PubMed · 10148447
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I Ziment, H Flaster. 1993. Using bronchodilators effectively.. https://pubmed.ncbi.nlm.nih.gov/10148447/
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The present paper describes the synthesis and characterisation of new hydrogel systems designed for colon targeting. The gels were composed of methacrylated inulin (MA-IN), copolymerized with the aromatic azo agent bis(methacryloylamino)azobenzene (BMAAB) and 2-hydroxyethyl methacrylate (HEMA) or methacrylic acid (MA). The gels were assessed by studying the influence of various parameters on the dynamic and equilibrium degree of swelling. It was shown that the uptake of water in the gels was inversely proportional to the MA-IN feed concentration, the degree of substitution of the inulin backbone, and the concentration of BMAAB. The latter can probably be explained by the hydrophobic nature and rigidity of the aromatic azo agent. Incorporation of the hydrophilic monomers HEMA or MA also reduced the equilibrium degree of swelling. An increasing network density and hydrogen bonding propensity, can suggested to be responsible for this observation. It was shown that water uptake in the hydrogels was controlled by both relaxation and diffusion mechanisms (anomalous behaviour). When the release of the model drug prednisolone was studied in phosphate buffer, it was shown that >80% of the drug was released during the first 3 h from hydrogels of MA-IN:HEMA. Although drug release decreased significantly from MA-IN:HEMA:BMAAB hydrogels, it remained too high: approximately 50% of the drug was released after 5 h. The same observation was made for hydrogels containing MA instead of HEMA. These results clearly point out the difficulty in finding the optimal balance between swelling to allow degradation in the colon (high swelling of the gels) and low premature drug release before the colonic environment is reached (low swelling properties).
BACKGROUND: Budesonide is a synthetic glucocorticoid used in the Crohns's disease (CD) and ulcerative colitis (UC). The aim of the study was to evaluate its efficacy in inducing and maintaining remission of CD in oral administration and in inducing endoscopic and histologic remission in distal UC when was given as enema. MATERIAL AND METHOD: Systematic review of controlled clinical trials was made and meta-analysis were performed using the Peto method. Eight studies provided data regarding CD (4 in induction of remission and 4 in maintenance therapy) and 4 regarding UC. RESULTS: CD-inducing remission: in total 560 patients were involved; 280 received 9 mg/d of budesonide and 280 received 40-46 mg/d of prednisolone. Clinical remission was similar in both groups [0.76 (0.54-1.06)] [0R (CI 95%)] and adverse events were more frequent in patients treated with prednisolone [0.42 (0.30-0.58)]. Plasma cortisol was evaluated in 292 patients (146 each group); values were significantly lower in prednisolone group [0.32 (0.20-0.50)]. CD-maintaining remission: in total 449 patients were enrolled; 174 and 90 received 3 mg/d or 6 mg/d of budesonide respectively and 185 received placebo. There were not significant differences between placebo and budesonide 3 mg/d [1.04 (0.56-1.92)]. Budesonide 6 mg/d was also similar to placebo group [0.91 (0.59-1.39)]. UC: 325 patients were included, 156 received budesonide and 169 were given conventional glucocorticoids. No significant differences were found between both groups in endoscopic remission rates [1.15 (0.71-1.88)]. CONCLUSIONS: Budesonide is as useful as prednisolone in treatment of active CD and it has a lower impact in serum cortisol levels. Nevertheless, at evaluated dose, it is not useful for maintenance therapy. In UC is as effective as conventional glucocorticoids.
Idiopathic pulmonary fibrosis is a progressive and usually fatal lung disease characterized by fibroblast proliferation and extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture. Although the pathogenetic mechanisms remain to be determined, the prevailing hypothesis holds that fibrosis is preceded and provoked by a chronic inflammatory process that injures the lung and modulates lung fibrogenesis, leading to the end-stage fibrotic scar. However, there is little evidence that inflammation is prominent in early disease, and it is unclear whether inflammation is relevant to the development of the fibrotic process. Evidence suggests that inflammation does not play a pivotal role. Inflammation is not a prominent histopathologic finding, and epithelial injury in the absence of ongoing inflammation is sufficient to stimulate the development of fibrosis. In addition, the inflammatory response to a lung fibrogenic insult is not necessarily related to the fibrotic response. Clinical measurements of inflammation fail to correlate with stage or outcome, and potent anti-inflammatory therapy does not improve outcome. This review presents a growing body of evidence suggesting that idiopathic pulmonary fibrosis involves abnormal wound healing in response to multiple, microscopic sites of ongoing alveolar epithelial injury and activation associated with the formation of patchy fibroblast-myofibroblast foci, which evolve to fibrosis. Progress in understanding the fibrogenic mechanisms in the lung is likely to yield more effective therapies.