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Perioperative management of bariatric surgery patients: Focus on metabolic bone disease

Cleveland Clinic Journal of Medicine. 2008 May;75(5):333-334, 336, 338, 342-346, 349
May 1, 2008|Cleveland Clinic Journal of Medicine
Susan E. Williams, MD, MS, RD, CNSP, CCD;Karen Cooper, DO;Bradford Richmond, MD;Philip Schauer, MD
Author and Disclosure Information

Susan E. Williams, MD, MS, RD, CNSP, CCD
Director, Center for Nutrition and Metabolic Medicine, Greene Memorial Hospital Advanced Medical Group, Xenia, OH; Assistant Professor of Clinical Medicine, Department of Internal Medicine, Wright State University Boonshoft School of Medicine, Dayton, OH; Chair-elect, Certification Council, International Society of Clinical Densitometry

Karen Cooper, DO
Bariatric and Metabolic Institute, Cleveland Clinic

Bradford Richmond, MD
Director, Musculoskeletal Radiology Fellowship Program, Department of Diagnostic Radiology, Cleveland Clinic; Associate Profesor of Radiology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University

Philip Schauer, MD
Director, Advanced Laparoscopic and Bariatric Surgery, Bariatric and Metabolic Institute, Cleveland Clinic; Professor of Surgery, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University

Address: Susan Williams, MD, Center for Nutrition & Metabolic Medicine, Greene Memorial Hospital Health Center, 50 North Progress Drive, Xenia, OH 45385; e-mail swilliams@greenehealth.org

Dr. Richmond has disclosed that he has received honoraria from Procter and Gamble for teaching and speaking.

Dr. Schauer has disclosed that he is a consultant for or on the scientific advisory boards of Bard-Davol, Barosense, Baxter, Ethicon Endosurgery, Gore, and Stryker Endoscopy; is on the board of directors and is a partner in Remedy MD; and has received grant support from Invacare.

ABSTRACTChronic vitamin D deficiency, inadequate calcium intake, and secondary hyperparathyroidism are common in obese individuals, placing them at risk for low bone mass and metabolic bone disease. After bariatric surgery, they are at even higher risk, owing to malabsorption and decreased oral intake. Meticulous preoperative screening, judicious use of vitamin and mineral supplements, addressing modifiable risk factors, and monitoring the absorption of key nutrients postoperatively are essential in preventing metabolic bone disease in bariatric surgery patients.

KEY POINTS

  • Metabolic bone disease in obese patients is multifactorial: causes include sequestration of vitamin D in the adipocytes, inadequate nutrition due to chronic dieting, and lack of physical activity.
  • Before bariatric surgery, one must look for and treat preexisting nutritional deficiencies.
  • In the immediate postoperative period, aggressive strategies (ie, giving multivitamins and minerals intravenously and orally) can prevent nutritional deficiencies and secondary bone disease.
  • Postoperatively, many bariatric patients require chewable or liquid supplements to facilitate adequate absorption.
  • Clinical suspicion, timely interventions, and lifelong monitoring can prevent metabolic bone disease in bariatric surgery patients.

Voluntary weight loss, involuntary bone loss

When overweight or obese people lose weight—whether by dieting or by bariatric surgery—they also lose bone: a voluntary loss of approximately 10% of body weight results in a loss of 1% to 2% of bone at all sites. This loss appears to vary among populations: premenopausal women younger than 45 years may be able to lose a moderate amount of weight without a significant increase in fracture risk, while a study of overweight men found that a 7% weight loss resulted in a 1% bone loss.15

The percentage of bone lost correlates strongly with how fast the weight is lost. A recent study found that losing 0.7 kg/week was more detrimental to bone than a slower loss of 0.3 kg/week, due to the activation of the calcium-PTH axis.16

After bariatric surgery, many patients rapidly lose 50 kg—some even lose 100 kg or more. This rapid weight loss, combined with severely restricted oral intake, decreased calcium absorption, and vitamin D deficiency places these patients at extremely high risk of rapidly developing metabolic bone disease.3,8,9 In one large study, metabolic bone disease developed in more than 70% of patients who underwent a malabsorptive procedure, while in a second study, markers of bone resorption were elevated as soon as 8 weeks after bariatric surgery, regardless of whether the patient underwent a malabsorptive or restrictive bariatric procedure.13 Yet another study found that 48% of patients had a statistically significant bone mineral reduction of more than 3% 12 months after undergoing gastric banding.10

ESSENTIAL NUTRIENTS FOR BONE HEALTH

A number of nutrients are essential for bone health; we will limit our discussion to the major ones directly affected by obesity and bariatric surgery (Table 1). Other nutrients often affected by obesity and bariatric surgery will be discussed in a subsequent article.

Protein

Dietary protein is needed to maintain bone structure, and although there is a link between high protein intake, calciuria, and fracture risk, the potentially harmful effects appear to be ameliorated when high protein intake is coupled with adequate calcium.17–20 This fact is of particular importance after bariatric surgery because once the patient can consume enough fluids to maintain hemodynamic stability, he or she is given a relatively high-protein diet to prevent protein malnutrition.21

Inadequate protein intake also has a detrimental effect on bone; therefore, it is essential to assess postoperative protein intake.22 Rizzoli and Bonjour23 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. In two 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.24,25 And a systematic review of protein and bone health concluded that diets containing 1.0 to 1.5 g protein/kg are best for bone health.26 This is particularly worrisome, since the current recommended dietary allowance for protein is only 0.8 g/kg, which may be insufficient to promote calcium homeostasis.26,27

Vitamin D

Vitamin D is essential for calcium absorption, stimulation of osteoblast activity, and normal bone mineralization throughout the life span.27 Dietary vitamin D is mainly absorbed by passive diffusion in the proximal and mid small intestine in a process that is highly dependent on bile salts.28–30 Dietary sources of vitamin D are clinically important because exposure to ultraviolet B radiation is often insufficient, especially in northern latitudes.27

Up to 84% of morbidly obese patients have vitamin D deficiency.2,3,5,2,29,31 The mechanism of vitamin D deficiency and secondary hyperparathyroidism in the morbidly obese remains unclear, although one study concluded they were likely due to sequestration of vitamin D in adipose tissue and subsequent limited bioavailability.32

Correction of vitamin D deficiency requires more than just an over-the-counter multivitamin, but standard multivitamins also contain vitamin A, so taking more than one tablet a day increases the risk of vitamin A excess.33 Repletion can often be safely achieved orally by giving 50,000 IU of vitamin D weekly for 8 weeks, followed by a maintenance dose of one 50,000 IU tablet every 2 weeks. If a repeat serum level shows suboptimal repletion (less than 32 ng/mL), an additional 8-week course is recommended.29 For patients who cannot tolerate or adequately absorb oral supplements, exposure to sunlight is still the best source of vitamin D and is an effective alternative.29,33

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