Ulcerative intestinal tuberculosis case as a complication of treatment by infliximab for intestinal Behçet's disease: A case report.

RATIONALE: Intestinal Behçet's disease (BD) is characterized by intestinal ulcerations and gastrointestinal symptoms. Ulcerative intestinal tuberculosis (TB) is usually with dyspepsia, abdominal pain, vomiting, and weight loss. The 2 diseases exhibit similar clinical manifestations, but the most critical aspects of their clinical courses and required treatments are not at all similar. PATIENT CONCERNS: We present a case in which a patient with intestinal Behçet's disease developed a de novo ulcerative intestinal TB infection after the start of anti-tumor necrosis factor-α treatment. This was despite histopathologic examination without caseous necrosis granuloma and negative for acid-fast staining and latent TB screen. DIAGNOSES: Intestinal Behçet's disease and intestinal TB. INTERVENTIONS: The patient was treated with quadruple antituberculous chemotherapy, comprising rifapentine, isoniazid, ethambutol, and pyrazinamide. OUTCOMES: At follow-up about 3 months, the therapy of oral antituberculous drugs and thalidomide was continued and the patient's condition had stabilized. LESSONS: This case illustrates the importance of closely monitoring patients who are on infliximab for possible onset of TB, even without abdominal symptoms, and with negative screening results for latent TB.

Tuberculosis and Crohn's Disease Revisited.

Crohn's Disease (CD) and Intestinal Tuberculosis (ITB) share confusingly similar clinical, endoscopic, radiological and pathological manifestations. There is no simple test for differentiating ITB from CD. Although there are a number of sensitive and specific parameters for distinguishing between CD and ITB, the differential diagnosis still remains challenging and both clinical suspicion and appropriate clinical and laboratory studies are required to establish the diagnosis. Correct diagnosis is crucial because the therapy strategies of the two diseases are dramatically different. Treatment of ITB with immunosuppressive agents would lead to worsening of the patients' condition. Likewise, unnecessary antituberculosis therapy would delay the treatment of CD. Another important consideration is the risk of reactivation TB in patients with inflammatory bowel diseases which has been significantly increased following the widespread use of anti-Tumor Necrosis Factor Alpha (TNF-α) therapy. The majority of reactivation cases are extrapulmonary or disseminated TB. And it is widely recommended that patients with IBD who are to receive TNF inhibitor therapy should be screened for evidence of latent TB. This paper mainly reviews current literature on differential diagnosis between CD and ITB, and summarizes strategies to reduce the TB risk among candidates for TNF antagonist therapy in this specific patient population.

Study of fibrotic complications and hydroxyproline content in mouse liver at different stages of generalized BCG-induced granulomatosis.

Generalized BCG-induced granulomatous was simulated in BALB/c male mice. The number of tuberculous granulomas in the liver and their size as well as the number of hepatocytes showing vacuolar degeneration increased from day 3 to 180 postinfection. Necrotic changes in hepatocytes were most pronounced at the acute phase of inflammation (days 3 to 30). Proliferative processes in the liver parenchyma in the experimental group were less marked than in the control. Increased content of collagen fibers in the liver was determined by excessive collagen synthesis in necrotic areas as well as increased amount of granulomas and fibroblasts. Enhanced proliferative and fibroplastic activity of fibroblasts in granulomas and liver parenchyma was evidently determined by activated granuloma macrophages. These shifts determined changes in the liver content of hydroxyproline during the acute and chronic periods of the disease.

Gastrointestinal tuberculosis is not associated with proton pump inhibitors: a retrospective cohort study.

AIM: To evaluate the effect of proton pump inhibitors (PPIs) on the development of gastrointestinal tuberculosis. METHODS: All patients who were more than 20 years old and who had received a prescription for PPIs among those who visited Seoul National University Hospital from January 1, 2005 to December 31, 2009 were identified. Due to the low sensitivity of the microbiologic test and the nonspecific pathologic findings, the diagnosis of gastrointestinal tuberculosis was confirmed through the presence of active ulcerations and the responses to anti-tuberculosis medications. The patients were divided into two groups according to treatment duration (group 1: ≤ 3 mo; group 2: > 3 mo) and were followed up from the time they took the first prescription of PPIs until their last visit. Logistic regression analysis was used to calculate the relative risks (RR) and 95%CI, adjusting for covariates. RESULTS: Among the 61, 834 patients exposed to PPIs (50,534 in group 1; 11,300 in group 2), 21 patients were diagnosed with PPI-associated gastrointestinal tuberculosis during 124,274 person-years of follow-up. Of 21 patients, the 12 who revealed only scar changes in the colonoscopy were excluded from the statistical analyses. Of those who remained, 2 were excluded because they underwent gastrointestinal endoscopy within 4 wk of the first prescription for PPIs. Longer exposure to PPI was associated with a higher mean age (55.0 ± 14.5 in group 1 vs 58.2 ± 13.3 in group 2, P < 0.001) and a higher Charlson co-morbidity index (0.50 ± 0.93 in group 1 vs 0.77 ± 1.14 in group 2, P < 0.001). The true incidence of active gastrointestinal tuberculosis was 0.65 per 1000 person-years in group 1 and 0.03 per 1 000 person-years in group 2. Like the less-than-three-month PPI treatment period in group 1, the over-three-month PPI therapy period in group 2 was not associated with increased risk of acquiring gastrointestinal tuberculosis, after adjusting for age and co-morbidities, whereas the Charlson co-morbidity index was associated with increased risk of acquiring gastrointestinal tuberculosis based on the score [RR: (reference 1) in group 1 vs 1.518 in group 2; 95% CI: 1.040-2.216, P = 0.03]. CONCLUSION: Long-term PPI therapy does not seem to be associated with increased risk of acquiring gastrointestinal tuberculosis, but a higher Charlson co-morbidity index is associated with such.