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Bone Guidelines Excerpted From New IDSA Guidelines- pdf of full paper attachedĘ
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Download the PDF here
Clinical Infectious Diseases Sept 1 2009;49:651-681
IDSA GUIDELINES
Primary Care Guidelines for the Management of Persons Infected with Human Immunodeficiency Virus: 2009 Update by the HIV Medicine Association of the Infectious Diseases Society of America
Judith A. Aberg,1 Jonathan E. Kaplan,2 Howard Libman,3 Patricia Emmanuel,5 Jean R. Anderson,6 Valerie E. Stone,4 James M. Oleske,7 Judith S. Currier,8 and Joel E. Gallant6
1New York University School of Medicine, Bellevue Hospital Center, New York; 2Centers for Disease Control and Prevention, Atlanta, Georgia; 3Beth Israel Deaconess Medical Center and 4Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; 5University of South Florida, Tampa; 6Johns Hopkins University School of Medicine, Baltimore, Maryland; 7University of Medicine and Dentistry of New Jersey, Newark; and 8University of California, Los Angeles
INTRODUCTION to full guidelines:
Evidence-based guidelines for the management of persons infected with human immunodeficiency virus (HIV) were prepared by an expert panel of the HIV Medicine Association of the Infectious Diseases Society of America. These updated guidelines replace those published in 2004. The guidelines are intended for use by health care providers who care for HIV-infected patients or patients who may be at risk for acquiring HIV infection. Since 2004, new antiretroviral drugs and classes have become available, and the prognosis of persons with HIV infection continues to improve. However, with fewer complications and increased survival, HIV-infected persons are increasingly developing common health problems that also affect the general population. Some of these conditions may be related to HIV infection itself and its treatment. HIV-infected persons should be managed and monitored for all relevant age- and gender-specific health problems. New information based on publications from the period 2003-2008 has been incorporated into this document.
BONE GUIDELINES
Baseline bone densitometry should be performed in postmenopausal women aged >65 years and in younger postmenopausal women with >1 additional risk factor(s) (other than being female and postmenopausal) for premature bone loss. Baseline bone densitometry should be considered in HIV-infected persons aged >50 years, especially if they have 1 risk factor(s) for premature bone loss. If the test demonstrates osteopenia or if the patient has a history of fragility or fracture, intervention with a bisphosphonate or other medical therapy should be considered. Bisphosponates appear to be effective in improving bone density in small studies of HIV-infected patients, but the data are limited [77, 78]. A follow-up study 1 year later to monitor the response to therapy is advised. Patients should be reminded of the health benefits of regular exercise and adequate calcium and vitamin D intake. They should also be counseled about the risks of cigarette smoking and excessive alcohol consumption. Secondary causes of decreased bone density, such as hypogonadism and vitamin D deficiency, should be investigated and treated accordingly.
Routine radiographic monitoring for avascular necrosis in asymptomatic persons is not recommended, but for patients presenting with persistent hip pain who have normal standard radiologic studies, magnetic resonance imaging is the preferred method of diagnosis, and both sides should be imaged. Most patients with symptomatic avascular necrosis will ultimately require hip replacement.
Recommendations:
Baseline bone densitometry measurement should be obtained in postmenopausal women aged 65 years and in younger postmenopausal women who have >1 risk factor for premature bone loss (B-III).
Routine screening for osteoporosis in HIV-infected patients without other risk factors for premature bone loss is not recommended at this time, on the basis of available data, but it should be considered in persons aged >50 years, especially if they have 1 risk factor for premature bone loss (B-III).
VIII. What Are the Long-Term Metabolic Complications Associated with Antiretroviral Therapy?
The major abnormalities that complicate the management of HIV infection include body morphology changes (lipohypertrophy and lipoatrophy), serum lipid abnormalities, dysregulation of glucose metabolism, lactic acidemia, and bone disorders (reduced bone mineral density and avascular necrosis). Concern has been expressed about long-term cardiovascular morbidity in patients who experience increases in atherogenic serum lipids levels, glucose intolerance, and body fat distribution changes, but as of yet, this risk is not well defined. In general, it appears that the benefits of antiretroviral therapy used in accordance with published guidelines outweigh the risk of cardiovascular disease associated with long-term exposure [69, 70]. Guidelines have been developed to assist providers in the identification and management of lipid abnormalities and metabolic complications [12, 16].
Evidence Summary
Recommendations
Fasting glucose and lipid levels should be monitored prior to and within 4-6 weeks after starting antiretroviral therapy (A-III). Patients with diabetes mellitus should have a hemoglobin A1c level monitored every 6 months with a goal of <7%, in accordance with the American Diabetes Association Guidelines. Patients with abnormal lipid levels should be managed according to the National Cholesterol Education Program Guidelines, with special consideration for persons with HIV infection.
There is no rationale for ordering lactic acid tests for asymptomatic patients at any time during HIV care (A-II).
Interruption of nucleoside reverse-transcriptase inhibitor (NRTI) therapy is recommended for symptomatic patients with a venous lactate level of >5 mmol/L (B-II).
Baseline bone densitometry measurement should be obtained in postmenopausal women aged 65 years and in younger postmenopausal women who have >1 risk factor for premature bone loss (B-III).
Routine screening for osteoporosis in HIV-infected patients without other risk factors for premature bone loss is not recommended at this time, on the basis of available data, but it should be considered in persons aged >50 years, especially if they have >1 risk factor for premature bone loss (B-III).
Insulin resistance has been associated with traditional risk factors, antiretroviral drugs, and possibly HIV infection itself. Diabetes mellitus is reported in 0.5%-6% of HIV-infected patients, but impaired glucose tolerance is considerably more common, occurring in 15%-20% of individuals. The Multicenter AIDS Cohort Study conducted during the period 1999-2003 indicated a 4-fold increased risk of diabetes mellitus in HIV-infected men receiving antiretroviral therapy [71]. A prospective study comparing glucose intolerance between HIV-infected pregnant women who were receiving protease inhibitor (PI)-based therapy and those not receiving PIs demonstrated that 38% of pregnant women developed impaired glucose tolerance and 9% had confirmed gestational diabetes mellitus, with no differences reported between those who received PIs and those who did not [72]. This is considerably higher than the expected normal percentages of 20%-25% and 2%-5% respectively, in the general obstetric population. HCV-infected patients are known to have an increased risk of insulin resistance and type 2 diabetes mellitus, and HIV- and HCV-coinfected patients have a 5-fold greater risk of developing hyperglycemia, compared with those with HIV infection alone.
The mechanisms behind insulin abnormalities in HIV-infected individuals are not fully defined. However, there is a known link between glucose intolerance and lipodystrophy in HIV infection, which is believed to be related to a failure of the pancreatic ß cells to fully compensate for decrements in insulin sensitivity despite simultaneous reduction in insulin clearance. This mechanism may partially explain the association of insulin resistance and thymidine NRTIs. The association between PI use and insulin abnormalities was described in early studies. Indinavir is known to have the greatest effect on insulin sensitivity, presumably through inhibition of the insulin-regulated glucose transporter, GLUT-4, a molecule involved in insulin-mediated glucose uptake by cells. Other PIs have a modest impact, and the effect is usually temporary. This transient impairment of insulin sensitivity does not appear to have an important clinical implication, because <5% of individuals treated with PIs experience clinical hyperglycemia. In most cases, blood glucose abnormalities can be effectively managed by lifestyle changes that include weight loss, increased exercise, and dietary modification. However, if therapeutic intervention is needed, insulin-sensitizing agents are preferred. Patients should be managed according to the American Diabetes Association guidelines [6]. The substitution of antiretroviral drugs that do promote insulin resistance with those that do not affect glucose metabolism may normalize blood glucose levels and prevent progression to diabetes mellitus, but the available evidence is inconclusive. There are no data suggesting that switching antiretroviral drugs is beneficial to patients who have impaired glucose tolerance associated with HIV infection itself or traditional risk factors.
Similar to the reports on insulin resistance, dyslipidemia has been associated with traditional risk factors, HIV infection itself, and antiretroviral drugs. It is recommended that all patients be assessed for coronary heart disease risk, and those with >2 risk factors should be further evaluated and managed according to the HIVMA and National Cholesterol Education Program guidelines [12, 38]. All patients should be encouraged to stop smoking regardless of cardiovascular risk, and hypertension and diabetes mellitus should be managed as appropriate.
Consideration should be given to switching antiretroviral therapy or using lipid-lowering therapy on an individualized basis [73, 74]. Although one should be aware of the potential for drug interactions and adverse effects from lipid-lowering therapy, its benefits may exceed the small but potential risk of virologic failure when antiretroviral therapy is modified. Results from the SMART trial indicated that patients in the CD4 cell-guided, intermittent treatment group were at increased risk for evidence of cardiac disease, and therefore, it is not recommended that antiretroviral therapy be stopped to improve lipid profiles [70].
Patient self-report of body shape changes may be sufficient for clinical practice screening for body morphology changes. Anthropometry (measurements of skin-fold thickness and circumference of the waist and hip) does not differentiate subcutaneous from visceral fat and requires training to perform. Although dual-energy X-ray absorptiometry has been used in research studies to evaluate regional body composition, it cannot distinguish subcutaneous from visceral fat but can compare limb fat with truncal fat. Computed tomography scanning at L4/5 can be used to assess visceral fat and quantitate subcutaneous fat. The body mass index assesses lean body mass but cannot determine fat distribution. None of these tools is currently recommended for clinical practice.
Polylactic acid and calcium hydroxylapatite have been approved for treatment of facial lipoatrophy, but these interventions may provide only short-term benefit in some patients. Cosmetic surgery (eg, liposuction) may be warranted for disfiguring cases of lipohypertrophy. Modification of antiretroviral drug therapy (ie, substitution of another drug for stavudine or zidovudine in a patient with facial lipoatrophy) can partially reverse lipoatrophy.
The incidence of lactic acidosis in clinical practice has decreased because abacavir and tenofovir have largely replaced didanosine, stavudine, and zidovudine use in combination antiretroviral therapy. The clinical manifestations of hyperlactatemia without acidosis (normal arterial pH) are variable and nonspecific. Some patients may report fatigue, nausea, vomiting, abdominal pain, and/or diarrhea. Serum transaminase abnormalities are common, usually as a result of associated hepatic steatosis. Patients starting NRTI treatment should be made aware of the symptoms of lactic acidemia and asked to report them promptly to their health care provider. A serum venous lactate level should be determined in the case of unexplained symptoms. If the level is abnormal, the measurement should be repeated, and an arterial blood gas measurement should be performed. For patients with a serum venous lactate level of 2-5 mmol/L, close monitoring is advised. No intervention is necessary for patients with a level of <2 mmol/L. Lactic acidemia will generally resolve once treatment with the offending drug(s) is stopped [75, 76]. The safety of resuming NRTI treatment in this setting has not been clearly established but may be considered with non-thymidine analog NRTIs.
Baseline bone densitometry should be performed in postmenopausal women aged 65 years and in younger postmenopausal women with >1 additional risk factor(s) (other than being female and postmenopausal) for premature bone loss. Baseline bone densitometry should be considered in HIV-infected persons aged >50 years, especially if they have >1 risk factor(s) for premature bone loss. If the test demonstrates osteopenia or if the patient has a history of fragility or fracture, intervention with a bisphosphonate or other medical therapy should be considered. Bisphosponates appear to be effective in improving bone density in small studies of HIV-infected patients, but the data are limited [77, 78]. A follow-up study 1 year later to monitor the response to therapy is advised. Patients should be reminded of the health benefits of regular exercise and adequate calcium and vitamin D intake. They should also be counseled about the risks of cigarette smoking and excessive alcohol consumption. Secondary causes of decreased bone density, such as hypogonadism and vitamin D deficiency, should be investigated and treated accordingly.
Routine radiographic monitoring for avascular necrosis in asymptomatic persons is not recommended, but for patients presenting with persistent hip pain who have normal standard radiologic studies, magnetic resonance imaging is the preferred method of diagnosis, and both sides should be imaged. Most patients with symptomatic avascular necrosis will ultimately require hip replacement.
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