Inflammatory bowel disease and mycobacteria: how much can we trust isoniazid prophylaxis during antitumor necrosis factor therapy?

OBJECTIVES: Isoniazid (INH) prophylaxis is recommended for the prevention of tuberculosis (TB) reactivation before or/and during initiation of treatment with tumour necrosis factor antagonists (anti-TNF agents). Nonetheless, the long-term effectiveness of chemoprophylaxis is not clear. In this study, we aimed to evaluate the characteristics of patients who developed TB reactivation in spite of INH prophylaxis associated with anti-TNF treatment. PATIENTS AND METHODS: In this retrospective study, medical records of 1263 patients with inflammatory bowel disease were reviewed. Baseline TB screening tests (purified protein derivative test and/or QuantiFERON-TB Gold test) were performed on all patients before initiation of anti-TNF therapy. Patients with purified protein derivative of more than 5 mm and/or a positive result of the QuantiFERON-TB Gold test received INH prophylaxis for 9 months. We analysed the data of patients diagnosed with TB reactivation during the anti-TNF treatment despite INH chemoprophylaxis. RESULTS: Overall, 175 patients underwent anti-TNF treatment. Sixty of these 175 patients had pretreatment testing showing latent TB infection and therefore were treated concomitantly with INH for 9 months in addition to their anti-TNF treatment. TB reactivation occurred in four of these 60 co-INH/anti-TNF treated patients. Active TB was diagnosed after 37.5±27 (range: 18-84) months of anti-TNF treatment. In two of the four patients that active TB was diagnosed, was also detected other Mycobacterium spp.: M. bovis in one patient and M. genavense in the other one. CONCLUSION: INH chemoprophylaxis may not prevent the reactivation of TB during anti-TNF therapy in the long-term. Patients should be carefully and periodically screened for TB reactivation during anti-TNF therapy.

[Fungal and tuberculous peritonitis in patients on peritoneal dialysis: characteristics, therapy and outcome].

Peritonitis is a serious clinical complication in patients with terminal chronic renal failure (CRF) on peritoneal dialysis (PD). The incidence of peritonitis varies from center to center, and during the last decade it occurs approximately in one patient during 24-60 therapeutical months, which is the result of good education of patients, but also of employing the new systems for PD. Fungi as well as Mycobacterium tuberculosis are rare causes of peritonitis in patients on PD therapy. The incidence of peritonitis with these two causes varies: 1-15% and 0.7-3%, respectively. The most frequent causes of fungal peritonitis are yeasts (Candida species 70-100%, with most frequent C. parapsilosis), but rarely filamentous fungi such as: Aspergillus, Paecilomyces, Penicillium, Zygomycetes, etc. Gram stains are helpful for diagnosis, as well as the culture of peritoneal effluent. There are various kinds of treatment protocols: withdrawal of peritoneal catheters and application of antimicotic drugs such as amphotericin B (which has recently been abandoned), oral flucytosine, oral or intraperitoneal fluconazole (imidazol) or itraconazol in the case of resistance. Although clinical signs disappear, most of these patients cannot continue with peritoneal dialysis therapy because of peritoneal adhesions, abscesses, fibrosis or progressive sclerosing peritonitis. Percentage of death is 12-44%. The incidence of tuberculosis is higher in patients with CRF in comparison with the entire population, and tuberculous peritonitis can develop in patients who had infection with Mycobacterium tuberculosis which was not treated adequately. Diagnosis can be made by detecting mycobacterium in peritoneal effluent (cultivation for 6 weeks) and/or acidophilic bacillus or typical granuloma in peritoneal biopsy. Therapy consists of removing the peritoneal catheter and long lasting antituberculotic therapy: izoniazid, rifampicin, pyrazinamide, pyridoxin (6-12 months). Streptomycin and ethambutol are to be avoided because of side effects in these patients. In spite of therapy, possible consequences are: ultrafiltration loss, obstruction of intestines because of adhesions, abdominal abscesses, fistulae, ending PD therapy, and even death.

[Abdominal tuberculosis in childhood: the clinical manifestations]. / Tuberculosis abdominal en la infancia: manifestaciones clíncas.

The authors reviewed the histories of 133 patients with abdominal tuberculosis in Instituto Nacional de Salud del Niño (Children's Hospital), Lima, Perú, between 1989 and 1991. We found morbidity higher in scholars (67.4%). Weight lost were present in all cases and malaise in 95.3%, abdominal distension in 83.72% and abdominal pain in 79.06%. Anaemia in 76.06%, ratio albumin/globulin were altered in 74.41% leukocytosis in 67.44%. Evidence of tuberculosis on chest X-ray were detected only in 62.5%.

Protective value of BCG vaccination in children in Bangkok, Thailand.

The protective effect of bacille Calmette-Guérin (BCG) vaccination against tuberculosis is controversial. In a study, 330 patients less than 12 years of age with tuberculosis, 52.1% of whom had had BCG vaccination, were compared with a control group of 1106 patients free of tuberculosis, 81% of whom had BCG vaccination. The occurrence of disseminated forms of tuberculosis, tuberculous meningitis, tuberculous peritonitis, and tuberculosis of bone and joints in BCG-vaccinated patients was quite low. With BCG vaccination, the incidence of the disseminated form of tuberculosis was significantly lower than that of pulmonary tuberculosis with pulmonary parenchymal lesions, primary pulmonary complexes, and pleural effusion. Tuberculous peritonitis was significantly less frequent than pulmonary tuberculosis with pulmonary parenchymal lesions, enlarged hilar glands, pulmonary primary complex, and pleural effusions. The study demonstrated that BCG gave an overall protective effect of 74% and that a major effect of this immunity was to produce a localized form of tuberculosis.