• Zhengwei Dong, Jingyun Shi, Anca Dorhoi, Jie Zhang, Adiilah K Soodeen-Lalloo, WenLing Tan, Hongyun Yin, Wei Sha, Weitong Li, Ruijuan Zheng, Zhonghua Liu, Hua Yang, Lianhua Qin, Jie Wang, Xiaochen Huang, Chunyan Wu, Kaufmann Stefan H E SHE Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany., and Yonghong Feng.
• Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University, School of Medicine, Shanghai, China; Department of Pathology, Shanghai Pulmonary Hospital, Tongji University, School of Medicine, Shanghai, China.
• Chest. 2018 May 1; 153 (5): 1187-1200.

BackgroundExacerbated immunopathology is a frequent consequence of TB that is complicated by diabetes mellitus (DM); however, the underlying mechanisms are still poorly defined.MethodsIn the two groups of age- and sex-matched patients with TB and DM (DM-TB) and with TB and without DM, we microscopically evaluated the areas of caseous necrosis and graded the extent of perinecrotic fibrosis in lung biopsies from the sputum smear-negative (SN) patients. We scored acid-fast bacilli in sputum smear-positive (SP) patients and compiled CT scan data from both the SN and SP patients. We compared inflammatory biomarkers and routine hematologic and biochemical parameters. Binary logistic regression analyses were applied to define the indices associated with the extent of lung injury.ResultsEnlarged caseous necrotic areas with exacerbated fibrotic encapsulations were found in SN patients with DM-TB, consistent with the higher ratio of thick-walled cavities and more bacilli in the sputum from SP patients with DM-TB. Larger necrotic foci were detected in men compared with women within the SN TB groups. Significantly higher fibrinogen and lower high-density lipoprotein cholesterol (HDL-C) were observed in SN patients with DM-TB. Regression analyses revealed that diabetes, activation of the coagulation pathway (shown by increased platelet distribution width, decreased mean platelet volume, and shortened prothrombin time), and dyslipidemia (shown by decreased low-density lipoprotein cholesterol, HDL-C, and apolipoprotein A) are risk factors for severe lung lesions in both SN and SP patients with TB.ConclusionsHemostasis and dyslipidemia are associated with granuloma necrosis and fibroplasia leading to exacerbated lung damage in TB, especially in patients with DM-TB.Copyright © 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

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