This article describes the history of knowledge management with special reference to primary and secondary osteoporosis, its epidemiology and diagnostics of different forms of this disease. The discussion is focused on therapeutic modalities for the treatment of osteoporosis based on the principles of evidence-based medicine. Special attention is given to the choice of optimal medicinal preparations for the management of primary osteoporosis taking into account results of multicenter randomized placebo-controlled clinical studies and the results of evaluation of the efficacy of various pharmaceutical for the treatment of secondary osteoporosis and its mixed forms. Some of these studies are carried out based at the Endocrinological Research Centre. Peculiarities of analysis of their results are discussed along with comparative characteristics of selected pharmaceuticals.
The present guidelines on diagnostics, differential diagnostics, and methods of treatment of Cushing’s disease have been developed by a group of Russian specialists.
The present study included patients with confirmed diagnosis of ACTH-dependent hypercorticism admitted to the Department of Neuroendocrinology and Osteopathies, Endocrinological Research Centre, between 2008 and 2012. Selective blood sampling from the inferior petrosal sinuses was performed with the stimulation by decompressin administered intravenously at a dose of 8 mcg. The normalized ACTH/prolactin ratio was calculated by dividing the maximum ACTH gradient following decompressin stimulation by the ipsilateral prolactin gradient. The cut off values were calculated from the operating characteristic curves as follows: 1.5 for the prolactin gradient (sensitivity 92.5%, specificity 100%) and 1.18 for the normalized ACTH/prolactin ratio (sensitivity 85.9%; 95% CI 76.8-93.4, specificity 100%; 95% CI 60.9-100). In the study cohort (n=70), the normalized ACTH/prolactin ratio proved to be a more specific but less sensitive parameter than the routine analysis of the ACTH gradient (sensitivity 98.4%, specificity 83.3%). Areas under the operating characteristic curves were on the whole identical. However, comparison of the diagnostic value of selective blood sampling from the inferior petrosal sinuses in combination of the determination of the prolactin gradient and normalized ACTH/prolactin ratio with the results obtained in the patients in whom the catheter position was not controlled (n=47) revealed the advantages of the former approach in terms of both the number of unverified causes of hypercorticism (1 versus 6) and the area under the operating characteristic curves 0.964 (95% CI 0.897-1.032) among 70 patients and 0.910 (95% CI 0.821-0.998) among the first 47 patients (included in the analysis confined to the confirmed cases). It is concluded that the determination of the prolactin gradient and calculation of the normalized ACTH/prolactin ratio allow to increase the diagnostic value of selective blood sampling from the inferior petrosal sinuses under decompressin stimulation. This inference is especially true of doubtful cases.
The present review is concerned with the up-to-date methods currently available for diagnostics of endogenous hypercorticism. The clinical picture of this condition is considered in conjunction with the epidemiological data, identification of risk groups and the choice of the patients for the screening studies. The main attention is given to the diagnostic modalities of the highest informative value, technically simple and providing readily interpretable results, viz. measurement of cortisol in daily urine, minor dexamethasone test, determination of cortisol in evening saliva). The estimation of sensitivity of these techniques, their specificity, and cut-off values is discussed. The procedures and limitations of each test are described in much detail. In addition, an algorithm for the performance of two or more tests is proposed allowing to lower the maximum sensitivity and specificity levels of the determination. The methods of screening are presented in such a way as to facilitate their practical application by the general practitioners and specialists in related disciplines for the establishment of diagnosis of endogenous hypercorticism (but not elucidation of its origin).
ВВеДениеВ эндокринологии принято рассматривать кость в качестве органа-мишени для таких гормо-нов, как половые гормоны, гормон роста, парати-реоидный гормон (ПТГ), D-гормон, кальцитонин, а также целый ряд других гормонов, осуществля-ющих регуляцию костного обмена [1,2]. Однако исследо-вания последних лет показывают, что кость обладает само-стоятельной эндокринной функцией, секретируя, по мень-шей мере, два гормона -фактор роста фибробластов 23 и остеокальцин.Фактор роста фибробластов 23 (ФРФ23) синтезирует-ся остеоцитами и является основным регулятором обмена фосфора в организме. Остеокальцин секретируется преиму-щественно остеобластами и в декарбоксилированном виде, способен связываться с собственным рецептором на бета-клетках поджелудочной железы и клетках Лейдига яичек. Таким образом, декарбоксилированная форма остеокальци-на участвует в регуляции энергетического обмена и половой функции у мужчин [3]. регуляция фосфорно-кальциевого обменаТрадиционно считается, что за регуляцию фосфорно-кальциевого обмена отвечает биологическая ось ПТГ/ви-тамин D. В ответ на снижение уровня кальция в сыворотке крови в околощитовидных железах увеличивается продук-ция ПТГ. Воздействуя на почечные канальцы, ПТГ активи-рует фермент 1a-гидроксилазу, в результате чего 25-гидрок-сиколекальциферол превращается в активный 1,25-дигидро-колекальциферол (1,25(ОН)2D), или D-гормон. D-гормон увеличивает всасывание кальция и фосфора в желудочно-кишечном тракте. Кроме того, за счет влияния на рецепторы остеобластов и остеокластов, ПТГ стимулирует ремодели-рование кости, в процессе которого из костной ткани высво-бождаются соли кальция (Рисунок 1).Открытие ФРФ23 позволило расширить современные представления о фосфорно-кальциевом обмене и включить данный гормон в ось ПТГ/витамин D в качестве контр-регулирующего элемента, приводящего к снижению уровня 1,25(ОН)2D и увеличению выведения фосфатов почками (Рисунок 2). Кроме ФРФ23 обнаружены и другие новые . В настоящее время биологическая роль ФРФ23 активно изучается в связи с его влиянием на метаболизм фосфатов при хронической болезни почек (ХБП) и развитие вторич-ного гиперпаратиреоза. ФРФ23 рассматривается как воз-можный предиктор развития минерально-костных осложне-ний ХБП на доклинической стадии для ранней коррекции нарушений и замедления их прогрессирования. Возможно, ФРФ23 и его ко-рецептор Клото вовлечены в механизмы раз-вития атеросклероза у пациентов с почечной недостаточно-стью. Соответственно изучаются перспективы фармаколо-гического влияния на ФРФ23, которое может открыть новые перспективы в лечении осложнений ХБП [5,6]. Проводятся исследования влияния ФРФ23 на процессы, не связанные с фосфорно-кальциевым обменом, так, на данный момент, из-вестно об участии гормона в развитии гипертрофии левого желудочка [7]. Общие сведения о ФрФ23ФРФ23 в основном секретируется остеоцитами в кости, однако, в небольшом количестве экспрессируется в слюн-ных железах, желудке, скелетных мышцах, головном мозге, молочных железах, печени и сердце. На молекулярном уров-не ФРФ23 представляет собой белок молекуля...
This review of the literature has been dedicated to experimental and clinical studies of mechanism of action and efficacy of 1—34 amino acid fragment of parathyroid hormone — teriparatide as well as others contries experience of its prescribtion. Teriparatide is an osteoanabolic agent which stimulates bone formation by affecting bone modeling and by stimulating bone remodeling. The effects on modeling lead to increased bone formation whereas the effects on bone remodeling lead to increased bone turnover. Thus, in its mode of action teriparatide differs from all others medicines currently available to treat osteoporosis. Daily subcutaneous injections of teriparatide are proved to be effective to prevent low-traumatic vertebral and non-vertebral fractures in postmenopausal women with the history of vertebral fractures. Teriparatide is effective to treat osteoporosis in male and even more effective than alendronate to treat glucocorticoid-induced osteoporosis. Due to high cost and some restriction related to the duration of therapy (up to 18 months in Russia and 24 months in others countries) teriparatide should be recommended to treat severe osteoporosis in patients with a history >1 moderate clinical vertebral fracture or two or more vertebral fragility fractures or in case the previous treatment was not effective. Teriparatide should be prescribed after bisphosphonates or other antiosteoporotic treatment, but not in the combination with bisphosphonates. The prescribtion of bisphosphonates after teriparatide is effective to maintaine and further improve the effect. Thus, teriparatide is effective to treat severe osteoporosis and osteoporosis resistant to other therapy.
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