Glucocorticoid treatment of tuberculous meningitis secondary research.docVIP

 PAGE \* MERGEFORMAT 17 Glucocorticoid treatment of tuberculous meningitis secondary research [Keywords:] glucocorticoid adjuvant treatment of tuberculous meningitis research Tuberculosis in many countries remains a serious public health problem, approximately 900 million people infected with TB, of which about 2 million people dead and a high incidence in Southeast Asia and Africa, in parts of South Africa the incidence is as high as 1% [1] . Tuberculous meningitis (tuberculous meningitis, TBM) is the most serious of TB, accounting for 6% of extrapulmonary TB, the prognosis is poor, high fatality rate, the remaining survivors varying degrees of neurological sequelae, such as mental and (or) movement barriers need to support long-term care of others [2]. TBM is not treatment, case fatality rate of 100%, streptomycin invention, the fatality rate dropped to 63%, with isoniazid, rifampicin, pyrazinamide, ethambutol advent of the case fatality rate is more reduced, but the there is still more than 50% will die or the legacy of serious neurological sequelae [3]. As early as 50 years in the 20th century, the researchers speculated that the anti-inflammatory effects of glucocorticoid can improve the prognosis and began trying to support the use of glucocorticoid treatment of TBM. After many years of clinical practice, corticosteroids TBM, in particular, the efficacy of HIV-negative patients, many researchers have been recognized and confirmed. A glucocorticoid treatment mechanism of TBM 1.1 TBM pathogenesis TBM is a Mycobacterium tuberculosis caused by hematogenous spread. Reach the subarachnoid space Mycobacterium tuberculosis, causing allergic inflammation. Inflammatory exudation of oppression and damage caused by the corresponding cranial nerve symptoms caused by obstructive hydrocephalus, Central pool. Brain artery involvement leading to tuberculous endarteritis in weight from cerebral infarction and brain softening occurs. Duration of post-inflammatory adhe