Jann S, Comini A, Pellegrini G
Clinica Neurologica II, Università di Milano.
Ital J Neurol Sci. 1988 Feb;9(1):83-8. doi: 10.1007/BF02334413.
We describe a patient with leptomeningeal carcinomatosis in whom no primary malignancy was found in spite of extensive laboratory investigations. The diagnosis was supported, however, by cytological and biochemical CSF examination. Of particular interest in this setting was the low level of glycorrhachia. In order to understand better the mechanism of hypoglycorrhachia, the patient was subjected to I.V. glucose loading; serial samples of blood and CSF were obtained to determine glucose and lactic acid levels. We found that: 1) The low CSF glucose concentration was not increased by I.V. infusion of sugar; 2) the high basal CSF lactic acid level was not further stimulated by I.V. glucose loading. These data suggest that hypoglycorrhachia was not due to an increased utilization of glucose by neoplastic cells that infiltrate the meninges but to abnormal transport of glucose from blood to CSF.
我们描述了一名患有柔脑膜癌病的患者，尽管进行了广泛的实验室检查，但未发现原发性恶性肿瘤。然而，脑脊液的细胞学和生化检查支持了该诊断。在这种情况下，特别令人感兴趣的是脑脊液中糖含量较低。为了更好地理解脑脊液低糖的机制，对该患者进行了静脉注射葡萄糖负荷试验；采集了血液和脑脊液的系列样本以测定葡萄糖和乳酸水平。我们发现：1）静脉输注糖并未使脑脊液中低葡萄糖浓度升高；2）静脉注射葡萄糖负荷并未进一步刺激脑脊液中基础乳酸水平升高。这些数据表明，脑脊液低糖并非由于浸润脑膜的肿瘤细胞对葡萄糖利用增加所致，而是由于葡萄糖从血液到脑脊液的转运异常。
