Цель. Сравнительный анализ клинической эффективности, длительности госпитализации и фармакоэкономической целесообразности различных схем антибактериальной терапии при тяжёлых циститах в республике Беларусь в сопоставлении с практикой в Российской Федерации. Методика. Исследование выполнено на базе урологического отделения УЗ «Городская клиническая больница скорой медицинской помощи» г. Гродно в период с марта 2023 по февраль 2024 года. В исследование включено 112 пациентов (84 женщины и 28 мужчин) в возрасте от 18 до 70 лет с диагнозом «тяжёлый острый цистит». Результаты. Комбинация цефиксим+амикацин может быть предпочтительной с точки зрения клинических результатов и экономических затрат на лечение Заключение. Тяжёлые формы цистита требуют агрессивной стартовой антибактериальной терапии с обязательным контролем лабораторных маркеров воспаления. Поскольку рост резистентности уропатогенов ограничивает эффективность монотерапии пероральными антибиотиками при тяжёлых формах заболевания, то комбинация цефиксим+амикацин может быть предпочтительной с точки зрения клинических результатов и экономических затрат на лечение. Objective. This study analyzes the efficacy, rationality, and cost-effectiveness of various antibacterial therapy regimens. Methods. The study was performed at the Urology Department of the Grodno City Clinical Emergency Hospital from March 2023 to February 2024 and included 112 patients (84 female and 28 male patients) aged 18 to 70 years with diagnosed severe acute cystitis. Results. The combination of cefixime + amikacin may be preferable in terms of clinical outcomes and treatment costs. Conclusion. Severe cystitis requires aggressive initial antibacterial therapy with mandatory monitoring of laboratory markers of inflammation. Since increasing resistance of uropathogens limits the effectiveness of oral antibiotic monotherapy in severe forms of the disease, the combination of cefixime + amikacin may be more preferable in terms of clinical outcomes and treatment costs.
Cerebrovascular diseases (CVDs) are one of the leading causes of death and disability In Russia: they rank second in the structure of mortality from diseases of the circulatory system and in the overall mortality of the population. Successful treatment of CVD involves an integrated approach to the problem, taking into account the compensation of cardiovascular disorders, the elimination of neurological and psychopathological syndromes, the improvement of cerebral circulation and the use of neuroprotective agents that increase the resistance of brain tissue to hypoxia and ischemia. Insufficient clinical efficacy of neuroprotectors is due to a number of objective reasons, of which only two are universal. The first of these reasons is the timing of the start of therapy in the clinic, as a rule, is outside the «therapeutic window»; the second reason is the fact that disturbance of the patency of the cerebral vessels in the affected area makes it difficult or impossible to deliver the drug to the penumbra area. The way out of this situation is the intranasal route of drug administration, which is characteristic for the analogs of regulatory peptides such as for H-Met-Glu-His-Phe-Pro-Gly-Pro-OH (MGHPPGP). The review of clinical studies indicates that MGHPPGP is clinically effective in the treatment of ischemic stroke both in the acute period of stroke and in the recovery period. The clinical efficacy of MGHPPGP was shown both in atherothrombotic and cardioembolic subtypes of stroke, against the background of blood flow disturbances in both the carotid and vertebrobasilar systems.
Болезнь Паркинсона (БП) – прогрессирующее нейродегенеративное заболевание, характеризующееся снижением уровня дофамина в substantia nigra, что приводит к типичным двигательным проявлениям (тремор в покое и ригидность мышц), а также к немоторным нарушениям (нервно-психические симптомы, нарушения сна, вегетативные дисфункции и сенсорные нарушения). Лечение заболевания проводится пожизненно, схему начальной терапии формируют с учетом возраста пациента и состояния его психических функций. При дебюте болезни до 70 лет лечение начинают с ингибиторов МАО-В или с агонистов дофаминовых рецепторов (АДР). На поздних стадиях БП (особенно у пожилых людей) целесообразно назначение комбинированных препаратов леводопы. Механизм терапевтического действия ингибиторов МАО-B связан с уменьшением степени и скорости распада дофамина, который в норме катализируется моноаминоксидазной реакцией. Препараты этой группы назначаются в качестве моно- терапии начальных стадий БП, хотя при непереносимости леводопы и АДР могут назначаться и на более поздних стадиях заболевания. Они лучше переносятся, чем леводопа и АДР, и часто назначаются совместно с ними. В настоящее время в клинике используются необратимые ингибиторы МАО-В (селегилин и разагилин), а также ингибиторы МАО-В плюс с двойным механизмом терапевтического действия, включающим ингибирование натриевых и кальциевых каналов с последующим угнетением высвобождения глутамата – сафинамид и зонисамид, являющиеся обратимыми ингибиторами МАО-В. Ингибиторы МАО-В занимают важную нишу в терапии БП. У пациентов на ранних стадиях заболевания они позволяют отсрочить момент назначения леводопа-содержащих препаратов, косвенно снижая риск развития клинически значимых поздних лекарственных осложнений, таких как флуктуации и дискинезии. При лечении БП на развернутых стадиях ингибиторы МАО-В сочетаются с леводопой и агонистами дофаминовых рецепторов, при этом не только усиливают их клиническую эффективность, но и повышают безопасность их приема. Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by decreased dopamine levels in the substantia nigra, leading to typical motor manifestations (resting tremor and muscle rigidity), as well as to non-motor disorders (neuropsychiatric symptoms, sleep disorders, autonomic dysfunctions and sensory impairments). The disease is being managed for lifelong; the initial therapy regimen is prescribed taking into account patients’ age and their mental functions state. At the disease onset before the age of 70, the therapy is started with MAO-B inhibitors or dopamine receptor agonists (DRA). In late stages of PD (especially in the elderly) it is advisable to prescribe combined levodopa formulations. The mechanism of MAO-B inhibitors therapeutic action is associated with a decrease in the extent and rate of dopamine breakdown, which is catalyzed in norm by monoamine oxidase reaction. Medicinal products of this group are administered as monotherapy at the initial stages of PD, although in case of levodopa and DRAs intolerance to they can be administered at later stages of the disease. They are better tolerated than levodopa and DRA, and are often prescribed in concomitance with them. Currently, irreversible MAO-B inhibitors selegiline and razagiline, as well as MAO-B plus inhibitors with a dual mechanism of therapeutic action, including inhibition of sodium and calcium channels with subsequent inhibition of glutamate (safinamide and zonisamide) release, which are reversible MAO-B inhibitors, are used in the clinic. MAO-B inhibitors occupy a major niche in PD therapy. In early-stage patients, they allow delaying the timing for levodopa-containing drugs initiation, indirectly reducing the risk of clinically significant late drug-associated complications, such as fluctuations and dyskinesias. In PD treatment at advanced stages, MAO-B inhibitors are combined with levodopa and dopamine receptor agonists, thus not only enhancing their clinical efficacy, but also increasing their safety.
Background: the process of studying at a medical university is associated with emotional stress, which can lead to stress and anxiety. Aim: to study the range of medications used by medical students for anxiety and (or) stress and the factors influencing their choice. Material and methods: survey of 106 students of the Medical University (GrSMU) of both sexes (74.5% female and 25.5% male) aged 17 to 25 years. Results: when feeling anxious or stressed, most students use herbal sedatives, for example, valerian tincture, etc. (51%). The second most popular are glycine (39%) and phenibut (33%). Adaptol (mebicar) and Magne B6 are also very popular (26% each, respectively). In addition, Afobazole (fabomotizole) (14%), the homeopathic drug Tenoten (10%) and (less than 3% of respondents each): Dapten (mebicar), Noofen (phenibut), paroxetine, Grandaxin (tofisopam), chamomile herbal tea. Conclusions: The vast majority of students do not use medications to reduce anxiety, which may indicate that the level of stress and anxiety in most students is low. Due to easier access to treatment, students prefer over-the-counter medications.
Treatment of rheumatoid arthritis is a complex and time-consuming process that does not always lead to significant results both due to poor effectiveness of drugs and drug toxicity. It means we need to search for new pharmacological targets to influence the pathological process, one of which is inhibition of proteinase-activated receptors 2 (PAR2 receptors) activity. In 2016–2019, synthesis of low-molecular-weight antagonists of PAR2 receptors belonging to 4,5-dihydroisoxazole-5-carboxamide derivatives was carried out, and in 2023 their anti-inflammatory efficacy was examined using the formaldehyde edema model. The most effective laboratory R004 compound was tested on a model of autoimmune pristane-induced inflammation in rats. During treatment of chronic inflammation in rats, R004 inhibited significant development of edema of feet, damage to small joints, and specific changes in the formula of white blood, and according to biochemical blood test led to normalization of liver and kidney functions and energy metabolism. R004 turned out to be more effective and safer than the comparator drugs such as diclofenac sodium and dexamethasone.
Glaucoma is a disease associated with increased intraocular pressure (IOP). Of the pharmacological agents for treating glaucoma, there are drugs of the first (most effective and safe) and second-line treatment. First-line treatment includes prostaglandin analogs and beta-blockers. The currently used prostaglandin analogs (latanoprost, bimatoprost, tafluprost and travoprost) are PG F2α analogs that act through stimulation of FP receptors. They are distinguished by the optimal ratio of effectiveness and risk of side effects. They are convenient for the patient because for the therapeutic effect, it is enough to prescribe 1 time per day. As a result, it is rational to start the treatment of glaucoma with a drug in this group. In terms of pharmacoeconomics, the most affordable prostaglandin drug is latanoprost, which is generally as effective as other prostaglandin analogs. β-adrenergic blockers reduce the production of intraocular fluid, the formation of which is controlled by β1- and β2-adrenergic receptors. Therefore, non-selective β-blockers (timolol, levobunolol, metipranolol, and carteolol) have a pharmacodynamic advantage over selective β1-adrenergic antagonists (betaxolol). Conducted clinical studies of β-blockers have shown that given the cost, efficacy and safety, timolol was the most preferable treatment for glaucoma. In the presence of medical contraindications to the use of first-line drugs or to enhance their effectiveness, α2-agonists (apraclonidine and brimonidine), carbonic anhydrase inhibitors (usually local action: dorzolamide and brinzolamide), M-cholinomimetics (pilocarpine, carbachol and echothiopate), and also Rho-kinase inhibitors (ripasudil)
Glaucoma is the leading cause of irreversible blindness. Its leading symptom and the most important initial link of the disease pathogenesis is represented by an increase of intraocular pressure (IOP). Decrease of IOP is a basic notion in the therapy of glaucoma. Drug-induced therapy is currently the most widely spread initial intervention to decrease IOP. Prostaglandin analogues are referred to the basic group of pharmacotherapeutic agents, because they are the most effective and well tolerated. Beta-blocking agents are selected as an alternative. Other medicinal products to treat glaucoma include inhibitors of carbonic anhydrase for systemic (acetazolamide and methazolamide) and local (dorzolamide and brinzolamide) use. Systemic inhibitors of carbonic anhydrase are, on the one hand, more active than non-systemic medicinal preparations, and, on the other hand, have numerous side effects which are not safe for humans. Thus, medicinal preparations for local use are most frequently applied in the therapy of glaucoma. If necessary, they are combined with beta-blocking agents or alpha-adrenergic agonists.
Selective blocking of individual isoforms of carbonic anhydrase (CA) is now one of the main directions in the development of its inhibitors. The new 1,2,4-oxadiazole-containing sulfonamides B12 and B13 predominantly block CA II and CA IX. The study of acute toxicity of B12 and B13 showed their safety. Substance B13 caused a relatively short-term, but rapid (within 30 min) decrease in the intraocular pressure in rabbits, which indicates the promise of its use for the emergency decrease in the intraocular pressure in medical practice. Analysis of the effects of sulfonamides on the functions of CNS showed that compound B12 probably exhibit tranquilizing activity; B13 is promising for the creation of drugs that have an antidepressant effect and at the same time increase the mental and physical performance.
In developed countries, mortality from cerebrovascular diseases (CVD) is about 12%, which is second only to mortality from cardiovascular diseases. In order to make treatment of CVD successful, a complex approach to the problem is required with compensation for cardiovascular diseases (atherosclerosis, arterial hypertension, rheological properties of blood, etc.), elimination of neurological and psychopathological syndromes, improvement of cerebral circulation and use of neurotropic agents. The use of neurotropic agents by a practicing physician is complicated due to the lack of a clear classification reflecting their position and significance in CVD treatment. It is suggested that taking into account the predominant mechanism of action targeting for a pathological process, neurotropic agents should be divided into 4 groups such as neuroprotectors, neurometabolics, nootropics and neurotrophic agents (direct activators of neutrophin synthesis in the brain). The last group is related to analogues of regulatory peptides and shares positive properties with medicinal agents from other groups: they have the properties of primary and secondary neuroprotectors, neurometabolics, and produce a positive effect on cognitive functions of a healthy and sick person. Heptapeptide Semax is a typical agent belonging to this group.
Background. The purpose of the study was to calculate the cost of lowering blood pressure (BP) in the complex antihypertensive therapy of arterial hypertension (AH) with and without Cholecalciferol. Materials and methods. 154 patients with grade II AH were divided into the AH(+)CH group receiving combined antihypertensive therapy plus Cholecalciferol in a dose of 2000 IU / day and into the comparison group — AH(–)CH. Office BP and total Vitamin D levels were measured. The costs of medication were calculated. Results. During the follow-up examination, the blood level of Vtamin D increased; in the AH(+)CH group getting higher (p = 0.0000001) than in the AH(–)CH group. The per capita cost of medication in the AH(+)CH group was higher than in the AH(–)CH group ($ 106.8 and $91.5, respectively); however, the cost of SBP reduction by 1 mmHg in the AH(+)CH group was $ 3.9 lower than in the AH(–)CH group. The Cholecalciferol dose of 2000 IU/day for 3 months results in an optimum level of Vitamin D for 83 % cases, irrespective of antihypertensive therapy. The Cholecalciferol dose of 2000 IU/day from 6.5 to 12 months results in an optimum level of Vitamin D for 100 % cases. The greatest dynamics of increase in the level of 25(OH)D achieved in response to taking cholecalciferol occurs when its initial level is < 20 ng/ml. Conclusions. The economic costs of reducing SBP, with a more frequent achievement of its target values, were the lowest in combination therapy with Cholecalciferol, especially in combination with a diuretic. In addition, with complex therapy, we received not only a correction of blood pressure, but also of the Vitamin D status.
Background. The purpose of the study was to calculate the cost of lowering blood pressure (BP) in the complex antihypertensive therapy of arterial hypertension (AH) with and without Cholecalciferol. Materials and methods. 154 patients with grade II AH were divided into the AH(+)CH group receiving combined antihypertensive therapy plus Cholecalciferol in a dose of 2000 IU / day and into the comparison group — AH(–)CH. Office BP and total Vitamin D levels were measured. The costs of medication were calculated. Results. During the follow-up examination, the blood level of Vtamin D increased; in the AH(+)CH group getting higher (p = 0.0000001) than in the AH(–)CH group. The per capita cost of medication in the AH(+)CH group was higher than in the AH(–)CH group ($ 106.8 and $91.5, respectively); however, the cost of SBP reduction by 1 mmHg in the AH(+)CH group was $ 3.9 lower than in the AH(–)CH group. The Cholecalciferol dose of 2000 IU/day for 3 months results in an optimum level of Vitamin D for 83 % cases, irrespective of antihypertensive therapy. The Cholecalciferol dose of 2000 IU/day from 6.5 to 12 months results in an optimum level of Vitamin D for 100 % cases. The greatest dynamics of increase in the level of 25(OH)D achieved in response to taking cholecalciferol occurs when its initial level is < 20 ng/ml. Conclusions. The economic costs of reducing SBP, with a more frequent achievement of its target values, were the lowest in combination therapy with Cholecalciferol, especially in combination with a diuretic. In addition, with complex therapy, we received not only a correction of blood pressure, but also of the Vitamin D status.
Исследовали противосудорожную активность 10 производных декагидрохинолина на модели острой никотиновой интоксикации у мышей. Среди изученных 10 производных декагидрохинолина противосудорожной активностью обладают 3 соединения: ФАВ-66, ФАВ-69 и ФАВ-70. В дозе 1/4 LD50 они укорачивают продолжительность никотиновой интоксикации в среднем на 22,2 %, p < 0,005, увеличивают латентный период судорог в среднем на 48,9 %, p < 0,005, понижают стадию судорог, оцениваемую по 4-балльной шкале, в среднем на 60,7 %, p < 0,005, а также уменьшают продолжительность судорог в среднем на 42,4 % при p < 0,005. Эффекты ФАВ-66 более выражены и сохраняются в дозе вплоть до 1/8 LD50. Способность ФАВ-66 в эксперименте ослаблять токсическое действие никотина, вероятно, связана с блокадой н-холинорецепторов.