China
Africa
Explore chapters and articles related to this topic
Hyperparathyroidism
Published in Pallavi Iyer, Herbert Chen, Thyroid and Parathyroid Disorders in Children, 2020
Kimberly Ramonell, Erin Partington Buczek
When only one allele is inactivated at this locus on the CaSR gene, the result is a milder and often asymptomatic form of primary HPT known as familial hypocalciuric hypercalcemia (FHH). In FHH, PTH and calcium levels are usually only modestly elevated. The defining feature, hypocalciuria, occurs due to the impaired function of renally expressed CaSR which alters calcium reabsorption in the thick ascending limb (7). The presence of hypocalciuria (usually <100 mg/day) is protective against the development of nephrolithiasis and nephrocalcinosis and helps distinguish FHH from other etiologies of primary HPT.
Parathyroid surgery
Published in Demetrius Pertsemlidis, William B. Inabnet III, Michel Gagner, Endocrine Surgery, 2017
Additional testing may be useful for patients whose calcium and PTH levels are borderline, to either confirm the diagnosis of hyperparathyroidism or determine the severity of end-organ manifestations. For example, an ionized calcium level may give a more accurate assessment of the physiologic calcium level in the bloodstream. Twenty-four-hour urine calcium should be done routinely to rule out the rare condition of familial hypercalcemic hypocalciuria, which is a relative contraindication to surgery [1]. A high urine calcium level may also help to measure the severity of hyperparathyroidism. Finally, bone densitometry is useful to determine the degree of bone loss and may help in determining the need for surgery. It should be noted, however, that bone density naturally decreases over time, thus the older the patient, the less useful the test becomes in determining the usefulness of surgery.
Surgical Failure and Reoperative Surgery
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Schelto Kruijff, Leigh Delbridge
The diagnosis of PHPT can only be made again if other causes of hypercalcaemia are excluded. In the first place serum analysis and 24-hour urine should be repeated to look for raised PTH and calcium to confirm the diagnosis of PHPT. Elevated PTH with normal calcium can occur in up to 30% post-op due to hungry bone syndrome (secondary response to bone remineralization), low vitamin D levels, impaired renal hydroxylation of vitamin D-25 or decreased peripheral PTH sensitivity or an impaired renal function. Elevated calcium in the presence of suppressed PTH suggests a misdiagnosis such as bone metastases. A modestly elevated serum calcium and serum PTH can be seen in familial hypocalciuric hypercalcaemia (FHH), which mimics PHPT and is a well-recognized cause of failure in an index case. It is of crucial importance to assess a family history properly to be able to exclude FHH because the disorder is not cured by parathyroidectomy. FHH is caused by various mutations in the gene coding for the Ca SR. The CaSR responds to serum calcium and mediates feedback inhibition of PTH release. A loss-of-function mutation results in a rising of the calcium threshold that triggers reduction of PTH secretion. Serum concentration of calcium is thus maintained at higher levels since more calcium is needed to trigger negative feedback. This results in hypercalcaemia, and since more calcium is sequestered in the serum, this often results in hypocalcuria.20 FHH is excluded by demonstration of a 24-hour urinary calcium/creatinine ratio greater than 2%. A family history of PHPT should be sought in order to exclude not only FHH but also other familial endocrinopathies such as MEN 1 and MEN 2A.
Bone mineral density in primary care patients related to serum calcium concentrations: a longitudinal cohort study from Sweden
Published in Scandinavian Journal of Primary Health Care, 2018
Sofia Dalemo, Robert Eggertsen, Per Hjerpe, Erik G. Almqvist, Kristina Bengtsson Boström
There has been increasing interest around the world in recent years in a variant of pHPT that seems to be little known in primary care; a mild type of pHPT where the patient has an elevated calcium concentration with a normal, non-suppressed PTH concentration [4]. The normal physiological reaction to elevated calcium should be a very low or undetectable PTH concentration [10,29]. Measurement of BMD in patients with elevated calcium concentrations and normal PTH concentrations, who do not seem to be candidates for parathyroidectomy, could lead to an early diagnosis of osteoporosis before fractures develop. By using 24-hour urine calcium sampling is it possible to distinguish these patients from patients with the unusual, congenital and benign condition of familial hypercalcaemic hypocalciuria, which is not ameliorated by surgery [10].
A pilot dynamic analysis of formative factors of nephrolithiasis related to metabolic syndrome: evidence in a rat model
Published in Renal Failure, 2022
Qiqi He, Yangguo Tang, Yuzhuo Li, Fei Wang, Junsheng Bao, Sanjay Gupta
Hypocalciuria was notably observed in the MS rats in our study, which is not consistent with the general risk factors theory of hypercalciuria in the regular stone pathogenic mechanism. To our knowledge, no literature has demonstrated and explained this manifestation and general mechanism. Only one clinical study has shown that urinary calcium has a very weak correlation with components of MS [22]. Due to limited literature, we hypothesize that the hypocalciuria in our study might be related to large amounts of ROS released in tissue. We also hypothesize that the long-term effects of excessive ROS would cause lipid peroxidation on the cell membrane and increase the permeability of the cell membrane and influx of calcium ions (Ca2+). All these circumstances induce continuous depolarization of mitochondria, inhibition of ATP production, and overload of intracellular Ca2+. Continuous Ca2+ influx might cause hypocalciuria, mitochondrial fragmentation, and inflammatory responses. Consistently, one recent study [23] indicated that mitochondrial dysfunction and fragmentation induced by excessive reactive oxygen species (ROS) in MS might promote calcium deposition on the surface of renal tubular epithelial cells and aggregation into crystals. Hypercalciuria is usually secondary to renal tubular acidosis and hyperparathyroidism. It leads to disturbances in calcium homeostasis and is recognized as a risk factor for nephrolithiasis. This finding might be more accurate and reliable with an increase in sample size. Due to ammonium chloride administration, lower urine pH levels were observed in both drug administration groups.
Effect of parathyroidectomy on osteopontin and undercarboxylated osteocalcin in patients with primary hyperparathyroidism
Published in Endocrine Research, 2018
Raelene E. Maser, M. James Lenhard, Ryan T. Pohlig, P. Babu Balagopal, Raafat Abdel-Misih
Weight and height were measured using a stadiometer. Body mass index (BMI) was calculated as body weight divided by height squared (kg/m2). Blood pressure was monitored electronically in the supine posture using an oscillometric automatic recorder. Twenty-four participants performed a 24 h urine collection for calcium. Results from an earlier 24 h collection, performed prior to enrollment in this study, were utilized for 15 participants. The median time of collection before the baseline visit was approximately 2.8 months. No participants had hypocalciuria. Specimens were not obtained for six participants due to refusal, insufficient time before surgery, or incomplete urine collection. The mean calcium level was 5.0 ± 2.1 (mean±SD) mg/kg/24 h.