Objective To summarize the research progress in antitumor mechanism of non-steroidal anti-inflam-matory drugs. Methods The domestic and international published literatures about antitumor mechanism of non-steroidal anti-inflammatory drugs in recent years were reviewed. Results The antitumor mechanism of non-steroidal anti-inflam-matory drugs was multistrata and multidigit. Conclusion Non-steroidal anti-inflammatory drugs can be used to prevent the development of colorectal cancer and also be a adjuvant therapy after radical operation for colorectal cancer.
Objective To improve the knowledge of epidemiology, diagnosis and treatment of aspirin induced asthma ( AIA) in China. Methods Thirty-six cases with AIA who were reported in 30 papers in recent 10 years were analyzed retrospectively. Results The drugs which induced AIA in China mainly included acetylsalicylic acid ( aspirin) , ibuprofen ( Fenbid, ibuprofen) , while acetaminophen ( paracetamol,Bufferin, Tylenol ) , phenylpropanoid thiazide ( Piroxicam) , methoxy-naphthalene C acid ( naproxen) ,diclofenac in rare cases. 28. 6% ( 8 /28) of AIA patients were complicated with nasal disease . AIA could occur at all ages, especially for those over 40 years ( 72. 2% , 26 /36) . No significant difference of prevalencein male and female. The onset time of AIA was less than 60min in 71. 4% and gt;120min in 38. 6% . Most patients took the medications by oral ( 83. 3% ,30/36) , but the AIA onset time was not different by different administration route. Conclusions The incidence of AIA increases in recent years because of widely use of NSAIDs. However, no awareness of NSAIDs induced asthma is common in patients and physicians. For asthma patients it must be caution to take antipyretic analgesic anti-inflammatory drugs. If necessary,methoxy-naphthalene C acid ( naproxen) and diclofenac could be better choice.
Objective To assess the effect of nonsteroidal anti-inflammatory drugs (NSAIDs) for the prevention of colorectal neoplasia. Methods A systematic review of all relevant randomized controlled trials and quasi-randomized controlled trials of NSAIDs for prevention of colorectal neoplasms was performed by using The Cochrane Collaboration recommended methods. Results Nine trials were included and assessed. There was sufficient evidence for aspirin to prevent the development of colorectal adenomas compared with placebo in three trials of high quality and large sample size with relative risk (RR) 0.81, 95% confidence interval (CI) 0.72 to 0.91 and P=0.000 5 . No adequate evidence supported aspirin in the prevention of development of colorectal cancer (RR 0.97, 95% CI 0.79 to 1.20, P= 0.79). However, there was no evidence to support sulindac and celecoxib curing or preventing colorectal adenomas or familial adenomatous polyposis (RR 0.71, 95% CI 0.49 to 1.03, P= 0.07 and RR 0.90, 95% CI 0.76 to 1.07, P=0.23). No evidence on the dose of NSAIDs was used for prevention of colorectal adenomas at present. No significant difference was seen in the number of adverse events between patients taking NSAIDs and those taking placebo (P=0.9). Conclusions Aspirin may prevent the development of colorectal adenomas and may avoid polypectomy for 1 in every 10 to 18 persons but we don’t know whether aspirin can be substituted for endoscopically removed colorectal polyps. However, the true clinical benefit for prevention of colorectal neoplasia of NSAIDs should be considered.
Objective To assess the efficacy of topical non-steroidal anti-inflammatory drugs （NSAIDs） in the treatment of osteoarthritis （OA）. Methods MEDLINE, EMBASE, Scientific Citation Index, CINAHL, The Cochrane Library, CBMdisc and abstracts from conference were searched from 1966 to March 30, 2005. Randomized controlled trials （R.CT） comparing topical non-steroidal anti-inflammatory drug （NSAIDs） with placebo or oral NSAIDs in OA were induded. Effect size （ES） was calculated for pain, function and stiffness. Relative risk （RR） was calculated for dichotomous data such as clinical response rate and adverse effect rate. Number needed to treat to obtain the clinical response was estimated. The quality of trials was assessed and sensitivity analyses were undertaken. Results Topical NSAIDs were superior to placebo in relieving pain due to osteoarthritis only in the first 2 weeks of treatment; ES （95% CI） were 0.41 （0. 16 to 0.66） and 0.40 （0.15 to 0.65） at week 1 and 2 respectively. However, the effects were short-lived and no benefit was observed over placebo at the third and fourth week. A similar pattern was observed with function, stiflhess and clinical response RR and number needed to treat. Topical NSAIDs were inferior to oral NSAIDs at week 1, and associated with more local side effects such as rash, itch or burning （RR 5.29, 95% CI 1.14 to 24. 51 ）. Conclusions Only very shortterm （less than 4 weeks） RCTs have assessed topical NSAID efficacy in OA ; after 2 weeks no efficacy above placebo has been obsevrved. There are no trial data to support the long-term use of topical NSAIDs in osteoarthritis.
Objective To investigate the medication advancement of gastrointestinal polyposis in patients with Peutz-Jeghers syndrome (PJS). Methods Literatures about the medication advancement on gastrointestinal polyposis of PJS were reviewed and analyzed. The recent development of targeting drugs, especially the data of cyclooxygenase-2 selective inhibitors and rapamycin, were emphatically summarized. Results With the deep investigation of PJS and application of selective drugs, the medication of gastrointestinal polyposis in cases of PJS has got more advancement. The extensive use of synthetic cyclooxygenase-2 inhibitors and rapamycin in clinic developed a new way to treat gastrointestinal polyposis of PJS. Conclusion The cyclooxygenase-2 selective inhibitors and rapamycin have the following features: noninvasive, high selectivity and good curative effects. They have splendid prospects in the clinical treatment of gastrointestinal polyposis in patients with PJS and are bring the treatment of gastrointestinal polyposis in cases of PJS into a targeting therapy phase.
ObjectiveTo compare the effect of bromfenac sodium hydrate ophthalmic solution and fluorometholone following sub-bowmans keratomileusis (SBK) from the aspects of subjective visual perception, ophthalmic signs and intraocular pressure. MethodsFifty myopic patients (94 eyes) who underwent SBK from April to May 2013 were divided into two groups according to the different postoperative drug treatment. Patients in group A were treated with bromfenac sodium hydrate (51 eyes), and patients in group B were treated with fluorometholone (43 eyes). To compare the effects of two kinds of drugs after SBK, results of the routine examination were recorded including uncorrected visual acuity (UCVA), refractive status, visual symptoms and signs, intraocular pressure (IOP) and Haze under Corneal Epithelium (HAZE) on pre-operational and postoperative day 1, 7, and 30. ResultsOn the 30th day, IOP in group A and group B were (9.88±2.34) mm Hg (1 mm Hg=0.133 kPa) and (11.00±2.27) mm Hg, respectively, and the difference between the two groups was statistically significant (P<0.05), but there were no statistically significant differences at other time points. There was no statistically significant difference in UCVA, refractive status, visual symptoms and signs, and corneal epithelial staining between the two groups (on day 1, 7, and 30). ConclusionBromfenac sodium and fluorometholone have the same effect in the control of postoperative visual acuity and ophthalmic inflammation. Bromfenac sodium has greater advantages in IOP control. Therefore, bromfenac sodium can substitute fluorometholone in resisting inflammation after SBK.
ObjectiveTo observe the efficacy and safety of etofenamate gel (foscavir+tramadoli hydrochloridum+gabapentin) in the treatment of acute herpes zoster. MethodsForty patients with acute herpes zoster neuralgia treated between January 2013 and June 2014 were randomly divided into two groups:control group and treatment group, with 20 in each. The patients had a visual analogue scale (VAS) pain score of seven or higher. Patients in the control group accepted conventional treatment, while those in the treatment group were treated with conventional treatment combined with etofenamate gel. Two weeks after treatment, VAS score, quality of life and sleep score, and the degree of improvement in skin paresthesia were evaluated and compared between the two groups. ResultsThe VAS score decreased significantly in both the two groups after treatment (P < 0.05), and the decrease in the treatment group was significantly more obvious (P < 0.05). The quality of life, sleep score and the degree of improvement in skin paresthesia were ameliorated significantly after treatment (P < 0.05), and the amelioration in the treatment group was significantly greater (P < 0.05). ConclusionThe early application of Ordofen can strengthen analgesia effect of the conventional treatment, improve the quality of life and sleep, and reduce skin paresthesia.
ObjectivesTo systematically review the efficacy of non-steroidal anti-inflammatory drugs (NSAIDs) on tennis elbow.MethodsPubMed, EMbase, The Cochrane Library, VIP, CNKI and WanFang Data databases were electronically searched to collect randomized controlled trials (RCTs) on NSAIDs for tennis elbow from inception to May 2019. Two reviewers independently screened literature, extracted data and assessed risk of bias of included studies, then, meta-analysis was performed by using RevMan 5.3 software.ResultsA total of 8 RCTs involving 595 patients were included. The results of meta-analysis showed that there were no significant differences in the therapeutic effect between NSAIDs and the placebo group (RR=1.10, 95%CI 0.89 to 1.35, P=0.39) or non-placebo control group (RR=0.88, 95%CI 0.77 to 1.00, P=0.06). Compared with non-placebo control group, NSAIDs group had lower VAS score difference (MD=−1.41, 95%CI −2.28 to −0.53, P=0.002).ConclusionsCurrent evidence shows that the effect of NSAIDs on tennis elbow is still uncertain. The improvement of symptoms with NSAIDs may be superior to placebo, but inferior to other treatment methods. Due to the limited quantity and quality of included studies, the above conclusions are required to be verified by more high-quality studies.
Objective To develop a diclofenac sodium-loaded gelatin scaffold with anti-inflammatory activity and provide a new avenue for alleviating the inflammatory response and enhancing cartilage regeneration in vivo. Methods Diclofenac sodium was homogeneously mixed with gelatin to prepare a diclofenac sodium-loaded porous gelatin scaffold by freeze-drying method as the experimental group, and a pristine porous gelatin scaffold was served as a control group. The general morphology of the scaffold was observed, the pore size of the scaffold was measured by scanning electron microscopy, the porosity of the scaffold was calculated by drainage method, the loading of diclofenac sodium into the gelatin scaffold was detected by fourier transform infrared spectrometer and X-ray diffraction examinations, and the release kinetics of diclofenac sodium from gelatin scaffold was tested using an in vitro release assay. The two scaffolds were co-cultured with lipopolysaccharide-predisposed RAW264.7 in vitro, and the expressions of interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) were detected by reverse transcription polymerase chain reaction (RT-PCR), enzyme-linked immuno sorbent assay, and Western blot, to detect the in vitro anti-inflammatory effect of the drug-loaded scaffold. Thereafter, the second generation chondrocytes of New Zealand white rabbits were inoculated on the two groups of scaffolds for in vitro culture, and the cytocompatibility of the scaffold was tested by live/dead staining and cell counting kit 8 assay, the feasibility of in vitro cartilage regeneration of the scaffold was evaluated via gross observation, HE staining, Safranin-O staining, and immunohistochemical collagen type Ⅱ staining, as well as biochemical quantitative analyses. Finally, the two groups of chondrocyte-scaffolds were implanted subcutaneously into New Zealand white rabbits, and after 4 weeks, the general observation, HE staining, safranin O staining, immunohistochemical collagen type Ⅱ staining, and biochemical quantitative analyses were performed to verify the cartilage regeneration in vivo, and the expression of inflammation-related genes CD3 and CD68 was detected by RT-PCR to comprehensively evaluate the anti-inflammatory performance of the scaffolds in vivo. Results The two scaffolds exhibited similar gross, microporous structure, pore size, and porosity, showing no significant difference (P>0.05). Diclofenac sodium was successfully loaded into gelatin scaffold. Data from in vitro anti-inflammatory assay suggested that diclofenac sodium-loaded gelatin scaffold showed alleviated gene and protein expressions of IL-1β and TNF-α when compared with gelatin scaffold (P<0.05). The evaluation of cartilage regeneration in vitro showed that the number of living cells increased significantly with the extension of culture time, and there was no significant difference between the two groups at each time point (P>0.05). White cartilage-like tissue was regenerated from the scaffolds in both groups, histological observation showed typical cartilage lacuna structure and specific cartilage extracellular matrix secretion. There was no significant difference in the content of cartilage-specific glycosaminoglycan (GAG) and collagen type Ⅱ between the two groups (P>0.05). In vivo experiments showed that the samples in the experimental group had porcelain white cartilage like morphology, histologic staining showed obvious cartilage lacuna structure and cartilage specific extracellular matrix, the contents of GAG and collagen type Ⅱ were significantly higher than those in the control group, and the protein and mRNA expressions of CD3 and CD68 were significantly lower than those in the control group, with significant differences (P<0.05). ConclusionThe diclofenac sodium-loaded gelatin scaffold presents suitable pore size, porosity, and cytocompatibility, as well as exhibited satisfactory anti-inflammatory ability, providing a reliable scheme for alleviating the inflammatory reaction of regenerated cartilage tissue after in vivo implantation and promoting cartilage regeneration in vivo.