ABSTRACT
Objective To explore the effect of Ginkgo leaf extract and dipyridamole injection combined with methylcobalam on nerve conduction velocity of nerve entrapment sites in the upper limbs in patients with diabetic peripheral neuropathy (DPN).Methods Two hundred and eight type 2 diabetic patients with DPN,admitted to our hospital from January 2008 to June 2011,were selected in our study,and randomly divided into an observation group (n=103) and a control group (n=105).Dietary regulation,exercises and glucose control were conducted in both groups.In the control group,patients were given methylcobalamin at the dose of 1000 μg,three times a day.In the observation group,patients were given methylcobalamin (1000 μg,three times a day) plus Ginkgo leaf extract and dipyridamole injection of 20 mL once a day.All treatments lasted for four weeks.The sensory conduction velocity (SCV),motor conduction velocity (MCV) and sensory nerve action potential (SNAP),compound muscle action potential (CMAP) and distal motor latency (DML) of median and ulnar nerves were measured and compared before and four weeks after the treatments.Results The DML was shortened,and SCV and amplitude of median nerve were improved.Segmental MCV of above-below elbow,SCV and amplitude of ulnar nerve were significantly improved in both groups after the treatments as compared with those before treatment (P＜0.05); the total effective rate of the observation group was significantly higher than that of the control group (P＜0.05).Conclusion The nerve electrophysiological characteristics of nerve compression sites in the upper limbs is sensitive for assessing injury and treatment effect in patients with DPN; the combination of Ginkgo leaf extract and dipyfidamole injection and methylcobalam is superior than methylcobalam alone in improving the nerve conduction of diabetic patients.
ABSTRACT
Objective To investigate the correlation of serum cystatin C and creatinine levels with cerebral infarction. Methods Eighty-four patients with cerebral infarction diagnosed by clinical manifestations, CT and (or) MRI and 76 healthy subjects were selected. Cystatin C level was tested by enzyme-linked immunosorbent assay (ELISA) and creatinine level was tested by the method of nitroxanthic acid. The correlation of cystatin C and creatinine levels with cerebral infarction was explored. Results The level of serum cystatin C in the cerebral infarction group (1.69±0.60 mg/L) was significantly lower as compared with that in the control group (2.00±0.67 mg/L) (t=-3.084, P=0.002); the level of serum creatinine in the cerebral infarction group (86.62±14.02 μmol/L) was significantly higher as compared with that in the control group (80.88±13.71 μmol/L) (t=2.611, P=0.010). Negative correlation between level of serum cystain C and cerebral infarction was noted (r=-0.238, P=0.002),while the level of serum creatinine was positively related to cerebral infarction (r=0.208, P=0.010).Conclusion A close correlation between cerebral infarction and both the levels of cystain C and creatinine exists, with cystatin C being a protective factor and creatinine being a risk factor for clinical cerebral infarction.