Circulating leptin and adiponectin levels in patients with primary hyperparathyroidism

Delfini, Enrica; Petramala, Luigi; Caliumi, Chiara; Cotesta, D.; Toma, Giorgio De; Cavallaro, Giuseppe; Pannone, Giuseppe; Diacinti, Daniele; Minisola, Savatore; Erasmo, Emilio D'; Mazzuoli, G. F.; Letizia, Claudio

doi:10.1016/j.metabol.2006.08.019

Cited by 42 publications

(32 citation statements)

References 45 publications

(52 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Univariate analysis indicates that PTH and total calcium levels are significantly associated with plasma glucose, while total calcium is associated with triglycerides and LDL cholesterol levels. These findings partially fit with those already reported by other authors [10,11,17,24,25], though only two [11,25] compare results with a local control group. Noteworthy, among PHPT patients subgrouped according to clinical presentation only those with low-risk asymptomatic form have a higher frequency of MS in comparison to controls, differently from intermediate-high CRS.…”

Section: Discussionsupporting

confidence: 91%

“…Among cardiovascular alterations, increased arterial stiffness and carotid intima-media thickness, endothelial dysfunction, hypertension, left ventricular hypertrophy, and diastolic dysfunction have been reported [4,5]. Among metabolic disorders, impaired insulin sensitivity, high prevalence of type 2 diabetes mellitus (Type 2 DM), dyslipidemia, hyperuricemia, increased body weight, and metabolic syndrome (MS) have been shown [6][7][8][9][10][11][12]. So far, it remains to be fully elucidated the pathogenetic link between PHPT and cardiometabolic morbidity and mortality which might be ascribed potentially to the contributory role of hypercalcemia, high serum PTH levels and vitamin D deficiency [4,6,13,14] .…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, hypertension and metabolic alterations, known to be inter-related, have been investigated mostly separately and only few studies focusing on the prevalence of MS reported inconsistent findings about its size and relationship with different clinical presentation of PHPT [10,11,17].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cardiovascular risk and metabolic syndrome in primary hyperparathyroidism and their correlation to different clinical forms

et al. 2013

View full text Add to dashboard Cite

Cardiometabolic disorders have been associated with primary hyperparathyroidism (PHPT), while the relationship of cardiovascular risk score (CRS) and metabolic syndrome (MS) with different clinical presentation of PHPT remains undefined. Our aim was to evaluate CRS, MS and its components in PHPT looking for their correlation to different clinical forms. In 68 consecutive PHPT patients and 68 matched controls, CRS, MS and its components were assessed to perform an observational case-control study at an ambulatory referral center for Bone Metabolism Diseases. Patients were stratified in symptomatic and asymptomatic PHPT; these latter were divided in high-risk and low-risk subgroups for end-organ damage. An increased proportion of PHPT patients had intermediate-high CRS and MS (mean, 95 % Confidence Interval (CI) 51.5 %, 39.6-63.3 and 20.6 %, 11.0-30.2, respectively, p < 0.02 vs. controls). Intermediate-high CRS was prevalent both in symptomatic and low-risk asymptomatic PHPT while MS resulted prevalent in low-risk asymptomatic but not in symptomatic PHPT. Type 2 DM, IFG, mixed dyslipidemia, hypertriglyceridemia, HDL-hypocholesterolemia, and LDL-hypercholesterolemia predominated in low-risk asymptomatic, while only LDL-hypercholesterolemia prevailed also in symptomatic PHPT. In patients and controls without cardiometabolic risk factors, HOMA-IR index was significantly increased in PHPT vs. controls (p < 0.03) and associated to total calcium (R = 0.73; p < 0.001). By multivariate analysis low-risk asymptomatic PHPT predicted MS after adjusting for age, sex, and BMI. Our data show an increased frequency of intermediate-high CRS both in symptomatic and low-risk asymptomatic PHPT while MS prevails in low-risk asymptomatic PHPT, supporting the potential for cardiovascular morbidity and mortality also in this form.

show abstract

Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Cardiovascular risk and metabolic syndrome in primary hyperparathyroidism and their correlation to different clinical forms

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Their data are in line with several previous studies that reported an increased coronary artery and cerebrovascular morbidity in PHPT [7,8]. By means of a multivariate analysis, they also showed that, PHPT status predicts the presence of intermediate-high CRS and metabolic syndrome [9], while elevated calcium levels predict altered glucose tolerance among the components of metabolic syndrome.…”

supporting

confidence: 90%

Emerging data on cardiovascular risk in primary hyperparathyroidism

et al. 2014

View full text Add to dashboard Cite

The cardiovascular risk profile of patients affected by primary hyperparathyroidism (PHPT) has been an issue of debate over the last years. Studies regarding the potential damages caused by increased serum levels of parathyroid hormone (PTH) and/or calcium, have yielded controversial results, suggesting either the presence or the absence of damage [1,2].It is interesting to note that the answer to this question is further complicated by the changing clinical presentation of PHPT over the last decade. Indeed, once considered a symptomatic disorder characterized by significant hypercalcemia with kidney stones and/or bone involvement [3][4][5], today PHPT is most commonly seen in asymptomatic individuals with milder hypercalcemia, due to the large availability of routine serum calcium measurements and developments in assay systems. A new presentation is now emerging, characterized by normocalcemia and elevated serum parathyroid hormone levels (the so-called ''normocalcemic primary hyperparathyroidism'').Recently in this Journal, Procopio et al. reported an increased prevalence of intermediate-high cardiovascular risk score (CRS), both in symptomatic and asymptomatic PHPT patients, as compared to healthy controls [6]. Their data are in line with several previous studies that reported an increased coronary artery and cerebrovascular morbidity in PHPT [7,8]. By means of a multivariate analysis, they also showed that, PHPT status predicts the presence of intermediate-high CRS and metabolic syndrome [9], while elevated calcium levels predict altered glucose tolerance among the components of metabolic syndrome.Procopio et al. added new information on an emerging aspect of patients with this glandular disorder; however, there are also some limitations that should be kept in mind when interpreting the results obtained. For example, the classification of patients is somewhat arbitrary. Asymptomatic patients with complications should no longer be considered as such; indeed, future classifications should be based on the presence or absence of complications. Just to make an example, patients may be asymptomatic, but can be incidentally discovered to have a kidney stone by ultrasound; in such a case she/he is asymptomatic but already has a complication of the disease. In essence, the term asymptomatic does not mean without complications; in this context, also a vertebral fracture may be asymptomatic but represents a complication. Secondly, the paper does not include any follow-up after surgery; this could have added meaningful information about the possible reversible effects of a restored biochemical calcium metabolism on cardiovascular risk factors. The current data conflict on this last issue [10,11], possibly due to the different timing of surgery. For example in the case of hypertensive patients, it is entirely possible that parathyroidectomy would be effective only if performed in an early phase of the disease, when structural abnormalities are not present. A similar situation can be observed in other endocrine disorders ...

show abstract

“…It has also been reported that serum leptin correlates with urinary magnesium/creatinine concentration in patients suffering from type I diabetes with hyperglycemia. Hyperleptinemia could lead to hypomagnesemia by inducing increased diuresis and natriuresis [9,29,30].…”

Section: Diabetes Mellitusmentioning

confidence: 99%

Magnesium metabolism in health and disease

2009

View full text Add to dashboard Cite

Magnesium (Mg) is the main intracellular divalent cation, and under basal conditions the small intestine absorbs 30-50% of its intake. Normal serum Mg ranges between 1.7-2.3 mg/dl (0.75-0.95 mmol/l), at any age. Even though eighty percent of serum Mg is filtered at the glomerulus, only 3% of it is finally excreted in the urine. Altered magnesium balance can be found in diabetes mellitus, chronic renal failure, nephrolithiasis, osteoporosis, aplastic osteopathy, and heart and vascular disease. Three physiopathologic mechanisms can induce Mg deficiency: reduced intestinal absorption, increased urinary losses, or intracellular shift of this cation. Intravenous or oral Mg repletion is the main treatment, and potassium-sparing diuretics may also induce renal Mg saving. Because the kidney has a very large capacity for Mg excretion, hypermagnesemia usually occurs in the setting of renal insufficiency and excessive Mg intake. Body excretion of Mg can be enhanced by use of saline diuresis, furosemide, or dialysis depending on the clinical situation.

show abstract

Circulating leptin and adiponectin levels in patients with primary hyperparathyroidism

Cited by 42 publications

References 45 publications

Cardiovascular risk and metabolic syndrome in primary hyperparathyroidism and their correlation to different clinical forms

Cardiovascular risk and metabolic syndrome in primary hyperparathyroidism and their correlation to different clinical forms

Emerging data on cardiovascular risk in primary hyperparathyroidism

Magnesium metabolism in health and disease

Contact Info

Product

Resources

About