KU-57788 clinical trial Systeme Internationale conversion factors: GH (μg/L), X 3.0?=?mUI/L; IGF-I (μg/L), X 0.131?=?nmol/L. a Nineteen were analyzed in the Acrostudy Italy; b GH nadir?=?value observed after oral glucose tolerance test (OGTT); c Baseline: End of SSA monotherapy, immediately before PEGV was started. d

Expressed as averages of GH day curve (4 points over 2 hours). e Level observed at diagnosis minus level observed at baseline. * p? Intragroup differences involving continuous variables were analyzed with the Wilcoxon buy AZD9291 rank sum test; the Mann–Whitney U test when data from different groups were being compared. For discontinuous variables, the chi-squared test was used. Multivariate logistic regression analysis was used to identify factors related to the decision to prescribe PEGV?+?SSA vs. PEGV monotherapy. Standard and stepwise multiple linear regression analyses were used to identify variables that best predicted the end-of-follow-up PEGV dose. P values selleck chemical <0.05 were regarded as significant. Results The study population included 62 patients with acromegaly caused by GH-secreting adenomas (Table 1). The vast majority had presented with macroadenomas. Almost all had already undergone surgery, but at baseline 2/3 had detectable residual adenoma. Three patients were treated with SSA as primary therapy:

in two cases because the neurosurgery was contraindicated due to severe cardiomyopathy and respiratory comorbidities and in the last case the patient refused surgery. All had received?≥?2 years of SSA monotherapy. All patients were on SSA treatment [octreotide LAR n?=?23 (37%), lanreotide ATG n?=?39 (63%)] before PEGV replaced or was added to SSA. Laboratory data obtained right before this treatment was discontinued (i.e., baseline) revealed the persistence of markedly elevated GH (median nadir 18 μg/L) and IGF-I levels (median 621 μg/L). The mean IGF-I ∆ was 132 μg/L PLEK2 (range −411 to 872). Thirty-five of the patients

had been treated with PEGV alone (Group 1) and 27 were receiving PEGV?+?SSA (Group 2), continuing the previous SSA treatment. As shown in Table 1, median GH and IGF-I levels documented at the time of diagnosis were significantly higher in Group 2 (p?Lanreotide ATG?=?21 (69%) patients; Group 2: octreotide LAR?=?9 (33%), Lanreotide ATG?=?18 (67%)]. However, Group 2 had significantly higher residual tumor rates and (as at diagnosis) GH levels that were nnearly twice as high as those of Group 1. Baseline IGF-I levels in both groups still clearly exceeded normal ranges. However, the IGF-I ∆ values (SDS) in Group 2 were 3–4 times higher than that of Group 1. As a result, when SSA monotherapy was discontinued (i.e., baseline), the IGF-I elevations in the two groups were not significantly different (Table 1). Multivariate logistic regression analyses revealed that the decision to prescribe PEGV?+?SSA vs.