ENTERITIS TUBERCULOSA PDF

Tutaxe Med Clin North Am. Response to antituberculous therapy is favorable and similar to that of patients without HIV infection, although adverse drug reactions occur more tuberclosa in those with HIV infection. Directly observed therapy is strongly recommended to encourage medication compliance. Create a free personal account to download free article PDFs, sign up for alerts, customize your interests, and more. Address correspondence to Holenarasipur R.

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Tuberculous enteritis Hypertrophic 10 percent , characterized by scarring, fibrosis, and pseudotumor lesions Ulcerohypertrophic 30 percent , characterized by an inflammatory mass around the ileocecal valve with thickened and ulcerated intestinal walls.

The ulcerohypertrophic form is more commonly observed in ileocecal disease than with TB involving other segments of the gastrointestinal tract. The presentation can be acute, chronic, or acute-on-chronic with a chronic presentation of weeks to months being most common.

As a result, the diagnosis of ileocecal tuberculosis TB can be difficult and requires a high index of suspicion, especially in high-risk groups. Symptoms Nonspecific chronic abdominal pain is the most common symptom, occurring in 80 to 90 percent of patients.

Anorexia, fatigue, fever, night sweats, weight loss, diarrhea, constipation, or blood in the stool may be present. A palpable right lower quadrant abdominal mass is present in 25 to 50 percent of patients [5,6].

The presence of ascites may help to distinguish ileocecal TB from Crohn disease, since ascites is uncommon in Crohn disease. Fistula and intestinal stricture may occur. Bowel obstruction is the most common complication and may be due to progressive stricture or adhesions [].

Laboratory tests Routine laboratory tests demonstrate mild anemia and increased sedimentation rate in 50 to 80 percent of patients [7]. The white blood count is usually normal. A tuberculin skin test is positive in the majority of patients with intestinal TB but is of limited value because it does not differentiate between active disease and previous sensitization by contact or vaccination [7].

Similarly, a positive interferon gamma release assay may be observed but cannot be used to distinguish between latent and active disease.

Imaging Oral and intravenous contrast-enhanced computed tomography CT is the most helpful imaging modality to assess intraluminal and extraluminal pathology and extent of disease []. The most common CT finding is concentric mural thickening of the ileocecal region, with or without proximal intestinal dilatation image 1. Occasionally, asymmetric thickening of the medial cecal wall is seen. Characteristic lymphadenopathy with hypodense centers, representing caseous liquefaction, may be present in the adjacent mesentery.

Findings more suggestive of TB than Crohn disease include mural thickening with contiguous ileocecal valve involvement and hypodense lymph nodes with peripheral enhancement in the mesentery and retroperitoneum. Abdominal radiograph findings are generally nonspecific.

However, chest radiographs are positive for active or healed TB in less than 50 percent of patients []. Definitive diagnosis is based on a combination of histology and culture of biopsy material; these can establish the diagnosis in up to 80 percent of patients [17]. Colonoscopy with biopsy is the most useful nonoperative diagnostic procedure to obtain material for histology and culture [,]. Biopsy is also useful for investigation of the diseases that compose the differential diagnosis of TB enteritis.

In the setting of ileocecal TB, endoscopic fine needle aspiration for cytology may be positive even if the biopsy is negative [22]. The main differential diagnosis at endoscopy is Crohn disease CD. The endoscopic finding of aphthous ulcers with normal surrounding mucosa, linear ulcers, or the presence of cobblestoning favors the diagnosis of CD; these lesions are rarely seen with TB. However, diffusely inflamed mucosa may be seen with severe inflammation due to CD.

Ulcers due to TB tend to be circumferential picture 1 and are usually surrounded by inflamed mucosa. A patulous valve with surrounding heaped-up folds or a destroyed valve with a fish mouth opening is more likely to be caused by TB than CD picture 2.

TB granulomas are often submucosal; CD granulomas are typically mucosal, though submucosal granulomas may also be seen [24]. Therefore, deep endoscopic biopsies should be taken from ulcers and their margins. Care must be taken to avoid perforation in the setting of significant inflammation or deep ulcerations. A TB isolation mask should be worn by all individuals in the endoscopy suite when a colonoscopy is performed on a patient for whom there is suspicion of intestinal TB.

Histopathology Granulomas associated with TB tend to be large and confluent, often with caseation necrosis. Ulcers are lined by aggregate epithelioid histiocytes, and disproportionate submucosal inflammation is seen. In contrast, granulomas associated with CD are infrequent, small, nonconfluent, and noncaseating.

CD is also characterized by focally enhanced colitis and a high prevalence of chronic inflammation in endoscopically normal-appearing areas [25]. Typical histologic features of TB such as caseation granulomas and positive acid-fast stain are found in less than 33 percent of cases [15,23]. Differential diagnosis The differential diagnosis of ileocecal TB includes CD, actinomycosis, histoplasmosis, amebiasis, yersiniosis, typhlitis, lymphoma, colon cancer, mucoceles, and drug-induced lesions such as lesions due to nonsteroidal antiinflammatory drugs [27].

Biopsy for culture and histopathology evaluation can be useful to definitively distinguish between these entities. The differentiation between CD and tuberculous enteritis is becoming increasingly important with the reemergence of TB in Western countries in the wake of the AIDS epidemic, migration from developing countries, and the emergence of CD in Asian countries, possibly as a result of Westernization [28].

This distinction is also of utmost importance because the use of steroids or antitumor necrosis factor drugs in the setting of an incorrect diagnosis of CD may have disastrous consequences in patients with TB enteritis [7,11]. However, there can be marked overlap between the features of CD and intestinal TB, making the differentiation between the two conditions difficult.

A combination of clinical, radiographic, endoscopic, and biopsy findings are used to distinguish between them table 1 [13,]. In another study involving 43 patients with confirmed diagnosis of intestinal TB and 53 patients with CD, the most important clinical features to differentiate CD from intestinal TB were night sweats, longitudinal ulcers, and granulomas [33].

Clinical approach with uncertain diagnosis The diagnosis of tuberculous enteritis can be difficult to establish. Patients with tuberculous enteritis generally demonstrate clinical improvement within two weeks on empiric therapy [35] and, in one study, colonoscopic follow-up after two to three months of anti-TB therapy showed complete healing of active ulcers and erosions [36]. In the absence of clinical response, surgical exploration may be warranted to evaluate for alternative diagnoses such as Crohn disease, lymphoma, or malignancy [7].

Similarly, for situations in which the index of suspicion for tuberculous enteritis is moderate or low and the diagnostic approach described above is unrevealing, laparoscopic exploration and possible laparotomy may be warranted to evaluate for alternative diagnoses. In the presence of closed loop bowel obstruction, intestinal ischemia, bowel perforation, massive bleeding, or peritonitis, emergent surgical exploration with targeted treatment is warranted [6,7,17].

Subsequently, antituberculous therapy should be initiated once the patient has stabilized from the operation. In the subacute setting, initiation of antituberculous therapy can result in a relatively prompt clinical response with improvement of symptoms in less than two weeks [37].

However, cases of worsening of strictures due to scar tissue formation have been reported. In general, the medical treatment of tuberculous enteritis is similar to treatment of pulmonary TB [7], with conventional antituberculous chemotherapy RIPE: rifampicin, isoniazid, pyrazinamide, and ethambutol for two months, followed by rifampicin plus isoniazid RI for an additional four to seven months. Most countries adhere to the World Health Organization guidelines of directly observed treatment, short course DOTS given on a daily or thriceweekly basis.

In one prospective, randomized trial, both DOTS RIPE thrice weekly for two months followed by RI thrice weekly for four months and daily chemotherapy RIPE for two months followed by RI for seven months were equally effective at healing ileocecal and colonic tuberculosis in 79 and 75 percent of patients, respectively [35].

The initiation of therapy, modification of the drug regimen based on drug susceptibility testing, and monitoring of therapy and drug toxicity are discussed in detail separately. See "Treatment of pulmonary tuberculosis in HIV-uninfected patients". Patients with low-grade obstruction and fistulas may respond to antituberculous therapy, and most with mild to moderate intestinal strictures can be managed nonoperatively.

Bowel obstruction is the most common complication and may be due to progressive stricture or adhesions [10]. Healing in the setting of antituberculous therapy can also result in symptomatic scarring.

See "Overview of enteric fistulas" and "Overview of management of mechanical small bowel obstruction in adults". The surgical resection should be conservative; in some cases, multiple strictures of the small bowel may be amenable to strictureplasty to avoid major resection [17]. Bypass surgery for obstructing lesions should be avoided because of complications related to blind loop syndrome.

Colonoscopic balloon dilation may be an alternative to surgery; it may be used to manage symptomatic short ileal strictures, although experience with this technique is limited [38].

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