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FAQ

Frequently Asked Questions and Answers

  1. What is acromegaly?
  2. What are the goals of treatment for acromegaly?
  3. What is first-line treatment for acromegaly?
  4. How are patients with acromegaly refractory to surgical intervention managed?
  5. What types of medical therapy are suitable for acromegaly?
  6. What is Sandostatin®?
  7. When is it appropriate to treat acromegaly with Sandostatin®?
  8. What are the recommendations for dosage and administration of Sandostatin® LAR® in patients with acromegaly?
  9. How does Sandostatin® LAR® differ from subcutaneous Sandostatin®?
  10. What are the clinical benefits of Sandostatin® for patients with acromegaly?
  11. Does Sandostatin® LAR® affect tumour growth and size?
  12. What are the side effects of Sandostatin® therapy?

1. What is acromegaly?

Acromegaly is a rare chronic disorder caused by a pituitary adenoma, which results in the hypersecretion of growth hormone (GH) and subsequent elevation of circulating and locally produced insulin-like growth factor-1 levels (IGF-1). The clinical presentation of acromegaly is characterised by skeletal overgrowth deformities, particularly of the hands, feet, and face; cardiovascular disease; neuropathy; and respiratory obstruction. If left untreated, acromegaly is associated with substantial morbidity and mortality rates, 2 to 4 times higher than those found in the general population.1-3

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2. What are the goals of treatment for acromegaly?

Treatment goals in acromegaly include control of GH and normalisation of IGF-1 levels, reduction in tumour size, prevention of tumour recurrence, and alleviation of significant comorbid features, particularly cardiovascular, pulmonary, and metastatic derangements.4,5 Considerable debate has taken place on the appropriate level of GH to be achieved when treating acromegaly.6 Normalisation of GH levels to less than 1 ng/mL within 2 hours after a glucose load has been proposed as the primary measure of biochemical control.4 Compelling evidence suggests that lowering GH levels to a target concentration of <2.5 ng/mL reverses the mortality associated with acromegaly.7

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3. What is first-line treatment for acromegaly?

Transsphenoidal surgical excision of the pituitary adenoma is usually first-line treatment in acromegaly. The procedure is associated with an overall remission rate of 72% for noninvasive adenomas following primary surgery.8 Surgical remission rates are lower in patients with macroadenomas because these tumours are large, fibrous, and frequently invasive, making complete resection unlikely.9,10 Unfortunately, macroadenomas constitute the majority of tumours detected in patients with acromegaly on initial presentation. These patients will likely be placed on medical therapy such as Sandostatin® LAR®.

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4. How are patients with acromegaly refractory to surgical intervention managed?

For patients with acromegaly who are not candidates for surgery, or for whom surgery has been unsuccessful, alternative approaches are required, such as pharmacological therapy and radiation therapy. In recent years, the use of pituitary irradiation has remarkably declined. Pharmacological therapy is indicated for second-line use following surgery.5 Radiation therapy is recommended for third-line treatment but is rarely used for first- or second-line therapy.7

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5. What types of medical therapy are suitable for acromegaly?

Medication for acromegaly decreases the secretion of GH and controls subsequent production of IGF-1, reduces the size of the tumour, and controls symptoms.11 Drug therapy has been used to shrink large tumours before surgery.11 Long-acting somatostatin analogues, such as octreotide acetate (Sandostatin®), are the mainstay of pharmacological treatment.12 Octreotide is a synthetic form of somatostatin used in the treatment of acromegaly.12 Sandostatin® LAR®, a longer-acting slow-release form of octreotide, is available for the treatment of acromegaly.13 Although oral dopamine agonists, such as cabergoline, constitute another therapeutic option, it is effective in less than 10% of patients and in patients with marginally elevated GH and IGF-I levels.12,14 The goals of medical therapy are to reduce GH levels to <1 ng/mL and to normalise IGF-1 production, reduce tumour volume, and provide symptom relief—Sandostatin LAR provides proven efficacy in acromegaly.15

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6. What is Sandostatin®?

Sandostatin® is a long-acting synthetic analogue of somatostatin that binds with maximum affinity to the somatostatin receptors.12 Through this interaction, Sandostatin exerts a number of physiological effects, including alteration of the expression of several hormones.12 Of note in acromegaly is the potent suppression of GH release, which is at least 45 times more potent than that achieved with naturally occurring somatostatin.1

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7. When is it appropriate to treat acromegaly with Sandostatin®?

Sandostatin® is typically used as second-line treatment in patients whose GH levels remain elevated after surgery, or in those patients for whom surgical resection is not an option.5 Based on the results of independent investigations, it has been proposed that it should also be considered as first-line treatment in patients with acromegaly caused by a macroadenoma, in whom the chances of surgical cure are reduced.16 Recent treatment guidelines also suggest that selected patients with unacceptable anesthetic risk, or cardiovascular and/or pulmonary complications may benefit from primary therapy with Sandostatin.5 In addition, studies have shown that preoperative treatment of patients with Sandostatin can improve surgical outcome, shrinking and softening tumours, facilitating their resection.10,17,18 In one recent study, Sandostatin given to newly diagnosed, acromegalic patients with macroademona as a pretreatment before transsphenoidal surgery led to a demonstrated increase in surgical cure rate.19

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8. What are the recommendations for dosage and administration of Sandostatin® LAR® in patients with acromegaly?

Patients Currently Receiving Sandostatin20
Patients who are currently receiving the standard formulation of Sandostatin can be switched directly to the slow-release depot formulation, Sandostatin LAR, using a dosage of 20 mg administered intragluteally at 4-week intervals for the initial 3 months. After 3-month treatment, if GH is not controlled and/or IGF-I is still elevated, the dose of Sandostatin LAR should be uptitraed to 30 mg w28d. Symptoms and levels of IGF-1 and GH should be monitored over time (ie, follow-ups at 3 months, 6 months, and 1 year). (Dosage may need to be increased up to 30 mg if symptoms and biochemical control are not achieved during follow-ups).

Patients Currently Not Receiving Sandostatin20
In patients who are not currently receiving Sandostatin, the standard injection formulation should be given subcutaneously at an initial dose of 50 μg 3 times a day. Dosage titration can be based on multiple GH measurements between 0 and 8 hours after administration.

  • Most patients require a dosage of 100 μg to 200 μg 3 times a day for the maximum effect of normalising GH and IGF-1
  • Some patients may require up to 500 μg 3 times a day

Patients should be maintained on this formulation for at least 2 weeks to determine their response and tolerability to Sandostatin.

Patients who tolerate the drug and are considered to be responders to the therapy based on GH and IGF-1 levels can be switched to Sandostatin LAR. The dosage should be 20 mg administered intragluteally at 4-week intervals for the initial 3 months. After 3-month treatment, if GH is not controlled and/or IGF-I is still elevated, the dose of Sandostatin LAR should be uptitrated to 30 mg w28d. Frequent monitoring of symptoms and levels of IGF-1 and GH over time (ie, follow-ups at 3 months, 6 months, and 1 year) is recommended to determine whether dosage adjustments are necessary. (Dosage may need to be increased up to 30 mg if symptoms and biochemical control are not achieved during follow-ups).

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9. How does Sandostatin® LAR® differ from subcutaneous Sandostatin®?

The long-acting repeatable (LAR) formulation of octreotide (Sandostatin LAR) consists of octreotide acetate incorporated into microspheres of a biodegradable polymer. It is administered as a single intramuscular injection into the gluteal muscle every 4 weeks, eliminating the need for multiple, daily injections. Drug release is governed by the slow degradation of the microspheres in the muscle, but once present in the systemic circulation, Sandostatin LAR appears to maintain the pharmacological characteristics of subcutaneous Sandostatin.21 Sandostatin LAR is indicated for long-term maintenance therapy in patients with acromegaly for whom medical treatment is appropriate and who have been shown to respond to and tolerate subcutaneous Sandostatin.20

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10. What are the clinical benefits of Sandostatin® for patients with acromegaly?

Treatment with Sandostatin is proven to control GH secretion and normalise IGF-1 levels, reduce tumour size, and control the symptoms of acromegaly including paraesthesias, headache, perspiration, joint pains, and fatigue.13 Most importantly, control of GH and IGF-1 levels in acromegaly patients has been shown to reduce their risk of mortality from cardiovascular complications associated with the condition.22 Long-term studies with both Sandostatin and Sandostatin® LAR® have shown that biochemical control in terms of GH and IGF-1 levels is associated with improved cardiac performance in patients with acromegaly.22

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11. Does Sandostatin® LAR® affect tumour growth and size?

Clinical evidence has shown that a reduction in tumour size occurs in patients treated with Sandostatin LAR. The effect is evident after Week 24 of therapy. During a recent study with 68 treatment-naïve patients who were administered Sandostatin LAR, tumour shrinkage was observed in 63% of patients after 24 weeks of treatment and in 75% of patients after 48 weeks of treatment.15 Reduction in tumour volume was greater in patients with microadenomas than those with macroadenomas.15

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12. What are the side effects of Sandostatin® therapy?

Sandostatin and Sandostatin® LAR® are generally well tolerated. The most frequent side effects are transient burning at the injection site and gastrointestinal complications, such as loose stools, abdominal cramping, nausea, and flatulence. Gastrointestinal complications will often resolve within 10 days with the continuation of therapy.23 In the meantime, reassuring the patient that this is a transient effect, avoiding administration close to mealtime, starting with a smaller dose and then increasing to the effective therapeutic level, can help to minimise any discomfort. Pain at the injection site can be alleviated by rotation of injection sites. Adverse drug reactions that should be monitored include development of gallstones, glucose homeostasis, and thyroid function. In clinical trials, hypoglycemia and hyperglycemia occurred in 3% and 16% of patients with acromegaly, respectively. These effects are a result of the mechanism of action of Sandostatin, which alters the balance between insulin, glucagon, and GH.

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References: 1. Melmed S. Acromegaly. N Engl J Med. 1990;322:966-977. 2. Acromegaly therapy consensus development panel. Consensus statement: Benefit versus risk of medical therapy for acromegaly. Am J Med. 1994;97:468-473. 3. Bates. Does treatment of acromegaly affect life expectancy? Metabolism. 1995;44(Suppl.1):1-5. 4. Melmed S, et al. Current treatment guidelines for acromegaly. J Clin Endocrinol Metab. 1998;83:2646-2652. 5. Melmed S, et al. Guidelines for acromegaly management. J Clin Endocrinol Metab. 2002;87:4054-4058. 6. Trainer PJ. Editorial: acromegaly - consensus, what consensus? J Clin Endocrinol Metab. 2002;87:3534-3536. 7. Melmed S, Colao A, Barkan A, et al. Guidelines for acromegaly management: an update. J Clin Endocrinol Metab. 2009;94:1509-1517. 8. Nomikos P, Buchfelder M, Fahlbusch R. The outcome of surgery in 668 patients with acromegaly using current criteria of biochemical 'cure'. Eur J Endocrinol. 2005;152:379-387. 9. Swearingen B, et al. Long-term mortality after transsphenoidal surgery and adjunctive therapy for acromegaly. J Clin Endocrinol Metab. 1998;83:3419-3426. 10. Abe T, Ludecke DK. Effects of pre-operative octreotide treatment on different subtypes of 90 growth hormone secreting pituitary adenomas and outcome in one surgical center. Eur J Endocrinol. 2001;145:137-145. 11. Giustina A, Barkan A, Casanueva FF, et al. Criteria for cure of acromegaly: a consensus statement. J Clin Endocrinol Metab. 2000;85:526-529. 12. Melmed S. Medical progress: Acromegaly. N Engl J Med. 2006;355:2558-2573. 13. About Sandostatin Website. Novartis Core Labeling Text. Available at: http://www.sandostatin.com/about_sandostatin/novartis_core_summary/index.html. Accessed March 16, 2009. 14. Paisley AN, Trainer PJ. Medical treatment in acromegaly. Curr Opin Pharmacol. 2003;3:672-677. 15. Mercado M, Borges F, Bouterfa H, et al; for the SMS995B2401 Study Group. A prospective, multicentre study to investigate the efficacy, safety and tolerability of octreotide LAR (long-acting repeatable octreotide) in the primary therapy of patients with acromegaly. Clin Endocrinol. 2007;66:859-868. 16. Ferone D, et al. Treatment options in acromegaly: pharmacotherapy or surgery as primary treatment for acromegaly? Drugs & Aging. 2000;17:81-92. 17. Spinas GA, et al. Pre-operative treatment of 5 acromegalics with a somatostatin analogue: endocrine and clinical observations. Acta Endocrinol. 1987;114:249-256. 18. Colao A, et al. Effect of octreotide pretreatment on surgical outcome in acromegaly. J Clin Endocrinol Metab. 1997;82:3308-3314. 19. Carlsen SM, Lund-Johansen M, Schreiner T, et al. Preoperative octreotide treatment in newly diagnosed acromegalic patients with macroadenomas increases cure short-term postoperative rates: a prospective, randomized trial. J Clin Endocrinol Metab. 2008;93:2984-2990. 20. Sandostatin LAR® [prescribing information]. East Hanover, NJ: Novartis Pharmaceuticals Corporation; 2008. 21. Chen TC, et al. Pharmacokinetics and pharmacodynamics and safety of microencapsulated Sandostatin® LAR® acetate in healthy subjects. J Clin Pharmacol. 2000;40:475-481. 22. Colao A, Spinelli L, Cuocolo A, et al. Cardiovascular consequences of early-onset growth hormone excess. J Clin Endocrinol Metab. 2002;87:3097-3104. 23. Melmed S. Consensus statement: benefits versus risks of medical therapy for acromegaly. Am J Med. 1994;97:468-473.