Treatment Options

The goals of acromegaly treatment are to:¹

Eliminate the tumor, including the mass effect and to reverse associated neurologic problems (optic compression and headaches) and prevent recurrence¹
Restore and maintain normal pituitary function¹
Normalize IGF-1 and GH levels (GH ≤ 2.5 ng/mL; if possible, lower to 1 ng/mL) in order to reduce the comorbidities and symptoms associated with active acromegaly¹

A variety of options are available for the treatment of acromegaly. The range of treatment options encompasses:

Surgery is the recommended first-line therapy for many patients with acromegaly. It is intended to remove GH-secreting microadenomas, and to decompress mass effects on vital structures—particularly the optic tracts.

Surgery may not be indicated for patients who:¹¹

Present with an invasive tumor, sinus extension, or suprasellar extension, and whose pituitary lesion does not compress vital structures¹¹
Have risk factors that make surgery or anesthesia unacceptable¹¹
Have major systemic manifestations of acromegaly, including cardiomyopathy, severe hypertension, and uncontrolled diabetes¹¹
Refuse to undergo surgery¹¹

Medical therapy may be used subsequent to surgery to control GH and IGF-1 levels and their associated comorbidities.

Pharmacological treatment may involve:¹

Somastatin analogs (SSAs), which can help control GH oversecretion at the site of a pituitary tumor, and which are recommended by the American Association of Clinical Endocrinologists as the drugs of first choice in the medical treatment of acromegaly. SSAs may be considered for patients with persistently nonsuppressible high GH and IGF-1 levels after a pituitary surgical procedure, or as primary therapy for patients who are not candidates for therapy.¹
A GH antagonist, which can help block the reception of GH produced at the pituitary, helping to normalize IGF-1 levels, but not effecting GH levels¹
Dopamine agonists, which have been shown to suppress GH production in some patients¹

Radiation therapy may be used after surgery. Up to 80% of patients at the time of diagnosis of acromegaly have a large tumor with dural, bone, or cavernous sinus invasion, which could indicate that multimodality therapy will be necessary for achievement of clinical remission and a normal serum IGF-1 concentration. Radiation may take 10 to 20 years to adequately reduce serum levels of GH and IGF-1.¹

Radiation may also be used if surgery involves unacceptable risks.

Conventional radiation therapy may be used if the tumor is near the optic chiasm, but focused radiation methods are only used if the residual tumor and optic chiasm/nerve is more than 5 mm.¹
Not all patients are candidates for stereotactic radiotherapy due to the concern about radiation exposure to the optic apparatus. Another potential complication is the loss of pituitary function, which would necessitate the need for hormone replacement.¹

Epidemiology & Pathophysiology
Learn about the incidence and causes of acromegaly Find out more »

Screening & Diagnosis
Understand the various ways in which acromegaly may be identified and assessed Learn more »

Indication and Important Safety Information

Somatuline^® Depot (lanreotide) Injection is a somatostatin analog indicated for the long-term treatment of patients with acromegaly who have had an inadequate response to or cannot be treated with surgery and/or radiotherapy.

CONTRAINDICATIONS

None.

WARNINGS & PRECAUTIONS

Somatuline Depot may reduce gallbladder motility and lead to gallstone formation; therefore, patients may need to be monitored periodically.
Somatuline Depot and other somatostatin analogs can inhibit the secretion of insulin and glucagon. Patients treated with Somatuline Depot may experience hypoglycemia or hyperglycemia.
Antidiabetic treatment may need to be adjusted when Somatuline Depot treatment is initiated or when the dose is altered.
Slight decreases in thyroid function have been seen during treatment with Somatuline Depot. Thyroid function tests are recommended where clinically indicated.
The most common cardiac adverse reactions observed in patients in 3 pooled cardiac studies were sinus bradycardia (5.5%), bradycardia (2.8%), and hypertension (5.6%).

In patients without underlying cardiac disease, Somatuline Depot may lead to a decrease in heart rate without necessarily reaching the threshold of bradycardia.
In patients suffering from cardiac disorders prior to Somatuline Depot treatment, sinus bradycardia may occur. Care should be taken when initiating Somatuline Depot treatment in patients with bradycardia.

The pharmacological gastrointestinal effects of Somatuline Depot may reduce the intestinal absorption of concomitant drugs.
Somatuline Depot may decrease the relative bioavailability of cyclosporine. Cyclosporine dose may need to be adjusted to maintain levels.

SPECIAL POPULATIONS

Patients with moderate and severe renal impairment or moderate and severe hepatic impairment should begin treatment with Somatuline Depot 60 mg. Caution should be exercised when considering these patients for an extended dosing interval of Somatuline Depot 120 mg every 6 or 8 weeks.
There are no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human responses, Somatuline Depot should be used during pregnancy only if the potential benefit justifies potential risk to the fetus.
A decision should be made whether to discontinue nursing or discontinue Somatuline Depot taking into account the importance of the drug to the mother.
Patients receiving beta-blockers, calcium channel blockers, or other drugs that affect heart rate may need dose adjustments to those drugs. Somatuline Depot may reduce the intestinal absorption of coadministered drugs. Caution should be used.

ADVERSE EVENTS

In pooled studies (N = 416), the most common adverse reactions (incidence > 5%) were diarrhea (37%), cholelithiasis (20%), abdominal pain (19%), nausea (11%), injection–site reaction (9%), constipation (8%), flatulence (7%), headaches (7%), arthralgia (7%),vomiting (7%), and loose stools (6%).
Gastrointestinal adverse reactions were mild to moderate and typically resolved within 8 to 10 weeks.

1% of patients in the pooled studies with Somatuline Depot discontinued treatment due to gastrointestinal adverse events.

Occasional cases of pancreatitis have been reported.
Injection-site pain (4.1%) and injection-site mass (1.7%) were the most frequently reported local adverse reactions.
Local side effects were more common at the start of treatment and less common as treatment continued.

Injection–site reactions were usually mild to moderate but did lead to withdrawal from clinical studies in two patients.

For Full Prescribing Information, click here.