Tolperizone is a central type of muscle relaxant that is widely used in clinical practice for the treatment of patients with acute and chronic nonspecific lower back pain(LBP), inflammatory and degenerative-dystrophic joint diseases, and is used in the treatment of myofascial pain syndrome (MPS).The Russian market widely used drug tolperizone, which is comparable in its clinical and anti-inflammatory activity with the original tolperizone, as well as with non-steroidal anti-inflammatory drugs (NSAIDs). Tolperizone is prescribed mainly in complex therapy, as well as as monotherapy.In some studies, based on the clinical efficacy of tolperizone (200 mg 3 times a day), it is concluded that tolperizone can be considered as a promising treatment for acute muscle spasm, without causing drowsiness. In the treatment of pain syndromes and osteoarthritis (OA) of various localization, the optimal dosage regimen of tolperizone is currently recommended: oral 150-300 mg per day for a course of 14 days, or according to a 2-stage scheme of administration, first intramuscularly 1.0 ml 2 times a day for 5 injections, then switching to oral administration of 150 mg 3 times a day; with MPS, a single local intramuscular injection of tolperizone is prescribed at the trigger point. The addition of tolperizone (150 mg/s) to the scheme of complex therapy allows to achieve an earlier clinical effect in OA of the hip and ankle joints, suppressing further progression of the disease. When included in the therapy regimen of tolperizone (150 mg/s, 14 days) OA of the ankle joint, with ultrasound examination, there is a statistically significant decrease in the signs of synovitis.
Understanding the major pathological pathways and the key molecules involved in the pathogenesis of inflammatory processes in joints, particularly in osteoarthritis (OA), is crucial for drug and pharmaconutraceuticals development. OA is a degenerative joint disease that predominantly affects articular cartilage. Destruction of hyaline cartilage and restructuring of subchondral bone are accompanied by synovial inflammation in the joint, including the facet joint of the spine, manifested by pain in the joint, low back pain (LBP), and limitation of functional activity. The article discusses the relationship between immune and inflammatory mechanisms in OA of any location, including the joints of the spine. One of the mechanisms for the formation of a “vicious circle of inflammation” during the activation of discoidin receptors by endogenous type II collagen is discussed, leading to the induction of the synthesis of pro-inflammatory mediators: tumor necrosis factor α(TNFα), metalloproteinases (MMPs) 1 and 13, interleukins (IL) 1 and 6. Inflammation, in turn, leads to a decrease in the synthesis and destruction of endogenous type II collagen and, subsequently, to cartilage destruction. Cartilage fragments entering the joint space of the intercellular matrix enhance the synthesis of TNFα, IL, and MMP and exacerbate the inflammatory process. Oral ingestion of exogenous undenatured type II collagen(NK-II) helps, first, to inactivate the binding of fragments of destroyed endogenous type II collagen to discoidin receptors and to break the "vicious circle of inflammation"; secondly, through the mechanism of oral/intestinal tolerance via the lymphoid system in Peyer's patches of the small intestine, leads to the activation of immune cells (T-lymphocytes) and initiation of the immune response – the synthesis of anti-inflammatory mediators (transforming growth factor β, IL4 and IL10). The new pharmaconutraceutical Chondroguard®TRIO, which contains chondroprotectors (chondroitin sulfate and glucosamine sulfate) as well as NK-II, will make it possible to influence the key sites of the pathological process in OA.
Background. Primary immunodeficiencies (PIDs), now known as inborn errors of immunity, are a group of inherited diseases caused by defects in the genes that control the immune response. Patients with PIDs have risks of developing a severe course and/or death in COVID-19. Passive immunization with long-acting monoclonal antibodies (MABs) to SARS-CoV-2 should be considered as pre-exposure prophylaxis in patients with PIDs. Tixagevimab/cilgavimab is a combination of MABs that bind to the SARS-CoV-2 spike protein. Aim. To evaluate the efficacy and safety of pre-exposure prophylaxis of new SARS-CoV-2 infection in PIDs with the combination of tixagevimab/cilgavimab. Materials and methods. Forty eight patients diagnosed with PIDs were included in the study. Median follow-up after drug administration was 174 days. The total number of confirmed coronavirus infections in patients with PIDs as well as 6 months before and after administration of MAT were assessed. Results. In the analyzed cohort, the overall incidence of COVID-19 from pandemic onset to MABs administration was 75% (36/48), with 31% (11/36) of over-infected patients having had the infection more than once. The incidence of COVID-19 immediately 6 months before the introduction of tixagevimab/cilgavimab was 40%. All patients who had COVID-19 after pre-exposure prophylaxis had a mild infection. The incidence of COVID-19 6 months after tixagevimab/cilgavimab administration significantly decreased compared to the incidence 6 months before administration (7 and 40%, respectively; p0.001). Conclusion. The use of tixagevimab/cilgavimab in patients with PIDs is effective as pre-exposure prophylaxis and reduces the risk of severe COVID-19.
Cerebrovascular diseases (CVD) are one of the main causes of mortality and permanent disability in patients. Chronic brain ischemia (CBI) is a slowly progressive dysfunction of the brain with gradually increasing defects in its functioning, which is accompanied by energy deficiency. Early use of energy correctors, one of the representatives of which is ethylmethylhydroxypyridine succinate (EMHPS), is recommended to preserve the viability of nervous tissue in patients with CBI. A number of experimental, clinical, and randomized studies have shown that medicinal preparation (MP) containing EMHPS improve brain metabolism and blood supply, improve microcirculation, and reduce platelet aggregation. The main mechanisms of action are: antioxidant and membranotropic effects, the ability to reduce glutamate excitotoxicity, modulate the functioning of receptors and membrane-bound enzymes, restore neurotransmitter balance, and increase the energy status of the cell. The liberal MP EMHPS included in the standards of medical care for patients with stroke, angina pectoris, acute myocardial infarction. The presented data from the results of numerous studies and our own observation indicate that it is possible to correct cognitive, motor, coordination, and adaptive capabilities while taking EMGPS. Used for today the scheme of appointment of EMHPS in patients with CBI: starting from 500 mg once a day intravenously (i/v) in drip for 14 days, followed by a transition to oral reception (o/r) at a dose of 250 mg 3 times a day, a course of 60 days.
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