease
    INFLAMMATORY BOWEL DISEASE: A PRACTICAL APPROACH, SERIES #15 Seymour Katz, M.D., Series Editor Practical Approach to Microscopic Colitis and Inflammatory Bowel Disease by Noel R. Fajardo and Darrell S. Pardi INTRODUCTION The prevalence of IBD, on the other hand, is higher nflammatory disorders of the intestines can be than microscopic colitis, reflecting the younger age of divided into those with macroscopic mucosal onset in patients with IBD. Ichanges (the traditional inflammatory bowel dis- In North America, the incidence of microscopic eases: ulcerative colitis and Crohn’s disease) and those colitis was 0.8/100,000 person-years from 1985 to with primarily microscopic changes. 1989, and this increased significantly to19.1/100,000 Microscopic colitis is a chronic diarrheal condi- from 1998 to 2001 (1). The incidence of collagenous tion that is separated into two main subtypes: collage- colitis and lymphocytic colitis was 5.1 and 9.8/100,000 nous colitis and lymphocytic colitis. These two condi- person-years, and the prevalence was 36 and tions have similar clinical and histologic features, but 64/100,000 persons, respectively (1). In Europe, the are distinguished by the presence or absence of a incidence of collagenous and lymphocytic colitis ranges thickened subepithelial collagen band. Inflammatory from 0.6 to 5.2/100,000 person-years with a prevalence bowel disease (IBD) is traditionally separated into two between 10 to 16/100,000 persons (2). The reason for distinct clinical entities: Crohn’s disease and ulcera- the significantly higher incidence and prevalence of MC tive colitis. Although there is considerable symptom in North America compared with Europe is not known, overlap between these diseases, there are several fea- though increasing recognition may play a role.
    [Show full text]
  • Chronic Viral Hepatitis in a Cohort of Inflammatory Bowel Disease
    pathogens Article Chronic Viral Hepatitis in a Cohort of Inflammatory Bowel Disease Patients from Southern Italy: A Case-Control Study Giuseppe Losurdo 1,2 , Andrea Iannone 1, Antonella Contaldo 1, Michele Barone 1 , Enzo Ierardi 1 , Alfredo Di Leo 1,* and Mariabeatrice Principi 1 1 Section of Gastroenterology, Department of Emergency and Organ Transplantation, University “Aldo Moro” of Bari, 70124 Bari, Italy; [email protected] (G.L.); [email protected] (A.I.); [email protected] (A.C.); [email protected] (M.B.); [email protected] (E.I.); [email protected] (M.P.) 2 Ph.D. Course in Organs and Tissues Transplantation and Cellular Therapies, Department of Emergency and Organ Transplantation, University “Aldo Moro” of Bari, 70124 Bari, Italy * Correspondence: [email protected]; Tel.: +39-080-559-2925 Received: 14 September 2020; Accepted: 21 October 2020; Published: 23 October 2020 Abstract: We performed an epidemiologic study to assess the prevalence of chronic viral hepatitis in inflammatory bowel disease (IBD) and to detect their possible relationships. Methods: It was a single centre cohort cross-sectional study, during October 2016 and October 2017. Consecutive IBD adult patients and a control group of non-IBD subjects were recruited. All patients underwent laboratory investigations to detect chronic hepatitis B (HBV) and C (HCV) infection. Parameters of liver function, elastography and IBD features were collected. Univariate analysis was performed by Student’s t or chi-square test. Multivariate analysis was performed by binomial logistic regression and odds ratios (ORs) were calculated. We enrolled 807 IBD patients and 189 controls. Thirty-five (4.3%) had chronic viral hepatitis: 28 HCV (3.4%, versus 5.3% in controls, p = 0.24) and 7 HBV (0.9% versus 0.5% in controls, p = 0.64).
    [Show full text]
  • Gastritis - Symptoms and Causes - Mayo Clinic Visited 11/22/2019
    Gastritis - Symptoms and causes - Mayo Clinic Visited 11/22/2019 Request an Appointment Find a Doctor MENU Find a Job Give Now Log in to Patient Account English Patient Care & Health Information Diseases & Conditions Request an Gastritis Appointment Symptoms & causes Diagnosis & treatment Doctors & departments Overview Print Advertisement Gastritis is a general term for a group Mayo Clinic does not endorse companies or of conditions with one thing in common: products. Advertising revenue supports our not- inflammation of the lining of the for-profit mission. stomach. The inflammation of gastritis Advertising & Sponsorship is most often the result of infection with Policy Opportunities Ad Choices the same bacterium that causes most stomach ulcers. Regular use of certain Stomach and pain relievers and drinking too much pyloric valve Mayo Clinic Marketplace alcohol also can contribute to gastritis. Check out these best-sellers and special offers on books and newsletters from Mayo Clinic. Gastritis may occur suddenly (acute gastritis), or appear slowly over time (chronic gastritis). In some cases, gastritis NEW – Guide to Fibromyalgia can lead to ulcers and an increased risk of stomach cancer. Instant access – Mayo Clinic Health Letter For most people, however, gastritis isn't serious and improves quickly with treatment. Diabetes? This diet works … Stop osteoporosis in its tracks The Mayo Clinic Diet Online Products & Services Book: Mayo Clinic on Digestive Health https://www.mayoclinic.org/diseases-conditions/gastritis/symptoms-causes/syc-20355807[11/22/2019 4:16:25 PM] Gastritis - Symptoms and causes - Mayo Clinic Visited 11/22/2019 Symptoms The signs and symptoms of gastritis include: Gnawing or burning ache or pain (indigestion) in your upper abdomen that may become either worse or better with eating Nausea Vomiting A feeling of fullness in your upper abdomen after eating Gastritis doesn't always cause signs and symptoms.
    [Show full text]
  • Gastroesophageal Reflux Disease (GERD)
    Guidelines for Clinical Care Quality Department Ambulatory GERD Gastroesophageal Reflux Disease (GERD) Guideline Team Team Leader Patient population: Adults Joel J Heidelbaugh, MD Objective: To implement a cost-effective and evidence-based strategy for the diagnosis and Family Medicine treatment of gastroesophageal reflux disease (GERD). Team Members Key Points: R Van Harrison, PhD Diagnosis Learning Health Sciences Mark A McQuillan, MD History. If classic symptoms of heartburn and acid regurgitation dominate a patient’s history, then General Medicine they can help establish the diagnosis of GERD with sufficiently high specificity, although sensitivity Timothy T Nostrant, MD remains low compared to 24-hour pH monitoring. The presence of atypical symptoms (Table 1), Gastroenterology although common, cannot sufficiently support the clinical diagnosis of GERD [B*]. Testing. No gold standard exists for the diagnosis of GERD [A*]. Although 24-hour pH monitoring Initial Release is accepted as the standard with a sensitivity of 85% and specificity of 95%, false positives and false March 2002 negatives still exist [II B*]. Endoscopy lacks sensitivity in determining pathologic reflux but can Most Recent Major Update identify complications (eg, strictures, erosive esophagitis, Barrett’s esophagus) [I A]. Barium May 2012 radiography has limited usefulness in the diagnosis of GERD and is not recommended [III B*]. Content Reviewed Therapeutic trial. An empiric trial of anti-secretory therapy can identify patients with GERD who March 2018 lack alarm or warning symptoms (Table 2) [I A*] and may be helpful in the evaluation of those with atypical manifestations of GERD, specifically non-cardiac chest pain [II B*]. Treatment Ambulatory Clinical Lifestyle modifications.
    [Show full text]
  • Ulcerative Colitis: Diagnosis and Treatment ROBERT C
    Ulcerative Colitis: Diagnosis and Treatment ROBERT C. LANGAN, MD; PATRICIA B. GOTSCH, MD; MICHAEL A. KRAFCZYK, MD; and DAVID D. SKILLINGE, DO, St. Luke’s Family Medicine Residency, Bethlehem, Pennsylvania Ulcerative colitis is a chronic disease with recurrent symptoms and significant morbidity. The precise etiology is still unknown. As many as 25 percent of patients with ulcerative colitis have extraintestinal manifestations. The diagnosis is made endoscopically. Tests such as perinuclear antineutrophilic cytoplasmic antibodies and anti-Saccharomyces cerevisiae antibodies are promising, but not yet recommended for routine use. Treatment is based on the extent and severity of the disease. Rectal therapy with 5-aminosalicylic acid compounds is used for proc- titis. More extensive disease requires treatment with oral 5-aminosalicylic acid compounds and oral corticosteroids. The side effects of steroids limit their usefulness for chronic therapy. Patients who do not respond to treatment with oral corticosteroids require hospitalization and intravenous steroids. Refractory symptoms may be treated with azathioprine or infliximab. Surgical treatment of ulcerative colitis is reserved for patients who fail medical therapy or who develop severe hemorrhage, perforation, or cancer. Longstanding ulcerative colitis is associated with an increased risk of colon cancer. Patients should receive an initial screening colonos- copy eight years after the onset of pancolitis and 12 to 15 years after the onset of left-sided dis- ease; follow-up colonoscopy should be repeated every two to three years. (Am Fam Physician 2007;76:1323-30, 1331. Copyright © 2007 American Academy of Family Physicians.) This article exempli- lcerative colitis is a chronic dis- of ulcerative colitis is not well understood.
    [Show full text]
  • Liver Disease in Ulcerative Colitis: an Epidemiological and Follow up Study
    84 Gut 1994; 35:84-89 Liver disease in ulcerative colitis: an epidemiological and follow up study in the county of Stockholm Gut: first published as 10.1136/gut.35.1.84 on 1 January 1994. Downloaded from U Broome, H Glaumann, G Hellers, B Nilsson, J Sorstad, R Hultcrantz Abstract sclerosing cholangitis (PSC) are said to be more In an epidemiological study ofthe incidence of common in patients with UC.47 The incidence of ulcerative colitis (UC) in the county of Stock- these complications varies in different studies holm between 1955 and 1979, 1274 patients depending on selection criteria and on the with UC were discovered. Almost all these definition of hepatobiliary disease.89 The true patients had regularly been investigated with incidence of hepatobiliary dysfunction in UC, liver function tests; 142 (11%) of them showed however, can only be obtained by tests of liver signs of hepatobiliary disease. A follow up function tests such as transaminases, alkaline study on all 142 patients with abnormal liver phosphatases, and bilirubin made routinely in function and UC was made between 1989 and unselected groups of patients with UC. Because 1991 to evaluate the cause of the liver abnor- the cause of hepatic involvement in UC is mality and to find out if the liver disease had enigmatic it is important to find out if the rate affected the survival rates. At follow up, eight of this complication is increasing, because of patients were reclassified as having Crohn's factors unrelated to UC, or if it mirrors the disease, 60 had developed normal liver func- incidence ofUC in itself.
    [Show full text]
  • Familial Occurrence of Lymphocytic Colitis
    BRIEF COMMUNICATION Familial occurrence of lymphocytic colitis Hugh J Freeman MD HJ Freeman. Familial occurrence of lymphocytic colitis. Can J Occurrence familiale de la colite Gastroenterol 2001;15(11):757-760. The familial occurrence lymphocytaire of lymphocytic colitis in a female parent and her two female children is reported. No other genetically based disorder, includ- RÉSUMÉ : On fait ici état de l’occurrence familiale de la colite lym- ing celiac disease, was evident. For both children, the age of phocytaire chez une patiente et ses deux filles. Aucune autre maladie diagnosis was more than two decades younger than the age of d’origine génétique, comme la maladie cæliaque, ne s’est manifestée. recognition of disease in the parent, and some clinical features, Pour les deux enfants, le diagnostic a été posé plus d’une vingtaine d’an- including the requirement for pharmacological agents in both nées avant l’âge qu’avait la mère au moment de son diagnostic et cer- taines caractéristiques cliniques, dont le traitement pharmacologique children, suggested that their disease severity was more signifi- chez les deux enfants, donnent à penser que leur maladie est plus grave cant than that of the involved parent. These characteristics of a que chez le parent atteint. Ces caractéristiques de la maladie familiale familial disease have been previously reported and labelled ont déjà été mentionnées et ont été appelées "anticipation génétique" ‘genetic anticipation’ in some monogenetic forms of neurologi- dans le cas de certaines formes monogénétiques de maladies neu- cal disease, as well as in other types of inflammatory bowel dis- rologiques, de même que dans d’autres types de maladies inflammatoires eases, including Crohn’s disease.
    [Show full text]
  • In Patients with Crohn's Disease Gut: First Published As 10.1136/Gut.38.3.379 on 1 March 1996
    Gut 1996; 38: 379-383 379 High frequency of helicobacter negative gastritis in patients with Crohn's disease Gut: first published as 10.1136/gut.38.3.379 on 1 March 1996. Downloaded from L Halme, P Karkkainen, H Rautelin, T U Kosunen, P Sipponen Abstract In a previous study we described upper gastro- The frequency of gastric Crohn's disease intestinal lesions characteristic of CD in 17% has been considered low. This study was of patients with ileocolonic manifestations of undertaken to determine the prevalence of the disease.10 Furthermore, 40% of these chronic gastritis and Helicobacter pylori patients had chronic, non-specific gastritis. infection in patients with Crohn's disease. This study aimed to determine the prevalence Oesophagogastroduodenoscopy was per- of chronic gastritis and that of H pylori infec- formed on 62 consecutive patients suffer- tion in patients with CD who had undergone ing from ileocolonic Crohn's disease. oesophagogastroduodenoscopy (OGDS) at the Biopsy specimens from the antrum and Fourth Department of Surgery, Helsinki corpus were processed for both histological University Hospital between 1989 and 1994. and bacteriological examinations. Hpylori antibodies of IgG and IgA classes were measured in serum samples by enzyme Patients and methods immunoassay. Six patients (9.70/o) were During a five year period from September 1989 infected with H pylorn, as shown by histo- to August 1994, OGDS was performed on 62 logy, and in five of them the infection consecutive patients with CD to establish the was also verified by serology. Twenty one distribution of their disease. During the study patients (32%) had chronic H pyloni period, the OGDS was repeated (one to seven negative gastritis (negative by both times) - on three patients because of anaemia histology and serology) and one of them and on five patients because of upper gastroin- also had atrophy in the antrum and corpus.
    [Show full text]