Magnetic resonance imaging as a predictor of therapeutic response to pasireotide in acromegaly.

OBJECTIVE: Hyperintensity signal in T2-weighted magnetic resonance imaging (MRI) has been related to better therapeutic response during pasireotide treatment in acromegaly. The aim of the study was to evaluate T2 MRI signal intensity and its relation with pasireotide therapeutic effectiveness in real-life clinical practice. DESIGN, PATIENTS AND MEASUREMENTS: Retrospective multicentre study including acromegaly patients treated with pasireotide. Adenoma T2-weighted MRI signal at diagnosis was qualitatively classified as iso-hyperintense or hypointense. Insulin-like growth factor (IGF-I), growth hormone (GH) and tumour volume reduction were assessed after 6 and 12 months of treatment and its effectiveness evaluated according to baseline MRI signal. Hormonal response was considered 'complete' when normalization of IGF-I levels was achieved. Significant tumour shrinkage was defined as a volume reduction of ≥25% from baseline. RESULTS: Eighty-one patients were included (48% women, 50 ± 1.5 years); 93% had previously received somatostatin receptor ligands (SRLs) treatment. MRI signal was hypointense in 25 (31%) and hyperintense in 56 (69%) cases. At 12 months of follow-up, 42/73 cases (58%) showed normalization of IGF-I and 37% both GH and IGF-I. MRI signal intensity was not associated with hormonal control. 19/51 cases (37%) presented a significant tumour volume shrinkage, 16 (41%) from the hyperintense group and 3 (25%) from the hypointense. CONCLUSIONS: T2-signal hyperintensity was more frequently observed in pasireotide treated patients. Almost 60% of SRLs resistant patients showed a complete normalization of IGF-I after 1 year of pasireotide treatment, regardless of the MRI signal. There was also no difference in the percentage tumour shrinkage over basal residual volume between the two groups.

Intensification of Basal Insulin Therapy with Lixisenatide in Patients with Type 2 Diabetes in a Real-World Setting: The BASAL-LIXI Study.

BACKGROUND: Basal insulin reduces fasting blood glucose levels, but postprandial blood glucose levels may remain higher. Traditional strategies with rapid insulin intensification can cause hypoglycemic episodes and weight gain. Glucagon-like peptide-1 receptor agonists, such as the short-acting lixisenatide, are able to control postprandial excursions, without weight gain, and with a low risk of hypoglycemic events. OBJECTIVE: Due to the limited data on the combination of lixisenatide with basal insulin (with or without oral antidiabetes drugs) in clinical practice, this study evaluated changes in parameters associated with glycemic control and anthropometric data after 24 weeks of this therapy intensification. METHODS: This was a multicenter, retrospective observational study of 129 patients with type 2 diabetes that was uncontrolled by basal insulin. Their treatment was intensified by the addition of lixisenatide at least 24 weeks before being included in the study. Data were retrospectively collected to determine changes in glycated hemoglobin (HbA1c) levels, blood glucose levels, weight, and body mass index. Adverse reactions and hypoglycemic events were also recorded. RESULTS: After 24 weeks of therapy intensification with lixisenatide, a significant reduction in HbA1c levels was observed (-1.1%; P < 0.001). An HbA1c <7% was achieved in 30.2% of patients, and 17.1% reached an HbA1c <6.5%. There was a reduction in fasting blood glucose (31.8 [60.3] mg/dL; P < 0.001) and postprandial blood glucose (55.0 [49] mg/dL; P < 0.001) levels, as well as body weight (4.0 [5.4] kg; P < 0.001) and body mass index (1.5 [1.9]; P < 0.001). The most commonly observed adverse reactions were nausea (n = 9), in line with previous studies. Hypoglycemia events were rare; only reported in 2 patients. CONCLUSIONS: Intensification strategy based on lixisenatide added to basal insulin (with or without oral antidiabetes drugs) can be an effective treatment option in patients with uncontrolled type 2 diabetes. In this small, selected population, glycemic control was significantly improved in terms of HbA1, fasting blood glucose levels, and postprandial glucose levels, with a reduction of body weight and low risk of hypoglycemic events. (Curr Ther Res Clin Exp. 2018; 79:XXX-XXX).

A case of lipoatrophy with insulin detemir.

Lipoatrophy is a rare cutaneous side-effect that can develop at the site of insulin injection. Since the introduction of human recombinant insulin the number of cases has decreased although cases have been reported in association with the use of rapid acting insulin analogues and continuous subcutaneous insulin infusion (CSII), recently one case has been reported with the use of insulin glargine. Insulin-induced lipoatrophy is a subcutaneous fat atrophy at the sites of injection which is relevant not only because of the cosmetic problem, but also because of the variability of absorption it causes in the site of injection. This report describes a patient with a type 1 diabetes mellitus who develops a lipoatrophy induced by insulin detemir. To our understanding this is one of the first reported cases of lipoatrophy induced by insulin detemir.

Severe hypoglycemia after gastric bypass surgery for morbid obesity.

Recently, hypoglycemia with endogenous hyperinsulinemia has been described after undergoing bariatric surgery because of morbid obesity. It has been theorized that after a gastric bypass surgery, some trophic factors affecting pancreatic beta cells could emerge. The authors present a case of morbidly obese patient with severe hypoglycemia 3 months after bariatric surgery. An abdominal helicoidally computed tomography scan showed a 1.7 cm tumor in the tail of the pancreas. Histopathology revealed an insulinoma with well-defined contours surrounded by pancreatic tissue with atrophic signs and with hyperplasia and hypertrophic phenomena compatible with nesidioblastosis in adjacent islets of the pancreatic duct. Authors hypothesize that maintenance of the stimulus produces hyperplasia/hypertrophy of the pancreatic islets and reemphasizes the dynamic qualities of pancreatic beta cells and the possibility of producing hyperplasia from the extreme resistance to insulin present in morbidly obese patients.