Health Questions and Answers

Chron’s Disease

What are the usual symptoms and signs suggestive of Crohn’s disease?
The symptoms of Crohn’s disease are determined by the site and type of involvement, that is, inflammatory, stenotic, or fistulizing. The most common site of involvement is ileocolitis. These patients present with diarrhea; abdominal pain that is usually insidious in the right lower quadrant, triggered or aggravated frequently after meals; weight loss; and an association with a tender, inflammatory mass in the right lower quadrant. The diarrhea is usually nonbloody, and this may be one of the clues in clinical history that helps differentiate Crohn’s disease from ulcerative colitis, where bloody diarrhea is almost universal. Patients frequently have fever, weight loss, perianal fistulas and/or fissures, and extra-intestinal manifestations, such as aphthous stomatitis, arthritis, and erythema nodosum. Patients with isolated colonic disease present usually with diarrhea, abdominal pain, and weight loss.
Perianal skin tags are very common and, at times, mistaken for external hemorrhoids; it is not until these are excised and the course is complicated by a nonhealing wound that the diagnosis of Crohn’s disease is entertained. At times the main symptoms are related to perianal fistulas and/or abscess, even though most of these patients have other areas of involvement by Crohn’s disease. Gastroduodenal Crohn’s disease is less common and can mimic complicated peptic ulcer disease with abdominal pain, early gastric satiety, or symptoms of duodenal obstruction.
Patients can present with mild, moderate, or severe disease. This is a clinical judgment based on factors such as the severity of diarrhea, abdominal pain, the presence or absence of dehydration, anemia, malnutrition, and tachycardia. For clinical trials, the Crohn’s Disease Activity Index (CDAI) has been developed. Calculation of the CDAI combines weighted scores of clinical and laboratory variables. CDAI scores less than 150 indicate a clinical remission, and scores over 450 indicate severely active disease. Even though the CDAI is subjective and cumbersome, it is currently the standard measure of disease activity for all clinical trials.

How is the diagnosis of Crohn’s disease established?
The diagnosis of Crohn’s disease is established by history, physical examination, endoscopy, biopsies, x-rays, and laboratory tests. Crohn’s disease presents more commonly between ages 15 and 25 years. The diagnosis should be suspected in patients with chronic diarrhea, finding characteristic intestinal ulcerations and excluding alternative diagnoses. The ulcerations of Crohn’s disease may be aphthoid but could be deep and serpiginous along the longitudinal axis of the bowel. Skip areas, cobblestoning, and rectal sparing are characteristic findings. Air contrast barium enema, small bowel series with or without a per-oral pneumocolon, or colonoscopy each may demonstrate these typical lesions. On a small bowel series, Crohn’s disease often leads to separation of bowel loops, a narrowed and ulcerated terminal ileum and, in advanced cases, the so-called string sign. The biopsies of involved areas have architectural distortion and a chronic inflammatory infiltrate, and in about 10-30% of cases of Crohn’s colitis there are noncaseating granulomas that are usually diagnostic. Typical lesions of Crohn’s disease may also be seen in the upper gastrointestinal tract. The inflammation is localized to the ileocecal region in approximately 50% of cases, the small bowel in approximately 25% of cases, the colon in 20% of cases, and the upper gastrointestinal tract or perirectum in 5%.

Which diseases can mimic the symptoms and signs of Crohn’s disease?
The differential diagnosis of Crohn’s disease is long. The most common mimics of Crohn’s colitis are ulcerative colitis, ischemic colitis, diverticulitis, or colorectal cancer. For Crohn’s ileitis, infection with Yersinia enterocolitica or Mycobacterium tuberculosis may mimic disease. In immunosuppressed patients, viral infections such as cytomegalovirus (CMV) can mimic Crohn’s disease. Other important diseases in the differential diagnosis of Crohn’s disease include the irritable bowel syndrome, intestinal lymphoma, celiac sprue, radiation enteropathy, and nonsteroidal anti-inflammatory drug-induced enteropathy.

What serologic tests can help establish the diagnosis?
Clinical, endoscopic, and histologic findings can establish the diagnosis and differentiate between Crohn’s disease and ulcerative colitis in 85-90% of patients. Still, in the 10-15% of patients with indeterminate colitis, where the diagnosis is important to determine optimal medical or surgical therapy, serologic testing may be helpful. Anti-Saccharomyces cerevisiae antibody (ASCA) is seen in over 60% of patients with Crohn’s disease (sensitivity) and in less than 10% of patients with other gastrointestinal diseases, such as ulcerative colitis and irritable bowel syndrome. Saccharomyces cerevisiae, or baker’s yeast, becomes antigenic when there is increased intestinal permeability, as there is in Crohn’s disease patients. When coupled with the perinuclear antineutrophil cytoplasmic antibody (pANCA), a test with a 70% sensitivity for ulcerative colitis and a 10% sensitivity for Crohn’s disease, ASCA and pANCA, testing together, have a sensitivity and specificity of over 90%.

References
BIBLIOGRAPHY

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4 Responses to “Chron’s Disease”

  1. Hans-Peter Schulz Says:

    Hello!
    You speek about Yersinia enterocolitica, that can mimic the symptoms of chron’s disease.
    So I want to ask, if it cannot be the reason of it?
    The base of this question is:
    – Yersinia enterocolitica is capable to live intracellular in epithelial cells
    – It can defend active against mechanisms of the defence of the body
    – In an environement beside of rooms with osmotic gradients, the link to signal infectious processes via proteines etc. can be redirected to this rooms. The information of an infection to the immune system is interrupted.
    – So a “silent infection” without immune reaction seems to be possible.
    – But, if infected endothelial cells became immune presenting cells, further bacteria and antigenes are released. A phase of an active immunologic process begins!
    – This problem is supported too by the ability of yersinia enterocolitica to escape the phagocytosis in som cell types
    – It can increase as long, as the immune system release more and more bacteria and bacterial trash from the work of defense!
    – The process ends finally for this phase, when all bacteria are removed from the area of infection
    – with immune processes can do this – but if the bacteria can escape and hide themselves in other endothelial cell, with active suppression of signalling the intracellular infection, a new reservoir for the next phases of the disease will grow!

    Is this a possible way to understand the problem?

    I would be happy, if I could get an answer!

    I have no chance to check this idea myself.

    Thanks

    Hans-Peter Schulz

  2. rtrafaelmd Says:

    Dear Hans-Peter Schulz

    Noninfectious inflammatory bowel disease (Chron’s Disease and Ulcerative Colitis) is distinguished from infectious entities by exclusion: recurrent episodes of mucopurulent (ie, containing mucus and white cells) bloody diarrhea characterized by lack of positive cultures for infectious organisms and failure to respond to antibiotics alone.
    The cause of noninfectious inflammatory bowel disease (Chron’s Disease and Ulcerative colitis) is unknown despite progress in understanding its pathogenesis

    You can exclude Yersinia enterocolitica by giving antibiotics like Ciprofloxacin , Ampicillin, Chloramphenicol and Polymyxin. Ergo Yersinia e. cannot be the reason for Chron’s Disease

    Some of the manifestation of Chron’s Disease that you cant find in Yersenia;
    Renal disorders, especially nephrolithiasis, are observed in one third of patients with Crohn’s disease, probably related to increased oxalate absorption associated with steatorrhea. Amyloidosis is a serious complication of Crohn’s disease, as is thromboembolic disease. Both of these complications are probably reflections of the systemic character of the inflammatory process. Patients are often malnourished and show evidence of nutrient deficiency states.

    Reference:
    Pathophysiology of Disease
    An Introduction to Clinical Medicine
    6th Edition
    Stephen J McPhee
    Garry D. Hammer

    Dr Rafael

  3. freakshare premium Says:

    interesting web log. It would be great if you can provide more details about it. Thanks you.

  4. rtrafaelmd Says:

    Hi! may I know what about Chron’s will you like me to discuss?

    Regards

    Rtrafaelmd

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