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Osteoporosis: You Could Be At Risk
By Mary Jane Detroyer, MS, RD, CDN

Osteoporosis is a progressive and silent disease that weakens bones by making them porous. Osteopenia is a state of lower than normal bone mass. Weak bones break easily. Most people are unaware they have osteoporosis until they experience a loss of height due to collapsing vertebrae, pain, or suspicious fractures. The only way to diagnose osteoporosis is to have your bone density measured by dual-energy x-ray absorptiometry (DEXA). Bone is dynamic and changes continuously throughout your lifetime through a process called remodeling in which old bone is removed (resorption) and new bone is formed. In healthy bone, the removal and formation of bone is in balance. Osteoporosis occurs when too much bone is removed, when not enough bone is formed, or when both defective processes occur in combination.

Women are more susceptible to osteoporosis than men because they lose bone very rapidly at menopause as estrogen levels decline. After the age of 65, men and women lose bone at a similar rate. However, with men decreased testosterone levels increased the risk of fractures.

Risk Factors

Many risk factors can interfere with bone remodeling and lead to osteoporosis. Some risk factors such as sex, age, body-frame size, ethnicity and heredity are beyond any control. So being female, elderly, small-boned or naturally thin, having a mother or father with osteoporosis, or being Caucasian or of Japanese or Chinese descent increases risk. Controllable factors include smoking, abnormally low body weight, diet, sex hormone levels, lack of exercise, and alcohol. Certain medications, medical conditions, chronic inflammatory diseases, and gastrointestinal problems such as malabsorption can also increase risk of osteoporosis.

HIV Infection

Being infected with human immunodeficiency virus (HIV) may increase the risk of developing osteoporosis. Abnormal bone metabolism was reported as early as 1993 in a study that compared serum osteocalcin levels (a marker of bone formation) and bone mass in 16 HIV+ patients and 27 healthy controls living in Spain.1 Serum osteocalcin levels were significantly lower than normal in the HIV+ patients. Bone mass was also lower, but the difference was not significant. Factors associated with HIV that may be responsible for increased risk of bone disease are malnutrition, medications, malabsorption, cytokine activity, low levels of sex hormones, physical inactivity, infection of bone building cells by HIV, and decreased levels of Vitamin D.
In 1995, investigators conducted a study to see if there was a relationship between the severity of HIV infection and bone disturbances.2 After carefully eliminating factors that might confound results, they found that serum osteocalcin was lower in patients with more advanced HIV infection as classified by the Centers for Disease Control and Prevention (CDC). They found no difference in bone density between patients and seronegative controls. In 1997, Paton et al measured bone mineral density (BMD) in 45 HIV+ men and compared their results with those of age-matched controls to determine if HIV infection was associated with decreased BMD.3 The HIV patients had slightly lower BMD at the lumbar spine compared with controls, but no difference in total or hip BMD. The authors performed repeat scans on 21 patients at 15 months to see if there were changes in BMD. The follow-up scans revealed a slight decrease in total BMD but no change in spine or hip BMD.

Teichman and colleagues looked at male and female patients to see whether HIV infection had an influence on bone formation.4 All patients had low bone mineral content. Females with a history of long-term heroin use had a more severe reduction. Serum osteocalcin was reduced in all patients, and the reduction was significantly correlated with progressive loss of CD4 cells.

Sex Hormones

Hypogonadism (abnormally low levels of testosterone) is quite prevalent in men living with AIDS5 and is also seen in women with AIDS.6 Reduced levels of plasma 1,25®¢dihydroxyvitamin D and calcium malabsorption, which are needed for proper bone formation, were seen in hypogonadal men. Testosterone replacement in these hypogonadal men resulted in a significant increase in total and free 1,25 (OH) 2D, improved calcium absorption, and increased retention of calcium and bone formation.7 Sublingual testosterone replacement in hypogonadal men (5 mg three times a day for 6 months) resulted in an increase in lean muscle mass and muscle strength and a decrease in bone resorption and urinary calcium excretion.8 Other studies showing reduced BMD in hypogonadal men support the role of testosterone replacement for increasing BMD.9,10

Medications

It has been suggested that protease inhibitors (PIs) may be related to reduced BMD. Tebas et al found that men on PI therapy had lower lumbar spine and proximal femur (upper leg bone) BMD compared to HIV-negative and HIV-positive men not on PIs.11 Fifty percent of those on PIs were classified as either osteoporotic or osteopenic. Carr and colleagues measured bone density, by DEXA, in 221 HIV-infected men and found seven men had osteoporosis and 44 had osteopenia.12 High lactate levels and low-weight prior to antiretroviral therapy were the only factors associated with osteopenia and osteoporosis. McDermott et al found that HIV+ men on highly active antiretroviral therapy (HAART) had lower total and regional bone mass than HIV+ men not on HAART.13

In contrast, Aukrust and coauthors found that during 24 months of HAART, the viral loads of HIV+ patients fell dramatically while their serum osteocalcin levels rose significantly and C-telopeptide decreased. This indicates a trend toward normalization of bone remodeling associated with HAART.14 Nolan and colleagues found no signs of accelerated bone loss in patients taking nelfinavir or indinavir and a possible positive effect on BMD with indinavir over time. They did find that a lower body mass index (BMI) prior to treatment with HAART was strongly associated with reduced bone density.15 Retrospective data on 10,000 HIV+ patients who participated in pharmaceutical trials on PI and non-PI regimens found no difference in the number of fracture rates in the patients on PIs than in those not on PI therapy.16 They found a large number of those who experienced fractures (20%®¢30%) were currently taking corticosteroids or had taken them in the past. No data was gathered on corticosteroid intake on those without fractures, which makes it difficult to accurately interpret this information. However, long-term intake of corticosteroids increases risk of osteoporosis.

Controllable Lifestyle Habits

It is probable that many of the controllable behaviors that increase risk of osteoporosis are contributing to the reduced bone density in HIV+ individuals. Longitudinal data was collected on 128 HIV+ patients. Some were on HAART (68%); others had never taken HIV medications. Bone mineral density T scores, measured by DEXA, indicated that 46% of the patients had osteopenia or osteoporosis. Notably, 70% of the patients were consuming less than 1,000 mg of calcium daily, the recommended dose for healthy individuals age 19®¢50 years to prevent deficiency. They also found that low body weight, low body mass index, history of weight loss or wasting, history of steroid use, and a current or past history of smoking were associated with low BMD. When they looked at medications, only length of antiviral therapy, not type, was significantly associated with increased risk of BMD.17

Prevention

The best way to decrease the risk of developing osteoporosis is prevention. Patient education
and risk assessment is essential. The National Osteoporosis Foundation recommends a
combination of these four steps to help prevent
osteoporosis:

"Eat a balanced diet with adequate calcium and vitamin D.
"Participate in regular weight-bearing exercise.
"Stop smoking and limit your alcohol intake.
"Patients and clinicians should consider a bone density test and medications for osteoporosis when appropriate.

Exercise

Participating in weight-bearing exercise is something that should already be incorporated on a regular basis to maintain muscle mass, decrease stress, improve immunity, improve cardiac health and cholesterol levels, and prevent glucose intolerance and diabetes. Patients with osteopenia can continue to exercise following their normal routine.

Patients diagnosed with osteoporosis need to be more cautious. To avoid falls and risk of fractures, they should avoid high impact, explosive movements like those involved in jogging, volley ball, and martial arts and they should also avoid fast, jerky movements that force a rapid change in direction. Weight training, however, can be very beneficial. It increases bone density and strengthens the muscles that support joints, improving balance and preventing falls.

To find out more information on osteoporosis, visit the National Osteoporosis FoundationÕs website at <www.nof.org> and request a copy of their publication ÒBoning Up on Osteoporosis:
A Guide to Prevention and TreatmentÓ as well as their video ÒBe Bone WiseªÑExercise.Ó The video shows exercises to improve bone density, posture, and balance and comes with a resistance band. You can also access information at the National Institutes of Health Osteoporosis and Related Bone Diseases Resource Center at <www.osteo.org>.

Mary Jane Detroyer is a registered dietitian and exercise physiologist who has been working with clients for over 15 years to improve their health through diet, exercise, and simple lifestyle changes. She is a professional speaker and has a private practice in Manhattan specializing in HIV/AIDS, WomanÕs Wellness, Weight Management, and Prevention. You can contact her at <>. 

References

1.   Hernandez J, Ortego N, Munoz-Torres M, Martinez MA, Higuera JM. Alterations in bone turnover in HIV-positive patients. Infection. 1993;21(4):.
2.   Serrano S, Marinoso ML, Soriaano JC, Rubie-Prat J, Aubia J, Coll J, Bosch J, Del Rio L, Vila J, Goday A, et al. Bone remodeling in human immunodeficiency virus-1-infected patients. A histomorphometric study. Bone. 1995;16(2):.
3.   Paton NI, Macallan DC, Griffin GE, Pazianas M. Bone mineral density in patients with human immunodefieicney virus infection. Calcif Tissue Int. 1997;61(1):30-32.
4.   Teichman J, Stephan E, Discher T, Lange U, Federlin K, Stracke H, Friese G, Lohmeyer J, Bretzel RG. Changes in calciotropic hormones and biochemical markers of bone metabolism in patients with human immunodeficiency virus infection. Metabolism. 2000;49(9):.
5.   Grinspoon S, Corcoran C, Askari H, Schoenfeld D, Wolf L, Burrows B, Walsh M, Hayden D, Parlman K, Anderson E, Basgoz N, Klibanski A. Effects of androgen administration in men with the AIDS wasting syndrome. A randomized, double-blind, placebo-controlled trial. Ann Intern Med. 1998;129(1):18-26.
6.   Huang JS, Wilkie SJ, Sullivan MP, Grinspoon S. Reduced bone density in androgen-deficient women with acquired immune deficiency syndrome wasting. J Clin Endocrino Metab. 2001;86(8):.
7.   Francis RM, Peacock M, Aaron JE, Selby PL, Taylor GA, Thompson J, Marshall DH, Horsman A. Osteroporosis in hypogonadal men: role of decreased plasma 1,25-dihydroxyvitamin D, calcium malabsorption, and low bone formation. Bone. 1986;7(4):.
8.   Wang C, Eyre DR, Clark R, Kleinberg D, Newman C, Iranmanesh A, Veldhuis J, Dudley RE, Berman N, Davidson T, Barstow TJ, Sinow R, Alexander G, Swerdloff RS. Sublingual testosterone replacement improves muscle mass and strength, decreases bone resorption, and increases bone formation markers in hypogonadal men in a clinical research center study. J Clin Endocrinol Metab. 1996;81(10):.
9.   Katznelson L, Finkelstein JS, Schoenfeld DA, Rosenthal DI, Anderson EJ, Klibanski A. Increase in bone density and lean body mass during testosterone administration in men with acquired hypogonadism. J Clin Endocrinol Metab. 1996;81(12):.
10. Behre HM, Kliesch S, Leifke E, Link TM, Nieschlag E. Long-term effect of testosterone therapy on bone mineral density in hypogonadal men. J Clin Endocrinol Metab. 1997;82 (8):.
11. Tebas P, Powderly WG, Claxton S, Marin D, Tantisiriwat W, Teitelbaum SL, Yatasheski KE. Accelerated bone mineral loss in HIV-infected patients receiving potent antiretroviral therapy. AIDS. 2000;14(4):F63-F67.
12. Carr A. Miller J, Eisman JA, Cooper DA. Osteopenia in HIV-infected men: association with asymptomatic lactic academia and lower weight pre-antiretroviral therapy. AIDS. 2001:15(6):.
13. McDermott A, Shevits A, Knox T, Roubenoff R, Kehayias J, Gorbach S. Effect of highly active antiretroviral therapy on fat, lean, and bone mass in HIV-seropositive men and women. Am J Clin Nutr. 2001;74(5):.
14. Aukrust P, Haug CJ, Ueland T, Lien E, Muller F, Espevik T, Bollerslev J, Froland SS. Decreased bone formative and enhanced resorptive markers in human immunodeficiency virus infection: indication of normalization of the bone-remodeling process during highly active antiretroviral therapy.
J Clin Endocrinol Metab. 1999;84(1):.
15. Nolan D, Upton R, McKinnnon E, John M, James I, Adler B, Roff G, Vasikaran S, Mallal S. Stable or increasing bone mineral density in HIV-infected patients treated with nelfinavir or indinavir. AIDS. 2001;15(10):.
16. Struble K, Murray J, Schneider B, Soon G. Bone fracture (FX) rates in HIV+ patients receiving PI vs non-PI regimens. Program and Abstracts of the 41st Interscience Conference on Antimicrobial Agents and Chemotherapy; 2001; Chicago, IL. [Abstract I-1329]
17. Mondy K, Lassa-Claxton S, Hoffmann M, Yarasheski K, Powderly W, Tebas P. Longitudinal evolution of bone mineral density (BMD) and bone markers in HIV-infected individuals. Program and abstracts of the 9th Conference on Retroviruses and Opportunistic Infections; 2002; Seattle, WA. [Abstract 718]

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