Effect of low dose denosumab on bone mineral density in postmenopausal women with osteoporosis after a transition from 60 mg dose: a prospective observational study.

INTRODUCTION: Denosumab is an effective antiresorptive molecule and reduces the risk of fracture in postmenopausal osteoporosis. Cessation of denosumab therapy however is associated with rapid declines in bone mineral density (BMD), rises in bone remodeling, and an increased risk of fracture. We evaluated the effect of low dose denosumab (30 mg every 6 months) on the prevention of bone loss following a switch from standard dose (60 mg of denosumab every 6 months) in a prospective observational study. METHODS: We recruited 114 women 50-90 years of age with postmenopausal osteoporosis at a moderate fracture risk without prior fragility fractures, who had been on denosumab 60 mg every 6 month. These women switched to low dose denosumab 30 mg every 6 months. Mean percentage change in lumbar spine (LS), femoral neck (FN), total hip (TH) and 1/3 distal radius (1/3RAD) BMD at 12 and 24 months were evaluated. Predictors for change in BMD were explored. Subgroup analysis for patients on denosumab 60 mg every 6 months for <3 years and for ≥3 years before switching to low dose denosumab 30 mg was evaluated. RESULTS: At 12 months following a switch from 60 mg to 30 mg of denosumab every 6 months we observed an increase in LS BMD mean percentage change (+2.03%, 95% CI 1.18-2.88, p < 0.001). BMD was stable at the hip and radial sites. Age was found to be a predictor of the mean percentage change in LS BMD for the overall sample. At 24 months, there was a further increase in LS BMD mean percentage change (+3.44%, 95% CI 1.74-5.12, p < 0.001), with stable BMD at other skeletal sites. The 12 month mean BMD percentage change at the LS (p = 0.015), FN (p < 0.001), TH (p < 0.001), and 1/3 RAD (p < 0.001) were found to be predictors of the 24 month mean BMD percentage change. No clinical fractures were reported during 24 months of follow up. CONCLUSION: We observed stable BMD following a switch from denosumab 60 mg every 6 months to 30 mg every 6 months in this prospective observational study conducted in postmenopausal women at a moderate fracture risk.

Hypoparathyroidism.

The regulation of plasma calcium levels is essential for the normal physiologic function of every cell. Parathyroid hormone (PTH) is the principal regulator of serum calcium and phosphate homeostasis. PTH is synthesized and secreted by the parathyroid chief cells in the parathyroid glands primarily in response to a decline in serum calcium levels. The causes of hypocalcemia can be broadly classified as inadequate PTH or vitamin D production, PTH resistance, or miscellaneous causes. The term "hypoparathyroidism" refers to a metabolic disorder in which hypocalcemia and hyperphosphatemia occur either from a failure of the parathyroid glands to secrete sufficient amounts of biologically active PTH, or from an inability of PTH to appropriately induce a biological response in its target tissues. The most common cause of acquired hypoparathyroidism is surgery, accounting for 75% of all cases. Nonsurgical causes of hypoparathyroidism include autoimmune, genetic variants, infiltrative, metastatic, radiation, mineral deposition, magnesium deficiency or excess or idiopathic. The objective of this chapter is to provide a comprehensive review of the physiology of calcium homeostasis, the causes of hypocalcemia, and the epidemiology of hypoparathyroidism. It is very important to determine the underlying cause of the hypoparathyroidism in order to effectively treat our patients and improve quality of life.

Medical Hypoparathyroidism.

Hypoparathyroidism is a metabolic disorder characterized by hypocalcemia, hyperphosphatemia, and inadequate levels of or function of parathyroid hormone (PTH). The authors review the nonsurgical or medical causes of hypoparathyroidism. The most common of the nonsurgical causes is autoimmune destruction of the parathyroid. Magnesium deficiency or excess can cause a functional hypoparathyroidism. Genetic conditions result in hypoparathyroidism as part of a syndrome or in isolation. Pseudohypoparathyroidism reflects a resistance to PTH. Infiltrative, metastatic, radiation destruction, mineral deposition, or idiopathic are uncommon causes of hypoparathyroidism. This article reviews the causes of hypoparathyroidism and an approach to the evaluation of this condition.

Clinical and epidemiological characteristics of pituitary tumours in a single centre in Saudi Arabia.

PURPOSE: Pituitary tumours are slowly progressing tumours, mostly benign, with a reported global prevalence of 16.7% (22.5% in radiologic studies and 14.4% in autopsy studies). Clinical and epidemiological data on pituitary adenomas in Saudi Arabia are lacking. We aimed to utilise our database variables to determine clinical and epidemiological characteristics as well as treatment outcomes of pituitary tumours among Saudi patients. METHODS: This retrospective study was conducted in King Fahad Medical City, Riyadh, Saudi Arabia, in patients with pituitary tumours. Data were collected between 2006 and 2017. RESULTS: Overall, 284 patients (females: 38.1 ± 13.9 years; males: 44.1 ± 15.4 years) with pituitary tumours were included. Common pituitary tumours were prolactin-secreting adenomas (45%), non-functioning pituitary adenomas (NFPAs: 35.6%), growth hormone (GH)-secreting adenomas (10.6%), craniopharyngiomas (7%), and adrenocorticotropic hormone (ACTH)-secreting adenomas (1.8%). Prolactin-secreting adenomas were more frequently microadenomas and were common among females. Headaches and visual symptoms occurred commonly in NFPA patients (62.4 and 45.5%, respectively) than in those with prolactin-secreting adenomas (56.3 and 32.8%, respectively) or GH-secreting adenomas (40 and 16.6%, respectively). Medical treatment was the mainstay for prolactin-secreting adenoma patients (69%). Pituitary surgery was the primary therapy in NFPA patients (43.6%) and GH-secreting adenomas (86.7%). CONCLUSION: This study identified the pattern of pituitary tumours in Saudi patients and management strategies. Further, the study highlights the need for a nationwide registry to improve surveillance and physicians' knowledge in Saudi Arabia.

Transient Thyroiditis after Surgery for Tertiary Hyperparathyroidism: A Case Report.

Parathyroid (PTH) exploration surgery carries the risk of developing post-operative thyroiditis due to vigorous manual manipulation of the thyroid gland during surgery. Post-operative thyroiditis has a wide spectrum of clinical manifestations. However, it remains underreported. Here, we describe a case of post-operative transient thyroiditis in a 33-year-old male who developed 3 days after parathyroidectomy for PTH hyperplasia. We review the limited literature regarding this interesting entity.