Guest guest Posted October 20, 2004 Report Share Posted October 20, 2004 http://www.pharma.us.novartis.com/product/pi/pdf/sandostatin_inj.pdf Sandostatin General Sandostatin® (octreotide acetate) alters the balance between the counter-regulatory hormones, insulin, glucagon and growth hormone, which may result in hypoglycemia or hyperglycemia. Sandostatin® (octreotide acetate) also suppresses secretion of thyroid stimulating hormone, which may result in hypothyroidism. Cardiac conduction abnormalities have also occurred during treatment with Sandostatin® (octreotide acetate). However, the incidence of these adverse events during long-term therapy was determined vigorously only in acromegaly patients who, due to their underlying disease and/or the subsequent treatment they receive, are at an increased risk for the development of diabetes mellitus, hypothyroidism, and cardiovascular disease. Although the degree to which these abnormalities are related to Sandostatin® (octreotide acetate) therapy is not clear, new abnormalities of glycemic control, thyroid function and ECG developed during Sandostatin® (octreotide acetate) therapy as described below. The hypoglycemia or hyperglycemia which occurs during Sandostatin® (octreotide acetate) therapy is usually mild, but may result in overt diabetes mellitus or necessitate dose changes in insulin or other hypoglycemic agents. Hypoglycemia and hyperglycemia occurred Page 5 on Sandostatin® (octreotide acetate) in 3% and 16% of acromegalic patients, respectively. Severe hyperglycemia, subsequent pneumonia, and death following initiation of Sandostatin® (octreotide acetate) therapy was reported in one patient with no history of hyperglycemia. In acromegalic patients, 12% developed biochemical hypothyroidism only, 8% developed goiter, and 4% required initiation of thyroid replacement therapy while receiving Sandostatin® (octreotide acetate). Baseline and periodic assessment of thyroid function (TSH, total and/or free T4) is recommended during chronic therapy. In acromegalics, bradycardia (<50 bpm) developed in 25%; conduction abnormalities occurred in 10% and arrhythmias occurred in 9% of patients during Sandostatin® (octreotide acetate) therapy. Other EKG changes observed included QT prolongation, axis shifts, early repolarization, low voltage, R/S transition, and early R wave progression. These ECG changes are not uncommon in acromegalic patients. Dose adjustments in drugs such as beta-blockers that have bradycardia effects may be necessary. In one acromegalic patient with severe congestive heart failure, initiation of Sandostatin® (octreotide acetate) therapy resulted in worsening of CHF with improvement when drug was discontinued. Confirmation of a drug effect was obtained with a positive rechallenge. Several cases of pancreatitis have been reported in patients receiving Sandostatin® (octreotide acetate) therapy. Sandostatin® (octreotide acetate) may alter absorption of dietary fats in some patients. In patients with severe renal failure requiring dialysis, the half-life of Sandostatin® (octreotide acetate) may be increased, necessitating adjustment of the maintenance dosage. Depressed vitamin B12 levels and abnormal Schilling's tests have been observed in some patients receiving Sandostatin® (octreotide acetate) therapy, and monitoring of vitamin B12 levels is recommended during chronic Sandostatin® (octreotide acetate) therapy. I hope this finds you and yours well Mark E. Armstrong casca@... www.top5plus5.com PAI NW Rep ICQ #59196115 Quote Link to comment Share on other sites More sharing options...
Recommended Posts
Join the conversation
You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.