Carlini S M, Beyers N, Schoeman J F, Nel E D, Truter E J, Donald P R
Department of Paediatrics and Child Health, University of Stellenbosch, South Africa.
Scand J Infect Dis. 1997;29(3):275-80. doi: 10.3109/00365549709019042.
Cerebrospinal fluid (CSF) adenylate kinase activity was determined in 88 children (mean age 32.6 months) at stage II (n = 40) and stage III (n = 48) tuberculous meningitis (TBM) at, or shortly after, the initiation of treatment, and at weekly intervals thereafter for the first month of treatment, and in 60 children (mean age 40 months) investigated for, but later considered not to have meningitis. CSF adenylate kinase activity in this latter group ranged from 0 to 1.27 u/l (mean 0.59 u/l). Mean CSF adenylate kinase activity during the first week of therapy in children at stage II TBM (2.95 u/l; range 0-9.22 u/l) differed significantly (p = 0.03) from that in children at stage III TBM (5.62 u/l; range 0-18.93 u/l). CSF adenylate kinase activity did not differ between children at stage II and stage III TBM during any of the 3 subsequent weeks. CSF adenylate kinase activity was not related to CSF cell count, total protein or glucose concentration or intracranial pressure at any point during the first month of treatment, but was related to CSF lactate during the first week of therapy (p = 0.001). Consecutive determinations of CSF adenylate kinase activity were available in 34 children. Although CSF adenylate kinase activity tended to increase or decrease in keeping with changes in clinical condition this was not always the case. The close relationship of CSF adenylate kinase activity and lactate concentrations suggests that adenylate kinase activity reflects hypoxic cerebral metabolism and it was unusual for children with increased CSF adenylate kinase activity at the time of diagnosis to be clinically normal on completion of 6 months of antituberculosis treatment. Any treatment modality which significantly reduced CSF adenylate kinase activity in children early in the course of TBM would probably be of clinical benefit to the patients.
在88名儿童（平均年龄32.6个月）中测定了脑脊液（CSF）腺苷酸激酶活性，这些儿童处于II期（n = 40）和III期（n = 48）结核性脑膜炎（TBM），在开始治疗时或治疗后不久进行测定，在治疗的第一个月内此后每周测定一次；并在60名儿童（平均年龄40个月）中进行了测定，这些儿童最初被怀疑患有脑膜炎，但后来被认为没有脑膜炎。后一组儿童的脑脊液腺苷酸激酶活性范围为0至1.27 u/l（平均0.59 u/l）。II期TBM儿童在治疗第一周的脑脊液腺苷酸激酶平均活性（2.95 u/l；范围0 - 9.22 u/l）与III期TBM儿童（5.62 u/l；范围0 - 18.93 u/l）有显著差异（p = 0.03）。在随后的3周中的任何一周，II期和III期TBM儿童的脑脊液腺苷酸激酶活性均无差异。在治疗的第一个月内的任何时间点，脑脊液腺苷酸激酶活性均与脑脊液细胞计数、总蛋白或葡萄糖浓度或颅内压无关，但在治疗的第一周与脑脊液乳酸有关（p = 0.001）。34名儿童可进行脑脊液腺苷酸激酶活性的连续测定。虽然脑脊液腺苷酸激酶活性往往会随着临床状况的变化而增加或降低，但情况并非总是如此。脑脊液腺苷酸激酶活性与乳酸浓度的密切关系表明，腺苷酸激酶活性反映了缺氧性脑代谢，并且在诊断时脑脊液腺苷酸激酶活性升高的儿童在完成6个月抗结核治疗后临床症状正常的情况并不常见。任何能在TBM病程早期显著降低儿童脑脊液腺苷酸激酶活性的治疗方式可能对患者具有临床益处。
