Disease relevance of Tuberculosis, Meningeal

• A simple latex particle agglutination test for the rapid detection of Mycobacterium tuberculosis plasma membrane antigen in cerebrospinal fluid was evaluated in 18 children with tuberculous meningitis and 134 control children with other disorders [1].
• Of the remaining 12 patients who had negative CSF by microscopy, PCR, and culture, 11 were diagnosed as having tuberculous meningitis on the basis of the response to treatment (three had active pulmonary tuberculosis) and one had mycobacteria other than M tuberculosis in sputum and urine [2].
• The diagnoses included Chiari malformation, Dandy-Walker syndrome, external hydrocephalus, cerebellar tumor, CNS histoplasmosis, and tuberculous meningitis [3].
• Five cases of lymphocytic meningitis are described where a Bromide Partition Test was performed and proved positive at levels usually considered consistent with tuberculous meningitis [4].
• Hydrocephalus in tuberculous meningitis in children: treatment with acetazolamide and repeated lumbar puncture [5].

High impact information on Tuberculosis, Meningeal

• Urea therapy for inappropriate antidiuretic hormone secretion from tuberculous meningitis [6].
• Rapid diagnosis of tuberculous meningitis by polymerase chain reaction [7].
• Diagnosis of tuberculous meningitis by detection of tuberculostearic acid in cerebrospinal fluid [8].
• Serum streptomycin levels in tuberculous meningitis in an infant [9].
• Rapid diagnosis of tuberculous meningitis by latex particle agglutination [1].

Chemical compound and disease context of Tuberculosis, Meningeal

• Tuberculostearic acid as a diagnostic marker in tuberculous meningitis [10].
• In bacterial and tuberculous meningitis the supply of glucose to the brain seems to be inadequate for its demands which are increased as a consequence of increased cerebral glycolysis [11].
• Inappropriate secretion of ADH corrected by ethanol in tuberculous meningitis [12].
• We previously reported that rabbits with experimental tuberculous meningitis were protected from death by a combination of antibiotics and thalidomide therapy [13].
• The clinical benefit of adjunctive dexamethasone in tuberculous meningitis is not associated with measurable attenuation of peripheral or local immune responses [14].

Biological context of Tuberculosis, Meningeal

• Using a rapid and highly sensitive method for the diagnosis of tuberculous meningitis by polymerase chain reaction (PCR), we detected the Mycobacterium tuberculosis genome in CSF of 5 of 6 patients with clinically diagnosed tuberculous meningitis [15].
• Cerebrospinal fluid ethionamide concentrations were determined in 18 children (median age 26.5 months) with tuberculous meningitis complicated by raised intracranial pressure [16].
• Cerebrospinal fluid isoniazid concentrations in children with tuberculous meningitis: the influence of dosage and acetylation status [17].
• Isoniazid resistance, mycobacterial genotype and outcome in Vietnamese adults with tuberculous meningitis [18].
• Kinetics of isoniazid transfer into cerebrospinal fluid in patients with tuberculous meningitis [19].

Anatomical context of Tuberculosis, Meningeal

• This is functionally significant, since MMP-9 concentrations per CSF leukocyte (but not TIMP-1 concentrations) were elevated in fatal tuberculous meningitis and in patients with signs of cerebral tissue damage (unconsciousness, confusion, or neurological deficit; p < 0.05) [20].
• Vascular endothelial growth factor and blood-brain barrier disruption in tuberculous meningitis [21].
• From a patient with tuberculous meningitis, T lymphocyte clones were obtained that showed tuberculin (PPD) specific proliferative responses restricted by a single HLA-DR antigen [22].
• Tuberculostearic acid (10-Methyloctadecanoic acid) is a lipid component of the mycobacterial cell wall and its presence in cerebrospinal fluid can serve as a diagnostic marker for tuberculous meningitis [23].
• In 10 patients with tuberculous meningitis both T and B lymphocyte activation was observed in the CSF from clinical onset of disease [24].

Gene context of Tuberculosis, Meningeal

• These finding may have therapeutic implication for the treatment of human diseases characterized by acute and extensive TNF alpha production such as tuberculous meningitis or toxic shock [25].
• The concentrations of the chemokines IL-8, monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein-1alpha (MIP-1alpha) were measured in 120 CSF samples from 23 patients with pyogenic meningitis and from 11 patients with tuberculous meningitis (TBM) and in 10 CSF from subjects with non-infectious neurological diseases [26].
• The ratio of concentrations of IL-1 receptor antagonist to IL-1 beta was 3.2 in acute bacterial meningitis, 6.9 in tuberculous meningitis and 8.3 in viral meningitis.(ABSTRACT TRUNCATED AT 250 WORDS)[27]
• The level of tumor necrosis factor (TNF)-alpha, soluble TNF receptors p75 (sTNFR-75) and sTNFR-55, interferon (IFN)-gamma, and interleukin (IL)-10 and IL-12 were measured in 59 cerebrospinal fluid (CSF) samples from 15 patients with tuberculous meningitis (TBM) [28].
• We found the expression of VEGF in tuberculous meningitis and think that VEGF reflects its activity [29].

Analytical, diagnostic and therapeutic context of Tuberculosis, Meningeal

• In serial CSF samples from patients with tuberculous meningitis tuberculostearic acid was still present after 8 months of continuous supervised chemotherapy [8].
• Nested polymerase chain reaction for diagnosis and monitoring treatment response in AIDS patients with tuberculous meningitis [30].
• Early diagnosis of tuberculous meningitis by polymerase chain reaction [2].
• Acid-fast smears of CSF and the tuberculin skin test were of little help diagnostically, being positive in only 18% and 31%, respectively, of patients with tuberculous meningitis [31].
• This study shows that M tuberculosis DNA can exist in the CSF of a patient with tuberculous meningitis for three weeks after treatment and that PCR can still be a sensitive method to detect M tuberculosis DNA in the CSF after the start of treatment in patients with tuberculous meningitis [32].

References