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Mem Inst Oswaldo Cruz. 2002 Dec;97(8):1225-30. Epub 2003 Jan 20.
Clinical presentation and survival of smear-positive pulmonary tuberculosis patients of a university general hospital in a developing country.

Carvalho AC, Nunes ZB, Martins M, Araujo RO, Comelli M, Marinoni A, Kritski AL.

Unidade de Pesquisa em Tuberculose, Servi o de Pneumologia, Hospital Universit rio Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-590, Brasil.

From January 1995 to August 1997 we evaluated prospectively the clinical presentation, laboratory findings and short-term survival of smear-positive pulmonary tuberculosis (TB) patients who sought care at our hospital. After providing informed, written consent, the patients were interviewed and laboratory tests were performed. Information about survivorship and death was collected through September 1998. Eighty-six smear-positive pulmonary TB patients were enrolled; 26.7% were HIV-seropositive. Seventeen HIV-seronegative pulmonary TB patients (19.8%) presented chronic diseases in addition to TB. In the multiple logistic regression analysis a CD4+ cell count <= 200 cell/mm was independently associated with HIV seropositivity. In the Cox regression model, fitted to all patients, HIV seropositivity and age > or = 50 years were independently associated with decreased survival. Among HIV-seronegative persons, the presence of an additional disease increased the risk of death of almost six-fold. Use of antiretroviral drugs was associated with a lower risk of death among HIV-seropositive smear-positive pulmonary TB patients (RH = 0.32, 95% CI 0.10-0.92). In our study smear-positive pulmonary TB patients had a low short-term survival rate that was strongly associated with HIV infection, age and co-morbidities. Therapy with antiretroviral drugs reduced the short-term risk of death among HIV-seropositive patients after TB diagnosis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12563494&dopt=Abstract

Pediatr Infect Dis J. 2002 Nov;21(11):1088-90.
Cerebral hemorrhage associated with vitamin K deficiency in congenital tuberculosis treated with isoniazid and rifampin.

Kobayashi K, Haruta T, Maeda H, Kubota M, Nishio T.

Department of Pediatrics, Kobe City General Hospital, Japan.

We report a male infant with congenital tuberculosis who developed cerebral hemorrhage associated with vitamin K deficiency during treatment with isoniazid and rifampin. Despite an absence of risk factors for vitamin K deficiency, the severe hemorrhagic disorder occurred at 4 months of age. We speculate that vitamin K deficiency in the present case may have resulted from a synergic effect of antituberculosis agents and immaturity of vitamin K metabolism and/or its absorption.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12458578&dopt=Abstract

Cancer Res. 2002 Dec 1;62(23):6924-7.
A mycobacterial iron chelator, desferri-exochelin, induces hypoxia-inducible factors 1 and 2, NIP3, and vascular endothelial growth factor in cancer cell lines.

Chong TW, Horwitz LD, Moore JW, Sowter HM, Harris AL.

Cancer Research United Kingdom, Molecular Oncology Laboratories, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom.

Hypoxia is a key phenomenon in tumor behavior, selecting for resistance to apoptosis, conferring resistance to radiotherapy and chemotherapy, and also inducing angiogenic factors such as vascular endothelial growth factor (VEGF). Exochelins are naturally evolved iron chelators produced by Mycobacterium tuberculosis. Because iron chelation has been reported to activate the hypoxia-inducible factor (HIF), we investigated the effects of an exochelin [desferri-exochelin (DFE) 772SM] on this hypoxia-inducible pathway and downstream target genes. DFE induced HIF-1alpha and HIF-2alpha transcription factors regulating the hypoxic response in the breast tumor cell line MDA468. DFE was 10 times more potent and more rapid in onset of effect than the clinically used iron chelator deferoxamine. The expression of downstream hypoxia-responsive target genes VEGF and the proapoptotic protein NIP3 was activated by transcription. MDA468 proliferation was inhibited via HIF-independent pathways, related to other effects of iron chelation. DFE inhibited effects of VEGF on endothelial cell proliferation. DFE potentially could be useful in cancer therapy by inducing apoptosis via NIP3 in conjunction with other non-HIF-related growth inhibitory pathways and blocking endothelial proliferation despite the presence of VEGF.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12460908&dopt=Abstract

J Antimicrob Chemother. 2002 Dec;50(6):1011-5.
Rifampicin concentrations in bronchial mucosa, epithelial lining fluid, alveolar macrophages and serum following a single 600 mg oral dose in patients undergoing fibre-optic bronchoscopy.

Ziglam HM, Baldwin DR, Daniels I, Andrew JM, Finch RG.

Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK.

The concentrations of rifampicin in epithelial lining fluid (ELF), human alveolar macrophages (AM), bronchial mucosal biopsies and serum were measured after a single oral dose of 600 mg rifampicin from 15 patients undergoing fibre-optic bronchoscopy. The samples of ELF, AM, the bronchial mucosal biopsies and serum were obtained approximately 2-5 h after dosing. The mean concentrations (mean +/- standard error) were 5.25 mg/L (+/-0.67) in ELF, 7.93 mg/kg (+/-1.61) in bronchial biopsies, 15.48 mg/L (+/-1.41) in serum and 251.8 mg/L (+/-65.92) in alveolar macrophages. These site concentrations exceeded the MIC90 for common respiratory pathogens including Mycobacterium tuberculosis and support the observed clinical efficacy of rifampicin in the treatment of a wide range of respiratory tract infections.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12461025&dopt=Abstract

J Exp Med. 2002 Dec 2;196(11):1473-81.
HLA-E-dependent presentation of Mtb-derived antigen to human CD8+ T cells.

Heinzel AS, Grotzke JE, Lines RA, Lewinsohn DA, McNabb AL, Streblow DN, Braud VM, Grieser HJ, Belisle JT, Lewinsohn DM.

Division of Pulmonary & Critical Care Medicine, Portland VA Medical Center, Oregon Health Sciences University, Portland, OR 97201, USA.

Previous studies in mice and humans have suggested an important role for CD8+ T cells in host defense to Mtb. Recently, we have described human, Mtb-specific CD8+ cells that are neither HLA-A, B, or C nor group 1 CD1 restricted, and have found that these cells comprise the dominant CD8+ T cell response in latently infected individuals. In this report, three independent methods are used to demonstrate the ability of these cells to recognize Mtb-derived antigen in the context of the monomorphic HLA-E molecule. This is the first demonstration of the ability of HLA-E to present pathogen-derived antigen. Further definition of the HLA-E specific response may aid development of an effective vaccine against tuberculosis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12461082&dopt=Abstract

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