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Kandeel, A.

The Effect of Cyclophosphamide on the Primary Humoral Immune Response. The Immunological Priming

Kay, M. Kolar, G. Lazuardi, L. Linterman, M. Meneghelli, V. Basel , , vol. Meredith, P. Mustafa, A. Ogura, I. Popp, D. Ageing Dev. Rahman, M. Scher, I.

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Smaniotto, S. Szczesny, G. Thyaga, R. Twohig, J. Vered, M. Metastasis , , vol. Xiao, S. Xu, Y. Yung, R. Zheng, B. Maiborodin 1 Email author M. Agzaev 1 T. Ragimova 1 I.


Maiborodin 2 1. Personalised recommendations. Two recent studies have investigated the role of intensified therapy for TBM. The first was randomized controlled trial with three parallel arms that compared the effect of adding a fluoroquinolone ciprofloxacin, levofloxacin or gatifloxacin with standard therapy in 61 Vietnamese adults with TBM. Surprisingly, worse outcomes were recorded in patients with lower and higher fluoroquinolone exposures, than those with intermediate exposures.

Those with high exposures were older and tended to have more severe disease, which may have resulted in greater blood—brain barrier breakdown. A second study conducted in Indonesia investigated the use of high mg or standard mg dose rifampicin and high mg or standard mg dose moxifloxacin in 60 Indonesian adults with TBM. A large randomized controlled trial of high-dose rifampicin and levofloxacin versus standard therapy is underway in Vietnam and expected to report soon.

Of note, all patients received adjunctive corticosteroids during the first 6—8 weeks of the study, which may have prevented the development of IRIS. Over the past 60 years, a number of studies have investigated the use of adjunctive corticosteroids in the treatment of TBM. The peripheral blood monocyte and T cell responses to M. Thus, dexamethasone did not appear to improve survival from TBM by attenuating immunological mediators of inflammation in the CSF, nor by suppressing peripheral T cell responses to mycobacterial antigens, challenging previously held views of the pathogenesis of TBM.

A study that looked at the long-term outcome recruited to the Vietnamese study found that adjunctive dexamethasone appeared to improve the survival in patients with TBM, until at least 2 years of follow-up, but failed to demonstrate a 5-year survival benefit. Two recent studies have examined the possible benefits of aspirin in TBM treatment. The first study was a randomized controlled trial of aspirin versus placebo in Indian adults.

The effects of aspirin are difficult to interpret, however, as prednisolone was also given to some patients such as those with severe disease at baseline, or those whose clinical condition worsened during treatment. The second study was a randomized controlled trial with three parallel arms low- and high-dose aspirin and placebo in South African children. Aspirin was well tolerated, but one death occurred and was probably related to aspirin.

Outcomes in the high-dose aspirin group compared favourably with the other treatment groups despite younger age and more severe neurological involvement. Despite advances in our understanding TBM over the past few years, it remains the most lethal form of tuberculosis. The best way to improve survival is by rapid accurate diagnosis and prompt initiation of therapy. The current rapid diagnostic methods for TBM are inadequate but some recent developments have shown promise. These include methods to improve the sensitivity of smear microscopy, the development of automated nucleic acid amplification platforms and the use of novel biomarkers to diagnose TBM, and these warrant further investigation.

The optimal antimicrobial treatment regimen for TBM has not been established in clinical trials, and current guidelines are extrapolated from treatment regimens for pulmonary tuberculosis. Ongoing trials of intensified therapy with rifampicin and fluoroquinolones are going some way towards addressing this deficiency. However, the role of other agents with good CSF penetration such linezolid or novel antituberculosis agents such as bedaquiline and PA warrants investigation. Adjunctive corticosteroids appear to improve survival in HIV-negative patients with TBM, but the mechanism by which they exert their beneficial effects are poorly understood.

The role of other adjunctive therapies such as thalidomide and aspirin remain controversial, although the latter may augment the response to corticosteroids. Recent studies have suggested that LTA4H genotype may module response to corticosteroids and offers the prospect of targeted immunomodulatory therapies based on patient genotype in the future. HIV-associated TBM remains a devastating condition with a dismal prognosis, and strategies to improve outcome are urgently required. The benefit of adjunctive corticosteroids in HIV-infected patients has not been established and is unlikely to be investigated in a large clinical trial.

The advances in diagnosis and treatment described in this review highlight the many challenges that clinicians face in managing this condition and a number of opportunities for research. Oxford University Press is a department of the University of Oxford.

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It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents. Pathogenesis of TBM. Host and pathogen genetics in TBM. Laboratory diagnosis of TBM. Treatment of TBM. Adjunctive anti-inflammatory therapies. Conflict of Interest statement.

Tuberculous meningitis: advances in diagnosis and treatment M. Oxford Academic. Google Scholar. Cite Citation.

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Worsening headache, vomiting, confusion, coma. Open in new tab. Growth detected by fluorescence resulting from consumption of oxygen by mycobacteria. Growth examined using an inverted microscope. Ability to detect M. Requires a containment Level 3 laboratory and laboratory expertise including PCR. Rapid, point-of-care test that can be conducted at community level. Two recent studies looking at other M. Google Preview. Tuberculous meningitis in the southwest United States: a community-based study.

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Tuberculous encephalopathy with and without meningitis. Clinical features and pathological correlations. Neurological and related syndromes in CNS tuberculosis. Clinical features and pathogenesis. A tuberculoma review with some personal experiences. Spinal cord and its coverings.

Tuberculous radiculomyelitis complicating tuberculous meningitis: case report and review.


Raised intracranial pressure, the syndrome of inappropriate antidiuretic hormone secretion, and arginine vasopressin in tuberculous meningitis. Hyponatremic natriuretic syndrome in tuberculous meningitis: the probable role of atrial natriuretic peptide. Plasma arginine vasopressin and the syndrome of inappropriate antidiuretic hormone secretion in tuberculous meningitis.

Serial MRI to determine the effect of dexamethasone on the cerebral pathology of tuberculous meningitis: an observational study. Tuberculous meningitis with acellular cerebrospinal fluid in AIDS patients. Pathophysiology and prognosis in vietnamese adults with tuberculous meningitis. Tumor necrosis factor and chemokine interactions in the formation and maintenance of granulomas in tuberculosis. Blood-brain barrier damage in patients with bacterial meningitis: association with tumor necrosis factor-alpha but not interleukin-1 beta.

Tumor necrosis factor alpha is a determinant of pathogenesis and disease progression in mycobacterial infection in the central nervous system. A combination of thalidomide plus antibiotics protects rabbits from mycobacterial meningitis-associated death. Adjunctive thalidomide therapy of childhood tuberculous meningitis: possible anti-inflammatory role.

Adjunctive thalidomide therapy for childhood tuberculous meningitis: results of a randomized study. Pretreatment intracerebral and peripheral blood immune responses in Vietnamese adults with tuberculous meningitis: diagnostic value and relationship to disease severity and outcome. The clinical benefit of adjunctive dexamethasone in tuberculous meningitis is not associated with measurable attenuation of peripheral or local immune responses.

The lta4h locus modulates susceptibility to mycobacterial infection in zebrafish and humans. Host genotype-specific therapies can optimize the inflammatory response to mycobacterial infections. A polymorphism in Toll-interleukin 1 receptor domain containing adaptor protein is associated with susceptibility to meningeal tuberculosis.

A polymorphism in human TLR2 is associated with increased susceptibility to tuberculous meningitis. The influence of host and bacterial genotype on the development of disseminated disease with Mycobacterium tuberculosis. Nicosia, G. Theory in Biosciences 93— CrossRef Google Scholar. Dasgupta, D.

Berlin, Germany: Springer-Verlag Tan, K. Coello Coello, C. ACM Computing Survey 32 — Garey, M. New York: Freeman Cutello, V. Honolulu, HI Mitchell, D. San Jose, CA —