ABSTRACT
BACKGROUND: The early stage of avascular necrosis of the femoral head is difficult to find, easy to be ignored and misdiagnosed. Due to the relatively poor medical conditions in some areas, the treatment is often delayed, resulting in a high rate of late disability. OBJECTIVE: To summarize the related literature in and outside China, and the research on the pathogenesis of hormonal osteonecrosis of the femoral head and related signal pathway so as to understand the pathogenesis. METHODS: The databases of CNKI, Wanfang and VIP were retrieved in Chinese with the key words of “necrosis of femoral head, glucocorticoid, pathogenesis, apoptosis, signal pathway, lipid metabolism disorder, BMSCs, Wnt/β-catenin”. PubMed and MEDLINE databases were retrieved in English with the key words of “ANFH, glucocortioids, pathogenesis, cell apoptosis, signal path, lipid metabolism disorder, BMSCs, Wnt/β-catenin”. The articles regarding the pathogenesis of hormonal osteonecrosis of the femoral head were collected. Finally, 57 articles were included according to the inclusion and exclusion criteria. RESULTS AND CONCLUSION: (1) The pathogenesis of steroid-induced femoral head necrosis is the result of a combination of multiple mechanisms and factors. Currently, the accepted theories mainly include intravascular coagulation, lipid metabolism disorder, osteoporosis and cell apoptosis. However, the pathological process has not yet been fully elucidated and further in-depth research is needed. (2) At present steroid-induced femoral head necrosis has not been completely cured because its pathogenesis has not been clearly identified. The reason for this difficulty may be that animal models in a large number of experiments at present cannot satisfactorily simulate the complex pathological changes and mechanisms of human femoral head necrosis. It is hoped that animal models of femoral head necrosis can be further improved in future experiments on steroid-induced femoral head necrosis. (3) On the basis of fully understanding the pathogenesis of steroid-induced femoral head necrosis, rational clinical use of glucocorticoids and preventive and intervention measures may be the key to prevent femoral head necrosis. In addition, speeding up the research on relevant signal pathways will help investigators find targets for the prevention and treatment of steroid-induced femoral head necrosis, and hopefully find more effective therapeutic schemes.
ABSTRACT
Amulticenter, randomized, controlled study to assess the efficacy and safety of MEBO [Julphar Gulf Pharmaceutical Industries, UAE, and SanTou MEBO Pharmaceutical CO., LTD., China] in healing of chronic pressure ulcers. Eighty seven patients with 182 chronic pressure ulcers treated at six hospitals from different areas in world, between January 2003 and January 2009, were randomized into 2 groups; those in group 1 [n=46] received MEBO while those in group 2 [n=41] received Fucidin [Leo Pharmaceutical Denmark]. Data collected prospectively included demographics, nutritional status, underlying predisposing disease and co-morbidities, Ulcer surface area [SA] and healing index [HI] were calculated and compared at two-week intervals for 12 weeks. Patients in both groups had similar demographic, clinical, biochemical features, and ulcer characteristics. There was a significant increase in HI and reduction in ulcer SA on weeks two and four respectively, that was maintained through 12 weeks in patients treated with MEBO. More than half of ulcers [56.5%] treated with MEBO had complete healing [HI=1] by 12 weeks, as opposed to only 19.6% of those treated with Fucidin [P<0.00l]. Moreover, none of the patients receiving MEBO had a HI of<50% of their ulcers by 12 weeks as compared to 26.8% of those receiving Fucidin [P<0.00l]. No adverse effects or allergic reactions of topical ointment were encountered in either group. In addition to its safety, MEBO significantly promotes the healing of chronic pressure ulcers with significant increase in HI of any given ulcer as early as two weeks following initiation of treatment, and complete healing of more than 50% of ulcers by 12 weeks