PubMed · 12001812
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2002. Profile summary.. https://doi.org/10.2165/00126839-200203020-00010
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PURPOSE: Antiresorptive therapy are usual treatment of osteoporosis, but they prevent no more than 40 or 60% of osteoporotic fracture. Thus, there is a need for osteoformative agents that can further augment bone mass and reduce risk fracture more substantially. CURRENT KNOWLEDGER AND KEYPOINTS: Daily injections of 1-34 aminoterminal fragment of PTH increase bone formation and bone mass. A randomized study recently demonstrated that PTH 1-34 decrease the risk of vertebral and non vertebral fracture, and the place of this treatment in the strategy of osteoporosis treatment is to demonstrate. Oral administration of strontium salt at low dosage level stimulate bone formation and decrease bone resorption. Preliminary data needs to be confirmed by a multicenter antifracture study. Retrospective results with statins in three international studies have not be confirmed by the only randomized clinical trial. Use of low dose intermittent fluoride therapy are still recommended by some authors. FUTURES PROSPECTS AND PROJECTS: Effects of insuline like growth factor I and other growing factor on bone turnover have to be confirmed in human, and pharmacological and tolerance problems have to be solved.
Ovarian cancer leads to more fatalities than any other form of gynaecological cancer in North America and Europe. Over the last 30 years survival figures have improved somewhat due to improvements in diagnosis, surgery and chemotherapy. Despite these advances, the majority of patients will die from their disease, with the overall 5-year survival being just 30%. The majority of patients with this disease will require treatment with cytotoxic chemotherapy. It is now well established that the platinum agents (cisplatin or carboplatin) are the most important drugs to be included in first-line regimens. More recently, randomised trials have confirmed the benefit of the addition of taxanes to platinum-containing regimens and the standard of care has become the combination of carboplatin and paclitaxel. Several unanswered questions remain regarding the optimal schedule, the optimum duration of treatment, possible benefits to be gained from the addition of other drugs and whether paclitaxel the best taxane. Despite high response rates to first line chemotherapy, the majority of patients with advanced ovarian cancer will relapse and will be candidates for further chemotherapy, which can palliate symptoms and improve survival even in recurrent disease. For a patient relapsing within six months of first-line treatment, studies have shown that there is little point in rechallenge with the same drugs. However, for patients who have a longer treatment-free interval the response rates to rechallenge with platinum is significant. A number of drugs have been shown to have activity in platinum- and taxane-refractory disease and are approved for this and/or other applications. These include topotecan, etoposide, pegylated liposomal doxorubicin, epirubicin, gemcitabine, altretamine, oxaliplatin and vinorelbine. Anti-oestrogens such as tamoxifen have a small but significant response rate. Recurrent ovarian cancer is a good setting to test investigational agents and compounds with promising activity including new platinums and taxoids, as well as a range of new compounds. Non-cytotoxic approaches that are showing promise include therapies designed to overcome drug resistance, signal transduction inhibitors, immunotherapy and gene therapy.
The information deduced from the genome sequence of Mycobacterium leprae is of immense value for the chemotherapy of leprosy. Knowing the complete set of genes, enzymes and proteins allows us to understand why some drugs are without effect whereas others are fully active. It may also enable better use to be made of existing drugs, such as beta-lactams, and opens new avenues for the development of novel compounds. M. leprae is relatively susceptible to a wide range of drugs, unlike the highly related tubercle bacillus, and several new multidrug regimens are in clinical trials. Genomics provides a number of possible explanations for this broader susceptibility as some of the genes encoding enzymes involved in antibiotic inactivation have decayed whereas the number of transporters available to contribute to drug efflux is considerably lower than in Mycobacterium tuberculosis. Several leads for new drug targets have been uncovered.