ABSTRACT
OBJECTIVE To analyze the situation and causes of the shortage of drugs in centralized volume-based procurement， and to put forward countermeasures and suggestions for optimizing centralized procurement rules and improving the drug shortage supply guarantee system. METHODS The shortage data of the first five batches of centralized purchasing drugs during January 2019 and December 2021 were collected from the Shortage Database of Chinese medicine economic information； descriptive statistical analysis was performed for shortage frequency， varieties and reasons. RESULTS & CONCLUSIONS After the first five batches of centralized volumetric procurement policy landed， the frequency of drug shortage reported for selected specifications and selected enterprises increased significantly， mainly drug shortage of selected enterprises. The shortage of some varieties from selected enterprises in the short term was obvious， and most of them were commonly used clinical drugs. The occurrence of drug shortages was affected by various links such as the production， circulation and use， and the main reasons were shortage or monopoly of raw materials. In order to ensure the drugs supply， the government should scientifically assess the risk of production interruption of enterprises， further optimize centralized procurement rules， improve the reporting system for drug shortages， and attach importance to the supply of key drugs； in addition， hospitals should take a variety of measures within the scopes of policies to flexibly respond to drug shortages so as to avoid delaying the treatment of patients.
ABSTRACT
24 cases of hypoparathyroidism, 24 cases of normal control were included. The levels of enzymes, concentration of Ca were measured in all cases. The electrocardiogram was carried out in the hypoparathyroidism group carries. The levels of CK, CK-MB, BHDH, LDH and AST were significantly higher in patients with hypoparathyroidism than in normal control cases(P＜0.05), especially the levels of CK and CK-MB (P＜0.01). After the treatment, the electrocardiogram and enzymes basically returned to normal. The changes of enzymes in patients with hypoparathyroidism may play a benchmark about the severity and treatment.
ABSTRACT
Objective: To analyze the chemical constituents of Polygonum multiflorum extract which may cause human liver cell damage and to explore the mechanism. Methods: Raw and processed Polygonum multiflorum were extracted by 70% ethanol, then raw and processed Polygonum multiflorum water-eluted material (RW and PW), 50% ethanol-eluted material (R50 and P50) and 95% ethanol-eluted material (R95 and P95) were obtained by absorbing through AB-8 macroporous resin, followed by water, 50% ethanol and 95% ethanol elution in order. The water extracts of raw and processed Polygonum multiflorum (RWE or PWE) were obtained by boiling them in water as usual. Normal human liver L02 cells were treated by different concentrations of eluted Polygonum multiflorum materials for different time, and the cell growth inhibition of each group was determined by methylthiazolyldiphenyl-tetrazolium bromide method. The chemical constituents which had a significant cytotoxicity to L02 cells were analyzed by high-performance liquid chromatography (HPLC). Morphological changes of L02 cells were observed by Giemsa staining and cell cycle distribution was observed by flow cytometry. Results: It was found that 95% ethanol-eluted extracts of raw and processed Polygonum multiflorum showed significant growth inhibition on normal human liver L02 cells, while the other components showed no significant inhibition on cell growth. HPLC analysis showed that the main component in 95% ethanol-eluted extract of raw and processed Polygonum multiflorum was emodin at content of (18.53+/-2.96)% and (10.28+/-1.34)% respectively. Cell cycle analysis showed that 95% ethanol-eluted material of Polygonum multiflorum and emodin had a similar significant effect of S phase arrest and all could induce L02 cell apoptosis. Conclusion: The main part of Polygonum multiflorum causing liver cell damage is the 95% ethanol-eluted extract, and emodin is one of the important chemical constituents leading to liver cell damage.