Life Extension Magazine August 2011
Increase of bone resorption and the parathyroid hormone in postmenopausal women in the long-term after Roux-en-Y gastric bypass.
BACKGROUND: The effects of Roux-en-Y Gastric Bypass (RYGB) on bone in the long-term remains unclear. We assessed bone metabolism and bone mineral density (BMD) 1 to 5 years after RYGB.METHODS: We designed a retrospective cohort study in 26 postmenopausal women (58.0+/-3.9 years old) with RYGB 3.5+/-1.1 years before (body mass index (BMI) 29.5+/-3.8 kg/m2, presurgery 43.6+/-5.5 kg/m2) and 26 nonoperated women (57.5+/-4.7 years old, BMI 29.2+/-4.1 kg/m2) matched by age and BMI. The main measures were BMD, serum carboxy telopeptide (CTx), total alkaline phosphatases (ALP), parathyroid hormone (PTH), 25-hydroxyvitamin D (25OHD), and ghrelin. RESULTS: RYGB group, compared to nonoperated women, had higher CTx (0.71+/-0.21 vs. 0.43+/-0.15 ng/ml; P<0.01) and PTH (68.3+/-35 vs. 49.4+/-16 pg/ml; P=0.02). There were no differences between RYGB and nonoperated women in: calcium and vitamin D intake (759+/-457 vs. 705+/-460 mg/day; 176+/-160 vs. 111+/-86 UI/day), ghrelin (763+/-336 vs. 621+/-274 pg/ml), ALP (101+/-22 vs. 94+/-25 UI/l), 25OHD (18.8+/-7.6 vs. 17.4 +/- 5.9 ng/ml), lumbar spine BMD (1.059+/-0.32 vs. 1.071+/-0.207 g/cm2), or femoral neck BMD (0.892+/-0.109 vs. 0.934+/-1.1 g/cm2). CONCLUSIONS: RYGB is associated to high bone resorption and hyperparathyroidism prevalence in postmenopausal women in the long-term. This occurs independently of the intake of calcium, vitamin D status, or ghrelin and does not seem to affect BMD after RYGB.
Obes Surg. 2009 Aug;19(8):1132-8
Metabolic bone disease after gastric bypass surgery for obesity.
BACKGROUND: The popularity of gastric bypass surgery for treatment of morbid obesity has been increasing in recent years. Osteomalacia and osteoporosis are commonly observed in patients who have had partial gastric resections for treatment of peptic ulcer disease. Recently, we encountered four patients with previous gastric bypass surgery who had metabolic bone disease similar to that reported in the older literature in patients who had partial gastrectomies. METHODS: Review of clinical data of four patients who developed osteomalacia and osteoporosis 9 to 12 years after gastric bypass surgery for morbid obesity.RESULTS: All subjects were women, 43 to 58 years old. Three had Roux-en-Y gastric bypass, and the other had a biliopancreatic diversion 9 to 12 years prior to presentation. Weight loss averaged 41.8 kg. Patients reported fatigue, myalgias, and arthralgias. They had symptoms for many months or years before the correct diagnosis was established. All were osteopenic or osteoporotic with hypocalcemia, very low or undetectable 25-hydroxyvitamin D levels, secondary hyperparathyroidism, increased 1,25-dihydroxyvitamin D levels, and increased serum alkaline phosphatase. CONCLUSIONS: Relatively little has been published in the general medical literature about this postoperative complication of bariatric surgery. Yet, nearly all patients after bariatric surgery will receive their long-term follow-up from a primary care physician. Physicians and patients need to be aware of this complication and take measures to identify and prevent it.
Am J Med Sci. 2005 Feb;329(2):57-61
Gastric banding or bypass? A systematic review comparing the two most popular bariatric procedures.
OBJECTIVE: Bariatric surgical procedures have increased exponentially in the United States. Laparoscopic adjustable gastric banding is now promoted as a safer, potentially reversible and effective alternative to Roux-en-Y gastric bypass, the current standard of care. This study evaluated the balance of patient-oriented clinical outcomes for laparoscopic adjustable gastric banding and Roux-en-Y gastric bypass. METHODS: The MEDLINE database (1966 to January 2007), Cochrane clinical trials database, Cochrane reviews database, and Database of Abstracts of Reviews of Effects were searched using the key terms gastroplasty, gastric bypass, laparoscopy, Swedish band, and gastric banding. Studies with at least 1 year of follow-up that directly compared laparoscopic adjustable gastric banding with Roux-en-Y gastric bypass were included. Resolution of obesity-related comorbidities, percentage of excess body weight loss, quality of life, perioperative complications, and long-term adverse events were the abstracted outcomes. RESULTS: The search identified 14 comparative studies (1 randomized trial). Few studies reported outcomes beyond 1 year. Excess body weight loss at 1 year was consistently greater for Roux-en-Y gastric bypass than laparoscopic adjustable gastric banding (median difference, 26%; range, 19%-34%; P < .001). Resolution of comorbidities was greater after Roux-en-Y gastric bypass. In the highest-quality study, excess body weight loss was 76% with Roux-en-Y gastric bypass versus 48% with laparoscopic adjustable gastric banding, and diabetes resolved in 78% versus 50% of cases, respectively. Both operating room time and length of hospitalization were shorter for those undergoing laparoscopic adjustable gastric banding. Adverse events were inconsistently reported. Operative mortality was less than 0.5% for both procedures. Perioperative complications were more common with Roux-en-Y gastric bypass (9% vs 5%), whereas long-term reoperation rates were lower after Roux-en-Y gastric bypass (16% vs 24%). Patient satisfaction favored Roux-en-Y gastric bypass (P=.006).CONCLUSION: Weight loss outcomes strongly favored Roux-en-Y gastric bypass over laparoscopic adjustable gastric banding. Patients treated with laparoscopic adjustable gastric banding had lower short-term morbidity than those treated with Roux-en-Y gastric bypass, but reoperation rates were higher among patients who received laparoscopic adjustable gastric banding. Gastric bypass should remain the primary bariatric procedure used to treat obesity in the United States.
Am J Med. 2008 Oct;121(10):885-93
The effects of obesity surgery on bone metabolism: what orthopedic surgeons need to know.
Morbid obesity affects approximately 9 million Americans. Obesity is associated with a reduced risk of osteoporosis, whereas weight loss decreases bone density. Obesity surgery has profound effects on bone, which are well described in the gastrointestinal literature; yet, there are virtually no reports in the orthopedic literature. The Roux-en-Y procedure is the leading bariatric operation performed in the United States. In this surgery, the primary sites for calcium absorption are bypassed. Patients become calcium- and Vitamin D-deficient, and the body then up-regulates parathyroid hormone, causing increased production of Vitamin D and increased calcium resorption from bone. Gastric banding utilizes a restrictive band and has not been shown to produce the same bone loss as the Roux-en-Y procedure, nor has there been evidence of secondary hyperparathyroidism. It is important for orthopedists to be aware of the types of obesity surgery and their sequelae on bone, as this may impact bone density, fracture risk, and fracture healing.
Am J Orthop (Belle Mead NJ). 2009 Feb;38(2):77-9
Bone and gastric bypass surgery: effects of dietary calcium and vitamin D.
OBJECTIVE: To examine bone mass and metabolism in women who had previously undergone Roux-en-Y gastric bypass (RYGB) and determine the effect of supplementation with calcium (Ca) and vitamin D. RESEARCH METHODS AND PROCEDURES: Bone mineral density and bone mineral content (BMC) were examined in 44 RYGB women (> or = 3 years post-surgery; 31% weight loss; BMI, 34 kg/m(2)) and compared with age- and weight-matched control (CNT) women (n = 65). In a separate analysis, RYGB women who presented with low bone mass (n = 13) were supplemented to a total 1.2 g Ca/d and 8 microg vitamin D/d over 6 months and compared with an unsupplemented CNT group (n = 13). Bone mass and turnover and serum parathyroid hormone (PTH) and 25-hydroxyvitamin D were measured. RESULTS: Bone mass did not differ between premenopausal RYGB and CNT women (42 +/- 5 years), whereas postmenopausal RYGB women (55 +/- 7 years) had higher bone mineral density and BMC at the lumbar spine and lower BMC at the femoral neck. Before and after dietary supplementation, bone mass was similar, and serum PTH and markers of bone resorption were higher (p < 0.001) in RYGB compared with CNT women and did not change significantly after supplementation. DISCUSSION: Postmenopausal RYGB women show evidence of secondary hyperparathyroidism, elevated bone resorption, and patterns of bone loss (reduced femoral neck and higher lumbar spine) similar to other subjects with hyperparathyroidism. Although a modest increase in Ca or vitamin D does not suppress PTH or bone resorption, it is possible that greater dietary supplementation may be beneficial.
Obes Res. 2004 Jan;12(1):40-7
Current understanding of osteoporosis associated with liver disease.
Osteoporosis is a common complication of many types of liver disease. Research into the pathogenesis of osteoporosis has revealed that the mechanisms of bone loss differ between different types of liver disease. This Review summarizes our current understanding of osteoporosis associated with liver disease and the new advances that have been made in this field. The different mechanisms by which cholestatic and parenchymal liver disease can lead to reduced bone mass, the prevalence of osteopenia and osteoporosis in patients with early and advanced liver disease, and the influence of osteoporotic fractures on patient survival are discussed along with the advances in our understanding of the molecular pathways associated with bone loss. The role of the CSF1-RANKL system and that of the liver molecule, oncofetal fibronectin, a protein that has traditionally been viewed as an extracellular matrix protein are also discussed. The potential impact that these advances may have for the treatment of osteoporosis associated with liver disease is also reviewed.
Nat Rev Gastroenterol Hepatol. 2009 Nov;6(11):660-70
Daily oral 25-hydroxycholecalciferol supplementation for vitamin D deficiency in haemodialysis patients: effects on mineral metabolism and bone markers.
BACKGROUND: Vitamin D deficiency is frequently observed in end-stage renal disease (ESRD) patients; however, the effects of vitamin D supplementation have rarely been reported. We aimed to assess the effects of daily 25(OH)D(3) supplementation on mineral metabolism, bone markers and Kidney Disease Outcomes Quality Initiative (KDOQI) targets in haemodialysis (HD) patients for a period of 6 months. METHODS: HD patients were included in this study if their serum 25(OH)D level was <75 mmol/L. Oral 25(OH)D(3) was administered daily at 10-30 microg/day based on the severity of the deficiency. Characteristics of the patients were compared from the baseline to 6 months on the basis of their response to 25(OH)D(3) administration and the patients were divided into three groups. Patients who showed partial response [serum 25(OH)D <75 nmol/L] were placed in group 1, those who showed normal response [serum 25(OH)D ranging from 75 to 150 nmol/L] were placed in group 2 and those who showed excessive response [serum 25(OH)D >150 nmol/L] were placed in group 3. RESULTS: Of the 253 HD patients, 225 (89%) showed vitamin D insufficiency or deficiency, 172 were included in the study and 149 patients completed the study. After 6 months of treatment [mean daily 25(OH)D(3): 16 +/- 5 microg/day], the serum 25(OH)D level increased (30 +/- 19 to 126 +/- 46 nmol/ L, P < 0.001), with 13% of patients in group 1, 57% in group 2 and 30% in group 3. The serum intact parathyroid hormone (iPTH) level decreased (235 +/- 186 to 189 +/- 137 pg/mL, P = 0.05), except in group 1. Bone alkaline phosphatase (BALP) showed a tendency to normalize (23 +/- 16 to 18.3 +/- 11 microg/L, P < 0.05), leading to a decrease in alfacalcidol administration from 66% to 43% (P < 0.05), except in group 1. The KDOQI targets achieved increased significantly for serum calcium (76% to 85%) and phosphate levels (66% to 77%) in all patients. The serum albumin level increased in all groups (34.6 +/- 4 to 36.8 +/- 4 g/L, P < 0.05), without any significant improvement in normalized protein catabolic rate (nPCR) or C-reactive proteins (CRP). CONCLUSION: With a daily dose ranging from 10 to 30 microg, daily oral 25(OH)D(3) supplementation corrects most vitamin D deficiencies or insufficiencies in HD patients, without any evident toxicity. The main effects observed included correction of excessive bone turnover, despite less alfacalcidol administration, increase in serum albumin level and increase in the percentage of patients with serum calcium and phosphorus levels within the recommendation of the KDOQI guidelines.
Nephrol Dial Transplant. 2008 Nov;23(11):3670-6
Evidence for persistent vitamin D 1-alpha-hydroxylation in hemodialysis patients: evolution of serum 1,25-dihydroxycholecalciferol after 6 months of 25-hydroxycholecalciferol treatment.
BACKGROUND: End-stage renal disease (ESRD) patients are thought to have impaired 1-alpha-hydroxylase capacity, but an extrarenal source of 1,25(OH)(2)D has been recognized. OBJECTIVE: The aim of this study was to assess the evolution of serum 1,25(OH)(2)D in hemodialysis (HD) patients with vitamin D deficiency after 6 months of 25(OH)D(3) supplementation, and to identify the factors associated with persistent 1,25(OH)(2)D production. METHODS: HD patients in a HD center with vitamin D deficiency (i.e. 25(OH)D <75 nmol/l) who were not receiving any vitamin D derivatives or calcimimetics were studied. Patients who had previously undergone parathyroidectomy or nephrectomy or those with uncontrolled hypercalcemia or hyperphosphatemia were excluded from this study. The patients were administrated a dose of 10-30 microg/day of oral 25(OH)D(3) based on the severity of their deficiency. The serum levels of 25(OH)D and 1,25(OH)(2)D evolution after 6 months were recorded. Responders were defined as patients with an increase in serum 1,25(OH)(2)D levels greater than the median value. Changes in mineral metabolism parameters were compared with those in the nonresponders. RESULTS: Of the 253 patients, 225 (89%) were vitamin D-deficient, and 43 met the inclusion criteria. The patients were 72.6 +/- 10 years old and had been on dialysis for 71 +/- 70 months; 39% of the patients were female and 45% were diabetics. From baseline to 6 months of treatment, serum 25(OH)D levels increased from 27.8 +/- 18 to 118 +/- 34 nmol/l (p < 0.001) and serum 1,25(OH)(2)D levels increased from 7.7 +/- 5 to 30.5 +/- 15 pmol/l (p < 0.001) with a median increase of 20 pmol/l. The mean serum calcium level increased from 2.19 +/- 0.1 to 2.25 +/- 0.1 mmol/l (p = 0.009), the intact parathyroid hormone (iPTH) level decreased from 144 +/- 108 to 108 +/- 63 pg/ml (p = 0.05), and the bone alkaline phosphatase (BALP) level remained unchanged. The serum phosphate level increased slightly from 1.22 +/- 0.3 to 1.34 +/- 0.2 mmol/l (p = 0.04) with reduced hypophosphatemia. Compared with the responders (n = 24), most of the nonresponders (n = 19) were diabetic (63 vs. 29%, p = 0.02) and had a lesser increase of their 25(OH)D serum level. The serum level of FGF-23 was not significant. A positive correlation was observed between serum 1,25(OH)(2)D and serum 25(OH)D levels after 6 months of 25(OH)D(3) treatment (p = 0.02). CONCLUSION: The Kidney Disease Outcomes Quality Improvement (KDOQI) guidelines do not recommend checking and treating vitamin D deficiency in chronic kidney disease (CKD) stage 5 patients due to the supposed lack of 1,25(OH)(2)D production. These data confirm persistent renal or extra-renal production of 1,25(OH)(2)D in HD patients after 6 months of 25(OH)D(3) administration. Diabetes is the main factor associated with impaired 1,25(OH)(2)D production. 25(OH)D(3 )administration corrects vitamin D deficiency with few effects on mineral metabolism and stability of bone turnover markers.
Nephron Clin Pract. 2008;110(1):c58-65
Liver disease in older women.
Clinicians are seeing increasing number of patients with chronic liver disease (CLD). The prevalence of diseases such as nonalcoholic fatty liver disease is increasing dramatically, our population is ageing and people with CLD are surviving into old age. Signs and symptoms of CLD in the older patient are often subtle and non-specific and a high index of suspicion is required in order to investigate. A number of diseases, which are predominate in women, tend to present in middle to older age. The menopause may render the liver more susceptible to disease progression and although hormone replacement appears safe in CLD but it is not recommended for liver protection. Osteoporosis is common in CLD but robust evidence is lacking on fracture prevention. Vigilance is required when interpreting investigations as there are no age-associated changes in clinical liver function testing. Management strategies are similar irrespective of age or gender, but evidence is lacking specific to older populations.
Maturitas. 2010 Mar;65(3):210-4
A new equation to estimate glomerular filtration rate.
BACKGROUND: Equations to estimate glomerular filtration rate (GFR) are routinely used to assess kidney function. Current equations have limited precision and systematically underestimate measured GFR at higher values. OBJECTIVE: To develop a new estimating equation for GFR: the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation.DESIGN: Cross-sectional analysis with separate pooled data sets for equation development and validation and a representative sample of the U.S. population for prevalence estimates. SETTING: Research studies and clinical populations (“studies”) with measured GFR and NHANES (National Health and Nutrition Examination Survey), 1999 to 2006. PARTICIPANTS: 8254 participants in 10 studies (equation development data set) and 3896 participants in 16 studies (validation data set). Prevalence estimates were based on 16,032 participants in NHANES. MEASUREMENTS: GFR, measured as the clearance of exogenous filtration markers (iothalamate in the development data set; iothalamate and other markers in the validation data set), and linear regression to estimate the logarithm of measured GFR from standardized creatinine levels, sex, race, and age. RESULTS: In the validation data set, the CKD-EPI equation performed better than the Modification of Diet in Renal Disease Study equation, especially at higher GFR (P < 0.001 for all subsequent comparisons), with less bias (median difference between measured and estimated GFR, 2.5 vs. 5.5 mL/min per 1.73 m(2)), improved precision (interquartile range [IQR] of the differences, 16.6 vs. 18.3 mL/min per 1.73 m(2)), and greater accuracy (percentage of estimated GFR within 30% of measured GFR, 84.1% vs. 80.6%). In NHANES, the median estimated GFR was 94.5 mL/min per 1.73 m(2) (IQR, 79.7 to 108.1) vs. 85.0 (IQR, 72.9 to 98.5) mL/min per 1.73 m(2), and the prevalence of chronic kidney disease was 11.5% (95% CI, 10.6% to 12.4%) versus 13.1% (CI, 12.1% to 14.0%). LIMITATION: The sample contained a limited number of elderly people and racial and ethnic minorities with measured GFR.CONCLUSION: The CKD-EPI creatinine equation is more accurate than the Modification of Diet in Renal Disease Study equation and could replace it for routine clinical use.
Ann Intern Med. 2009 May 5;150(9):604-12
Chronic liver disease in an ageing population.
The prevalence of chronic liver disease is increasing in the elderly population. With a mostly asymptomatic or non-specific presentation, these diseases may easily go undiagnosed. Abnormal liver function tests of unknown cause are a common reason for referral to secondary care. Investigating the older person with abnormal liver function is important; even with mild abnormalities, the same vigilance should be applied to an older person as in a young person. Liver biopsy is safe but often overlooked in this age group and may provide useful information to diagnose, direct therapy and prognosticate. Treatment options are similar for all age groups, with a few subtle differences, although further evidence is frequently required for the older population. Morbidity and age-adjusted mortality are often more severe in older people, and therefore early diagnosis and intervention is important. Presented here are the most common chronic liver diseases that geriatricians are likely to encounter in clinical practise. Their epidemiology, clinical features, investigation, treatment and mortality are described with a particular focus on the elderly population.
Age Ageing. 2009 Jan;38(1):11-8
Bone mineral density and disorders of mineral metabolism in chronic liver disease.
AIM: To estimate the prevalence and identify the risk factors for metabolic bone disease in patients with cirrhosis. METHODS: The study was performed on 72 Indian patients with cirrhosis (63 male, nine female; aged < 50 years). Etiology of cirrhosis was alcoholism (n = 37), hepatitis B (n = 25) and hepatitis C (n = 10). Twenty-three patients belonged to Child class A, while 39 were in class B and 10 in class C. Secondary causes for metabolic bone disease and osteoporosis were ruled out. Sunlight exposure, physical activity and dietary constituents were calculated. Complete metabolic profiles were derived, and bone mineral density (BMD) was measured using dual energy X ray absorptiometry. Low BMD was defined as a Z score below -2. RESULTS: Low BMD was found in 68% of patients. Lumbar spine was the most frequently and severely affected site. Risk factors for low BMD included low physical activity, decreased sunlight exposure, and low lean body mass. Calcium intake was adequate, with unfavorable calcium: protein ratio and calcium: phosphorus ratio. Vitamin D deficiency was highly prevalent (92%). There was a high incidence of hypogonadism (41%). Serum estradiol level was elevated significantly in patients with normal BMD. Insulin-like growth factor (IGF) 1 and IGF binding protein 3 levels were below the age-related normal range in both groups. IGF-1 was significantly lower in patients with low BMD. Serum osteocalcin level was low (68%) and urinary deoxypyridinoline to creatinine ratio was high (79%), which demonstrated low bone formation with high resorption. CONCLUSION: Patients with cirrhosis have low BMD. Contributory factors are reduced physical activity, low lean body mass, vitamin D deficiency and hypogonadism and low IGF-1 level.
World J Gastroenterol. 2009 Jul 28;15(28):3516-22
Vitamin D—a panacea in nephrology and beyond.
Vitamin D and its active analogues play an essential role in maintaining the calcium and phosphate homeostasis. Vitamin D deficiency may be a consequence of insufficient dietary supply, impaired intestinal absorption, insufficient exposure of the skin to the ultraviolet radiation, or liver and kidney failure. The consequences of mineral metabolism disorders and in particular vitamin D depletion are osteoporosis, increased cardiovascular diseases, immune system impairment and increased morbidity and mortality in patients with end stage of renal disease. These abnormalities are common in patients with chronic kidney disease. Recent clinical studies have shown that vitamin D supplementation in patients with its deficiency, contribute to decreased frequency of bone disorders, cardiovascular incidents, lower risk of several malignancies and to improvement of immune system response regardless of renal function.
Pol Merkur Lekarski. 2009 Nov;27(161):437-41
Chronic kidney disease-mineral-bone disorder: a new paradigm.
Disturbances in mineral and bone metabolism are prevalent in chronic kidney disease (CKD) and an important cause of morbidity, decreased quality of life, and extraskeletal calcification that have been associated with increased cardiovascular mortality. These disturbances have traditionally been termed renal osteodystrophy and classified on the basis of bone biopsy. Kidney Disease: Improving Global Outcomes (KDIGO) recently sponsored a Controversies Conference to evaluate this definition. The recommendations were that (1) the term renal osteodystrophy be used exclusively to define alterations in bone morphology associated with CKD and (2) the term CKD-mineral and bone disorder (CKD-MBD) be used to describe the broader clinical syndrome that develops as a systemic disorder of mineral and bone metabolism as a result of CKD. CKD-MBD is manifested by an abnormality of any one or a combination of the following: laboratory-abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism; bone-changes in bone turnover, mineralization, volume, linear growth, or strength; and calcification-vascular or other soft-tissue calcification. The pathogenesis and clinical manifestations of these components of CKD-MBD are described in detail in this issue of Advances in Chronic Kidney Disease.
Adv Chronic Kidney Dis. 2007 Jan;14(1):3-12
Age-related increases in parathyroid hormone may be antecedent to both osteoporosis and dementia.
BACKGROUND: Numerous studies have reported that age-induced increased parathyroid hormone plasma levels are associated with cognitive decline and dementia. Little is known about the correlation that may exist between neurological processing speed, cognition and bone density in cases of hyperparathyroidism. Thus, we decided to determine if parathyroid hormone levels correlate to processing speed and/or bone density. METHODS: The recruited subjects that met the inclusion criteria (n = 92, age-matched, age 18-90 years, mean = 58.85, SD = 15.47) were evaluated for plasma parathyroid hormone levels and these levels were statistically correlated with event-related P300 potentials. Groups were compared for age, bone density and P300 latency. One-tailed tests were used to ascertain the statistical significance of the correlations. The study groups were categorized and analyzed for differences of parathyroid hormone levels: parathyroid hormone levels <30 (n = 30, mean = 22.7 +/- 5.6 SD) and PTH levels >30 (n = 62, mean = 62.4 +/- 28.3 SD, p <or= 02). RESULTS: Patients with parathyroid hormone levels <30 showed statistically significantly less P300 latency (P300 = 332.7 +/- 4.8 SE) relative to those with parathyroid hormone levels >30, which demonstrated greater P300 latency (P300 = 345.7 +/- 3.6 SE, p = .02). Participants with parathyroid hormone values <30 (n = 26) were found to have statistically significantly higher bone density (M = -1.25 +/- .31 SE) than those with parathyroid hormone values >30 (n = 48, M = -1.85 +/- .19 SE, p = .04). CONCLUSION: Our findings of a statistically lower bone density and prolonged P300 in patients with high parathyroid hormone levels may suggest that increased parathyroid hormone levels coupled with prolonged P300 latency may become putative biological markers of both dementia and osteoporosis and warrant intensive investigation.
BMC Endocr Disord. 2009 Oct 13;9:21