Tuberculosis (TB) may produce abnormalities in the peripheral blood, including anemia. However, the evolution of TB-associated anemia with short-term combination anti-TB chemotherapy has not been well elucidated. The aim of this study was to characterize TB-associated anemia by clarifying its prevalence, characteristics, and evolution, through involving large numbers of patients with TB. The medical records of adult patients with TB diagnosed between June 2000 and May 2001 were reviewed. Among 880 patients with TB, 281 (31.9%) had anemia on diagnosis of TB, however, the hemoglobin concentration was less than 10 g/dL in only 45 patients (5.0%). Anemia was more frequently associated with the female and old age. Good treatment response, young age (≤65 yr-old) and initial high hemoglobin were the predictive factor for resolution of anemia. In 202 patients with anemia (71.9%), anemia was normocytic and normochromic. During or after anti-TB treatment, anemia was resolved in 175 (64.6%) out of 271 patients without iron intake. The mean duration of resolution from the initiation of anti-TB treatment was 118.8±113.2 days. In conclusion, anemia is a common hematological abnormality in patients with TB and close observation is sufficient for patients with TB-associated anemia, because TB-associated anemia is usually mild and resolves with anti-TB treatment.

C uring drug-sensitive tuberculosis (TB) takes 6 to 9 months of combination therapy despite the availability of antibiotics with potent in vitro activity, yet other pulmonary infectious diseases can be cured with single drugs that have similar mechanisms of action with only 3 to 14 days of treatment. One hypothesis used to explain the extended duration required with TB therapy is that subpopulations of bacteria become phenotypically drug tolerant in response to specific local microenvironmental conditions determined by the pathology of individual lesions (37). Understanding the features of these microenvironments and the conditions that generate tolerance may allow a rational design of drug regimens capable of shortening the time required to achieve a durable TB cure, but the methods used to evaluate new regimens have changed little and rely heavily on murine models of tuberculosis that typically have less complex lung pathology than human lesions. Premature discontinuation of treatment in humans results in disease relapse and the presence of cavities, and advanced lung pathology is strongly correlated with relapse (7,19,23). Only the rabbit and nonhuman primate models of pulmonary tuberculosis develop similar heterogeneous pathology, including the formation of cavitary disease. Guinea pigs, and some newer mouse models, develop more highly organized lesions, but these do not progress to cavities (for a comprehensive review of the comparative pathology of tuberculosis animal models, see reference 2).Nonterminal monitoring procedures, such as live imaging modalities, are increasingly being applied during TB drug efficacy experiments in animals and in human clinical trials (12,32,40,52). Structural and/or functional features observed in imaging modalities such as computed tomography (CT) and positron emission tomography (PET) are particularly attractive because they can be measured serially in a single subject at many time points during treatment. Computed tomography (CT) can add highly detailed information to the characteristic features of pulmonary tuberculosis visualized using conventional chest X-rays (1). CT scanning is typically used to monitor patients, assist in diagnosis, and assess surgical options for drug-resistant cases of disease (26), but there have been few examinations of the rate of change in CT findings during chemotherapy. The most detailed study of TB chemotherapy in patients (25) examined high-resolution CT scans from patients undergoing TB chemotherapy for up to 20 months. Old fibrotic lesions could be distinguished from active lesions, and criteria for the state of metabolic activity of lesions were proposed. However, that study did not sequentially

Uncontrolled diabetes is an independent risk factor for poor treatment response in PTB.

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