Questions & answers

Questions & answers

PH C CLINICAL REPORT QUESTIONS & ANSWERS L i n d a K . Jo n i d e s , B S , R N , C P N P 1. What additional patient and/or family history would yo...

28KB Sizes 1 Downloads 24 Views



QUESTIONS & ANSWERS L i n d a K . Jo n i d e s , B S , R N , C P N P

1. What additional patient and/or family history would you inquire about? Afamily history of osteoporosis and timing of menarche in the patient’s mother would be important. Dietary history, especially calcium intake, is important, as are any concerns about eating disorders. In the case of R. S., there is no family history of osteoporosis. According to R.S. and her mother, her calcium intake is “not the best” and never really has been very good. Otherwise, R. S. eats quite well, including a good variety of foods in her diet, and R. S. says she “never skips a meal.” Nothing in the patient’s history, physical examination, or questioning of the patient or her mother made one suspicious of an eating disorder. The patient’s pubertal progression of Tanner stages was within normal limits; however, onset of menses was late. The patient’s mother and her older sister both started their menses at age 12 years. The average age of menarche is 12.5 years, with more than 95% expecting menarche between the ages of 10.5 and 14.5 years. The mean age at menarche is highly dependent on ethnic background, socioeconomic factors, nutritional status, and perhaps physical activity. A body fat level of 17%, on average, is needed for menarche, and a level of about 22% is needed to initiate and maintain regular ovulatory cycles (White & Hergenroeder, 1990). The endocrinologist who evaluated R. S. suspects that her strenuous exercise suppressed her gonadotropin values and therefore caused altered bone density values. Most likely, the disruption of the release of gonadotropic hormones caused low levels of follicle-stimulating hormone and luteinizing hormone followed by low levels of estrogen and progesterone.


(Data on page 133.)

2. What causes or clinical considerations would you include when assessing this patient? It is important to consider factors that affect peak bone mass, factors that may affect bone loss, and other associated risk factors. Factors that may affect peak bone mass include gender, race, genetic factors, gonadal steroids, growth hormone, timing of puberty, calcium intake, and exercise. Bone density increases dramatically during puberty in response to


nsuring adequate

intake of dietary calcium and encouraging physical exercise that places stress on bones during childhood and adolescence are important strategies to promote the development of bone density and prevent osteoporosis.

gonadal steroids and eventually reaches values in young adults that are nearly double those in children. Of the factors listed that affect peak bone mass, genetic factors account for up to 80% of the variance in peak bone mass. This fact has been demonstrated in several ways: a. Bone density is lower in daughters of women with osteoporosis than in daughters of women without osteoporosis. b. The concordance of bone density is much higher among monozygotic twins than among dyzygotic twins. c. Recent data suggest that most of the genetic differences in bone density can be accounted for by a gene closely linked to the vitamin D receptor gene, perhaps the gene itself (Finkelstein, 1996). Development of bone density in the early years of life is dependent on mechanical loading, optimal calcium intake, and appropriate hormone, particularly estrogen, levels (Finkelstein, 1996). Therefore, ensuring adequate intake of dietary calcium and encouraging physical exercise that places stress on bones during childhood and adolescence are important strategies to promote the development of bone density and prevent osteoporosis. Osteopenia is a generalized bone loss. The diagnosis of osteoporosis is made when bone loss cannot be accounted for by other factors. At any point in time, bone density depends on both peak bone density achieved during development and subsequent adult bone loss. Osteo-

Reprint requests: Linda K. Jonides, BS, RN, CPNP, 911 Brown St, Ann Arbor, MI 48104. J Pediatr Health Care. (2000). 14, 144-146. Copyright © 2000 by the National Association of Pediatric Nurse Associates & Practitioners. 0891-5245/2000/$12.00 + 0 25/8/106003 doi:10.1067/mph.2000.106003

May/June 2000

PH CLINICAL INSIGHTS C penia can result from either deficient pubertal bone accretion, accelerated bone loss, or both (White & Hergenroeder, 1990). Currently it is not known at what age bone loss begins, but during the course of their lifetime, women lose 30% of cortical bone and 50% of trabecular bone. Men generally have a larger bone mass than women, which may make them less susceptible to osteoporosis. African Americans also have a higher bone density than do Whites. This may account for a lower incidence of osteoporotic fractures in men and African Americans (Finklestein, 1996). Factors that may affect bone loss and cause abnormal bone density values include decreased physical activity, malignancy, malnutrition, scurvy, malabsorption syndromes, genetic predisposition, systemic diseases such as diabetes, cholestatic liver disease, thyroid disorders, kidney failure, osteomalacia, hyperglucocorticoidism, and medications such as steroids, anticonvulsants, heparin, antacids with aluminum, and thyroid extract in doses larger than 3 g per day (White & Hergenroeder, 1990). R. S. had no systemic diseases, was not taking any medications regularly, and had no symptoms or physical findings to suspect malignancy. She had low body fat but was not malnourished, and she had no signs or symptoms of malabsorption problems. She engaged in considerable physical activity, but it was not weight bearing. Other associated risk factors include smoking, anorexia or disordered eating, and excessive alcohol or caffeine intake. Smoking and ingestion of alcohol and caffeine have negative effects on bone density. Unfortunately, the triad of disorders including disordered eating, amenorrhea, and osteoporosis in adolescent female athletes has become more prevalent in recent years, or, at least, awareness of the problem has increased (Yeager, Agostini, Nattiv, & Drinkwater, 1993). R. S. consumes minimal caffeine and denied smoking or alcohol use. As stated previously, neither the patient’s mother nor various health care providers now involved in her care suspected any eating disorders in R. S. 3. What would you include in your management plan? Hormone supplements would be one consideration for treatment. Although



hormone replacement therapy is known to be effective in maintaining bone mass and reducing the risk of fractures in menopausal women, little research about this treatment has been conducted among young estrogen-deficient women. Some studies are in process, however. No controlled trials have been conducted using either hormone replacement therapy or oral contraceptive pills specifically in amenorrheic female athletes. Reasons include difficulty in conducting truly blind controlled trials with either of these treatments because of withdrawal bleeding, and subjects not knowing if they are receiving contraception. However, in one study of anorexic women, it was reported that estrogen deficiency may have a detrimental effect on calcium metabolism and that in women with very low weights, an increase in weight may improve bone density (Sambrook & Naganathan, 1997).


everal cross-sectional

studies support the influence of dietary calcium during childhood and adolescence on attainment or maintenance of peak bone mass.

Addressing calcium intake would certainly be part of the treatment plan. Several cross-sectional studies support the influence of dietary calcium during childhood and adolescence on attainment or maintenance of peak bone mass. The current recommended daily allowance for calcium in North America is 800 mg during childhood and 1200 mg during adolescence. In amenorrheic persons, the recommendation is 1500 mg daily. Few randomized controlled trials have looked at the effect of calcium supplements in children and adolescents. Currently available data do not provide evidence to recommend widespread use

of calcium supplementation in addition to diet during childhood or adolescence (Sambrook & Naganathan, 1997). Optimal absorption of calcium occurs in whole foods compared with supplements, and supplements can interfere with iron absorption (White & Hergenroeder, 1990). As PNPs are well aware, dietary intake of calcium in adolescents is often significantly less than what is recommended. A thorough diet history with recommendations for adequate calcium intake and close follow-up are very important for this patient. Evaluating the current exercise regimen of R. S. and considering exercise recommendations that affect bone density need to be included in the plan. In vigorous athletes, such as R. S., reduction in training, both in duration and intensity, to a level at which normal menstrual cycles can occur is recommended. Substituting alternative sports might be an option for some athletes. A positive effect on bone density of physical activity, and in particular, weightbearing exercise, has been observed in several cross-sectional studies. There are reported beneficial effects on attainment of peak bone mass and prevention of bone loss in adolescence (Sambrook & Naganathan, 1997). Strength training is defined as the use of progressive resistance exercise methods specifically to increase one’s ability to exert muscular force against resistance. Isometric, isotonic, isokinetic, variable resistance, and pylometric (hops, medicine ball drills, jumping with weights) exercises are various types of strength training. Bone and muscle mass and strength are maintained by a constant application of mechanical force. Such exercises can affect bone density (White & Hergenroeder, 1990). Any strength training program should be undertaken with appropriate instruction and supervision. The use of bisphosphonates may become an additional treatment for osteoporosis in adolescents. Bisphosphonates are synthetic compounds that suppress bone resorption and reduce bone turnover. They were first introduced into clinical practice in the 1960s. They are effective in the treatment of patients with postmenopausal osteoporosis and have been shown to increase bone mass and significantly reduce the frequency of new vertebral fractures in controlled studies. At pre-

May/June 2000




sent, some bisphosphonates (alendronate is one) are registered for the treatment of postmenopausal osteoporosis worldwide. Little information is available about the use of these compounds in children or adolescents; however, some studies are in progress (Brumsen, Hamdy, & Papapoulos, 1997). Regarding the treatment plan for R. S., the endocrinologist initially prescribed a hormone supplement in the form of estrogen (Premarin) at 625 mg daily, which resulted in heavy bleeding. The estrogen was discontinued, and after a few weeks, she started to take oral contraceptives (Ortho-Cept), and she has had 3 periods since then. All of the health care providers with whom she has come in contact during this evaluation have reviewed her food intake and

provided recommendations for change, especially regarding calcium. R. S. reports that she is consuming more dairy products and is taking a calcium supplement, with the goal of a total daily calcium intake of 1500 mg. Her weight has been stable. After the bone density results were known, R. S. decreased her swimming schedule to every other day and began swimming about half the time/distance she was doing previously. She had already done some strength training exercises under the direction of her swim coach, but she is now doing that exercise 3 times a week with more direction from her physical therapist. Previously, during the off season from swimming, she jogged a few times a week; she is now jogging more consistently. R. S. is scheduled to have a fol-

low-up bone density scan 6 to 9 months after the initial study, and it is hoped that scan will show some improvement.

REFERENCES Brumsen, C., Hamdy, N. A., & Papapoulos, S. E. (1997). Long-term effects of bisphosphonates on the growing skeleton: Studies of young patients with severe osteoporosis. Medicine, 76, 266-283. Finkelstein, J. S. (1996). Osteoporosis. In R. L. Cecil, J. C. Bennett, & F. Plum (Eds.), Cecil Textbook of Medicine (20th ed.). Philadelphia: W. B. Saunders. Sambrook, P., & Naganathan, V. (1997). How do we manage specific types of osteoporosis? Ballieres Clinical Rheumatology, 8, 597-612. White, C. M., & Hergenroeder, A. C. (1990). Amenorrhea, osteopenia, and the female athlete. Pediatric Clinics of North America, 37, 1125-1141. Yeager, K. K., Agostini, R., Nattiv, A, & Drinkwater, B. (1993). The female athlete triad: Disordered eating, amenorrhea, osteoporosis. Medicine And Science in Sports And Exercise, 7, 775-777.

WANTED: CHILDREN’S DRAWINGS The Journal is interested in publishing children’s drawings of their responses to illness, treatment, or encounters with the health care system or personnel. Please send the drawings, along with the child’s age, gender, any pertinent information regarding the child’s condition, and written parental permission to print the drawing, to Bobbie Crew Nelms, PhD, RN, CPNP 3133 Barbara St San Pedro, CA 90731


Volume 14 Number 3