Obesity,Bariatric Surgery,and Vitamin D

The high prevalence of obesity is a worldwide problem associated with multiple comorbidities, including cardiovascular diseases. Vitamin D deficiency with secondary hyperparathyroidism is common in obese individuals and can be aggravated after bariatric surgery. Moreover, there is no consensus on the optimal supplementation dose of vitamin D in postbariatric surgical patients. We present new data on the variability of 25(OH)D response to supplementation in postmenopausal obese women. It is important to recognize and treat vitamin D deficiency before bariatric surgery to avoid postoperative complications, such as metabolic bone disease with associated high fracture risk. The objective of this article is to discuss the bone metabolism consequences of vitamin D deficiency after bariatric surgery.     

Vitamin D Therapy of Osteoporosis: Plain Vitamin D Therapy Versus Active Vitamin D Analog (D-Hormone) Therapy

Normal intestinal calcium (Ca) absorption is an essential feature of bone homeostasis. As with many other organ systems, intestinal Ca absorption declines with aging, and this is one pathological factor that has been identified as a cause of senile osteoporosis in the elderly. This abnormality leads to secondary hyperparathyroidism, which is characterized by high serum parathyroid hormone (PTH) and an increase in bone resorption. Secondary hyperparathyroidism due to poor intestinal Ca absorption has been implicated not only in senile osteoporosis but also in age-related bone loss. Accordingly, in population-based studies, there is a gradual increase in serum PTH from about 20 years of age onward, which constitutes a maximum increase at 80 years of age of 50% of the basal value seen at 30 years of age. The cause of the increase in PTH is thought to be partly due to impaired intestinal Ca absorption that is associated with aging, a cause that is not entirely clear but at least in some instances is related to some form of vitamin D deficiency. There are three types of vitamin D deficiency: (1) primary vitamin D deficiency, which is due to a deficiency of vitamin D, the parent compound; (2) a deficiency of 1,25(OH)₂D₃ resulting from decreased renal production of 1,25(OH)₂D₃; and (3) resistance to 1,25(OH)₂D₃ action owing to decreased responsiveness to 1,25(OH)₂D₃ of target tissues. The cause for the resistance to 1,25(OH)₂D₃ could be related to the finding that the vitamin D receptor level in the intestine tends to decrease with age. All three types of deficiencies can occur with aging, and each has been implicated as a potential cause of intestinal Ca malabsorption, secondary hyperparathyroidism, and senile osteoporosis. There are two forms of vitamin D replacement therapies: plain vitamin D therapy and active vitamin D analog (or D-hormone) therapy. Primary vitamin D deficiency can be corrected by vitamin supplements of 1000 U a day of plain vitamin D whereas 1,25(OH)₂D₃ deficiency/resistance requires active vitamin D analog therapy [1,25(OH)₂D₃ or 1α(OH)D₃] to correct the high serum PTH and the Ca malabsorption. In addition, in the elderly, there are patients with decreased intestinal Ca absorption but with apparently normal vitamin D metabolism. Although the cause of poor intestinal Ca absorption in these patients is unclear, these patients, as well as all other patients with secondary hyperparathyroidism (not due to decreased renal function), show a decrease in serum PTH and an increase in Ca absorption in response to therapy with 1,25(OH)₂D₃ or 1α(OH)D₃. In short, it is clear that some form of vitamin D therapy, either plain vitamin D or 1,25(OH)₂D₃ or 1α(OH)D₃, can be used to correct all types of age-dependent impairments in intestinal Ca absorption and secondary hyperparathyroidism during aging. However, from a clinical standpoint, it is important to recognize the type of vitamin D deficiency in patients with senile osteoporosis so that primary vitamin D deficiency can be appropriately treated with plain vitamin D therapy, whereas 1,25(OH)₂D₃ deficiency/resistance will be properly treated with 1,25(OH)₂D₃ or 1α(OH)D₃ therapy. With respect to postmenopausal osteoporosis, there is strong evidence that active vitamin D analogs (but not plain vitamin D) may have bone-sparing actions. However, these effects appear to be results of their pharmacologic actions on bone formation and resorption rather than through replenishing a deficiency.     

The effects of medications on bone

Medications taken for the treatment of arthritis and psychotropic and epileptic disorders, as well as anticoagulants, antacids, bisphosphonates, corticosteroids, and antineoplastic drugs, can profoundly affect bone metabolism. In some scenarios (eg, osteoporosis), these effects are intended; in others (eg, rickets, osteomalacia secondary to antiepileptic drugs), potentially adverse side effects of medications on bone may occur. Nonsteroidal anti-inflammatory drugs appear to delay fracture healing and bone ingrowth, although these effects are reversible. Disease-modifying antirheumatic drugs do not appear to affect bone metabolism adversely when taken in the low dosages currently prescribed. Bisphosphonates are useful in restoring bone mass in cases of postmenopausal osteoporosis, glucocorticoid-induced osteoporosis, Paget's disease, and neoplastic conditions with bone loss and hypercalcemia. Corticosteroids and cancer chemotherapeutic agents generally affect bone adversely and increase fracture risk.     

Relationship between vitamin D status, parathyroid hormone levels and bone mineral density in patients with chronic kidney disease stages 3 and 4

AIM: Low vitamin D status is associated with secondary hyperparathyroidism and increased bone turnover in the general population and can aggravate the hyperparathyroidism of chronic kidney disease (CKD) patients. It is also correlated to low bone mineral density (BMD), but this correlation is less clear in CKD patients. Aims of our study were to investigate these associations in CKD stages 3 and 4 patients, and to identify significant predictors of BMD in this population. METHODS: Serum 25-hydroxyvitamin D (25OHD) levels, BMD at the femur and radius, and bone mineral metabolism parameters were measured in 89 CKD stages 3 and 4 patients. Vitamin D status was defined according to the NKF/KDOQI guidelines. RESULTS: Mean 25OHD levels were 53.8+/-32.1 nmol/L and correlated to the severity of proteinuria. Thirty-five patients (39%) had vitamin D insufficiency, 29 (33%) had vitamin D deficiency and five (6%) had severe deficiency. Of the 89 patients, two had osteoporosis and 31 had osteopenia either at femur or radius. Independent predictors for the total femur BMD were the intact parathyroid hormone (iPTH) levels and the body mass index (BMI). For the total radius BMD, independent predictor was only the BMI. Serum 25OHD levels were not directly associated with BMD, but they were independent predictors of iPTH. CONCLUSION: Vitamin D insufficiency and deficiency are very common in CKD stages 3 and 4 population and may indirectly affect, via effects on iPTH, the BMD of these patients.     

Prevention and treatment of renal osteodystrophy in children with chronic renal insufficiency and end-stage renal disease

Histologic features associated with secondary hyperparathyroidism remain the predominant skeletal lesion in adults and children with chronic renal failure. When instituted early, vitamin D therapy has been shown to ameliorate the development and progression of the biochemical, radiographic, and histologic evidence of secondary hyperparathyroidism in patients with chronic renal insufficiency. Aggressive parathyroid hormone suppression, however, has led to the increased prevalence of adynamic bone. Adynamic bone has been attributed partly to aggressive calcitriol therapy, administration of high amounts of exogenous calcium either as a phosphate binding agent or during dialysis therapy, presence of diabetes, older age, or previous parathyroidectomy. Several vitamin D analogues are currently being evaluated in patients with chronic renal failure to prevent complications associated with calcitriol therapy. In addition, calcium-free phosphate binding agents and the use of calcimimetic drugs may play a significant role in the effective management of secondary hyperparathyroidism in children with chronic renal failure.     

Bsm1 Vitamin D Receptor Polymorphism and Calcium Homeostasis Following Bariatric Surgery

Purpose/Aim: To evaluate the association between the Bsm1 vitamin D receptor polymorphism and the calcium-vitamin D-parathormone axis following bariatric surgery. Materials and Methods: This cross-sectional study included 86 morbidly obese patients, who underwent either gastric bypass or sleeve gastrectomy, with a mean follow-up of four years. Calcium metabolism indices and bone turnover markers were assessed according to the presence of secondary hyperparathyroidism and the Bsm1 vitamin D receptor genotypes. Results: Secondary hyperparathyroidism (42.2% of sample) was associated with lower levels of 25hydroxyvitamin D and elevated markers of bone turnover. In subjects without secondary hyperparathyroidism, presence of the unfavorable B allele resulted in higher levels of parathormone (Bb and BB vs. bb genotype: 50.3 ± 8.2 pg/dl vs. 44.4 ± 10.7 pg/dl, p = .011, adjusted for weight loss, baseline body mass index, 25hydroxyvitamin D, surgical procedure, and duration after surgery). In the whole sample, patients bearing the unfavorable B allele exhibited lower weight loss, a parameter that was negatively associated with markers of bone resorption. Conclusions: Secondary hyperparathyroidism is highly prevalent after bariatric surgery. Bsm1 vitamin D receptor polymorphism may have an effect in early stages of calcium metabolism imbalance, while no association is detected in patients who have already developed secondary hyperparathyroidism. Moreover, vitamin D receptor polymorphism is associated with post-surgery weight loss, a process related to bone turnover.     

Hip fracture patients in India have vitamin D deficiency and secondary hyperparathyroidism

Summary

This study evaluated the parameters of bone mineral homeostasis including 25(OH)D and PTH in 90 Indian patients with hip fracture and 90 controls. Hypovitaminosis D, secondary hyperparathyroidism, and biochemical osteomalacia was present in 77, 69, and 50 % patients, respectively, significantly higher compared to controls. Vitamin D deficiency is an important risk factor for hip fracture.

Introduction

The prevalence of vitamin D deficiency is not well known in hip fracture patients from India. Therefore, the present study was conducted to evaluate the parameters of bone mineral homeostasis including 25(OH)D and intact PTH in hip fracture from North India.

Methods

Ninety consecutive patients with hip fracture and similar number of age- and sex-matched controls were enrolled in the study. The fasting venous samples were analyzed for 25-hydroxyvitamin D (25-OHD), intact parathyroid hormone (PTH), alkaline phosphatase (ALP), calcium, and phosphorus. Vitamin D deficiency was defined as serum 25-OHD of <20 ng/dl.

Results

The mean age of hip fracture subjects was 65.9?±?12.6 which was comparable in men and women. Majority of study subjects were women (70 women and 20 men). The serum 25(OH)D and calcium levels were significantly lower, whereas the intact PTH and ALP levels were significantly higher in patients compared to controls. There was significant negative correlation between serum 25(OH)D and PTH. In the hip fracture group, 76.7 % of the subjects had vitamin D deficiency, and 68.9 % had secondary hyperparathyroidism. In the control group, vitamin D deficiency and elevated PTH levels were seen in 32.3 and 42.2 %, respectively.

Conclusion

About three fourths of hip fracture patients have vitamin D deficiency, and two thirds have secondary hyperparathyroidism. Therefore, the serum 25-OHD level may be a useful index for the assessment of risk of hip fracture in India.     

Treatment of Epilepsy to Optimize Bone Health

When treating a person with epilepsy, one must consider many factors in addition to the obvious need to treat the seizures. Both epilepsy itself and treatment with antiepileptic drugs (AEDs) subject one to numerous potential secondary long-term health concerns. Poor bone health is one of these concerns. Studies suggest that persons with epilepsy treated with AEDs have an increased risk of fracture, low bone mineral density (BMD), and abnormalities in bone metabolism. Multiple factors likely contribute to the increased risk. Falls during generalized tonic-clonic seizures, secondary effects of AEDs on balance, inactivity, low BMD, reduced calcium intake, reduced active vitamin D metabolites, and a genetic predisposition to low BMD may all contribute. Studies suggest a differential influence of AEDs. Phenytoin, phenobarbital, and primidone are most consistently associated with a negative impact on bone. Carbamazepine and valproate may also result in bone abnormalities, but data are mixed. Current studies suggest that lamotrigine has limited (if any) effect, but again, data are inconsistent. Other AEDs have received limited study. Screening for poor bone health includes serologic testing of vitamin D metabolites (notably 25-hydroxyvitamin D) as well as BMD testing using dual energy x-ray absorptiometry. Optimizing intake of calcium and vitamin D is important for all persons with epilepsy treated with AEDs. Although many treatments for low BMD are available, these agents have not been studied in persons with epilepsy treated with AEDs. Overall, physicians treating persons with epilepsy must consider the potential effect of having epilepsy and its main treatment, AED therapy, on bone health. For patients in whom bone health is a particular concern (eg, those with diagnosed bone disease or with significant risk factors for bone disease, including glucocorticosteroid use), it is best to avoid AEDs known to negatively affect bone. In addition, practitioners should work with other treating physicians to optimize bone health in these patients.     

Vitamin D deficiency and secondary hyperparathyroidism and the association with bone mineral density in persons with Pakistani and Norwegian background living in Oslo, Norway, The Oslo Health Study

We studied the prevalence of poor vitamin D status and the association with bone density in men and women born in Norway (quoted as Norwegians, n = 869) and Pakistan (quoted as Pakistanis, n = 177) in the population-based Oslo Health Study, 2000-2001. We measured 25-hydroxyvitamin D, iPTH and ionized calcium in serum and bone mineral density at the forearm site with single energy X-ray absorptiometry. Mean 25-hydroxyvitamin D was 74.8 +/- 23.7 nmol/l in the Norwegians and 25.0 +/- 13.6 nmol/l in the Pakistanis (P = 0.000). The prevalence of secondary hyperparathyroidism (iPTH > or = 8.5 pmol/l, 25-hydroxyvitamin D < 50 nmol/l and Ca2+ < or = 1.35 mmol/l) was four times higher in Pakistani compared to Norwegian women. Also in Pakistani men, serious vitamin D deficiency defined as secondary hyperparathyroidism was prevalent, and five times as frequent as in Norwegian men. However, whereas BMD was significantly lower in Norwegian women with, compared to Norwegian women without, secondary hyperparathyroidism, there was no difference in BMD between Pakistani women with and without secondary hyperparathyroidism. In conclusion, vitamin D deficiency was prevalent among Pakistani immigrants, and in great contrast to the vitamin D replete Norwegians. Serious vitamin D deficiency was interestingly not associated with reduced forearm bone density among Pakistani women.     

Calcimimetics: a remedy for all problems of excess parathyroid hormone activity in chronic kidney disease?

PURPOSE OF REVIEW: Cinacalcet is a calcimimetic agent that is now available for use clinically to manage secondary hyperparathyroidism among patients undergoing dialysis regularly. It acts as an allosteric activator of the calcium-sensing receptor, the molecular mechanism that controls parathyroid hormone secretion. This mechanism of action differs fundamentally from that of the vitamin D sterols, which heretofore have been the only definitive pharmacological intervention for treating secondary hyperparathyroidism. RECENT FINDINGS: The ability of calcimimetic agents to enhance signaling through the calcium-sensing receptor in parathyroid cells affects several important components of parathyroid gland function. Results from several large clinical trials demonstrate that cinacalcet effectively lowers plasma parathyroid hormone levels in dialysis patients with secondary hyperparathyroidism when used either alone or together with vitamin D. Unlike the vitamin D sterols, which generally raise serum calcium and phosphorus levels, treatment with cinacalcet is associated with modest reductions in serum calcium and phosphorus concentrations. The impact of these biochemical changes on renal bone disease and on soft-tissue and vascular calcification during long-term treatment has yet to be characterized fully. Cinacalcet also diminishes parathyroid hormone gene expression, and studies in experimental animals indicate that its use retards the progression of parathyroid gland hyperplasia and increases bone mass. If confirmed in future clinical trials in patients with secondary hyperparathyroidism, these features represent potentially important ancillary therapeutic benefits. SUMMARY: Calcimimetic agents have diverse effects on parathyroid gland function that may enhance the overall medical management of secondary hyperparathyroidism in patients undergoing dialysis regularly.     

The impact of calcimimetics on mineral metabolism and secondary hyperparathyroidism in end-stage renal disease

The impact of calcimimetics on mineral metabolism and secondary hyperparathyroidism in end-stage renal disease. Secondary hyperparathyroidism is often complicated by elevations in calcium and phosphorus either as a result of the disease per se or due to toxicity from current therapeutic options. These disturbances in mineral metabolism limit the successfulness of therapy and have been implicated as contributing to the development and progression of vascular calcification, an important and often overlooked component of cardiovascular disease in patients on dialysis. Phosphorus, active vitamin D, and calcium all play important roles in the pathogenesis of secondary hyperparathyroidism; however, serum calcium is the primary regulator of minute-to-minute parathyroid hormone secretion. Small changes in serum calcium are detected by a cell surface calcium sensing receptor that has recently been cloned. Calcimimetic agents modulate the activity of the calcium-sensing receptor and result in profound reductions in levels of circulating parathyroid hormone. Additionally, these agents result in decreases in serum calcium, phosphorus, and calcium-phosphorus product. Recently completed phase 2 clinical trials with the second-generation calcimimetic agent cinacalcet HCl confirm that this agent represents a safe and effective novel therapeutic agent which has the potential to dramatically alter the treatment and complications associated with secondary hyperparathyroidism in patients on dialysis.     

Addressing the Musculoskeletal Components of Fracture Risk with Calcium and Vitamin D: A Review of the Evidence

Osteoporotic fractures are an extremely common and serious health problem in the elderly. This article presents the rationale for calcium and vitamin D supplementation in the prevention and treatment of osteoporotic fractures and reviews the literature evidence on the efficacy of this strategy. Two musculoskeletal risk factors are implicated in osteoporotic fractures in the elderly: the loss of bone mass due to secondary hyperparathyroidism and the increased propensity to falls. Calcium and vitamin D reverse secondary hyperparathyroidism with resultant beneficial effects on bone mineral density (BMD). Additionally, calcium and vitamin D supplementation significantly improves body sway and lower extremity strength, reducing the risk of falls. The effects of combined calcium and vitamin D on parathyroid function and BMD provide a strong rationale for the use of this therapy in the prevention and treatment of osteoporosis and osteoporotic fractures. There is general agreement that, in patients with documented osteoporosis, calcium and vitamin D supplementation should be an integral component of the management strategy, along with antiresorptive or anabolic treatment. Frail elderly individuals constitute another major target population for calcium and vitamin D because evidence from randomized studies in institutionalized elderly subjects demonstrates that these supplements reduce osteoporotic fracture risk, particularly in the presence of dietary deficiencies. However, the results of trials in community-dwelling subjects have been equivocal. Within the primary-care setting, further research is required to establish appropriate target subgroups for calcium and vitamin D supplementation; overall, the data are consistent with a benefit individuals with insufficient calcium and/or vitamin D, although patients with documented osteoporosis will derive further benefit in terms of fracture prevention from the addition of an antiresorptive agent.     

关注甲状旁腺功能增强和正常血钙型原发性甲状旁腺功能亢进症的防治

随着血钙及甲状旁腺素（PTH）等各种实验室检查技术的发展,大量无症状或正常血钙型原发性甲状旁腺功能亢进症（primary hyperparathyroidism,PHPT）得以早期诊断。PHPT已成为影响人类健康的第三大常见内分泌系统疾病。目前部分PHPT,尤其是多数正常血钙型PHPT,并非原发,可能是长期钙摄入不足和...     

Vitamin D status among patients with fractured neck of femur in Hong Kong

Vitamin D deficiency leads to secondary hyperparathyroidism initially and then to mild osteomalacia, both of which conditions may be aymptomatic and may predispose to bone fracture. To assess the importance of vitamin D deficiency in predisposing to fractured neck of femur, we studied the vitamin D status, dietary intake and socio-economic characteristics in 69 patients with fractured neck of femur (group A), 28 normal subjects with age above 60 (group B), and 101 normal volunteers (group C). Patients with fractured neck of femor had significantly lower levels of serum 25-hydroxy-cholecalciferol compared with subjects of groups B and C. There is no statistically significant difference in other biochemical parameters, including calcium, phosphate, and alkaline phosphatase. Patients with fractured neck of femur and with 25-hydroxycholecalciferol below 20 ng/mL were characterized by a home-bound and/or institutionalized life-style, smaller living place, and limited access to open space. To conclude, hypovitaminosis D is a common problem among elderly patients with fractured neck of femur in Hong Kong. The fact that such vitamin D deficiency is associated with muscle weakness may contribute to falls, and thus indirectly account for an increased rate of hip fractures over the normal control.     

Renal osteodystrophy: present and future

Evidence is accumulating to indicate that certain abnormalities in mineral metabolism and/or their clinical management can lead to the development of vascular and soft tissue calcifications in patients with end-stage renal disease. Although the long-term consequences of vascular calcification in chronic renal failure have yet to be fully defined, the disorder may contribute to the high mortality rate from cardiovascular causes in patients undergoing long-term dialysis. The relationship between vascular calcification and cardiovascular disease in those with end-stage renal disease needs to be thoroughly evaluated, and substantial changes in the clinical management of patients undergoing dialysis may be appropriate. Phosphate retention and hyperphosphatemia have long been recognized as contributors to vascular and soft tissue calcification in chronic renal failure. Several recent reports indicate, however, that the use of large oral doses of calcium as phosphate-binding agents particularly in patients with persistently elevated serum phosphorus levels, may increase the risk of vascular calcification. Concurrent therapy with supra-physiological doses of calcitriol and other vitamin D sterols to manage secondary hyperparathyroidism leads to episodes of hyperphosphatemia and hypercalcemia, which can further aggravate soft tissue and vascular calcification. The phosphate-binding ion exchange resin sevelamer is now available for clinical use in the United States. It does not contain either calcium or aluminum, and other calcium- and aluminum-free phosphate-binding agents are being developed. These compounds make it possible to manage phosphate retention in patients with chronic renal failure without the risks associated with the sustained ingestion of large daily doses of calcium or aluminum. Several new vitamin D analogs are now available to treat secondary hyperparathyroidism due to chronic renal failure. These compounds may be less likely than calcitriol to enhance intestinal calcium and phosphorus absorption and to promote calcium and phosphorus release from bone. The therapeutic use of new vitamin D sterols as alternatives to calcitriol may permit clinicians to effectively manage secondary hyperparathyroidism while reducing the risks of soft tissue calcification in patients who require vitamin D therapy. Received: July 27, 2000 / Accepted: July 27, 2000     

High prevalence of hypovitaminosis D in pregnant Japanese women with threatened premature delivery

Serum 25-hydroxyvitamin D (25-OHD) concentrations are thought to accurately reflect vitamin D stores, and vitamin D deficiency causes secondary hyperparathyroidism, irreversible bone loss, and increased risk of fracture. Recent studies suggest that decrease of serum 25-OHD level in mothers could increase the risk of preeclampsia, cesarean section, and craniotabes. Furthermore, this deficiency may affect bone mass and the incidence of neuromuscular diseases of their children in the future. In the present study, the serum concentration of 25-OHD in 93 pregnant women after the 30th week of their gestation was determined by direct radioimmunoassay. Mean 25-OHD levels in spring, summer, fall, and winter were 14.3 ± 5.1, 15.7 ± 6.4, 13.7 ± 5.1, and 13.9 ± 4.2 ng/ml, respectively. Severe vitamin D deficiency (25-OHD < 10 ng/ml) was found in 10 of these 93 women. Overall, hypovitaminosis D, which was defined as serum 25-OHD concentration equal to or less than 20 ng/ml, was revealed in 85 mothers (89.5%). Serum 25-OHD levels were not associated with either intact parathyroid hormone or corrected calcium concentrations, but were negatively associated with serum type I collagen N-terminal telopeptide and bone-specific alkaline phosphatase in these subjects. Mothers with threatened premature delivery had significantly lower 25-OHD levels (11.2 ± 3.2 ng/ml) than those in mothers with normal delivery (15.6 ± 5.1 ng/ml). In conclusion, the present data suggest a high prevalence of hypovitaminosis D in perinatal pregnant Japanese women throughout the year, which seems to affect bone metabolism and to be associated with threatened premature delivery.     

Regulation of parathyroid function in chronic kidney disease (CKD)

In chronic kidney disease (CKD), several abnormalities in bone and mineral metabolism develop in the majority of patients. The parathyroid plays a very important role in regulating bone and mineral metabolism; thus, control of parathyroid function is one of the main targets of the management of CKD-mineral and bone disorder (CKD-MBD). In the development of secondary hyperparathyroidism, it has recently been suggested that fibroblast growth factor 23 (FGF23) plays a crucial role, both as a phosphaturic factor and as a suppressor of active vitamin D (1,25D) production in the kidney. FGF23 is originally secreted to prevent hyperphosphatemia in CKD, but this occurs at the expense of low 1,25D and hyperparathyroidism (“trade-off” hypothesis revisited). Furthermore, recent data suggest that FGF23 could be another useful marker for the prognosis of hyperparathyroidism, because a high serum level may reflect the cumulative dose of vitamin D analogues previously administered. We have also demonstrated that severe hyperparathyroidism was associated with the production and secretion of a new form of parathyroid hormone (PTH) molecule, which can be detected by third-generation assays for PTH, but not by the second-generation assays. For the regression of already established nodular hyperplasia, the more advanced type of parathyroid hyperplasia, it is certainly necessary, in the near future, to develop new agents that specifically induce apoptosis in parathyroid cells. Until such agents are developed, prevention and early recognition of nodular hyperplasia is mandatory for the effective and safe management of hyperparathyroidism in CKD.     

Bone and mineral metabolism in patients undergoing Roux-en-Y gastric bypass

Summary

Despite effective weight reduction, the impact of bariatric surgery on bone is a major concern. Mechanisms include decreased mechanical loading, calcium and vitamin D malabsorption, deficiency in other nutrients, and alterations in fat- and gut-derived hormones. The evidence to support clinical care pathways to prevent bone loss and fractures is at this point weak.

Introduction

There is a growing concern regarding the potential deleterious impact of bariatric surgery on bone metabolism. This comprehensive review addresses this controversial topic.

Methods

We reviewed and analyzed articles evaluating bone metabolism and mechanisms for the ensuing putative bone loss in adult patients exclusively undergoing Roux-en-Y gastric bypass (RYGB) surgery, for the period spanning 1942 till September 2012.

Results

Mechanisms identified to contribute to alterations in bone metabolism after bypass surgery include: decreased mechanical loading, calcium and vitamin D malabsorption with secondary hyperparathyroidism, deficiency in other nutrients, in addition to alterations in adipokines, gonadal steroids, and gut-derived hormones favoring bone loss, with the exception of serotonin and glucagon-like peptide-1. The relative contribution of each of these hormones to changes in bone homeostasis after bypass surgery remains undefined. Bone loss reflected by a decline in bone mineral density (BMD) and an increase in bone turnover markers have been reported in many studies, limited for the most part by the exclusive use of dual energy X-ray absorptiometry. Well-designed long-term prospective trials with fractures as an outcome, and studies investigating the magnitude, reversibility, and impact of the observed metabolic changes on fracture outcomes are lacking.

Conclusion

Robust conclusions regarding bone loss and fracture outcome after RYGB surgery cannot be drawn at this time. Although not evidence based, baseline evaluation and sequential monitoring with measurement of BMD and calciotropic hormones seem appropriate, with adequate calcium and vitamin D replacement. Beneficial interventions remain unclear.     

Periosteal chondroma of the cuboid with secondary aneurysmal bone cyst in a setting of secondary hyperparathyroidism

We report the case of a 35-year-old woman with painful, nontender mass at the right lateral hindfoot. Computed tomography (CT) and magnetic resonance imaging (MRI) indicated the suspect of a chondroid tumour in the cuboid. The tumour was resected en bloc and histology revealed the presence of a periosteal (juxtacortical) chondroma with secondary aneurysmal bone cyst. Secondary hyperparathyroidism was detected in laboratory tests and put into context with the histopathologic findings. In conclusion, a rare case of periosteal chondroma of the cuboid with secondary aneurysmal bone cyst in a setting of secondary hyperparathyroidism due to vitamin D deficiency is presented.Level of clinical evidence: 4.