cholecalciferol and Hyperparathyroidism--Primary

In primary hyperparathyroidism, successful parathyroidectomy leads to improved bone mineral density in the majority of cases. Our aim was to further explore the relationship between hypercalciuria, kidney function, and bone recovery after parathyroidectomy.. Bone mineral density, estimated glomerular filtration rate, and 24-hour urinary calcium were analyzed before and one year after parathyroidectomy in a cohort of 150 primary hyperparathyroidism patients (119 women; median age 60 [range 30-80] years) taking part in a clinical trial. The patients were randomized to 1-year daily treatment with either cholecalciferol 1,600 IU and calcium carbonate 1,000 mg or calcium carbonate alone.. Baseline 24-hour urinary calcium correlated directly with s-calcium, parathyroid hormone, 25-OH-D, the bone markers beta C-terminal telopeptide of type 1 collagen and procollagen type 1 amino-terminal propeptide, and estimated glomerular filtration rate (r = 0.19-0.30; P < .05) and inversely with age (r = -0.25; P = .004); 24-hour urinary calcium decreased and bone mineral density in lumbar spine and hip increased similarly in the 2 groups. Baseline 24-hour urinary calcium in the highest quartile (>10 mmol/d) was associated with greater increases in all locations. In a multivariable model adjusting for age, sex, smoking, diabetes, body mass index, estimated glomerular filtration rate, baseline bone mineral density, and vitamin D group, the increase in total hip bone mineral density remained independently associated with baseline 24-hour urinary calcium in the highest quartile (>10 mmol/d) and with plasma parathyroid hormone. Patients with persistent increases in 24-hour urinary calcium at follow-up (14%) had similar bone mineral density improvement.. Overall, 24-hour urinary calcium > 10 mmol/d was an independent determinant of improvement in bone mineral density and should be taken into account when considering parathyroidectomy.

Topics: Adult; Aged; Aged, 80 and over; Antacids; Bone Density; Bone Density Conservation Agents; Calcium Carbonate; Cholecalciferol; Cohort Studies; Female; Glomerular Filtration Rate; Humans; Hypercalciuria; Hyperparathyroidism, Primary; Male; Middle Aged; Parathyroidectomy

No data on the pharmacological treatment of normocalcemic hyperparathyroidism (NPHPT) are available. We treated 30 NPHPT postmenopausal women with alendronate/cholecalciferol (treated group) or vitamin D alone (control group). Over 1 year, bone mineral density (BMD) increased significantly in treated group, but not in control group. Both treatments did not affect serum or urinary calcium.. Normocalcemic primary hyperparathyroidism (NPHPT) is defined by normal serum calcium and consistently elevated PTH levels after ruling out the causes of secondary hyperparathyroidism. It is likely that subjects with NPHPT may develop kidney and bone disease. As no data on the pharmacological treatment of NPHPT are available, we aimed to investigate the effects of alendronate and cholecalciferol on both BMD and bone biochemical markers in postmenopausal women with NPHPT. Safety of vitamin D was evaluated as secondary endpoint.. The study was a prospective open label randomized trial comparing 15 postmenopausal women with NPHPT (PMW-NPHPT), treated with oral alendronate plus cholecalciferol (treated group) and 15 PMW-NPHPT treated only with cholecalciferol (control group). Blood samples were obtained at baseline and after 3, 6, and 12 months. Bone turnover markers (BTM) were measured at baseline, 3, and 6 months, respectively. BMD was assessed at baseline and after 12 months.. After 1 year of treatment, BMD increased significantly at the lumbar, femoral neck, and hip level in the treated group, but not in the control group (p = 0.001). No differences were found between or within groups in serum calcium, PTH, and urinary calcium levels. BTM significantly decreased in the treated group but not in the control group, at 3 and 6 months (p < 0.001), respectively. No cases of hypercalcemia or hypercalciuria were detected during the study.. The results of this study indicate that alendronate/cholecalciferol increases BMD in postmenopausal women with NPHPT. Alendronate/cholecalciferol or vitamin D alone does not affect serum or urinary calcium.

Topics: Administration, Oral; Alendronate; Bone Density; Bone Density Conservation Agents; Calcium; Cholecalciferol; Drug Combinations; Female; Femur; Humans; Hyperparathyroidism, Primary; Lumbar Vertebrae; Middle Aged; Osteoporosis, Postmenopausal; Prospective Studies

Vitamin D insufficiency may increase the risk for cardio metabolic disturbances in patients with primary hyperparathyroidism (PHPT).. To analyze the vitamin D status and indices of the metabolic syndrome in PHPT patients and the effect of vitamin D supplementation after parathyroid adenomectomy (PTX).. Double-blinded, randomized clinical trial (ClinicalTrials.gov identifier: NCT00982722) performed at Karolinska University Hospital, Sweden, April 2008 to November 2011. One hundred and fifty consecutive patients with PHPT (119 women) were randomized after PTX, 75 to oral treatment with calcium carbonate 1000 mg daily and 75 to calcium carbonate 1000 mg and cholecalciferol 1600 IU daily over 12 months. Changes in metabolic profile and ambulatory blood pressure (BP) were analyzed. Main outcome measures were changes in metabolic factors, BP, and body composition.. The 25-hydroxyvitamin D (25-OH-D)-level was <50 nmol/l in 76% of the patients before PTX. After PTX, glucose, insulin, and IGF1 decreased, while the 25-OH-D and the IGF-binding protein 1 increased and remained unchanged at follow-up after study medication. One year of vitamin D supplementation resulted in lower parathyroid hormone (PTH) (40 (34-52) vs 49 (38-66) ng/l) and higher 25-OH-D (76 (65-93) vs 49 (40-62) nmol/l; P<0.05). Other laboratory parameters were stable compared with after PTX. Systolic BP decreased and total bone mineral content increased in both groups.. Except for the lowering of the PTH level, no additive effect of vitamin D supplementation was seen. However, PTX proved effective in reducing insulin resistance.

Topics: Adult; Aged; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Body Composition; Calcium Carbonate; Cholecalciferol; Double-Blind Method; Drug Administration Schedule; Female; Humans; Hyperparathyroidism, Primary; Insulin Resistance; Male; Middle Aged; Parathyroid Hormone; Parathyroidectomy; Risk Assessment; Risk Factors; Sweden; Treatment Outcome

The 25 hydroxyvitamin D [25(OH)D] is the major metabolite for ascertaining vitamin D status, which circulates bound to a specific carrier (vitamin D-binding protein - VDBP). A portion that circulates unbound vary according to the VDBP genotype. This study evaluates the behavior of different forms of 25(OH)D, before and after supplementation with 14,000 IU of vitamin D3, weekly for 12 weeks, in individuals with primary hyperparathyroidism and controls. Fifty-six patients with active primary hyperparathyroidism (PHPT) and 64 paired controls (CTRL), not taking vitamin D3 for the last three months, were enrolled. The genetic isotypes of VDBP were determined to calculate bioavailable and free 25(OH)D. A p < 0.05 was considered significant. There were no statistical differences in free, bioavailable, and total 25(OH)D levels between PHPT and CTRL groups at baseline. The distribution of VDBP haplotypes 1s/1s, 1f/1f, 1s/1f, 2/2, 1s/2, and 1f/2 was similar between groups. After supplementation, all three forms of 25(OH)D proportionally increased within each group, although the percentage increment was lower in the PHPT group (p < 0.05). Total 25(OH)D is better correlated with PTH in the PHPT group than bioavailable and free 25(OH)D (r = -0.41; p < 0.05). The concentrations of total, free, and bioavailable 25(OH)D were similar in both PHPT and CTRL groups, and all forms increased proportionally after supplementation, although this increment percentage was higher in the CTRL group, with a subsequent reduction of PTH and AP. Total 25(OH)D correlated better with PTH than other forms, suggesting no advantages in measuring free or bioavailable 25(OH)D in these situations.

Topics: Cholecalciferol; Dietary Supplements; Humans; Hyperparathyroidism, Primary; Vitamin D; Vitamin D-Binding Protein

Vitamin D (25-hydroxyvitamin D [25(ОН)D]) deficiency (<20 ng/mL) and insufficiency (20-29 ng/mL) are common in primary hyperparathyroidism (PHPT), but data regarding the vitamin D metabolism in this population is limited.. The aim of this study is to estimate the vitamin D metabolites and their relationship with the main parameters of phosphorus-calcium metabolism in patients with PHPT at baseline and on the background of a single dose of cholecalciferol 150,000 IU.. A single-center interventional, dynamic, prospective, comparative study has been carried out. The study included 54 participants, divided into two groups: the 1st group included 27 patients with confirmed PHPT, the 2nd control group (n = 27), matched on gender (p = 0.062). The study included 4 visits; the baseline laboratory examination and a bolus dose of cholecalciferol were performed at the visit 1, the subsequent visits included a dynamic laboratory examination.. Vitamin D deficiency (<20 ng/ml) was detected in 69% of patients with PHPT. In the PHPT group (before cholecalciferol therapy), there was a direct association of 1.25(OH)2 D3 with albumin-corrected and ionized calcium, as well as between the 25(OH)D3 /24.25(OH)2 D3 ratio with PTH and magnesium. After taking of cholecalciferol, the levels of 1.25(OH)2 D3 and 25(OH)D3 /24.25(OH)2 D3 were significantly increased, and the levels of 25(OH)D3 /1.25(OH)2 D3 were significantly declined at all visits among patients with PHPT. The common 25(OH)D level was comparable to the control group, however the levels of 1,25(OH)2 D3 in patients with PHPT were 55% higher at baseline, and after taking of cholecalciferol 150,000 IU. They remained increased by 3-7 days by an additional 23-36%, significantly higher than those in the control group: 44%, 74% and 65%, at visits 2, 3 and 4, respectively (p<0.05). The taking of 150,000 IU cholecalciferol in the PHPT group did not lead to a significant increase in hypercalcemia and hypercalciuria, which indicates the safety of this dose in patients with mild hypercalcemia (albumin corrected calcium <3 mmol/l). None of the study participants experienced any side effects.. The completely comprehensive assessment of vitamin D metabolites was carried out for the first time in patients with PHPT before and after using a bolus dose of cholecalciferol. The results confirmed the differences of vitamin D metabolism in chronic excessive secretion of PTH compared to control group, which is new data in the pathogenesis of the disease, and can be used to develop optimal regimens for cholecalciferol taking in this population.

Topics: Cholecalciferol; Humans; Hyperparathyroidism, Primary; Phosphorus; Prospective Studies; Vitamin D

There is ample evidence associating vitamin D deficiency in primary hyperparathyroidism (PHP) patients with more severe disease manifestations and increased risk of postoperative hypocalcemia. Yet, there is limited data regarding the safety of vitamin D repletion in these patients.. To assess the safety of vitamin D repletion in PHP patients in a real-world setting.. We included patients with asymptomatic PHP and few symptomatic patients who declined surgery, followed in our clinic, and treated on a routine basis with 2000 IU/day of vitamin D3.. Serum calcium (sCa), PTH, 25-hydroxyvitamin D, and 24 h urinary calcium (uCa) and creatinine collections were compared between the lowest and the highest vitamin D time points.. There were 40 patients of a mean age was 63 ± 10 years. 25(OH)D at lowest and highest vitamin D time points was 15.5 ± 6.2 ng/ml and 33.2 ± 8, respectively (P < 0.001). Serum calcium was not affected by the changes in vitamin D levels. In none of the patients did sCa exceed 11.5 mg/dL. uCa was 220 ± 110 mg/24 h at the lowest vitamin D time point and 260 ± 140 at the highest vitamin D time point (P = 0.14). uCa exceeded 400 mg/24 h in two vs. five patients (P = 0.23) at the lowest and highest vitamin D time points, respectively. PTH was not significantly different between the different vitamin D time points.. Vitamin D repletion in PHP seems safe. Considering the documented adverse influence of vitamin D deficiency in PHP, particularly on skeletal manifestations and on the postoperative course, vitamin D repletion is warranted.

Topics: Adult; Aged; Aged, 80 and over; Calcium; Cholecalciferol; Creatinine; Female; Humans; Hyperparathyroidism, Primary; Male; Middle Aged; Parathyroid Hormone; Retrospective Studies; Vitamin D; Vitamin D Deficiency

Revision parathyroid is challenging due to possible diagnostic uncertainty as well as the technical challenges it can present.. A multidisciplinary panel of distinguished experts from the American Head and Neck Society (AHNS) Endocrine Section, the British Association of Endocrine and Thyroid Surgeons (BAETS), and other invited experts have reviewed this topic with the purpose of making recommendations based on current best evidence. The literature was also reviewed on May 12, 2017. PubMed (1946-2017), Cochrane SR (2005-2017), CT databases (1997-2017), and Web of Science (1945-2017) were searched with the following strategy: revision and reoperative parathyroidectomy to ensure completeness.. Guideline recommendations were made in 3 domains: preoperative evaluation, surgical management, and alternatives to surgery. Eleven guideline recommendations are proposed.. Reoperative parathyroid surgery is best avoided if possible. Our literature search and subsequent recommendations found that these cases are best managed by experienced surgeons using precision preoperative localization, intraoperative parathyroid hormone (PTH), and the team approach.

Topics: Bone Density; Calcium; Cholecalciferol; Clinical Competence; Diagnosis, Differential; Hospitals, High-Volume; Humans; Hyperparathyroidism, Primary; Intraoperative Neurophysiological Monitoring; Medical History Taking; Parathyroid Glands; Parathyroidectomy; Patient Selection; Postoperative Complications; Preoperative Care; Recurrence; Reoperation; Societies, Medical; Vitamin D Deficiency; Vitamins

Long-term severe hyperparathyroidism leads to thinning of cortical bone and cystic bone defects referred to as osteitis fibrosa cystica. Cysts filled with hemosiderin deposits may appear colored as "brown tumors." Osteitis fibrosa cystica and brown tumors are occasionally visualized as multiple, potentially corticalis-disrupting bone lesions mimicking metastases by bone scintigraphy or. We report a case of a 72-year-old white woman who presented with malaise, weight loss, and hypercalcemia. She had a history of breast cancer 7 years before. The practitioner, suspecting bone metastases, initiated bone scintigraphy, which showed multiple bone lesions, and referred her to our hospital for further investigations. Laboratory investigations confirmed hypercalcemia but revealed a constellation of primary hyperparathyroidism and not hypercalcemia of malignancy; in the latter condition, a suppressed rather than an increased value of parathyroid hormone would have been expected. A parathyroid adenoma was found and surgically removed. The patient's postoperative course showed a hungry bone syndrome, and brown tumors were suspected. With the background of a previous breast cancer and lytic, partly corticalis-disrupting bone lesions, there was a great concern not to miss a concomitant malignant disease. Biopsies were not diagnostic for either malignancy or brown tumor. Six months after the patient's neck surgery, imaging showed healing of the bone lesions, and bone metastases could be excluded.. This case shows essential differential diagnosis in a patient with hypercalcemia and multiple bone lesions. Whenever multiple, fluorodeoxyglucose-avid bone lesions are found, malignancy and metabolic bone disease should both be included in the differential diagnosis. Fluorodeoxyglucose-avid and corticalis-disrupting lytic lesions also occur in benign bone disease. There may be very few similar cases with heterogeneous and widespread bone lesions reported in the literature, but we think our patient's case is particularly remarkable for its detailed imaging and the well-documented course.

Topics: Aged; Bone Neoplasms; Breast Neoplasms; Calcium; Cholecalciferol; Diagnosis, Differential; Female; Humans; Hypercalcemia; Hyperparathyroidism, Primary; Osteitis Fibrosa Cystica; Parathyroid Neoplasms; Parathyroidectomy; Positron Emission Tomography Computed Tomography; Treatment Outcome; Vitamins

Topics: Biomarkers; Calcium; Cholecalciferol; Dietary Supplements; Female; Humans; Hyperparathyroidism, Primary; Hypocalcemia; Hypoparathyroidism; Infant, Newborn; Infant, Newborn, Diseases; Male; Pregnancy; Recurrence; Risk Factors; Seizures; Tetany; Time Factors; Treatment Outcome

Epidemiological studies suggest that vitamin D deficiency is common in patients with primary hyperparathyroidism (PHPT). They have higher levels of serum parathyroid hormone (PTH) and markers of bone turnover and fractures are more frequent than vitamin D-replete patients. However, there are concerns that Vitamin D repletion might exacerbate pre-existent hypercalcaemia. Therefore, we aimed to determine if vitamin D replacement improved biochemical indices of calcium metabolism without worsening underlying hypercalcaemia.. This is a prospective, observational study based on routine clinical practice, set up in a secondary care centre. 45 consecutive patients with mild biochemical hypercalcaemia due to PHPT and hypovitaminosis D were enrolled. The mean age of the cohort was 61 years (range 25-85 years), predominately Asian (32 patients) and female (41 patients). They received 20,000 IU of oral cholecalciferol, once a week, for 3 months. Calcium, phosphate, alkaline phosphatase and PTH were measured at baseline, 4, 8 and 12 weeks following treatment. Vitamin D levels were obtained at baseline and at 12 weeks, after they completed their treatment.. Vitamin D levels normalised at week 12 (mean ± SD, 18.8 ± 9.4 versus 76 ± 20 nmol/L, p = 0.0001) and PTH levels improved following treatment completion (21.2 ± 10 versus 16.2 ± 6 pmol/L, p = 0.026). There was no significant increase in serum calcium levels during vitamin D supplementation.. High doses of oral cholecalciferol normalised vitamin D levels without worsening underlying hypercalcaemia in individuals with PHPT.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Calcifediol; Calcium; Cholecalciferol; Cohort Studies; Dietary Supplements; Female; Humans; Hypercalcemia; Hyperparathyroidism, Primary; Male; Middle Aged; Parathyroid Hormone; Secondary Care Centers; Severity of Illness Index; United Kingdom; Vitamin D Deficiency

Topics: Cholecalciferol; Dietary Supplements; Female; Humans; Hyperparathyroidism, Primary; Male; Vitamin D Deficiency

Fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH) are major players in the bone-parathyroid-kidney axis controlling phosphate homeostasis. In patients with primary hyperparathyroidism (PHPT), data on the relationship between PTH and FGF23 are scarce and not always concordant.. The aim of our study was to evaluate the relationship between PTH and FGF23 in patients with PHPT and in euparathyroid patients cured after successful parathyroidectomy (PTx).. Twenty-one patients with PHPT and 24 patients in long-term cure after successful PTx (EuPTH) were studied. All patients underwent biochemical evaluation of renal function, parathyroid status, vitamin D status, bone turnover markers, and serum intact FGF23 levels.. Mean serum FGF23 concentration was significantly higher in PHPT than in EuPTH patients (50.8±6.1 vs 33.1±2.6 pg/ml, P=0.01). FGF23 levels significantly correlated with PTH levels (r=0.361, P=0.02), also after correction for 1,25(OH)(2)D levels (r=0.419, P=0.01). FGF23 levels showed a significant negative correlation with 1,25(OH)(2)D, which was more pronounced in PHPT than in EuPTH patients (r=-0.674, P=0.001, vs r=-0.509, P=0.01).. Our findings suggest that in PHPT, FGF23 levels are increased independent of 1,25(OH)(2)D levels. The more pronounced negative relationship between FGF23 and 1,25(OH)(2)D in the presence of high circulating PTH levels suggests that the increase in FGF23 levels may be an adaptive mechanism to counteract the PTH-induced increase in 1,25(OH)(2)D levels, although not completely overriding it.

Topics: Adult; Cholecalciferol; Female; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Humans; Hyperparathyroidism, Primary; Male; Middle Aged; Parathyroid Hormone; Parathyroidectomy

Primary hyperparathyroidism (PHPT) is an uncommon cause of neuromuscular weakness which is often ignored due to non-specific nature of complaints. The authors present a case of PHPT with severe 25-hydroxyvitamin D (25(OH)D) deficiency which presented with quadriparesis. Normocalcaemic hyperparathyroidism with hypophosphatemia was documented initially and correction of 25(OH)D deficiency unmasked hypercalcaemia. A parathyroid adenoma causing PHPT was localised with radiology and scintigraphy of neck. An ectopic supernumerary parathyroid adenoma was identified and removed from the right tracheoesophageal groove during bilateral exploration of neck and the patient was completely cured after surgery.

Topics: Adenoma; Adult; Cholecalciferol; Female; Humans; Hyperparathyroidism, Primary; Parathyroid Neoplasms; Quadriplegia; Thyroxine; Vitamin D; Vitamin D Deficiency

In patients with primary hyperparathyroidism (PHPT) not suitable for surgical correction, a skeletal protection with bisphosphonates is considered a reasonable option, but the long-term effects after treatment discontinuation are not well known. Sixty postmenopausal women with PHPT were given 400-600 IU vitamin D(3) daily and 100 mg neridronate IV every 2 months for 2 years with 2 additional years of follow-up without antiresorptive therapies. Bone mineral density (BMD) progressively rose by 6.7 ± 7.6% (SD) and by 2.9 ± 4.5% at the spine and femoral neck, respectively. During follow-up, mean BMD progressively fell, but after 2 years it was still 3.9 ± 5.5% higher than baseline values at the spine. Bone alkaline phosphatase and serum C-telopeptide of type I collagen decreased significantly within 6 months (28 and 49% versus baseline, respectively) and rose to baseline values within 6-12 months during follow-up. Serum PTH significantly rose from baseline during treatment, but it remained significantly higher than baseline during follow-up. The PTH changes were significantly correlated with serum 25-hydroxyvitamin D (25OHD) levels. In conclusion, in this study we observed that in patients with mild PHPT treatment with bisphosphonates is associated with the expected changes in bone-turnover markers and that the significant increases of both hip and spine BMD are partially maintained for at least 2 years after treatment discontinuation at the vertebral site. The marked increases in serum PTH levels, particularly in subjects with low 25OHD levels, persist after treatment discontinuation and this raises the suspicion that this might reflect a worsening of PHPT.

Topics: Aged; Alkaline Phosphatase; Bone Density Conservation Agents; Cholecalciferol; Collagen Type I; Diphosphonates; Female; Femur Neck; Humans; Hyperparathyroidism, Primary; Middle Aged; Osteoporosis, Postmenopausal; Parathyroid Hormone; Peptides; Time