ABDOMINAL AND INTESTINAL TUBERCULOSIS - pediagenosis
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Sunday, September 28, 2025

ABDOMINAL AND INTESTINAL TUBERCULOSIS

ABDOMINAL AND INTESTINAL TUBERCULOSIS

APPEARANCE OF MUCOSA
APPEARANCE OF MUCOSA


Worldwide, tuberculosis presents with an incidence of 7 to 10 million new cases per year, with a prevalence of approximately 2 billion people. Tuberculosis accounts for 6% of global deaths. Intestinal tuberculosis is the sixth most prevalent extrapulmonary manifestation (EPTB); it mimics primary disease of the entire digestive tract presenting as Crohn ileocolitis. Tuberculosis can also manifest as a disease affecting the peritoneum, presenting as peritonitis. Multiple factors additively contribute to propagating tuberculosis, including poverty, malnutrition, overcrowding, immigrant status, and the presence of HIV coinfection. Patients with HIV coinfection demonstrate a deficient cellular immune response, poor immune reconstitution, and a risk for latent tuberculosis reactivation. Hence, a higher incidence of EPTB, increased severity of disease, and more rapid progression of disease may be observed.

The principal cause of intestinal tuberculosis is Mycobacterium tuberculosis. Intestinal tuberculosis may exist as a primary infection or as a secondary infection following reactivation from a Ghon focus. Routes of transmission directly to the gastrointestinal tract include ingestion of bacilli-infected sputum or hematogenous transit via the lymphatic system; a primary pulmonary focus may use either route. Continuous spread to direct adjacent organs is also observed.

M cells are found in the follicle-associated epithelium of intestinal Peyer patches of gut-associated lymphoid tissue. The M cells provide a route of entry for pathogens into the mucosa and can subsequently be a source of phagocytosis of tubercle bacilli. The ensuing inflammatory reaction is often indolent, with severe consequences resulting in both acute and subacute symptoms.

The ileocecal region is the most common site of involvement, with symptoms resulting from complications of ulcerative, hypertrophic/ulcerohypertrophic, or fibrous disease. Initially, abdominal discomfort, altered bowel habits, anemia, and constitutional symptoms herald insidious disease. Fibrous or hypertrophic disease can present with obstruction from stricture. The inflammatory reaction may result in obstruction purely from the mass effect (tuberculoma). Ulcerative disease may manifest with malabsorption or perforation, or both. In fact, peritoneal tuberculosis often manifests with ascites and/or fever of unknown origin. Though uncommon, esophageal tuberculosis may present as an esophageal pseudotumor. Gastroduodenal tuberculosis can masquerade as peptic ulcer disease. Alternatively, it can simulate an adenocarcinoma with pyloric mass obstruction. Enteric infections with amebiasis or caused by Yersinia enterocolitica can have intestinal manifestations similar to those of tuberculosis. Additionally, 10% of cases of intestinal tuberculosis are colonic. Hence, the disease may mimic carcinoma or ulcerative colitis. Rectal tuberculosis may manifest with bleeding, while anal tuberculosis presents commonly with fistulous complications. The similar clinical presentations of intestinal tuberculosis and Crohn disease are undeniable. Notably, the luminal appearance of intestinal tuberculosis is characterized by superficial to deep, circumferential ulcerations, as opposed to the deep, linear ulcers of Crohn disease. It has been suggested that tuberculosis and/or Mycobacterium spp. are the actual cause of Crohn disease but this has never been proved. In developing nations, enteric disease is unlikely to be Crohn disease; in developed nations, the small bowel findings are more likely to suggest Crohn disease, though tuberculosis should always be ruled out appropriately.

Initial diagnostic studies may include radiography with cross-sectional imaging. Imaging may reveal mesenteric or paraaortic lymphadenopathy, asymmetric bowel wall thickening (white bowel sign from lymphatic infiltration, sliced bread sign from bowel wall edema), ileal stricture, fistulas, masses, or ascites. Ultimately, confirmation of the diagnosis is predicated on tissue biopsy. Acid-fast staining, culture, and polymerase chain reaction testing are used extensively. Tissue sample diagnosis may be obtained via colonoscopy, laparotomy, or percutaneous biopsy of peritoneal nodes. Histologic analysis will classically reveal findings of caseating granuloma. When investigating the potential for peritoneal tuberculosis, either laparoscopic investigation or paracentesis will be necessary. On laparotomy, peritoneal tuberculosis will demonstrate multiple yellow-white tubercles on the peritoneal surface and/or visceral organs. A careful cell count of the paracentesis fluid will demonstrate a lymphocytic predominance (lymphocytes > 250 cells/mm3). Also, the ascites fluid will demonstrate a high serum ascites albumin gradient that is consistent with an exudative process. Subsequent adenosine deaminase assay testing is positive and is consistent with tuberculous ascites. A serum-based interferon-gamma release assay is more specific to latent and/or active tuberculosis infection. Early diagnosis, especially in nonendemic regions, is critical to prevent unnecessary surgical resection and intervention. Notably, inflammatory bowel disease patients taking immunosuppressive medications are at risk for acquiring tuberculosis and/or for its latent reactivation. These patients should be screened for tuberculosis annually while they are receiving immunosuppressant agents. Inflammatory bowel disorder patients with findings of latent tuberculosis and exposure should be treated for 3 months prior to induction of immuno-suppression.

CHRONIC PERITONITIS
CHRONIC PERITONITIS


Standard treatment for intestinal tuberculosis is extremely effective; it consists of chemotherapeutic regimens, including rifampicin, isoniazid, pyrazinamide, and ethambutol (RIPE), for 2 months, with rifampicin plus isoniazid daily or thrice weekly for 4 to 7 months more.

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