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ONCOLOGY Nurse Edition.
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LATE EFFECTS CLINIC 

Addressing Bone Loss in the Cancer Survivor

By MAUREEN E. O’ROURKE, RN, PhD
University of North Carolina, Greensboro School of Nursing
Wake Forest University School of Medicine
Winston-Salem, North Carolina

KATHY RUBLE, PhD(c), RN, CPNP, AOCN
Johns Hopkins University
Baltimore, Maryland
| February 11, 2009

Maureen E. O’Rourke is Clinical Professor of Nursing, University of North Carolina, Greensboro School of Nursing and Adjunct Assistant Professor of Medicine, Hematology-Oncology, Wake Forest University School of Medicine, Winston-Salem, North Carolina. Kathy Ruble is Coordinator, Long-Term Follow-up Program, Johns Hopkins University, Baltimore, Maryland.

Financial Disclosure:
The authors have no significant financial interest or other relationship with the manufacturers of any products or providers of any services mentioned in this article.


Osteoporosis, the most common late effect of cancer treatment in the US, occurs with greater frequency among cancer survivors than the general population. Survivors of breast cancer, prostate cancer, and childhood leukemia are at particularly high risk for changes in bone mineral density (BMD) / osteoporosis that can lead to fractures.[1] In breast and prostate cancer patients, bone effects are often the result of endocrine therapy–induced alterations in bone microarchitecture. They also can be caused by other types of cancer therapy, vitamin D deficiency, and other physiological changes that may or may not be related to cancer or its treatment. In childhood leukemia patients, bone effects can be caused by a variety of factors, including corticosteroid therapy, radiation therapy to the brain, and the disease itself.

Osteoporosis can exist for many years without symptoms, and the presence of a clinically symptomatic fracture may be the first indication that bone loss has occurred. Given that the majority of cancer cases occur in people over 65 years of age, and even healthy older people are at higher risk of bone changes than younger ones (eg, owing to hormonal changes, nutritional differences, lifestyle changes including reduced mobility and lack of exercise, etc), the health care team must be vigilant in screening, monitoring, and intervention for bone effects in the cancer survivor.

Naturally, bone loss in the growing adolescent also is devastating, as this is the time of life when peak bone mass normally is achieved. Efforts to preserve bone integrity are critically important in this patient population as well. In both adult and pediatric cases, patient management can be complicated by bone metastases.

Bone health in both childhood and adult cancer survivors is receiving increased attention. The American Society of Clinical Oncology (ASCO) recommends that “cancer survivors at risk for bone and joint problems, especially survivors of breast and prostate cancers and childhood leukemia, can lower their risk by not smoking, eating foods rich in calcium, participating in regular physical activity, and limiting the amount of alcohol(Drug information on alcohol) they drink.”[1]

Oncology nurses are well positioned to educate cancer survivors about newer agents (eg, bisphosphonates) and lifestyle changes that can help to protect against treatment- and disease-related bone loss. This article presents two case studies that highlight key risk factors for bone loss in pediatric and adult cancer survivors and provide guidance on appropriate assessment and nursing intervention.

PATIENT OVERVIEWS

Patient 1: Stage II Prostate Cancer Survivor
JM is a 60-year-old male who was diagnosed 6 years ago with prostate cancer, clinical stage II. The primary tumor was considered to be confined within the prostate, but with both lobes involved. His prostate specific antigen (PSA) level was 18 ng/mL and his Gleason score at diagnosis was 3+5, or 8, indicating the cells were poorly differentiated and his disease course was likely to be aggressive.[2] After carefully considering his treatment options, he chose radical prostatectomy. National Comprehensive Cancer Network (NCCN) guidelines indicate he was at high risk for recurrence (based on his high Gleason score).[3]

Following surgery, JM’s disease was reclassified as Stage IV, because cancer was detected in two lymph nodes. He was given the option of active surveillance or treatment with androgen-deprivation therapy (ADT). He underwent ADT using a combination of flutamide(Drug information on flutamide) (Eulexin) and leuprolide acetate (Lupron) for the purpose of medical castration.

JM experienced predictable side effects from his ADT regimen, including erectile dysfunction, hot flashes, and fatigue. One year following initiation of ADT, his dual energy X-ray absorptiometry (DXA) scan indicated a 2% loss in bone density in his hip and a 5% radial ulnar loss, compared with his baseline scan. This finding is consistent with the research literature, wherein BMD decreases ranging from 1.8% to 3.9% at the hip and up to 10% at the radius have been reported.[4]

Even greater losses have been documented at other sites such as the lumbar spine and femoral neck (7.1% and 6.6% respectively).[5] A review by Saad et al. of research related to BMD loss suggests bone density decreases progressively with increased duration of ADT, and fractures are independent adverse predictors of survival among prostate cancer patients.[6] The major risk factors for osteoporosis in men, aside from hypogonadism, include prior fracture after age 40, family history of osteoporotic fractures, low baseline bone density, advanced age (greater than 65 years), and apparent osteopenia on X-ray. Minor contributory risk factors include comorbidities such as chronic inflammatory disease (eg, rheumatoid arthritis, lupus), celiac disease, concomitant use of mediations such as heparin(Drug information on heparin), anticonvulsants, barbiturates, etc, weight < 57 kilograms, cigarette smoking, excessive alcohol intake (three or more drinks per day), low dietary calcium intake, and high caffeine intake.[6]

Along with his ADT, JM’s risk factors for osteoporosis and future fracture included a 20 pack-year history of smoking and one fracture sustained at age 41.

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