Originally published 2007, revised April 2010

Send Feedback

In this Issue

Bariatric Surgery And Skeletal Health

Susan E. Williams, MD, MS, CCD, FACN, FACP, Guest Author

Editor's Introduction

Obesity is a very serious public health issue that has reached pandemic proportions, and has been ranked the number-one threat to American health by the CDC since 2004. Results from the 2003-2004 National Health and Nutrition Examination Survey (NHANES) estimated that 33.8% of U.S. adults were obese (BMI ≥ 30), and the prevalence of overweight and obesity combined (BMI ≥ 25) is 68%[1].

According to a RAND Survey on the Health Risks of Obesity, rates are increasing dramatically. Since 1980 the percentage of Americans who are overweight (BMI ≥ 25) or obese (BMI ≥ 30) has been steadily increasing, with a dramatic 60% increase in obesity. Even worse, the rate of clinically severe, or morbid, obesity (self-reported BMI of 40 or above) was found to have risen three times faster, at a rate of 75% in that period of time.

Diet and exercise alone are typically not adequate to achieve a healthy weight in severely obese people, and for those few who do attain a healthy weight, less than 2% are able to maintain that weight beyond two years. Bariatric (weight loss) surgery is the only effective therapy for morbid obesity, it has been around since the 1940s but has undergone resurgence in the last two decades in response to the obesity pandemic and the need to address the myriad co-morbidities for which obesity is directly responsible. Recent data indicate that the number of bariatric surgeries performed in the U.S. rose from 13,365 in 1998 to an estimated 200,000 in 2007[3]. Advances in the field of bariatric surgery have addressed many of the more serious post-operative problems with severe malabsorption and subsequent metabolic derangements however; the consequences of bariatric surgery and dramatic weight loss on skeletal health are just now coming into focus.

In this issue of Osteoporosis Clinical Updates, we look at common contemporary bariatric surgical procedures, their effects on skeletal health, and highlight the need for lifelong surveillance in this patient population.

 

 

Case Study: 50-Year-Old Woman Who Had Roux-En-Y Gastric Bypass Surgery

The patient we will discuss is a 50-year-old woman who was referred for osteoporosis evaluation one year after undergoing Roux-en-Y gastric bypass (RNYGB) surgery. The patient reports having had weight problems since her teen years, she has lost and regained weight numerous times, each time ending up weighing more than when she started. At age 49, with hypertension, newly diagnosed diabetes, and painful knees due to arthritis, she underwent weight loss surgery. Her starting weight was 240 pounds, with a BMI of 42. Now, one year later and 102 pounds lighter, her BMI is 24 and she no longer requires routine medications.

Shortly after a natural menopause at age 46, her family physician obtained a baseline DXA. The spine was found to have the lower score with a BMD of 0.964 g/cm2, a T-score of -1.9 and a Z-score of 0.2. With the concern that the patient had experienced two minimal-trauma ankle fractures in her 30s, had not started hormone replacement therapy, and the patient's mother had been diagnosed with osteoporosis after experiencing multiple rib fractures, the physician prescribed alendronate.

The patient reported good compliance with alendronate until her surgery. She restarted the alendronate after her one-month postoperative check-up but discontinued it 3 weeks later due to cramping and abdominal pain. Five months after surgery, DXA was repeated and revealed a spine BMD of 0.914 g/cm2 and a Z-score of -1.2; DXA was repeated again one year post-operatively and revealed a spine BMD of 0.862 g/cm2 and a Z-score of -1.9. With the concern that these measurements revealed a 6% decline in bone mineral density in six months, with a previous 5% decline over three years, and worsening Z-scores, the patient was referred to a bone specialist.

Labs obtained at the consultation included albumin 3.1 g/mL, calcium 8.2 (normal 8.6-10.5 mg/dL), 25-hydroxyvitamin D low at 12 ng/mL, PTH 128 (normal 10 – 72 pg/mL), and magnesium 1.9 mg/dL (normal). Since her surgery, the patient has been taking a multivitamin tablet, 600 mg calcium carbonate with D, a B-50 complex tablet, and 1000 IU vitamin D3 daily.

Given the patient's surgical and weight loss history, what are her risks for bone loss?

Voluntary weight loss of approximately 10%, whether it is achieved because of bariatric surgery or dieting, results in bone loss at all skeletal sites of 1-2%[4-7]. Bone loss due to weight reduction is multifactorial and correlates strongly with the velocity at which the weight is lost. Decreased calcium, vitamin D, and protein intake during periods of caloric restriction result in decreased calcium absorption, a subsequent rise in PTH, and increased bone resorption. Proposed mechanisms include effects due to increased levels of circulating cortisol, and decreased levels of circulating estrogen, IGF-1, leptin, ghrelin, and GLP-2, particularly in patients who have undergone bariatric surgery[5].

Minerals essential to bone health such as calcium and magnesium are absorbed predominantly in the proximal small bowel, and are dependent upon an acidic environment for optimal solubility and uptake. Proteins and fats are absorbed in the proximal bowel after the prerequisite actions of pancreatic enzymes. Vitamin D is mainly absorbed in the proximal and mid small intestine in a process that is not fat-dependant per se but highly dependent on the presence of bile salts[8,9]. After RNYGB, the proximal small bowel is bypassed, the actions of bile acids and pancreatic enzymes are delayed and often inadequate due to their release in the bypassed duodenum, and the relatively neutral environment of the jejunum impedes calcium absorption.

Rapid weight loss of 100 pounds to greater than 200 pounds is not uncommon among successful bariatric surgery patients. And this, combined with severely restricted oral intake, decreased calcium absorption, and vitamin D deficiency, places these patients at extremely high risk for rapid bone loss[10-12]. One large study noted bone loss in greater than 70% of patients having undergone a malabsorptive procedure, while a second study detected increased markers of bone resorption as soon as 8 weeks after bariatric surgery, regardless of whether the patient underwent a malabsorptive or restrictive bariatric procedure. A third study that examined patients 12 months after undergoing gastric banding found that 48% had a statistically significant bone mineral reduction of greater than three percent[10,13,14].

What can be done to improve her bone health?

Calcium Supplementation

The optimal daily requirement of calcium defined by surgical procedure is currently unknown however, 1500 – 2000 mg/daily appears to be beneficial, particularly during periods of rapid weight loss[15,16] Attempts to protect the skeleton and mitigate the activation of the calcium-PTH axis during weight reduction with supplemental calcium have had mixed results. One current hypothesis supports the fact that the usual recommended intake of calcium is inadequate during weight loss and higher levels of 1600 – 1800 mg/day should be recommended[15,17]. Quantifying urine calcium can further assist in assessing the adequacy of calcium intake in that abnormally low urine calcium in the presence of normal renal function suggests inadequate absorption.

Calcium absorption, separate from the issue of compliance, can be problematic therefore, judicious monitoring is recommended. It is important to remember that calcium homeostasis is a tightly regulated process, maintained by a combination of gut absorption, bone resorption, and renal reabsorption. In the absence of adequate dietary calcium and/or absorption, calcium will be resorbed from bone in order to support calcium-dependant processes and attempt to maintain normal serum calcium levels

Vitamin D Supplementation

Correction of vitamin D deficiency in bariatric surgery patients requires more than just an over-the-counter supplement. Although the upper limit for daily oral vitamin D3 (cholecalciferol) is 10,000 IU, the effective daily dose for bariatric surgery patients can be extraordinarily high[18]. Repletion has been safely and efficaciously achieved by giving 50,000 IU to 100,000 IU cholecalciferol daily for one to two weeks followed by a maintenance dose of 50,000 one to three times weekly. Ergocalciferol as well as the various vitamin D analogs have not demonstrated the efficacy achieved with cholecalciferol in normalizing blood values[19,20].

The absorption of vitamin D is dependent upon the presence of bile acids therefore recommending that the patient take her vitamin D supplements with her largest meal of the day can prove beneficial. It is important to keep in mind that individual variability in absorption varies greatly therefore, specific guidelines need to be viewed with caution while recognizing that titrating the dose in response to the serum level is both appropriate and necessary

For patients who are unable to achieve or maintain normal serum levels with oral supplements, UV-B phototherapy administered by a dermatologist or obtained from a lamp specifically designed for home use is an effective alternative[21-24]. The increased risk of photoaging and skin cancer from tanning beds due to a 4- to 15-fold higher dose of UVA and 2-fold higher dose of UVB than summer, casual sun exposure precludes recommending the routine use of tanning beds[25,26].

The Importance of Dietary Protein

Inadequate dietary protein also has a detrimental effect on bone and likely plays a key role in this population[27]. Appropriate intake of lean protein should be highly emphasized as a bone sparing and body protein-sparing strategy however; tolerance, compliance, and malabsorption issues frequently result in inadequate intake and frank protein deficiency. Reliance on protein supplement powders and beverages is sometimes necessary however, the clinician needs to be mindful that there is also a link between excessively high protein intake, calciuria, and increased fracture risk[28,29].

Investigators Rizzoli and Bonjour noted that markers of bone turnover were higher with a low-protein diet (0.7 g protein per kg body weight) than with a diet containing 2.1 g protein per kg[30]. In trials examining graded levels of protein ingestion (0.7, 0.8, 0.9, and 1.0 g protein per kg body weight), decreased calcium absorption and an acute rise in PTH were noted by day 4 of the 0.7- and 0.8-g/kg diets but not during the 0.9- or 1.0-g/kg diets[31]. Moreover, a systematic review of protein and bone health concluded that diets containing 1.0-1.5 g/kg protein are typically optimal for bone health[32].

Our patient was prescribed 50,000 IU vitamin D3 daily for seven consecutive days then three times weekly. She was switched from calcium carbonate to calcium citrate and instructed to take 615 mg three times daily, her multivitamin was changed to a chewable form and doubled; and she was encouraged to consume an ounce or two of lean protein with each meal and snack. Follow-up labs eight weeks later revealed normal albumin, normal calcium, 25-hydroxyvitamin D 42 ng/mL, and PTH 71 pg/mL.

How should the patient be followed?

According to the American Association of Clinical Endocrinologists (www.aace.com), The Obesity Society (www.obesity.org), and American Society for Metabolic and Bariatric Surgery (www.asmbs.org) (AACE/TOS/ASMBS) joint medical guidelines for clinical practice for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient[3], bariatric surgery patients require meticulous lifetime surveillance.

Our patient should have biochemical indices including albumin, calcium, 25-hydroxyvitamin D, and PTH checked every 3 to 4 months until her labs stabilize, optimal vitamin D of greater than or equal to 50 ng/mL is achieved[38], and the PTH is appropriately suppressed. Once these goals have been met, compliant patients such as in this case can be safely monitored every 6 to 12 months. In addition to an annual physical exam specifically to assess for signs and symptoms of osteoporosis such as loss of height, postural changes and back pain, the AACE/TOS/ASMBS guidelines recommend annual DXA.

[ top ]

 

DXA Z-Scores In Bariatric Surgery Patients

Abnormal DXA results should never evoke a 'knee-jerk' reflex response on the part of the clinician to diagnose osteoporosis and start a bisphosphonate. Abnormal DXA does not always represent primary osteoporosis, nor does it delineate treatment options; and indiscriminate use of bisphosphonates particularly in this patient population can result in life-threatening complications – more on this in a moment.

Abnormal DXA in a bariatric surgery patient often represents secondary bone disease due to nutritional deficiencies. Recall that Z-scores for a reference population are matched to age as well as gender. If BMD had changed only because of normal aging, Z-scores would be expected to be zero, however if the Z-scores are significantly low, this should prompt additional investigation.

[ top ]

Bisphosphonate Use In Bariatric Surgery Patients

When osteoporosis is suspected in a bariatric surgery patient, secondary disease should be suspected first, and if present, should become the focus of treatment interventions. The etiology of the clinical presentation and biochemical indices such as vitamin D deficiency, hypocalcemia, elevated alkaline phosphatase, and secondary hyperparathyroidism should be clearly defined and appropriate treatment interventions initiated. Abnormal DXA may in fact be indicative of both primary and secondary disease however, aggressive treatment of the underlying cause of the secondary disease can result in significant improvements in BMD[34]. The addition of a bisphosphonate to the treatment regimen should only be considered after clinical and biochemical resolution of secondary metabolic bone disease (MBD).

Bisphosphonates inhibit bone resorption, slow calcium efflux from the skeleton and cause a compensatory rise in PTH. Administered in the presence of vitamin D deficiency such as that seen in our patient, normal serum calcium cannot be maintained despite dramatic increases in serum PTH, and life-threatening hypocalcemia can result[35-37]. Therefore, caution is advised when considering the use of oral bisphosphonates in this population due to the high prevalence of vitamin D deficiency and subclinical osteomalacia.

Oral bisphosphonate use in bariatric surgery patients should also be approached cautiously due to the lack of safety and efficacy data. Specifically, tolerance has not been established in the surgical gut, and risk of ulceration at surgical anastamosis has not been defined. Efficacy of oral bisphosphonates has also come into question following bariatric bypass procedures due to the high likelihood that the drug may not be adequately absorbed. It is for these reasons that if treatment for primary osteoporosis is indicated in a bariatric surgery patient, there should be no clinical or biochemical evidence of secondary bone disease, the patient should be taking daily calcium and vitamin D supplements, and intravenous bisphosphonates should be considered.

[ top ]

Bariatric Surgery: Implications for Bone Health

The first papers identifying metabolic bone disease following gastrointestinal surgeries were published in the 1970s, most notably following gastrectomy that rapidly became a well-known cause of osteomalacia[39]. Since then, publications citing a causal relationship between bariatric surgery and MBD number into the multiple of hundreds. The time from surgery to diagnosis of MBD ranges from a few weeks to greater than 32 years, and no bariatric procedure to date has been exempt[13,40-43]. However, the most profound and recent clinical findings that highlight the utmost importance of accurately diagnosing MBD have been in older patients who underwent weight loss surgery in the 1970s. These cases document subsequent treatment for chronic renal oxalate stones and “severe osteoporosis" when in fact chronic, severe long-standing malabsorption resulted in profound nutritional deficiencies and osteomalacia[10,34].

Present-day Bariatric Surgery

Today there are multiple, safe, effective bariatric procedures, and most are performed laproscopically, which has resulted in less postoperative pain, fewer complications, shorter hospital stays and recovery periods. Bariatric surgeries are classified by their predominant mechanism of action and include restrictive and combination restrictive-malabsorptive procedures. Restrictive procedures such as gastric banding and the sleeve gastrectomy promote weight loss by reducing the size of the stomach thereby severely limiting oral intake. Combination procedures, such as the Roux-en-Y gastric bypass, biliopancreatic diversion, and biliopancreatic diversion with duodenal switch promote weight loss by both restrictive and malabsorptive means by decreasing the size of the stomach as well as bypassing part of the small intestine.

Indications for Bariatric Surgery

The 1991 NIH Consensus Development Conference Panel established the following eligibility criteria: surgical candidates with BMI ≥ 40 kg/m[2]; and patients with BMI ≥ 35 kg/m[2]could be considered[ ]if they had high-risk obesity-related co morbidities[44,45]. Subsequently, Medicare further stipulated that patients with BMI ≥ 35 with co-morbid conditions had to submit evidence of unsuccessful attempts at medical management of their obesity.

A consensus does not currently exist regarding possible contraindications to bariatric surgery however, the AACE/TOS/ASMBS guidelines suggest exclusion of those patients who have an unacceptable surgical risk, active substance abuse, major psychopathology; and those who are unable or unwilling to commit to the required lifelong diet and lifestyle changes.

Types of Bariatric Surgery

Gastric Restriction

The goal of restrictive bariatric procedures is to produce early satiety, limit oral intake and thus promote weight loss. The laproscopic adjustable gastric band (LAGB) (Figure 1) also known as the 'lap band' has become a very popular procedure, is associated with weight loss maintenance far better than lifestyle changes alone, and has a very low operative mortality rate of 0.1%[46,47]. The sleeve gastrectomy, previously an investigational procedure, is now an accepted primary procedure and is often employed as the first half of a staged procedure for those patients at high risk for complications. The sleeve is created by performing a longitudinal gastrectomy (seen in figure 3 as part of the BPD/DS) and is known for promoting up to 45% loss of excess weight within the first postoperative year. Following weight loss and improvement in comorbidites, the patient can safely undergo either RNYGB or BPD/DS.

Exclusively restrictive procedures, formerly presumed not to alter bone metabolism, place the skeleton at risk due to inadequate intake and absorption of calcium, vitamin D, and protein[14,48]. Longitudinal studies in patients who have undergone LAGB are needed in order to determine the short- and long-term effects of the procedure on skeletal health, and to quantify any changes in osteoporosis and fracture risks.

Figure 1. Adjustable Gastric Band

Bariatric-BAND-FIG-1.jpg

Laparoscopic adjustable gastric band restricts food intake by creating a 15 to 45 mL gastric pouch and limiting the pouch outlet thereby promoting early satiety. The band can be adjusted by infusing or withdrawing saline into the band via a port that is placed subcutaneously and connected to the band via a small tube.

Graphic Source: U.S. National Library of Medicine. National Institutes of Health. MedlinePlus. Accessed online 03-19-2010.

Roux-en-Y Gastric Bypass (RNYGB)

The most commonly performed bariatric procedure in the United States is the Roux-en-Y gastric bypass (Figure 2), and accounts for more than 80% of bariatric operations although the proportion is changing with the advent of LAGB[3]. This combination procedure restricts oral intake by creating a 10 – 30 mL gastric pouch then limits nutrient absorption by bypassing the duodenum and proximal jejunum. The remaining 'roux' limb receives food directly from the gastric pouch, and bile acids and pancreatic enzymes from the bypassed segment. Patients who undergo RNYGB surgery often experience dramatic weight loss of up to 70% of excess body weight and the loss is typically sustained for more than 10 years[49,50].

As previously noted, the metabolic complications and resulting skeletal problems can be significant following RNYGB. Decreased absorption of essential minerals, inadequate protein intake, and delayed action of biliopancreatic juices often lead to frank malnutrition and begin to compromise bone health within the first few postoperative weeks. In addition to the malabsorption, the rapid, dramatic weight loss these patients experience appears to promote bone loss.

Several prospective studies have investigated the metabolic effects of RNYGB. One small study of 25 women found that following RNYGB, calcium absorption declined 24% - 36% and levels of serum estradiol decreased. Another study found decreased 25-hydroxyvitamin D, increased PTH, and increased CTX (serum C-terminal telopeptide, a marker of bone resorption) in both premenopausal women and postmenopausal women who had undergone RNYGB[51]. And a third study showed elevated PTH and a 3-fold increase in urine NTX(urinary N-telopeptide a marker of bone resorption) nine months after the procedure[52]. Research has also demonstrated detrimental skeletal effects. A study that followed 230 RNYGB patients noted declines in BMD in the spine, hip, and forearm by 9.3%, 4.5% and 0.6% respectively. During the second post-operative year forearm BMD declined an additional 3.6%[53].

Figure 2. Roux-en-Y Gastric Bypass

Bariatric-3.jpg

The Roux-en-Y gastric bypass procedure creates a small gastric pouch that is anastamosed to the proximal jejunum. The remainder of the stomach, duodenum, and proximal jejunum are bypassed, and rejoin the distal 'roux' limb in a 'Y' configuration.

Graphic Source: Google Images: U.S. National Library of Medicine. National Institutes of Health. MedlinePlus (caption added). Accessed online 03-19-2010.

Biliopancreatic Diversion (BPD) and Biliopancreatic Diversion with Duodenal Switch (BPD/DS)

Biliopancreatic diversion (BPD) and biliopancreatic diversion with duodenal switch (BPD/DS) (Figure 3) are also combination restrictive-malabsorptive procedures that result in weight loss predominantly due to calorie and fat malabsorption[3]. These procedures are typically done in patients who have super-morbid obesity and who need to lose multiples of hundreds of pounds.. Both procedures are associated with a variety of postsurgical nutritional and metabolic complications, including protein-calorie malnutrition, anemia, vitamin D deficiency that can be very resistant to oral repletion, and metabolic bone disease. Excess weight loss and severe malnutrition resistant to more conservative management with diet, supplements and oral pancreatic enzyme replacement can necessitate surgical revision to lengthen the absorptive channel in patients who have undergone one of these procedures.

Figure 3: Biliopancreatic diversion with duodenal switch

Bariatric-3.jpg

The biliopancreatic diversion with duodenal switch procedure includes creating a vertical (sleeve) gastrectomy that preserves the pylorus. The biliopancreatic limb is attached just distal to the pylorus and 50 cm from the ileo-cecal valve. Weight loss occurs predominantly because of calorie and fat malabsorption.

Graphic Source: U.S. National Library of Medicine National Institutes of Health. MedlinePlus (caption added). Accessed online 03-19-2010.

[ top ]

Recommendations For Monitoring And Promoting Skeletal Health After Bariatric Surgery

Patients who have had bariatric surgery should be screened for osteoporosis, undergo baseline and serial bone density testing, and be routinely checked for signs of malnutrition, malabsorption, vitamin and mineral deficiencies, and changes in height and posture. Specifically, patients should be have follow-up nutritional and metabolic consultations every one to three months for the first six months, every three to six months for the next six months and every three to 12 months in the second and subsequent years depending upon the procedure, degree of compliance, and the ability to maintain normal nutritional parameters. Routine lab testing should include albumin, serum calcium, magnesium, 25-hydroxyvitamin D, and PTH. Baseline and annual exams should include DXA, and measured height using a stadiometer.

Vitamin and mineral supplementation should be started as soon after surgery as is tolerated and should include a chewable adult multivitamin, calcium citrate, and vitamin D3. Intake of lean protein should begin as soon as the diet is advanced, with an initial goal of consuming an ounce of protein six times daily and gradually advancing to 1.0 to 1.2 grams of protein per Kg of adjusted body weight. Chewable supplements appear to be better tolerated and may facilitate absorption; the multivitamin should be dosed twice daily initially. The starting calcium dose should not be less than 1200 mg, taken in a divided dose, and will likely require frequent dose adjustments upward based on serum and urine indices. Vitamin D3 supplementation should be based on the serum level, with a minimum starting dose of 50,000 IU twice weekly taken with the patient's larger meal of the day.

Pharmacologic treatment for low bone mass, high bone turnover, or osteoporosis should only be initiated after all bone-related biochemical indices – serum calcium, 25-hydroxyvitamin D, and PTH - are normal. Clinicians need to remain mindful that bone loss due to nutritional deficiencies can substantially improve with aggressive oral repletion and in some cases, no additional interventions are indicated. Due to the risk of ulceration at surgical anastamoses and likelihood of inadequate oral drug absorption, intravenous administration of bisphosphonates is currently recommended.

Table 1

Recommended Daily Calcium and Vitamin D3 Intake for Obese and Bariatric Surgery Patients
Adult Women and Men Calcium[‡] Vitamin D3[*]
*Doses listed are for maintenance of normal levels. Repletion of vitamin D often requires significantly higher doses.
[‡]Calcium citrate has been demonstrated to have better bioavailability, superior fractional uptake in bone, and efficacy in normalizing markers of bone turnover when compared to other commercial calcium supplements[33].
During periods of rapid weight loss 1,500 – 2000 mg 1,000 IU
Morbidly obese patients 1,500 mg 2,000 IU
Post-Bariatric surgery patients 1,500 – 2000 mg 2,000 IU – 100,000+ IU

[ top ]

 

References

  1. Flegal KM, Carroll MD, Ogden CL, et al. Prevalence and trends in obesity among US adults, 1999-2008. JAMA 2010;303(3):235-241
  2. Sturm R. Increases in morbid obesity in the USA: 2000-2005. Public Health. 2007;121(7):492-496.
  3. Mechanick JI, Kushner RF, Sugerman HJ, et al. American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery Medical guidelines for clinical practice for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient. Endocr Pract 2008: Jul-Aug; 14(Suppl 1):1-83.
  4. Shapses SA, Cifuentes M. Body weight/composition and weight change: effects on bone health. In Holick MF, Dawson-Hughes B, editors. Nutrition and Bone Health. New Jersey: Humana Press; 2004. p. 549-573.
  5. Shapses SA, Riedt CS. Bone, body weight, and weight reduction: What are the concerns? J Nutr 2006;136:1453-1456.
  6. Chao D, Espeland MA, Farmer, D, et al. Effect of voluntary weight loss on bone mineral density in older overweight women. J Am Geriatr Soc 2000;48:753-759.
  7. Coates PS, Fernstrom JD, Fernstrom MH, et al. Gastric bypass surgery for morbid obesity leads to an increase in bone turnover and a decrease in bone mass. J Clin Endocrinol Metab 2004;89(3):1061-1065.
  8. Keitel V, Kubitz R, Haussinger D. Endocrine and paracrine role of bile acids. World J Gastroenterol 2008;14(37):5620-5629.
  9. Houten SM, Watanabe M, Auwerx J. Endocrine functions of bile acids. The EMBO Journal 2006;25:1419-1425.
  10. Haria DM, Sibonga JD, Taylor HC. Hypocalcemia, hypovitaminosis D osteopathy, osteopenia, and secondary hyperparathyroidism 32 years after jejunoileal bypass. Endocr Pract 2005; 11:335–340.
  11. Hamoui N, Anthone G, Crookes F. Calcium metabolism in the morbidly obese. Obes Surg 2004; 14:9–12.
  12. Newbery L, Dolan K, Hatzifotis M, et al. Calcium and vitamin D depletion and elevated parathyroid hormone following biliopancreatic diversion. Obes Surg 2003;13(6):893-895.
  13. Collazo-Clavell ML, Jimenez A, Hodgson SF, et al. Osteomalacia after Roux-en-Y gastric bypass. Endocr Pract 2004; 10:287–288.
  14. Pugnale N, Giusti V, Suter M, et al. Bone metabolism and risk of secondary hyperparathyroidism 12 months after gastric banding in obese pre menopausal women, Int J Obes Relat Metab Disord 2003; 27(1):110-116
  15. Jensen LB, Kollerup G, Quaade F, et al. Bone mineral changes in obese women during moderate weight loss with and without calcium supplementation. J Bone Miner Res 2001;16:141-147.
  16. Heaney RP. Sodium, Potassium, Phosphorus, and Magnesium. In Holick MF, Dawson-Hughes B, editors. Nutrition and Bone Health. New Jersey: Humana Press; 2004. p. 327-344.
  17. Ricci TA, Chowdhury HA, Heymsfield SB, et al. Calcium supplementation suppresses bone turnover during weight reduction in postmenopausal women. J Bone Miner Res 1998;13:1045-1050.
  18. Hathcock JH, Shaw A, Vieth R, Heaney RP. Risk assessment for vitamin D. Am J Clin Nutr 2007; 85:6-18
  19. Houghton LA, Vieth R. The case against ergocalciferol (vitamin D2) as a vitamin supplement. Am J Clin Nutr 2006;84:694-697.
  20. Lips P. Vitamin D deficiency and secondary hyperparathyroidism in the elderly: Consequences for bone loss and fractures and therapeutic implications. Endo Rev 2001;22(4):477-501
  21. Chel VGM, Ooms ME, Popp-Snijders C, et al. Ultraviolet irradiation corrects vitamin D deficiency and suppresses secondary hyperparathyroidism in the elderly. JBMR 1998;13(8):1238-1242.
  22. Holick MF. Vitamin D. In: Shils ME, Olsen JA, Shine M, et al. editors. Modern Nutrition in Health and Disease (9th ed.). Philadelphia: Lippincott Williams & Wilkins; 1999. p. 329-346.
  23. Rosen CJ. Vitamin D and bone health in adults and the elderly. In: Holick MF. Vitamin D: Physiology, molecular biology, and clinical applications. New Jersey: Humana Press; 1999. p. 287-306.
  24. Holick MF, Garabedian M. Vitamin D: Photobiology, metabolism, mechanism of action, and clinical applications. In: Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism (6th ed.). Washington D.C. American Society for Bone and Mineral Research, 2006. p. 106-114
  25. Levine JA, Sorace M, Spencer J, et al. The indoor UV tanning industry: A review of skin cancer risk, health benefit claims, and regulation. J Am Acad Dermatol 2005;53(6):1038-1044.
  26. Lim HW, Gilchrest BA, Cooper KD, et al. Sunlight, tanning booths, and vitamin D. J Am Acad Dermatol 2005;52(5):868-876.
  27. Conigrave AD, Brown EM, Rizzoli R. Dietary protein and bone health: roles of amino-acid receptors in the control of calcium metabolism and bone homeostasis. Annu Rev Nutr 2008;28:131-155.
  28. Krenitsky J. Adjusted body weight: Evidence to support the use of adjusted body weight in calculating calorie requirements. Nutr Clin Prac 2005;20(4): 468-473.
  29. Munger RG, Cerhan JR, Chiu BC. Prospective study of dietary protein intake and risk of hip fracture in postmenopausal women. Am J Clin Nutr 1999;69:147-152.
  30. Rizzoli R, Bonjour JP. Dietary protein and bone health. J Bone Miner Res 2004;19:527-531.
  31. Kerstetter JE, Svastisalee CM, Caseria DM, et al. A threshold for low-protein-diet-induced elevations in parathyroid hormone. Am J Clin Nutr 2000;72:168-173
  32. Ilich JZ, Kerstetter JE. Nutrition in bone health revisited: A story beyond calcium. J Am Coll Nutr 2000;19(6):715-737
  33. Harvey JA, Kenny P, Poindexter J, et al Superior calcium absorption from calcium citrate than calcium carbonate using external forearm counting. J Am Col Nutr 1990;9(6):583-587.
  34. Williams SE, Licata AA. Improved forearm bone mineral density after treatment with vitamin D3 in a patient 30 years after bariatric surgery. JBMR 2008;23:S226
  35. Recker RR, Lewiecki EM, Miller PD, et al. Safety of bisphosphonates in the treatment of osteoporosis. Am J Med 2009;122(2 Suppl):S22-32.
  36. Maalouf NM, Heller HJ, Odvina CV, et al. Bisphosphonate-induced hypocalcemia: Report of three cases and review of literature. Endo Pract 2006;12(1):48-53.
  37. Rosen CJ. Severe hypocalcemia after intravenous bisphosphonate therapy in occult vitamin D deficiency. NEJM 2003;348(15):1503-1504.
  38. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-81
  39. Eddy RL. Metabolic bone disease after gastrectomy. Am J Med 1971;50(4):442-449.
  40. De Prisco C, Levine SN. Metabolic bone disease after gastric bypass surgery for obesity. Am J Med Sci 2005;329:57–61.
  41. Parikh SJ, Edelman M, Uwaifo GI, et al. Gastric bypass surgery for morbid obesity leads to an increase in bone turnover and a decrease in bone mass. J Clin Endocrinol Metab 2004; 89:1196–1199.
  42. Goldner WS, O'Dorisio TM, Dillon JS, Mason EE. Severe metabolic bone disease as a long-term complication of obesity surgery. Obes Surg 2002; 12:685–692.
  43. Atreja A, Abacan C, Licata A. A 51-year-old woman with debilitating cramps 12 years after bariatric surgery. Cleve Clin J Med 2003; 70:417–426.
  44. Gastrointestinal surgery for severe obesity: National Institutes of Health Consensus Development Conference Statement. Am J Clin Nutr 1992;55(2 suppl):615S-619S
  45. Consensus Development Conference Panel. NIH conference: Gastrointestinal surgery for severe obesity. Ann Intern Med 1991;115:956-961
  46. Greenway FL. Surgery for obesity. Endocrinol Metab Clin North Am 1996;25:1005-1027
  47. O'Brien PE, Dixon JB, Laurie C, et al. Treatment of mild to moderate obesity with laparoscopic adjustable gastric banding or an intensive medical program: a randomized trial. Ann Intern Med. 2006;144:625-633.
  48. Guisti V, Gasteyger C, Suter M, et al. Gastric banding induces negative bone remodeling in the absence of secondary hyperparathyroidism: Potential role of serum C telopeptide for follow-up . Inter J Obes 2005;29 (12):1429-1435
  49. Brolin RE. Bariatric surgery and long-term control of morbid obesity. JAMA. 2002;288(22):2793-2796.
  50. Pories WJ, Swanson MS, MacDonald KG, et al. Who would have thought it? An operation proves to be the most effective therapy for adult onset diabetes mellitus. Ann Surg. 1995;222(3):339-352
  51. El-Kadre LJ, Rocha PR, de Almeida Tinoco AC,Tinoco RC. Calcium metabolism in pre- and postmenopausal morbidly obese women at baseline and after laparoscopic Roux-en-Y gastric bypass. Obes Surg. 2004;14(8):1062-1066.
  52. Coates PS, Fernstrom JD, Fernstrom MH, Schauer PR, Greenspan SL. Gastric bypass surgery for morbid obesity leads to an increase in bone turnover and a decrease in bone mass. J Clin Endocrinol Metab 2004;89(3):10611065.
  53. Johnson JM, Maher JW, Samuel I, et.al. Effects of gastric bypass procedures on bone mineral density, calcium, parathyroid hormone, and vitamin D. J Gastrointest Surg. 2005;9(8):1106-1110.

[ top ]

Measuring BMD in Bariatric Surgery Patients

Measuring BMD in patients over 250 pounds is complicated by weight limitations of common DXA tables currently in use, which range from 250 to 350 pounds. New machines that can accommodate people up to 400 pounds have recently been introduced, but are available in few locations.

In addition to machine size/weight limitations, BMD measurement in patients during weight change is further complicated by anomalies in BMD measurements associated with variables such as fat density and distribution and the DXA software used. [1,2] One study tested a wide range of DXA machines and found that all showed some degree of inconsistency in measuring total-body BMC and BMD measurements in individuals undergoing weight loss. As a result, the study's authors recommended that total body BMD measurements during weight change “be treated with suspicion." [3]

Standard central DXA can be used to measure forearm BMD in patients too heavy for full-body scans. In addition, peripheral BMD measurement can also be used for measuring bone density in patients over 400 pounds. Measurement at the forearm, heel, and finger is commonly performed using peripheral bone density techniques that include:

Peripheral DXA measurements at the phalanges and proximal/distal forearm have been shown in studies to correlate 75-90% to BMD measurements at the spine and hip by central DXA.[4] Peripheral QUS appears to be less closely correlated to hip and spine BMD by DXA.

All types of peripheral BMD measurement techniques are appropriate for screening and fracture risk predictions, but are not the gold standard for diagnosis and monitoring of treatment in patients with osteoporosis.

References

  1. Tothill P. Dual-energy x-ray absorptiometry measurements of total-body bone mineral during weight change. J Clin Densitom. 2005 Spring;8(1):31-8.
  2. Blake GM, Herd RJ, Patel R, Fogelman I. The effect of weight change on total body dual-energy X-ray absorptiometry: results from a clinical trial. Osteoporos Int. 2000;11(10):832-9.
  3. Tothill P, Laskey MA, Orphanidou CI, van Wijk M. Anomalies in dual energy X-ray absorptiometry measurements of total-body bone mineral during weight change using Lunar, Hologic and< Norland instruments. Br J Radiol. 1999 Jul;72(859):661-9.
  4. Picard D, Brown JP, Rosenthall L, et. al. Ability of peripheral DXA measurement to diagnose osteoporosis as assessed by central DXA measurement. J Clin Densitom. 2004 Spring;7(1):111-8.

[ top ]

Adjusted Body Weight

Not all excess adipose tissue in obese patients is metabolically active, in fact, only about 25% is considered metabolically active. Calculating the adjusted body weight accounts for this disparity, and can be used to help prevent over-supplementation.

First, the ideal body weight needs to be determined. To define the ideal body weight (IBW), use the rule of 5s and 6s: In women, allow 100 pounds for the first 60 inches in height then add 5 pounds for each additional inch. For men, allow 106 pounds for the first 60 inches then add 6 pounds for each inch. For example, a women who is 5'4" tall has an ideal body weight of 120 pounds, and for a 5'10" man, his ideal body weight is 166 pounds.

Keep in mind that the IBW is NOT what a person should strive to weigh but rather a tool for clinicians to use similar to the BMI to estimate the degree to which a patient is underweight, normal weight, or overweight.

Once the IBW has been calculated, to define the adjusted body weight use the following formula: Adjusted Body Weight = (( Actual weight – Ideal Body Weight) x 0.25) + IBW. A woman who is 5'4" tall and weighs 240 pounds – ((240 – 120) x 0.25) + IBW - has an adjusted body weight of 150 pounds.

References

Krenitsky J. Adjusted body weight: Evidence to support the use of adjusted body weight in calculating calorie requirements. Nutr Clin Prac 2005;20(4): 468-473.

[ top ]

Continuing Education

CE Credit

After participating in this activity, the reader has the option of taking a post-test to qualify for continuing education credit for this activity. It is estimated it will take 1.0 hour(s) to complete the reading and take the post-test. Continuing education credit will be available for two years from the date of publication.

The National Osteoporosis Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.  The National Osteoporosis Foundation designates this educational activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)TM. Physicians should only claim credit commensurate with the extent of their participation in the activity.

The National Osteoporosis Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation.

The National Osteoporosis Foundation designates this educational activity for a maximum of 1.0 continuing nursing education credit(s).

Other healthcare providers will also be able to receive a certificate of completion; nurse practitioners and physician assistants may request an AMA PRA Category 1 Credit(s)™ certificate.

If you wish to receive continuing education credit, please click here to access the Continuing Education Application. Print this form and complete offline. Complete the registration form then take the 10-question post test and circle your answers on the CE Reporting Form. Then complete the activity evaluation found at the bottom of the CE Reporting Form. You must complete the Post-Test and CE Reporting Form in order to receive credit.

There is a $10.00 fee for this continuing education activity. Payment may be made by check, VISA or MasterCard. We cannot accept any other forms of payment. Please complete the payment information on the CE Reporting Form.

Once the Continuing Education Application is complete, return it with your payment to NOF at the address indicated on the form. Your continuing education certificate will be emailed to you within 3 weeks of receipt.

Software Requirement: Adobe Acrobat Reader is required to read the text for this continuing education activity.

Editorial Board

The Osteoporosis Clinical Updates Editorial Board is comprised of medical specialists, nonspecialists, and a variety of other healthcare professionals involved in research in and management of osteoporosis.

DISCLOSURE OF COMMERCIAL SUPPORT
It is the policy of the National Osteoporosis Foundation (NOF) to ensure balance, independence, objectivity, and scientific rigor in all its sponsored publications and programs. NOF requires the disclosure of the existence of any significant financial interest or any other relationship the sponsor, Editorial Board or Guest Contributors have with the manufacturer(s) of any commercial product(s) discussed in an educational presentation. All authors and contributors to this continuing education activity have disclosed any real or apparent interest that may have direct bearing on the subject matter of this program.

Please be advised that NOF’s accreditation status with ACCME and ANCC does not imply endorsement by NOF, ACCME, or ANCC of any commercial products displayed in conjunction with this activity.

STATEMENT ON OFF-LABEL USE

Please be advised that any publication of the Osteoporosis Clinical Updates that discusses off-label use of any medications or devices will be disclosed to the participant.

EDITORIAL BOARD DISCLOSURES

Editor-in-Chief
Angelo Licata, MD, PhD
Director, Center Space Medicine
Department of Endocrinology
Cleveland Clinic 
Disclosures: Speaking/Teaching: Eli Lilly, Novartis, Amgen, Consulting: Merck

Adrienne Berarducci, PhD, ARNP, BC 
Associate Professor
University of South Florida and 
Azure Medical Group
Disclosure: No relationships to disclose

Carolyn J. Bolognese, RN, CDE
Bethesda Health Research Center
Disclosure: Consulting: Amgen, Merck
Speaking/Teaching: Amgen, Merck

JoAnn Caudill, RT, BD, CDT
Bone Health Program Manager
Redwood / Erickson Retirement Communities
Disclosures: No relationships to disclose

Peggy Doheny, PhD, RN, CNS, ONC
Professor and Adult CNS Program Director
Kent State University College of Nursing
Disclosures: No relationships to disclose

Patricia Graham, MD, PC
Owner, Physical Medicine and Rehabilitation / Integrative Medicine
Disclosures: No relationships to disclose

Craig Langman, MD
Head, Kidney Diseases
Childrens Memorial Hospital
Professor, Feinberg School of Medicine
Northwestern University
Disclosure: No relationships to disclose

Barbara Messinger-Rapport, MD, PhD
Director, Center for Geriatric Medicine of the Medicine Institute
Cleveland Clinic
Disclosure: No relationships to disclose

Paul D. Miller, MD
Distinguished Clinical Professor of Medicine
Colorado Center for Bone Research
Disclosures: Consulting: Warner Chilcott, Baxter, Genentech, Eli Lilly, Merck, Novartis, Amgen, GlaxoSmithKline
Speaking/Teaching: Warner Chilcott, Genentech, Eli Lilly, Merck, Novartis, Amgen
Advisory Committee: Warner Chilcott, Genentech, Eli Lilly, Merck, Novartis, Amgen
Research/Grants: Warner Chilcott, Eli Lilly, Merck, Novartis, Amgen

Jeri Nieves, PhD
Associate Professor of Clinical Epidemiology
Columbia University, Helen Hayes Hospital
Disclosure: Consulting: Merck

Mary Beth O’Connell, PharmD, BCPS
Associate Professor, Wayne State University
Eugene Applebaum College of Pharmacy and Health Sciences
Disclosures: Research Grants: Merck

Carol Sedlak, PhD, RN, CNS, ONC, CNE
Professor & Nurse Educator Program Director
Kent State University College of Nursing
Disclosures: No relationships to disclose

Kathy M. Shipp, PT, MHS, PhD 
Assistant Professor, Division of Physical Therapy 
Department of Community and Family Medicine 
Duke University School of Medicine 
Disclosure: Speaking/Teaching: Amgen

Andrea Sikon, MD, FACP, CCD, NCMP
Chair, Department of Internal Medicine
Cleveland Clinic
Disclosure: Stockholder: Amgen, Pfizer

Kelly Trippe, MA
Managing Editor, Osteoporosis Clinical Updates
National Osteoporosis Foundation
Disclosure: No relationships to disclose

Susan Randall, RN, MSN, FNP-BC
Senior Director, Science and Education
National Osteoporosis Foundation
Disclosure: No relationships to disclose

 

[ top ]