Therapy of tuberculous meningitis presents the problem of controlling the tuberculous infection without causing serious or permanent damage to the patient due to the undesirable side-effects of certain of the antituberculous drugs. The combined use of streptomycin, aminosalicylic acid (PAS), isoniazid (isonicotinic acid hydrazide, INAH), and hydrocortisone has changed dramatically the once-hopeless outlook in this disease.1
In the original clinical studies hydrocortisone was administered intrathecally; however, during the last two or three years intrathecal therapy has been abandoned generally as being unnecessary.1-3 Yet, although clinical evidence suggested that orally or intramuscularly administered hydrocortisone was passing into the cerebrospinal fluid, no reported measurements of 17-hydroxycorticosteroid levels in the cerebrospinal fluid of patients receiving oral or intramuscular hydrocortisone therapy could be found in the literature. Therefore, it was decided to determine whether steroids, as indicated by Porter-Silber chromogens, were present in the cerebrospinal fluid of patients four hours after the
CRANNY RL, KELLEY VC. The Use of Hydrocortisone in the Treatment of Tuberculous Meningitis: A Study of Steroid Concentrations in Cerebrospinal Fluid. AMA Am J Dis Child. 1958;96(2):165–168. doi:10.1001/archpedi.1958.02060060167006
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