We suggest that PDW, MPV and plateletcrit change in tuberculosis and that these changes may not reflect only acute phase reaction and disease activity. The potential role of platelet indices in tuberculosis immunopathogenesis remains to be investigated.

These results indicate that repetitive treatment with HBO may cause oxidative stress in critical tissues including the lung. Although HBO-mediated free radicals are accepted to be responsible for the benefits of this therapeutic modality, especially in cases with prolonged exposure, possible injurious effects of supranormal values of bio-oxidative products need to be considered.

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BackgroundChitotriosidase is an accepted marker of macrophage activation. In this study, we investigated serum chitotriosidase levels in pulmonary tuberculosis (PTB).MethodsForth-two patients with PTB and 30 healthy subjects were enrolled in the study. The radiological extent of PTB, radiological sequela after treatment, and the degree of smear positivity were assessed. Chitotriosidase levels were measured by a fluorometric method.ResultsThe serum chitotriosidase levels of the PTB patients were significantly higher than those of the control subjects (39.73±24.97 vs. 9.63±4.55 nmol/mL/h, P<0.001). After completion of the standard 6-month antituberculous treatment, chitotriosidase levels in PTB patients significantly decreased (10.47±4.54 nmol/mL/h, P<0.001). Chitotriosidase levels correlated significantly with the radiological extent of PTB, degree of smear positivity, and post-treatment radiological sequela score (r=0.439, r=0.449, and r=0.337, respectively).ConclusionsThis study demonstrated that serum chitotriosidase levels increase in PTB; therefore, chitotriosidase can be used as a marker of disease activity, severity, and response to treatment.

Among the most readily available chemical warfare agents, sulfur mustard (SM), also known as mustard gas, has been the most widely used chemical weapon. SM causes debilitating effects that can leave an exposed individual incapacitated for days to months; therefore delayed SM toxicity is of much greater importance than its ability to cause lethality. Although not fully understood, acute toxicity of SM is related to reactive oxygen and nitrogen species, oxidative stress, DNA damage, poly(ADP-ribose) polymerase (PARP) activation and energy depletion within the affected cell. Therefore several antioxidants and PARP inhibitors show beneficial effects against acute SM toxicity. The delayed toxicity of SM however, currently has no clear mechanistic explanation. One third of the 100,000 Iranian casualties are still suffering from the detrimental effects of SM in spite of the extensive treatment. We, therefore, made an attempt whether epigenetic aberrations may contribute to pathogenesis of mustard poisoning. Preliminary evidence reveals that mechlorethamine (a nitrogen mustard derivative) exposure may not only cause oxidative stress, DNA damage, but epigenetic perturbations as well. Epigenetic refers to the study of changes that influence the phenotype without causing alteration of the genotype. It involves changes in the properties of a cell that are inherited but do not involve a change in DNA sequence. It is now known that in addition to mutations, epimutations contribute to a variety of human diseases. Under light of preliminary results, the current hypothesis will focus on epigenetic regulations to clarify mustard toxicity and the use of drugs to correct possible epigenetic defects.