Concept: Parathyroid gland
The survival rate of dialysis patients, as determined by risk factors such as hypertension, nutritional status, and chronic inflammation, is lower than that of the general population. In addition, disorders of bone mineral metabolism are independently related to mortality and morbidity associated with cardiovascular disease and fracture in dialysis patients. Hyperphosphatemia is an important risk factor of, not only secondary hyperparathyroidism, but also cardiovascular disease. On the other hand, the risk of death reportedly increases with an increase in adjusted serum calcium level, while calcium levels below the recommended target are not associated with a worsened outcome. Thus, the significance of target levels of serum calcium in dialysis patients is debatable. The consensus on determining optimal parathyroid function in dialysis patients, however, is yet to be established. Therefore, the contribution of phosphorus and calcium levels to prognosis is perhaps more significant. Elevated fibroblast growth factor 23 levels have also been shown to be associated with cardiovascular events and death. In this review, we examine the associations between mineral metabolic abnormalities including serum phosphorus, calcium, and parathyroid hormone and mortality in dialysis patients.
Pharmacodynamic Actions of a Long-Acting PTH Analog (LA-PTH) in Thyroparathyroidectomized (TPTX) Rats and Normal Monkeys
- Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
- Published over 3 years ago
Hypoparathyroidism is a disease of chronic hypocalcemia and hyperphosphatemia due to a deficiency of parathyroid hormone (PTH). PTH and analogs of the hormone are of interest as potential therapies. Accordingly, we examined the pharmacological properties of a long-acting PTH analog, [Ala(1,3,12,18,22) , Gln(10) ,Arg(11) ,Trp(14) ,Lys(26) ]-PTH(1-14)/PTHrP(15-36) (LA-PTH) in thyroparathyroidectomized (TPTX) rats, a model of HP, as well as in normal monkeys. In TPTX rats, a single intra-venous administration of LA-PTH at a dose of 0.9 nmol/kg increased serum calcium (sCa) and decreased serum phosphate (sPi) to near-normal levels for longer than 48 hours, while PTH(1-34) and PTH(1-84), each injected at a dose 80-fold higher than that used for LA-PTH, increased sCa and decreased sPi only modestly and transiently (< 6 hours). LA-PTH also exhibited enhanced and prolonged efficacy versus PTH(1-34) and PTH(1-84) for elevating sCa when administered subcutaneously (SC) into monkeys. Daily SC administration of LA-PTH (1.8 nmol/kg) into TPTX rats for 28-days elevated sCa to near normal levels without causing hypercalciuria or increasing bone resorption markers, a desirable goal in the treatment of hypoparathyroidism. The results are supportive of further study of long-acting PTH analogs as potential therapies for patients with hypoparathyroidism. This article is protected by copyright. All rights reserved.
Lithium is a widely used and highly effective treatment for mood disorders, but causes poorly characterised adverse effects in kidney and endocrine systems. We aimed to analyse laboratory information system data to determine the incidence of renal, thyroid, and parathyroid dysfunction associated with lithium use.
Hungry bone syndrome: still a challenge in the post-operative management of primary hyperparathyroidism.A systemic review of the literature.
- European journal of endocrinology / European Federation of Endocrine Societies
- Published almost 7 years ago
Hungry bone syndrome refers to the rapid, profound and prolonged hypocalcaemia associated with hypophosphataemia and hypomagnesaemia and exacerbated by suppressed parathyroid hormone levels, which follows parathyroidectomy in patients with severe primary hyperparathyroidism and preoperative high bone turnover. It is a relatively uncommon, but serious adverse effect of parathyroidectomy. We conducted a literature search of all available studies reporting a “hungry bone syndrome” in patients who had a parathyroidectomy for primary hyperparathyroidism, to identify patients at risk and address the pitfalls in their management. The severe hypocalcaemia is believed to be due to increased influx of calcium into bone, due to the sudden removal of the effect of high circulating levels of PTH on osteoclastic resorption, leading to a decrease in the activation frequency of new remodelling sites and to a decrease in remodelling space, although there is no good documentation for this. Various risk factors have been suggested for the development of a hungry bone syndrome, including older age, weight/volume of the resected parathyroid glands, radiological evidence of bone disease and vitamin D deficiency. The syndrome is reported in 25-90% of patients with radiological evidence of hyperparathyroid bone disease versus only 0-6% of patients without skeletal involvement. There is insufficient data-based evidence on the best means to treat, minimize or prevent this severe complication of parathyroidectomy. Treatment is aimed at replenishing the severe calcium deficit by using high doses of calcium supplemented by high doses of active metabolites of vitamin D. Adequate correction of magnesium deficiency and normalization of bone turnover are required for resolution of the hypocalcaemia which may last for a number of months after successful surgery. Pre-operative treatment with bisphosphonates has been suggested to reduce postoperative hypocalcaemia, but there are to date no prospective studies addressing this issue.
- The Journal of clinical endocrinology and metabolism
- Published about 7 years ago
The underlying molecular alterations causing sporadic parathyroid adenomas that drive primary hyperparathyroidism have not been thoroughly defined.
The study is about the regulatory effects of estrogen and parathyroid hormone (PTH) on sclerostin, a protein that inhibits the Wnt/β-catenin pathway. The results indicate that estrogen may down-regulate sclerostin expression and that estrogen displays synergistic action with PTH. These results provide a new perspective on the relationship between estrogen and bone.
The treatment of primary hyperparathyroidism consists almost exclusively in the parathyroidectomy. The preoperative imaging (ultrasonography, 99mTc sestamibi scan) can allow to localize the pathologic gland and perform minimally-invasive focused techniques, but in presence of ectopic or intrathyroidal glands, parathyroid hyperplasia or coexistent thyroid disease, the sensitivity of these imaging techniques worsens. The present study shows a new technique of preoperative scintigraphic imaging and describes the early applications of this technique investigating if it is useful in improving the localization of the pathologic parathyroid.
Effective new therapies are still needed for people with osteoporosis. In 2002, the introduction of teriparatide, or recombinant parathyroid hormone (PTH [1-34]), opened a promising chapter in osteoporosis care.(1) For the first time, there was an anabolic agent that significantly increased bone mineral density (BMD), reduced fracture risk, and restored bone architecture back to, or close to, normal. However, despite an impressive track record of both safety and efficacy, teriparatide has had a limited clinical reach as compared with other agents, largely owing to its requirement for daily subcutaneous injection, a black-box warning about osteosarcoma in rats, and its high . . .
Therapy-refractory persistent hypoparathyroidism after extensive neck surgery is a rare but severe complication. Parathyroid allotransplantation may represent a definitive treatment option.
Parathyroidectomy is often challenging. This letter reports the use of intraoperative MRI integrated with real-time navigation to guide parathyroidectomy.