ABDOMINAL AND INTESTINAL TUBERCULOSIS
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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.
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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.