LAUSR

activity, also had a sterilizing effect. The ideal choice in this case was moxifloxacin. In subsequent visits, the patient reported good tolerance to the drugs, and no changes were detected on clinical laboratory tests. Some systemic diseases increase the risk of developing active TB, and CD is one of these risk factors.5 Although the mechanism has not been entirely clarified, it may be due to malabsorption and lack of vitamin D in individuals with this disease.6 Celiac patients often have persistent low-grade inflammation and vitamin deficiencies, even many years after the introduction of a gluten-free diet. This diet also tends to be low in vitamin D, increasing the risk of deficiency. Vitamin D has been shown to induce nitric oxide synthesis in the macrophages, suppressing intracellular M. tuberculosis growth. It also increases the effect of interferonin promoting the granulomatous process, and induces the differentiation of monocytes to epithelioid cells and multinucleated giant cells that form a major part of the granulomas.6,7 The strongest genetic links with CD are found in the MHC locus, and the correlation with HLA-DQ2 (DQA1*05/DQB1*02) is well established.6 Associations between TB and various HLA alleles have been documented, but they are not as strong as in CD.6 In northern Europeans, HLA-DQ2 is often part of the 8.1 ancestral haplotype8 that contains a number of genes, including specific alleles of class I and class II HLA molecules, and genes coding for TNFand C2 and C4 complement factors. Since the C2 molecule is important in the mycobacterial invasion of macrophages, a C2 allele in particular may promote TB infection in a patient subgroup.6 In addition to increasing the risk of developing TB, CD may be a risk factor for TB complications, increasing severity and the risk of death (up to 6-fold) due to TB.4 An additional complication is that patients with TB who have CD-mediated malabsorption may be at risk of developing resistance to anti-TB drugs, due to their lower bioavailability.6 As in our case, drug tolerance among CD patients may also be poor, since some medications such as isoniazid are formulated with ingredients containing gluten. By replacing some these first-line drugs with a second-line drug, we were able to improve tolerance, and to continue treatment. In conclusion, poor tolerance to TB medications in a celiac patient requires a review of the drug components to see if they contain gluten. If the problem persists after the gradual introduction of the drugs, first-line drugs can be replaced by second-line agents.