Relationship between forearm and vertebral mineral density in postmenopausal women with primary hyperparathyroidism

Wishart, J.

doi:10.1001/archinte.150.6.1329

Cited by 20 publications

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“…Bone density was significantly reduced in all the studies [33][34][35][36] except for one subgroup of "very mild" hypercalcemia (serum calcium < 2.74 mmol/ 1) [36]. Mitlak et al also found a significant reduction in a subgroup of patients without either osteitis fibrosa cystica or renal stones [34].…”

Section: Resultsmentioning

confidence: 91%

“…Studies on bone density (Table 3) All four studies on bone density used a crosssectional design in which bone density in PHPT patients with mild hypercalcemia was measured and compared with a reference value [33][34][35][36]. There was no intervention study on bone density.…”

Section: Resultsmentioning

confidence: 99%

“…The proportions of patients without either osteitis fibrosa cystica or renal stones were clearly indicated in two studies [33,34]. Two other studies limited their study populations to PHPT patients with mild hypercalcemia [35,36], and it was not explicitly mentioned whether some of the patients had the classical manifestations or not. Explicit criteria for inclusion and exclusion of study subjects were indicated in two studies [33,34].…”

Section: Resultsmentioning

confidence: 99%

“…Referral patterns of the patients were described in two studies [34,35]. Bone density was measured by single-photon absorptiometry (SPA) at the forearm [33][34][35][36] and quantitative computed tomography (QCT) at the spine [35].…”

Section: Resultsmentioning

confidence: 99%

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Psychiatric Symptoms, Bone Density and Non-Specific Symptoms in Patients with Mild Hypercalcemia due to Primary Hyperparathyroidism: A Systematic Overview of the Literature.

1997

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Abstract.To determine (1) the relationship between primary hyperparathyroidism with mild hypercalcemia and psychiatric disturbances, bone density, or non-specific symptoms, and (2) the effect of parathyroidectomy on these outcomes, a systematic and critical review of the literature was conducted. Relevant citations were identified using MEDLINE (1966( to August, 1995 and PsycINFO (1967 to August, 1995. Studies were included for the overview if they described patients with mild hypercalcemia (< 12 mg/dl), and if they dealt with at least one of the following outcomes: psychiatric disturbances, bone density, joint pain, constipation, polyuria/nocturia or weight loss. Either a calculated effect size or Z score was used to estimate the effect of the disease or parathyroidectomy on these outcomes. Seven studies met the inclusion criteria for this overview. Two out of three case-control studies on psychiatric symptoms found a significant association between primary hyperparathyroidism with mild hypercalcemia and psychiatric disturbances (effect sizes; 0.17, 1.2 and 1.6). One of the three studies also examined the effect of parathyroidectomy on psychiatric symptoms, and found an effect size of 1.5. All four cross-sectional studies that measured bone mass showed significantly reduced bone density in the forearm and the lumbar spine. The bone loss ranged from 0.9 to 1.4 standard deviation below the age-and sex-adjusted mean value in the forearm, and was 0.5 in the spine. There was no relevant study regarding non-specific symptoms. Among the seven studies, five did not explicitly indicate whether the patients had classical symptoms of either osteitis fibrosa cystica or renal stones. Primary hyperparathyroidism with mild hypercalcemia is associated with psychiatric disturbances and reduced bone density. Nevertheless, further research is needed to determine the symptoms, particularly for a group of patients without either classical bone disease or renal stones.The effects of parathyroidectomy on these outcomes also remain to be determined.

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Section: Resultsmentioning

confidence: 91%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Psychiatric Symptoms, Bone Density and Non-Specific Symptoms in Patients with Mild Hypercalcemia due to Primary Hyperparathyroidism: A Systematic Overview of the Literature.

1997

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“…Less specific features of PHPT are fatigue, proximal muscle weakness, mild cognitive disturbances, hypertension, left ventricular hypertrophy, valvular calcification, and cardiovascular mortality [2,10]. Classic skeletal lesions, which are bone resorption, bone cysts, brown tumors and generalized osteopenia, occur in less than 5% of cases [11]. PHPT affects compact bone more than trabecular bone with particular sensitivity in the cortices of long bones leading to subperiostal bone resorption (seen as periosteal elevation on plain radiography) [12].…”

mentioning

confidence: 99%

Primary hyperparathyroidism presented with peripheral brown tumor in the oral cavity: a case report

Elbüken¹,

Ozan²,

Öztürk³

et al. 2014

EJEA

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Introduction: Parathyroid hormone (PTH) is the chief regulator of calcium homeostasis in the human body. Primary hyperparathyroidism (PHPT) occurs in a setting of excessive PTH secretion with an autonomous parathyroid gland which resulting in hypercalcemia [1]. Most patients with PHPT have a single adenoma (about 80% of cases), but multigland disease can occur in 10%-15% of cases and double adenomas in 4%-5% [2]. Parathyroid carcinoma is a rare cause (usually less than 1% of patients) of hyperparathyroidism [3,4]. There is a great variation in the manifestations of PHPT. The clinical presentation of PHPT is changing from a severe disease with nephrolithiasis and metabolic bone disease to mild asymptomatic disease [5,6]. The most common clinical presentation of PHPT is asymptomatic hypercalcemia with an elevated or high-or normal intact PTH level. Patients with hypercalcemia may present with vague constitutional symptoms, anorexia, lethargy, or polydipsia and polyuria [7][8][9]. Less specific features of PHPT are fatigue, proximal muscle weakness, mild cognitive disturbances, hypertension, left ventricular hypertrophy, valvular calcification, and cardiovascular mortality [2,10]. Classic skeletal lesions, which are bone resorption, bone cysts, brown tumors and generalized osteopenia, occur in less than 5% of cases [11]. PHPT affects compact bone more than trabecular bone with particular sensitivity in the cortices of long bones leading to subperiostal bone resorption (seen as periosteal elevation on plain radiography) [12]. PHPT is prone to cause loss of the lamina dura [13].

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The Deletion of Hdac4 in Mouse Osteoblasts Influences Both Catabolic and Anabolic Effects in Bone

Nakatani

Chen

Johnson

et al. 2018

Journal of Bone and Mineral Research

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Histone deacetylase 4 (Hdac4) is known to control chondrocyte hypertrophy and bone formation. We have previously shown that parathyroid hormone (PTH) regulates many aspects of Hdac4 function in osteoblastic cells in vitro; however, in vivo confirmation was previously precluded by preweaning lethality of the Hdac4-deficient mice. To analyze the function of Hdac4 in bone in mature animals, we generated mice with osteoblast lineage-specific knockout of Hdac4 (Hdac4 ) by crossing transgenic mice expressing Cre recombinase under the control of a 2.3-kb fragment of the Col1a1 promoter with mice bearing loxP-Hdac4. The Hdac4 mice survive to adulthood and developed a mild skeletal phenotype. At age 12 weeks, they had short, irregularly shaped and stiff tails due to smaller tail vertebrae, with almost no growth plates. The tibial growth plate zone was also thinned, and Mmp13 and Sost mRNAs were increased in the distal femurs of Hdac4 mice. Immunohistochemistry showed that sclerostin was elevated in Hdac4 mice, suggesting that Hdac4 inhibits its gene and protein expression. To determine the effect of PTH in these mice, hPTH (1-34) or saline were delivered for 14 days with subcutaneously implanted devices in 8-week-old female Hdac4 and wild-type (Hdac4 ) mice. Serum CTX, a marker of bone resorption, was increased in Hdac4 mice with or without PTH treatment. Tibial cortical bone volume/total volume (BV/TV), cortical thickness (Ct.Th), and relative cortical area (RCA) were decreased in Hdac4 mice, but PTH caused no further decrease in Hdac4 mice. Tibial trabecular BV/TV and thickness were not changed significantly in Hdac4 mice but decreased with PTH treatment. These results indicate that Hdac4 inhibits bone resorption and has anabolic effects via inhibiting Mmp13 and Sost/sclerostin expression. Hdac4 influences cortical bone mass and thickness and knockout of Hdac4 prevents the catabolic effect of PTH in cortical bone. © 2018 American Society for Bone and Mineral Research.

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Relationship between forearm and vertebral mineral density in postmenopausal women with primary hyperparathyroidism

Cited by 20 publications

References 0 publications

Psychiatric Symptoms, Bone Density and Non-Specific Symptoms in Patients with Mild Hypercalcemia due to Primary Hyperparathyroidism: A Systematic Overview of the Literature.

Psychiatric Symptoms, Bone Density and Non-Specific Symptoms in Patients with Mild Hypercalcemia due to Primary Hyperparathyroidism: A Systematic Overview of the Literature.

Primary hyperparathyroidism presented with peripheral brown tumor in the oral cavity: a case report

The Deletion of Hdac4 in Mouse Osteoblasts Influences Both Catabolic and Anabolic Effects in Bone

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