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Pharmacological Management of Amyotrophic Lateral Sclerosis
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Shalini Mani, Chahat Kubba, Tanya Sharma, Manisha Singh
Treatment of ALS using anti-excitotoxins is still in active research phase and has shown a promising clinical outcome (Venkova-Hristova et al., 2017). The benzothiazole compound R-pramipexole came into view as a drug from research on Parkinson’s disease that can save dopaminergic neurons from glutamate excitotoxicity. The neuroprotective effects observed to be triggered downstream from the glutamate-gated receptors and further intended to perform action in the mitochondria (Izumi et al., 2007). Thus, potential neuroprotective compounds are hypothesized to have a considerable clinical benefit in ALS patients. Unsurprisingly, therapeutic approach that belongs to this class has recruited numerous patients in their respective phase 3 trials. Clinical trials with TCH346 (Miller et al., 2007) and olesoxime (Lenglet et al., 2014) have recruited more than 500 patients each, with dexpramipexole (Cudkowicz et al., 2011) and xaliproden (Lacomblezetal, 2004) recruiting more than 1000 and 2000 patients, respectively. Dexpramipexole falls under the category of compounds termed as benzothiazoles, which shows a broad range of biological activity. As per studies conducted in preclinical models, dexpramipexole has demonstrated its neuroprotective activity in CNS to be dependent on the function of mitochondrial (Alavian et al., 2012), including the improvement in survivability of SOD1G93A mouse model (Bennett et al., 2014). However, this compound was not capable to exhibit its therapeutic effects in ALS (Cudkowiczetal., 2013).
Metabolic Therapies in the Management of Heel Pain
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
Another common medication that causes complications in foot health are chemotherapeutic agents, including platinum drugs, taxanes, epothilones and vinca alkaloids.8 Chemotherapy-induced peripheral neuropathy is the most common podiatric side effect that is not only painful and uncomfortable for the patient but can lead to overuse of the plantar fascia and weakness in the intrinsic foot muscles. This can be quite distressing for patients; however, recent evidence from several small pilot studies has shown that the use of vitamin E might help prevent or lessen the side effects of chemotherapy-induced peripheral neuropathy and thus the risk of plantar fasciitis. Other agents that look promising in preliminary studies include glutamine, glutathione, N-acetylcysteine, oxcarbazepine and xaliproden.8
Development of palliative medicine in the United Kingdom and Ireland
Published in Eduardo Bruera, Irene Higginson, Charles F von Gunten, Tatsuya Morita, Textbook of Palliative Medicine and Supportive Care, 2015
Prevention is the best strategy against CIPN, but until now there is no intervention convincingly effective to prevent it. Vitamin E, intravenous infusions of calcium and magnesium, glutathione, glutamine, N-acetylcysteine, oxcarbazepine, amifostine, and xaliproden have been tested with conflicting results, as others have reviewed [7,8]. A Cochrane systemic review of interventions for preventing neuropathy by cisplatin and other platin compounds concluded that "At present, the data are insufficient to conclude that any of the Table 119.1 Classic chemotherapy drugs that can cause CINPo,c
Implications of spirometric reference values for amyotrophic lateral sclerosis
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2019
Ruben P.A. van Eijk, Jaap N.E. Bakers, Michael A. van Es, Marinus J.C. Eijkemans, Leonard H. van den Berg
We retrospectively determined the predicted FVC in liters according to five reference standards: Knudson ’76 (14), Knudson ’83 (15), European Community for Steel and Coal (ECSC) (16), National Health and Nutrition Examination Survey (NHANES) III (17), and GLI-2012 (4). The Knudson ’76, ’83, and ECSC reference standards are still used in ALS clinics (personal communication) and ALS clinical trials (e.g. the Ceftriaxone trial used Knudson ’83 (18), whereas the Xaliproden trials were using ECSC (19)), despite their known disadvantages (5). The GLI-2012, the most recent standard and based on >74,000 global control subjects (4), has been endorsed by both the American Thoracic Society (ATS) and European Respiratory Society (ERS) and will probably supersede previous reference standards (5). The observed FVC was standardized according to the prediction per reference standard and expressed as percentage from normal (%predicted FVC). Survival time was defined as the time from trial inclusion until death from any cause. Patients who remained alive during the trial were censored after their last follow-up visit. The severity of dyspnea symptoms was assessed using item 10 of the revised ALS functional rating scale (ALSFRS-R).
Treating cardiovascular complications of radiotherapy: a role for new pharmacotherapies
Published in Expert Opinion on Pharmacotherapy, 2018
Nathalie Donis, Cécile Oury, Marie Moonen, Patrizio Lancellotti
Since TGFβ1 is a key player in the development of long-term radiation-induced cardiac fibrosis, targeting its pathway could likely prevent RICVD. While Boerma et al. showed that xaliproden, a TGFβ1 inducer, worsens RICVD in rats, Rabender et al. reported that inhibiting TGFβ receptor I (TGFβRI) with IPW-5371 reduces radiation-induced mortality and cardiac fibrosis, in addition to preserving arterial oxygen saturation and cardiac contractility [53,112]. TGFβ signaling is also often deregulated in cancer, playing both pro-tumoral and antitumoral roles depending on cancer characteristics. Several studies are ongoing to evaluate the possibility to target this pathway as anticancer therapy. So, once again, further investigations are required in order to study how TGFβRI inhibitors might act in the complex situation of RICVD and cancer.
Persistent prevention of oxaliplatin-induced peripheral neuropathy using calmangafodipir (PledOx®): a placebo-controlled randomised phase II study (PLIANT)
Published in Acta Oncologica, 2018
Bengt Glimelius, Nebojsa Manojlovic, Per Pfeiffer, Baadur Mosidze, Galina Kurteva, Mia Karlberg, Devalingam Mahalingam, Peter Buhl Jensen, Jan Kowalski, Marie Bengtson, Malin Nittve, Jacques Näsström
This randomised placebo-controlled clinical study shows a clear decrease in OIPN. A few randomised trials have previously reported significant protection against peripheral neuropathy from an intervention perspective (intravenous calcium-magnesium, xaliproden, venlaflaxine, reduced glutathione and oral glutathione) [29–33]. However, a meta-analysis including 42 trials recently concluded that no intervention has favourably influenced the rate of CIPN, including that caused by oxaliplatin [11]. The neuroprotective effects seen here appear clinically meaningful, delaying both the onset and reducing the intensity, and were seen both in the acute and in the early chronic phase. Longer follow-up times are needed in future trials since the OIPN may remain for many years. At the same time, no toxicity could be registered to the active agent calmangafodipir and there were no signs of any tumour protective effect to the chemotherapy. A decrease in acute toxicity may, however, potentially mean that oxaliplatin dose reductions or actual termination are delayed, increasing late toxicity.