DOCSLIB.ORG

Ulcerative Colitis of the Appendix (‘Ulcerative Appendicitis’) Mimicking Acute Appendicitis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Ulcerative Colitis of the Appendix (‘Ulcerative Appendicitis’) Mimicking Acute Appendicitis BRIEF COMMUNICATION Ulcerative colitis of the appendix (‘ulcerative appendicitis’) mimicking acute appendicitis RL Barclay MD1, WT Depew MD1, KK Taguchi MD2, DJ Hurlbut MD3 RL Barclay, WT Depew, KK Taguchi, DJ Hurlbut. Ulcerative Colite ulcéreuse de l'appendice (« appendicite colitis of the appendix (‘ulcerative appendicitis’) mimicking acute appendicitis. Can J Gastroenterol 2001;15(3):201-204. ulcéreuse ») imitant l'appendicite aiguë Appendiceal involvement in ulcerative colitis may occur in the RÉSUMÉ : Dans certains cas de colites ulcéreuses, une atteinte de l'ap- setting of either diffuse or distal disease, and is usually diagnosed pendice peut survenir dans le contexte de maladies diffuses ou distales, et incidentally at the time of proctocolectomy. The present patient habituellement ce problème est constaté et diagnostiqué au cours de la had a rare case of ‘ulcerative appendicitis’ occurring on a back- proctocolectomie. Ce patient souffrait d'un cas rare d'« appendicite ground of clinically quiescent ulcerative colitis, and presented ulcéreuse », survenue dans un contexte de colite ulcéreuse clinique- with the signs and symptoms of acute appendicitis. ment inactive, et il se plaignait des signes et symptômes d'une appen- dicite aiguë. Key Words: Appendicitis; Ulcerative colitis lcerative colitis is a chronic, relapsing inflammatory toms resolved spontaneously until one year later, when he Udisorder of the large bowel. Its cardinal clinicopatho- developed intermittent, small volume rectal bleeding. Stool logical features are rectal bleeding, anemia and contiguous cultures were negative, and sigmoidoscopy showed proctitis mucosal involvement beginning in the rectum and extend- limited to the distal rectum. The bleeding responded to a ing proximally to varying extents. Appendiceal involve- short course of topical steroid therapy, but 16 months later, ment in ulcerative colitis may occur either in the setting of he developed persistent, bloody diarrhea associated with a continuous disease of the entire colon (pancolitis) (1) or as weight loss of 11.2 kg over a three-month period. His symp- discontinuous (‘skip’) appendiceal lesions, isolated from dis- toms resolved after a course of empirical prednisone, and tal disease (2). A rare case of active ulcerative disease of the repeat sigmoidoscopy three months later showed no active appendix is presented, in which the clinical presentation disease. Biopsies were compatible with chronic, inactive simulated acute appendicitis. ulcerative colitis. The patient was maintained on oral sul- fasalazine (Salazopyrin, Pharmacia & Upjohn) and entered CASE PRESENTATION a long (seven-year) period of clinical remission. In 1985, a 67-year-old man presented with rectal bleeding. In 1992, colon cancer in the patient’s sister prompted a Colonoscopy initially revealed only diverticulosis, and ran- screening colonoscopy in the authors’ patient, which sur- dom biopsies showed nonspecific inflammation. His symp- prisingly revealed diffuse, mucosal pseudopolyposis (repre- Departments of 1Medicine, 2Surgery and 3Pathology, Queen’s University at Kingston, Kingston, Ontario Correspondence and reprints: Dr William T Depew, Hotel Dieu Hospital, 166 Brock Street, Kingston, Ontario K7L 5G2. Telephone 613-544-3310 ext 2483, fax 613-544-3114, [email protected] Received for publication July 26, 1999. Accepted November 9, 1999 Can J Gastroenterol Vol 15 No 3 March 2001 201 Barclay et al Figure 1) A Appendix shows inflammation confined to the mucosa (20× magnification), without ulceration or deeper mural involvement. B The active inflammation is characterized by crypt epithelial infiltration with neutrophils (cryptitis) and numerous crypt abscesses (C 200× magnification; D 400× magnification). senting the sequelae of prior severe colitis) extending from appendicitis was made. At laparotomy, the appendix had a the sigmoid to the ascending colon; however, there was no normal gross appearance, and no other intra-abdominal macroscopically active inflammation. Extensive biopsies pathology was identified. The appendix was removed. from all segments showed chronic inflammatory changes. A Pathology showed acute inflammation confined to the single tubular adenoma was also identified and removed. mucosa, with neutrophilic crypt epithelial infiltration The patient remained in clinical remission and under- (cryptitis) and crypt abscesses consistent with appendiceal went yearly surveillance colonoscopy. There was no change involvement by ulcerative colitis (Figure 1). The inflam- in the disease pattern until 1995, when he had a reactiva- mation did not extend beyond the mucosa, and no fecalith tion of pancolitis, which settled after a short course of oral was identified. Following appendectomy, the patient made prednisone. Surveillance colonoscopy in December 1997 a rapid and uneventful recovery; he was asymptomatic one showed the aforementioned pseudopolyposis and no grossly day after the operation and was discharged home on day 2. active colitis. Multiple biopsies, including several speci- Six months later, the colitis remained in complete clinical mens obtained from the cecum, showed neither chronic nor remission, and there has been no recurrence of right lower acute inflammation. There was no evidence of gland quadrant symptoms. branching, chronic changes or dysplasia. Five months later, while still free of the typical symp- DISCUSSION toms of active colitis, he experienced acute onset of rapidly This was the first reported case of active ulcerative appen- progressive right lower quadrant pain lasting 12 h, which dicitis in which the clinical presentation simulated acute was associated with diaphoresis. Physical examination appendicitis. The most convincing evidence implicating revealed pyrexia and focal peritoneal irritation in the right the appendix as the source of this patient’s sudden illness lower quadrant. There was leukocytosis with a predomi- was his rapid and complete return to normal health almost nance of granulocytes, and a clinical diagnosis of acute immediately following appendectomy. It is possible that the 202 Can J Gastroenterol Vol 15 No 3 March 2001 ‘Ulcerative appendicitis’ mimicking acute appendicitis pathological finding of ulcerative appendicitis was an inci- (13), driven by a localized, active focus of ulcerative colitis. dentally detected marker of chronically active, diffuse coli- In contrast to the remainder of the colon, inflammation in tis, rather than a localized, inflammatory process. However, the vermiform appendix was incompletely suppressed, per- the patient had no symptoms of active luminal disease at haps due, in part, to suboptimal delivery of 5-aminosalicy- the time of presentation; also, random biopsies (including late therapy to the appendiceal lumen. The appendix is a several from the cecum) obtained shortly before presenta- highly vascular organ with a rich lymphoid complement of tion showed no evidence of inflammation. Furthermore, no B cells and CD4 T-helper cells, making it an important active cecal disease was evident on numerous previous sur- component of the gut-associated mucosal immune system veillance colonoscopies. These features thus support active (14,15). These immune cells participate in the mucosal ulcerative appendicitis, in the setting of remote and current- inflammation of ulcerative colitis through various mecha- ly inactive pancolitis, as the cause of his acute illness. nisms, including the elaboration of cytokines and vasoac- The appendix is affected in at least half of all cases of tive mediators (13). Both mucosal and systemic concentra- ulcerative colitis requiring surgery (3). Appendiceal skip tions of such substances are increased in active ulcerative lesions – namely, discontinuous involvement of the appen- colitis (16,17). In our patient, the markedly increased num- dix in which the remainder of the cecum is spared – was bers of neutrophils in the appendiceal mucosa could have once thought to be rare in ulcerative colitis (4). Davison reflected a response to local release of neutrophil chemo- and Dixon (5) questioned this perception by demonstrating tactic agents, such as leukotriene B4 (17). In addition, isolated ulcerative appendicitis in 21% of 62 proctocolecto- there is a close association between subepithelial neuroen- my specimens from ulcerative colitis patients. Our patient is docrine cells and nerve fibres of the mucous plexus in the another case of discontinuous ulcerative appendicitis and appendix (18). The mucosal release of serotonin, a potent is, to our knowledge, the first case detected at appendecto- vasoactive and neurogenic mediator, has been implicated in my, rather than incidentally at colectomy. the pathogenesis of acute appendiceal pain, even without Acute appendicitis is relatively uncommon in patients significant inflammation (19,20). with ulcerative colitis (6-8). While some authors (6) Thus, it seems plausible that with the degree of acute believe that appendectomy may confer protection against mucosal inflammation observed in our patient, the combi- ulcerative colitis, others (8) speculate that this lower fre- nation of cytokine release (17), localized ischemia mediat- quency of acute appendicitis may stem from a downregulat- ed by alterations in endothelial integrity (21) and ed immune response associated with chronic ulcerative activation of neurogenic inflammation could result in suffi- colitis, which may be less susceptible to stimulation by an ciently increased tension and spasm within the inflamed etiological,
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]
  • 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]
  • 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]
  • Peptic Ulceration in Crohn's Disease (Regional Gut: First Published As 10.1136/Gut.11.12.998 on 1 December 1970
    Gut, 1970, 11, 998-1000 Peptic ulceration in Crohn's disease (regional Gut: first published as 10.1136/gut.11.12.998 on 1 December 1970. Downloaded from enteritis) J. F. FIELDING AND W. T. COOKE From the Nutritional and Intestinal Unit, The General Hospital, Birmingham 4 SUMMARY The incidence of peptic ulceration in a personal series of 300 patients with Crohn's disease was 8%. Resection of 60 or more centimetres of the small intestine was associated with significantly increased acid output, both basally and following pentagastrin stimulation. Only five (4 %) of the 124 patients who received steroid therapy developed peptic ulceration. It is suggested that resection of the distal small bowel may be a factor in the probable increase of peptic ulceration in Crohn's disease. Peptic ulceration was observed in 4% of 600 1944 and 1969 for a mean period of 11-7 years patients with Crohn's disease by van Patter, with a mean duration of the disorder of 13.7 Bargen, Dockerty, Feldman, Mayo, and Waugh years. Fifty-one of these patients had Crohn's http://gut.bmj.com/ in 1954. Cooke (1955) stated that 11 of 90 patients colitis. Diagnosis in this series was based on with Crohn's disease had radiological evidence of macroscopic or histological criteria in 273 peptic ulceration whilst Chapin, Scudamore, patients, on clinical and radiological data in 25 Bagenstoss, and Bargen (1956) noted duodenal patients, and on clinical data together with minor ulceration in five of 39 (12.8%) successive radiological features in two patients with colonic patients with the disease who came to necropsy.
    [Show full text]
  • Crohn's Disease and Ulcerative Colitis in the Same Patient
    Gut: first published as 10.1136/gut.24.9.857 on 1 September 1983. Downloaded from Gut, 1983, 24, 857-862 Case report Crohn's disease and ulcerative colitis in the same patient C L WHITE III, S R HAMILTON, M P DIAMOND, AND J L CAMERON From the Departments ofPathology, Medicine, and Surgery, The Johns Hopkins University School of Medicine and Hospital, Baltimore, Maryland, USA SUMMARY A well documented case of a patient with both Crohn's disease and ulcerative colitis is presented. A 29 year old woman underwent resection of her terminal ileum and ascending colon for typical Crohn's disease with ileocolitis. Eleven years later, an ileoproctocolectomy was performed for typical ulcerative colitis involving the left colon. The resection specimen also showed evidence of colonic Crohn's disease near the anastomotic site. This unusual case shows that Crohn's disease and ulcerative colitis can occur in the same patient. The rarity of such cases supports the concept that Crohn's disease and ulcerative colitis are separate entities, rather than different manifestations of the same disease process. Crohn's disease and ulcerative colitis are the two healed with conservative measures. Four months well recognised forms of idiopathic inflammatory later she developed rectal bleeding. Proctoscopy bowel disease. As the aetiologies (or aetiology) of showed slightly inflamed rectal mucosa, but no idiopathic inflammatory bowel disease are biopsy was performed. Barium enema showed a unknown, these entities are distinguished on the stricture in the ascending colon; the caecum and basis of their pathologic and resulting clinical, and colon distal to the hepatic flexure were normal.
    [Show full text]
  • Acute Gastroenteritis: Adult ______Gastrointestinal
    Acute Gastroenteritis: Adult _____________________________ Gastrointestinal Clinical Decision Tool for RNs with Effective Date: December 1, 2019 Authorized Practice [RN(AAP)s] Review Date: December 1, 2022 Background Gastroenteritis, also known as enteritis or gastroenterocolitis, is an inflammation of the stomach and intestines that manifests as anorexia, nausea, vomiting, and diarrhea (Thomas, 2019). Gastroenteritis can be acute or chronic and can be caused by bacteria, viruses, parasites, injury to the bowel mucosa, inorganic poisons (sodium nitrate), organic poisons (mushrooms, shellfish), and drugs (Thomas, 2019). Chronic causes include food allergies and intolerances, stress, and lactase deficiency (Thomas, 2019). Gastroenteritis caused by bacterial toxins in food is often known as food poisoning and should be suspected when groups of individuals present with the same symptoms (Thomas, 2019). Immediate Consultation Requirements The RN(AAP) should seek immediate consultation from a physician/NP when any of the following circumstances exist: ● moderate dehydration (six to 10% loss of body weight), and blood pressure and mental status do not stabilize in the normal range within one hour of initiating rehydration therapy; ● severe dehydration (>10% loss of body weight); ● high fever and appears acutely ill; ● tachycardia or palpitations; ● hypotension; ● severe headache; ● blood or pus in stool; ● severe abdominal pain; ● abdominal distention; ● absent bowel sounds; ● altered mental status; ● older and immunocompromised clients; and/or ● severe vomiting (Interprofessional Advisory Group [IPAG], personal communication, October 20, 2019). GI | Acute Gastroenteritis - Adult The RN(AAP) should initiate an intravenous fluid replacement as ordered by the physician/NP or as contained in an applicable RN Clinical Protocol within RN Specialty Practices if any of the ​Immediate Consultation​ circumstances exist.
    [Show full text]
  • Ulcerative Colitis Fact Sheet
    Ulcerative Colitis What is Ulcerative Colitis? Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) that is characterized by an abnormal, prolonged immune response that creates long-lasting inflammation and ulcers (sores) in the mucosa (lining) of the large intenstine (colon), or rectum.1,2 UC and Crohn's disease both involve chronic inflammation of the intestines and classify as IBD.3 It is estimated that approximately 12.6 million people worldwide have IBD.4 Symptoms Signs and symptoms of ulcerative colitis can range from mild to severe. When the disease is active, symptoms may include:5,6 Patients with UC may experience ongoing disease symptoms, or have Fever episodes of symptom-free remission, Fatigue which can be followed by relapse or Nausea or loss flares.7 of appetite Weight loss Diarrhea Though UC is usually not a fatal (often with abdominal pain, disease, it is serious, and in some presence of blood, pus or mucus) cases, may cause life-threatening Extraintestinal manifestations (joint pain/soreness, eye complications, including an increased irritation, rash, sores risk of colorectal cancer (CRC), toxic in the mouth, etc.) megacolon/bowel obstruction and Rectal bleeding need for a colectomy.5,7 UC patients Urgent need for are almost 2.5 percent more likely to the restroom develop CRC than those without UC.8 Eect on Quality of Life Living with UC may severely aect quality of life, particularly during flares and relapses. Physical hurdles may include:9 Socio-psychological hurdles may include:9 • Pain, fatigue or discomfort
    [Show full text]
  • Gastroenteritis
    GASTROENTERITIS BASIC INFORMATION: DESCRIPTION: Irritation and infection of the digestive tract that can often cause sudden and sometimes violent upsets. Gastroenteritis may be confused with spastic colitis. It affects all ages, but is most severe in young children (1 to 5 years) and adults over 60. FREQUENT SIGNS AND SYMPTOMS: · Nausea that sometimes causes vomiting · Diarrhea that ranges from 2 to 3 loose stools to many watery stools · Abdominal cramps, pain or tenderness · Appetite loss · Fever · Weakness CAUSES: · A variety of viruses, bacteria or parasites that have contaminated food or water · Food poisoning · Use of harsh laxatives · Change in bacteria that normally live in the intestinal tract · Chemical toxins in certain plants, seafood, or contaminated food · Heavy metal poisoning RISK INCREASES WITH: · Adults over 60 · Newborns and infants · Improper Diet · Excess alcohol consumption · Use of drugs, such as aspirin, nonsteroidal anti-inflammatories, antibiotics, laxatives, cortisone or caffeine · Travel to foreign countries PREVENTIVE MEASURES: · Wash hands frequently if you or someone around you has gastroenteritis · Avoid as many causes and risks mentioned above as possible · Take care with food preparation EXPECTED OUTCOME: Vomiting and diarrhea usually disappear in 2 to 5 days, but adults may feel weak, fatigued for about one week. POSSIBLE COMPLICATIONS: · Serious dehydration that requires intravenous fluids · Serious illness that may be overlooked because symptoms of gastroenteritis mimic other disorders TREATMENT: GENERAL MEASURES: · Diagnostic tests may include laboratory studies of blood and stool · Treatment is usually supportive (rest, fluids) · Mild cases are usually treated at home · It is not necessary to isolate persons with gastroenteritis · Hospitalization, if dehydration is severe MEDICATION: · Medicine is usually not necessary.
    [Show full text]
  • Gastroenteritis ("Stomach Flu")
    GASTROENTERITIS Information From Your Health Care Provider (Stomach Flu) A BASIC INFORMATION B DIAGNOSIS & TREATMENT DESCRIPTION GENERAL MEASURES Gastroenteritis is an irritation and inflammation of the • In most cases, this disorder will be self-treated at stomach and intestines. It is a general term and is often home. Call your health care provider if symptoms are used when there is a nonspecific, uncertain, or severe or if they cause you any concern. unknown cause. The disorder can affect all ages, but is • Your health care provider may do a physical exam. most severe in young children (1 to 5 years). Adults usu- Medical tests may include studies of blood and stool. ally have mild cases, sometimes with no symptoms. • Treatment usually involves rest and fluids. There is no FREQUENT SIGNS & SYMPTOMS specific drug for viral infections. • Diarrhea is the main symptom, and sometimes, the • It is not necessary to keep persons with gastroenteri- only one. Diarrhea may range from 2 or 3 loose stools tis away from others in the family or household. Try to to many watery stools. avoid close contact if possible. • Nausea and vomiting. • Hospital care may be needed, if dehydration is severe. • Stomach cramps, pain, or tenderness. MEDICATIONS • Fever or chills. • Drugs are usually not needed for treatment. • Appetite loss. Antibiotics do not work for viral infections. • Weakness. • If symptoms are severe or prolonged, your health • Dehydration. care provider may recommend nonprescription drugs CAUSES for vomiting or diarrhea. • Viral infections are the most common cause. They are •Some infections may require specific drug treatment. spread by contact with an infected person or by touch- • If a drug you take is the cause of the problem, you ing an object that has germs on it.
    [Show full text]
  • Campylobacter Colitis: Histological Immuno- Histochemical and Ultrastructural Findings
    Gut: first published as 10.1136/gut.26.9.945 on 1 September 1985. Downloaded from Gut, 1985, 26, 945-951 Campylobacter colitis: histological immuno- histochemical and ultrastructural findings J P VAN SPREEUWEL, G C DUURSMA, C J L M MEIJER, R BAX, P C M ROSEKRANS, AND J LINDEMAN From the Department ofInternal Medicine, Division of Gastroenterology, St. Antonius Ziekenhuis, Nieuwegein, Department ofMicrobiology and Pathology, Stichting Samenwerking Delftse Ziekenhuizen, Delft, Department ofInternal Medicine, St. Elizabeth Ziekenhuis, Leiderdorp, and the Department of Pathology, Vrije Universiteit, Amsterdam, The Netherlands SUMMARY The colonic biopsy specimens of 22 patients with colitis and positive stool cultures for Campylobacter jejuni were studied in order to obtain histological and immunohistochemical criteria to differentiate Campylobacter colitis from chronic inflammatory bowel disease. In addition we tried to identify Campylobacter inclusions by means of immunohistochemistry and electron microscopy as evidence for invasion of the colonic mucosa. The results show that the majority of patients with Campylobacter colitis have the histological picture of acute infectious colitis with increased numbers of IgA and IgM containing plasma cells in the colonic mucosa in contrast with patients with active chronic inflammatory bowel disease who show increases of IgA and IgG (ulcerative colitis) or IgA-, IgM and IgG containing plasma cells (M Crohn) in their colonic biopsies. The results of immunohistochemical stainings with Campylobacter antiserum show invasion of Campylobacter in the colonic mucosa. These findings were confirmed ultrastructurally. http://gut.bmj.com/ In the past decade Campylobacter has emerged be indistinguishable from ulcerative colitis. Histo- from obscurity to become an important human logical examination of rectal biopsies has ranged pathogen.
    [Show full text]
  • Coexistence of Primary Biliary Cirrhosis and Inflammatory Bowel Disease Toru Shizuma* Department of Physiology, School of Medicine, Tokai University, Japan
    al of urn Li o ve J r Shizuma, J Liver 2014, 3:3 Journal of Liver DOI: 10.4172/2167-0889.1000154 ISSN: 2167-0889 Mini Review Open Access Coexistence of Primary Biliary Cirrhosis and Inflammatory Bowel Disease Toru Shizuma* Department of Physiology, School of Medicine, Tokai University, Japan Abstract The coexistence of Primary Biliary Cirrhosis (PBC) and Inflammatory Bowel Disease (IBD) is uncommon, although hepatobiliary complications in IBD patients are not rare. This report reviews the English and Japanese literature and covers reported cases of concomitant PBC and IBD. We identified 2 cases of concomitant PBC and Crohn’s Disease (CD) and 18 cases of concomitant PBC and Ulcerative Colitis (UC). In most instances (15/18), IBD (CD or UC) developed before PBC, with the exception of 2 cases that were almost simultaneously diagnosed with both conditions. There is no evidence that UC cases with concomitant PBC are more severe than those without; however, the clinical features of concomitant PBC and CD are unclear due to few reports. Keywords: Primary biliary cirrhosis; Inflammatory bowel disease; such as autoimmune hepatitis or PBC [15,19,21,23]. The incidence of Crohn’s disease; Ulcerative colitis hepatobiliary diseases with UC has been reported to be 3%-15% and up to 90% with abnormal liver histology at surgery or autopsy [16,24]. Introduction PSC is best known for hepatobiliary manifestation with UC, and the Inflammatory Bowel Diseases (IBD), including Crohn’s Disease frequency of incidence of patients with concomitant PSC and IBD (CD) and Ulcerative Colitis (UC), are chronic recurrent, and has been reported to be in the range of 2.4%-7.5% [10,16,23,25,26].
    [Show full text]