Osteitis Fibrosa Cystica
Charles Theisler in Adjuvant Medical Care, 2023
Osteitis fibrosa cystica (OFC), also known as Von Recklinghausen's disease, is a serious skeletal disorder and a complication of primary or secondary hyperparathyroidism. As a result, osteoclasts are activated to resorb bone. This results in fibrous tissue replacing calcified supporting structures. The loss of bone mass causes bone pain and susceptibility to fractures, especially in the arms, legs, or spine. Ultimately, sites of increased bone activity (i.e., phalanges, skull bones, ends of long bones, and trabecular bones of the vertebrae) are softened, weakened, and deformed.1 Advanced OFC results in lytic lesions due to defective remodeling called brown tumors, which are more severe in young adults. Persistent hypercalcemia and an elevated serum parathyroid hormone (PTH) level help confirm the diagnosis of primary hyperparathy-roidism. Whenever possible, the underlying cause of secondary hyperparathyroidism should be removed.
Parathyroid Hormone (Pth)
Fuad S. Ashkar, Lelio G. Colombetti in Radiobioassays, 2019
Secondary hyperparathyroidism is a common complication of chronic renal failure.255–260 In secondary hyperparathyroidism, the levels of PTH are markedly elevated, usually higher than those seen in primary hyperparathyroidism. In the successful treatment of the patient with renal failure, it is necessary to minimize the degree of secondary hyperparathyroidism since it can be responsible for many of the abnormalities of calcium and skeletal metabolism that occur in chronic renal disease.261–264 Therefore, the measurement of PTH, especially serial measurements during treatment regimens, can often be a valuable index of the effectiveness of therapy. However, the problems of assay interpretation discussed under the immunochemical heterogeneity of PTH are especially prominent in chronic renal failure.
Treating the Dysmetabolism Underlying Osteoporosis
Kohlstadt Ingrid, Cintron Kenneth in Metabolic Therapies in Orthopedics, Second Edition, 2018
In hyperparathyroidism, parathyroid hormone (PTH) stimulates a release of calcium from bone by an increase in osteoclast activity. It does so by increasing activation of 25-hydroxy vitamin D3 to 1.25-dihydroxy vitamin D3 which increases bone resorption. Primary hyperparathyroidism is frequently a consequence of a benign adenoma, yet may also be caused by a malignant tumor. In secondary hyperparathyroidism, the major causes are vitamin D deficiency and chronic kidney disease. Secondary hyperparathyroidism is the response to a lowered serum calcium level resulting in an increase in PTH levels and increased bone resorption. Consequences of hyperparathyroidism include hypercalciuria, hypercalcemia, hypophosphatemia, osteopenia/osteoporosis, osteomalacia, and kidney stones [67, 68].
A single-center experience of parathyroidectomy in 1500 cases for secondary hyperparathyroidism: a retrospective study
Published in Renal Failure, 2022
Shasha Zhao, Wei Gan, Wenjia Xie, Jinlong Cao, Liang Zhang, Ping Wen, Junwei Yang, Mingxia Xiong
Secondary hyperparathyroidism, a common complication of chronic kidney disease, has gradually become important for the prolonged survival of patients with end-stage renal disease and has been accompanied by improvements in medical care [1]. There have been many subsequent studies on this disease since it was initially reported in 1934 [2]. To date, hyperphosphatemia, hypocalcemia, vitamin D deficiency, dysfunction of the fibroblast growth factor 23-klotho axis and other factors [3] are presumed to be associated with secondary hyperparathyroidism, which causes renal osteodystrophy, disorders of calcium and phosphorus metabolism, cardiovascular calcification, ectopic calcification, pruritus, anemia, myopathy, malnutrition and neuropathy [4]. In addition, it results in worse quality of life, increased cardiovascular and all-cause mortality [5]. Combined conservative therapy composed of appropriate diet, dialysis and medication is widely adopted. Nevertheless, diet control and adjustment of dialysis prescription contribute only slightly. Calcium-based phosphorus binders, active vitamin D and analogs may lead to hypercalcemia, which increases the risk of cardiovascular and ectopic calcification [6,7]; however, noncalcium-based phosphorus binders, vitamin D receptor agonists and calcimimetics have limited therapeutic effects on refractory secondary hyperparathyroidism, and they are costly.
When and How to Diagnose and Treat Vitamin D Deficiency in Adults: A Practical and Clinical Update
Published in Journal of Dietary Supplements, 2020
Antoine Aoun, Jessica Maalouf, Myriam Fahed, Flora El Jabbour
In people with healthy kidneys and bones, normal serum levels of calcium and phosphorus are predominantly maintained through the interaction of two hormones: parathyroid hormone (PTH) and calcitriol. In the setting of vitamin D deficiency, secondary hyperparathyroidism causes both the release of calcium stored in the bone and the reabsorption of calcium by the kidneys to maintain normal serum calcium and phosphorus levels. Thus, vitamin D deficiency is usually accompanied by normal blood levels for calcium and phosphorus, high-normal or elevated levels of PTH, normal to elevated levels of total alkaline phosphatase, a low 24-hour urine calcium excretion rate, and low levels of total 25(OH)D. Patients with severe and long-standing vitamin D deficiency may present exceptionally with overt hypocalcemia and/or hypophosphatemia (Kennel et al. 2010).
Mineral and bone disorder in hemodialysis patients in the Tibetan Plateau: a multicenter cross-sectional study
Published in Renal Failure, 2019
Zong-Hui Dang, Chen Tang, Guo-Liang Li, Ciren Luobu, De Qing, Zhen-Hua Ma, Jing-Feng Qu, lamu Suolang, Li-Jun Liu
Logistic regression analysis also showed that the use of activated vitamin D as a protective factor was associated with hyperphosphatemia for local people, and patients taking vitamin D were less likely to develop hyperphosphatemia (Table 4). However, a meta-analysis concluded that vitamin D therapy cannot improve biochemical markers of MBD [20]. Generally, activated vitamin D can promote the absorption of calcium and phosphorus from the intestine but can also cause hypercalcemia and hyperphosphatemia in CKD [21]. In addition, current research suggests that vitamin D insufficiency and deficiency should be avoided in CKD and dialysis patients by using supplementation to prevent secondary hyperparathyroidism (SHPT) [22]. The findings of prolonged survival in some studies may be because patients prescribed vitamin D tended to be healthier overall than those who were not prescribed vitamin D, and therefore, the survival benefit may be due to the underlying health status of study participants rather than to the vitamin D treatment itself [4]. Hence, we assume this result may be due to similar reason: local patients were given vitamin D treatment on the premise that their blood phosphorus levels were controlled.