Practice Pearl 2: Differences Among the Somatostatin Analogues for NETs
Cecilia Lau, RPh, BCOP, APh, and Daneng Li, MD, review the differences among the somatostatin analogues, particularly the differences in PK data.
Daneng Li, MD: Cecilia, have you been able to see any differences between these agents that could help us tease out, at least a little, the differences and how that might impact someone undergoing treatment with either of these 2 somatostatin analogues [SSAs]?
Cecilia Lau, RPh, BCOP, APh: Both long-acting somatostatin analogues are generally dosed once every 4 weeks. Lanreotide is usually dosed at 120 mg every 4 weeks and given as a deep subcutaneous injection. Regarding octreotide and lanreotide, the starting dose can be 20 to 30mg, though it is usually 30 mg every 2 weeks as an IM [intramuscular] injection.
The main difference between the 2 is that lanreotide tends to peak a little earlier compared with octreotide-LAR, such that the patients who are initially starting on octreotide-LAR may actually have continued short-acting octreotide subcutaneous injections for the first couple of weeks to make sure they have control of their symptoms. That also means that for patients who are symptomatic, they may benefit from using lanreotide instead of octreotide-LAR [long-acting release].
As far as the use of either agent in special populations, lanreotide PK [pharmacokinetics] was studied in geriatric patients up to age 85, and it was shown that there was no change in PKs in terms of renal function. Mild to moderate renal impairment was shown not to have any effect on lanreotide PKs, but the drug was not studied in patients with severe renal impairment, meaning those with creatinine clearance less than 30 mL/min. Lanreotide was not studied, at least in the neuroendocrine arena, in patients with hepatic impairment.
As far as octreotide-LAR goes, I do not think it was studied specifically in geriatric patients. There are some—rather, there are no dosage adjustments recommended for patients with renal impairment, except for patients with end-stage renal disease on dialysis. We use a slower-starting dose and then titrate the dose according to symptoms. Likewise, for octreotide-LAR, there are no dosage adjustments for patients with hepatic impairment, except for the setting of cirrhosis, where the recommended starting dose would be lower, and then the dose should be titrated according to patient symptoms.
Daneng Li, MD: Those are all great data points for our colleagues to understand. Somatostatin analogue therapies are very well tolerated. It is good to know that we have some geriatric population data, because the incidence of neuroendocrine tumors has particularly increased most significantly in the 65-plus population.
That is very good and assuring to our colleagues who are potentially going to be using these medications to treat more and more patients with this disease.
I do completely agree that clinically, what we are seeing is that, as you mentioned, the lanreotide might have a faster peak time. There are benefits and potentially additional adverse effects, to monitor. As you mentioned, you might not need the short-acting doses for those patients who have carcinoid syndrome, those situations where you’re really trying to suppress the hormone release relatively quickly. At the same time, for patients who are nonfunctional—somatostatin is essentially a stop hormone in a way—those patients might have stat urea as a result. We caution them not to eat very fatty foods during that first week or to replace that with pancreatic enzymes to help them get through that initiation.