RESUMO
OBJECTIVE: To analyze the clinical features of occupational chronic toxic peripheral neuropathy caused by1-bromopropan( 1-BP). METHODS: Clinical data of 4 patients who suffered from occupational chronic toxic peripheral neuropathy caused by 1-BP were collected for retrospective analysis. RESULTS: The 4 male patients were ultrasonic cleaning operation workers in a hardware vacuum coating enterprise. They were exposed to high levels of 1-BP for 9-11 months. The main clinical manifestations were varying degrees of sensory disorder and dyskinesia. The main symptoms were progressive increase of numbness and fatigue in the lower extremities. These symptoms might be accompanied by unsteady gait.Physical examination showed muscle strength weakness in the double lower limbs. The hypalgesia,pselaphesia,topesthesia and pallesthesia decreased in the double lower limbs or 4 limbs. The bilateral achilles tendon reflex mainly showed reduced or disappeared. One case had sensory ataxia. Electroneuromyography examination showed different levels of peripheral nerve damage among the cases. The motor nerve conduction velocity and sensory nerve conduction velocity reduced commonly. The axon and myelin sheath damage were visible. On the basis of GBZ / T 247-2013 Diagnosis of Occupational Chronic Toxic Peripheral Neuropathy Caused by Chemicals,these cases were diagnosed as occupational chronic toxic peripheral neuropathy caused by 1-BP. CONCLUSION: Long-term exposure to high level 1-BP can lead to chronic poisoning with peripheral nervous system damage. The diagnosis can be made based on the 1-BP exposure history,clinical features and the neurogenic damage found in electroneuromyography examination.
RESUMO
OBJECTIVE: To investigate the effect of cadmium chloride on the expression of kidney injury molecule-1( KIM-1)in human renal tubular epithelial cells( HK-2 cells). METHODS: HK-2 cells at logarithmic phase were divided into a control group and 5 treatment groups that were treated with 5. 0,10. 0,20. 0,50. 0 and 100. 0 μmol / L of cadmium chloride dissolved in phosphate buffer solution. Cell pathology observation was carried out after 24 hours of cultivation. The methyl thiazolyl tetrazolium assay was used to calculate the survival rate of HK-2 cells. The expression of KIM-1 mRNA and protein were detected by the reverse transcription-polymerase chain reaction and Western blotting analysis respectively.RESULTS: There were no cellular morphologic change in HK-2 cells in the control group,the 5. 0 and 10. 0 μmol / L groups;the HK-2 cells showed different degree of swellings or vacuoles in the 20. 0 and 50. 0 μmol / L groups; a large number of cells were found dead in the 100. 0 μmol / L group. The cell survival rates of HK-2 cells in the 20. 0,50. 0 and 100. 0μmol /L groups were lower than those of control group,the 5. 0 and 10. 0 μmol /L groups( P < 0. 05). The pairwise comparison among survival rates of the 20. 0,50. 0 and 100. 0 μmol / L groups showed significant difference( P < 0. 05).The expression levels of KIM-1 mRNA and protein in the 20. 0 and 50. 0 μmol / L groups were higher than those of control group,the 5. 0 and 10. 0 μmol / L groups( P < 0. 05). The levels of KIM-1 mRNA and protein in the 50. 0 μmol / L group were higher than those of the 20. 0 μmol / L group( P < 0. 05). CONCLUSION: Cadmium chloride at certain concentration can increase the expression of KIM-1 mRNA and protein in HK-2 cells. Therefore,the expression of KIM-1 could be used as one of the effect biomarkers for cadmium induced kidney tubule injury.