Acromegaly Patient Care and Monitoring

1. Assess patient's clinical signs and symptoms to determine severity of acromegaly.

2. Review the biochemical disease markers to assess severity of acromegaly.

3. Review the available diagnostic data to determine pituitary tumor size and location. Determine if the patient has a coexisting prolactin secreting tumor. Determine if the tumor extends toward the optic chiasm or if it is continuous on the optic tracts.

4. Assess presence of acromegaly complications. Identify any significant comorbidit-ies associated with acromegaly that require immediate treatment or early diagnosis.

5. Determine what treatment options the patient has tried in the past.

6. Evaluate patient for presence of surgical contraindications to transsphenoidal microsurgery. Determine if the patient is able or willing to undergo surgical intervention.

7. Develop a formal plan to assess patient's response and complications to surgical intervention. Measure both GH and IGF-I levels.

8. If surgical intervention does not achieve satisfactory disease control, select subsequent appropriate pharmacologic therapy based on patient-specific factors. In se lecting therapy, be sure to consider if the patient has any contraindications or allergies to therapies.

9. Evaluate patient for presence of adverse drug reactions, drug allergies, and drug interactions.

10. Develop a plan to assess efficacy of pharmacologic therapy. Also consider if the patient's therapy requires any dose adjustments.

11. Assess biochemical markers annually once disease control is achieved.

12. Routinely assess acromegaly complications; include blood pressure, glucose tolerance, fasting lipid profile, cardiac evaluations (if clinically indicated), colono-scopy, dual energy x-ray absorptiometry (DEXA) scan (hypogonadal only), evaluation of residual pituitary function, and evaluation of sleep apnea.

13. Provide patient education in regards to disease state, nondrug and drug therapy. Discuss with the patient:

• Possible complications of acromegaly,

• How to reduce the modifiable cardiovascular and metabolic risk factors,

• Potential effectiveness and disadvantages of existing treatment options,

• Importance of adherence to therapy, and

• Potential adverse effects that may occur.

Childhood GH deficiency may or may not continue into adulthood. Most adults with GH deficiency have overt pituitary disease and present with nonspecific clinical disorders distinct from pediatric GH deficiency, thereby making diagnosis of GH deficiency in adults more difficult than in children. Additionally, adult GH deficiency presumably is associated with increased risk of death from cardiovascular diseases.35

Treatment Goals

The goal of treatment for GH deficiency is to correct associated clinical symptoms. In children, prompt diagnosis and early initiation of treatment are important to maximize final adult height. In adults, efforts should be made to achieve normal physiologic

GH levels in an attempt to reverse the metabolic, functional, and psychological abnor-


Pharmacologic Therapy

GH Therapy

® Recombinant GH therapy is the main pharmacologic treatment for GH deficiency in both children and adults. It promotes skeletal, visceral, and general body growth; stimulates protein anabolism; and affects bone, fat, and mineral metabolism (Table 46—1). GH therapy requires subcutaneous or intramuscular administrations. Since two-thirds of GH secretion normally occurs during sleep, it is recommended to administer injections in the evening.36 Many preparations of synthetic GH are available with a variety of injection devices to make administration more appealing and easier. Protropin (somatrem) and Tev-Tropin (somatropin) are approved by the FDA for use in children, whereas other somatropin products such as Nutropin, Nutropin AQ, Hu-matrope, Norditropin, Genotropin, Omnitrope, and Saizen are FDA approved in both children and adults.

Although comparative trials have not been conducted to date, recombinant GH products appear to have similar efficacy for treating GH deficiency as long as the regimen follows currently approved guidelines. GH secretion decreases with age. Therefore, older adults with GH deficiency often require substantially lower replacement doses than younger individuals. The optimal therapeutic approach is to initiate

GH therapy with lower doses. The recommended initial GH dose is 0.2 mg/day for

young men, 0.3 mg/day for young women, and 0.1 mg/day for older adults. Conventional weight-based regimens are not recommended in adults due to the lack of evidence supporting higher dosages in heavier individuals and greater potential for

32 35 37

adverse effects. ' Maintenance doses may be lower with chronic GH therapy. For elderly patients, lower GH replacement doses often are adequate because of increased

GH sensitivity. Carefully monitor patients requiring replacement therapy with estrogens, thyroid hormones, or glucocorticoids due to potential interactions with GH

therapy. In prepubertal children, the recommended replacement dose is 25 to 50 mcg/kg/day.3 Replacement doses should be titrated based on clinical and biochemic-

al responses. The conversion of international units (IU or mU) to mg is a 3:1 ratio. Selection of an injection device depends on patient preference because there is currently no difference in clinical outcomes among the various injection systems.38

Evidence has suggested that GH treatment in GH-deficient children can increase

short-term growth and improve final adult height. Beneficial effects of GH therapy in adults with GH deficiency have been demonstrated in subsequent studies to nor malize body composition and metabolic process; improve cardiac risk profile, bone mineral density, quality of life and psychological well-being; and increase muscle strength, and exercise capacity. Although long-term efficacy of GH replacement in

adults has been demonstrated in a 10-year prospective study, overall reduction in mortality with GH therapy remains to be established.

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