Treatment of high fracture risk patients in routine clinical practice

Lesnyak, Olga; Gladkova, E. N.; Aleksandrov, N. A.; Belaya, Zhanna; Belova, Ksenia; Bezlyudnaya, N V; Dobrovolskaya, O. V.; Dreval, A. V.; Ершова, О. Б.; Grebennikova, T. A.; Kryukova, I. V.; Мазуренко, С. О.; Priymak, Diana; ROZhINSKAYa, L Ya; Samigullina, R.; Solodovnikov, Alexander; Торопцова, Н. В.

doi:10.1007/s11657-020-00851-z

Cited by 4 publications

(5 citation statements)

References 22 publications

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“…Today, we are not able to distinguish to which factor was predominately responsible for the loss of BMD. The decision in favor of denosumab was made on the basis of the rapid onset of action [ 17 , 18 ], the expected reduction of vertebral fracture risk, and the fact that denosumab—unlike bisphosphonates—does not accumulate in bone and because the reluctance of the health care provider to cover the costs of teriparatide [ 19 ]. It will be interesting to further investigate the BMD changes in the 12 months after her 2nd pregnancy without denosumab treatment.…”

Section: Discussionmentioning

confidence: 99%

Influence of denosumab on bone mineral density in a severe case of pregnancy-associated osteoporosis

2021

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Pregnancy and lactation-associated osteoporosis (PLO) with predominantly subsequent vertebral fracture is a rare but severe disease with an estimated incidence of 0.4 in 100,000. In the past, patients with PLO have been predominantly treated with oral and i.v. bisphosphonates to reduce subsequent fracture risk. Hereby, the use of bisphosphonates in premenopausal women is controversial, as bisphosphonates know to persist in bone for many years and can be exposed and circulate in maternal serum and subsequently pass the placenta barrier and may have a detrimental effect on fetal bone health. Here we report the effects of denosumab on the bone mineral density (BMD) and subsequent fracture risk in PLO. In this case presentation, denosumab was administered postpartum with 3000 IE vitamin D and 1000 mg of calcium daily in a patient with PLO and vertebral fracture of L1 and L4. After 18 months of treatment with denosumab, we could demonstrate a clinical significant increase of BMD at the lumbar spine, femoral neck, and total hip of 32.2%, 13.0%, and 11.5% respectively with no further subsequent fractures. As the patient had regular menstrual cycles and considered a further pregnancy, denosumab treatment was terminated and soon a second pregnancy occurred. After the second pregnancy, BMD decreased at the lumbar spine, femur neck, and total hip by −8.8%, −6.9%, and −7.0% respectively compared to the maximum values during treatment with denosumab, but was still significantly higher compared to baseline levels with no further fractures.

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Section: Discussionmentioning

confidence: 99%

Influence of denosumab on bone mineral density in a severe case of pregnancy-associated osteoporosis

2021

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“…По поводу костных метастазов однократно назначалась терапия золедроновой кислотой. Хотя золедроновая кислота и деносумаб доказали свою эффективность в снижении скелетных осложнений при андроген-нечувствительной форме рака предстательной железы, их следует применять с осторожностью у пациентов с остеомаляцией [17][18][19]. Легкая и преходящая гипофосфатемия является частым побочным эффектом деносумаба и золедроновой кислоты.…”

Section: а B б гunclassified

“…Доброкачественные ФРФ23-опухоли обычно имеют диаметр не более 5 см, хотя были описаны и более крупные образования [19,29]. В РФ имеются описания отдельных клинических случаев доброкачественных ФРФ23-продуцирующих опухолей [1-3, 24, 30], однако первое описание принадлежит Родионовой С.С.…”

Section: а B б гunclassified

A clinical case of phosphopenic osteomalacia due to paraneoplastic secretion of metastatic prostate cance

et al. 2023

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Phosphaturic mesenchymal tumor can cause osteomalacia due to excessive secretion of fibroblast growth factor 23 (FGF23), which disrupts the metabolism of phosphate and vitamin D. These tumors are predominantly benign, but less than 5% of them are malignant forms. This article presents the first clinical case in the Russian Federation of a 69-year-old patient with severe hypophosphatemia due to metastatic prostate cancer. Increased secretion of FGF23 are described in the androgen-resistent prostate cancer, which led to pronounced disorders of mineral metabolism, accompanied by a clinical symptom of weakness, pain in the bones, immobilization of the patient. The condition was regarded as worsening against the background of the progression of the disease. However, symptomatic therapy aimed at increasing the level of phosphate significantly improved the patient’s general condition. The medical community should be aware of the possibility of developing hypophosphatemia in patients with weakness and bone pain, which are not always associated with the progression of metastatic prostate cancer.

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“…[8]). У пациентов наблюдаются выраженные боли в костях (до 99,3%), множественные переломы (до 79%), уменьшение в росте (до 69%), генерализованная миопатия (до 65%), а также ряд неспецифических симптомов [1,3,4,[9][10][11]. Визуализация опухолей с помощью мультиспираль-ной компьютерной томографии (МСКТ) или магнитно-резо-нансной томографии (МРТ) сложна из-за малых размеров, мезенхимальной природы образований и разнообраз-ной локализации, как внутри костей так и в мягких тканях.…”

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“…Вдобавок неспецифичность клинической картины и малая распространенность приводят к тому, что заболевание остается нераспознанным [10][11][12]. Активная диагностика началась с 2008 г., что связано с прогрессом инструментальных методов.…”

unclassified

FGF23 tumor induced osteomalacia

Gronskaia

Belaya

Мельниченко

2022

Probl Endokrinol (Mosk)

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Tumor induced osteomalacia is a rare acquired disease. The cause is a mesenchymal tumor secreting fibroblast growth factor 23 (FGF23). An excessive amount of FGF 23 disrupts the metabolism of phosphorus and vitamin D, which leads to severe paraneoplastic syndrome, manifested in the form of multiple fractures, severe pain in the bones and generalized myopathy. With oncogenic osteomalacia, a complete cure is possible with radical resection of the tumor. Unfortunately, localization, small size of formations and rare frequency of occurrence lead to the fact that the disease remains unrecognized for a long time and leads to severe, disabling consequences. A step-by-step approach to diagnosis improves treatment outcomes. First, a thorough anamnesis is collected, then functional visualization is performed and the diagnosis is confirmed by anatomical visualization of the tumor. After that, the method of choice is a surgical treatment. If resection is not possible, then conservative therapy with active metabolites of vitamin D and phosphorus salts is indicated. New therapeutic approaches, such as the antibody to FGF23 or the pan-inhibitor of receptors to FGF, are actively developing. This article provides an overview of modern approaches to the diagnosis and treatment of this disease.

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Treatment of high fracture risk patients in routine clinical practice

Cited by 4 publications

References 22 publications

Influence of denosumab on bone mineral density in a severe case of pregnancy-associated osteoporosis

Influence of denosumab on bone mineral density in a severe case of pregnancy-associated osteoporosis

A clinical case of phosphopenic osteomalacia due to paraneoplastic secretion of metastatic prostate cance

FGF23 tumor induced osteomalacia

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