octreotide
Sources réglementaires consultées
Indications approuvées
- Contrôle biochimique de l’acromégalie lorsque la chirurgie, la radiothérapie ou la bromocriptine sont insuffisantes ou impossibles ; contrôle symptomatique des tumeurs carcinoïdes métastatiques et des VIPomes.
Contre-indications
Absolues
- Hypersensibilité à l’octréotide ou à ses composants.
Mises en garde cliniques
- Mise en garde majeure · Surveiller la conduction cardiaque, surtout par voie IV ; une bradycardie, des arythmies ou un bloc AV complet peuvent survenir. — DailyMed, set_id 4e2c9856-1836-49f0-9472-4dbeeb408f39
- Mise en garde majeure · Surveiller la vésicule biliaire, la glycémie, la thyroïde et la vitamine B12. Rechercher une insuffisance pancréatique exocrine en cas de stéatorrhée, selles molles, ballonnements ou perte de poids. — DailyMed, set_id 4e2c9856-1836-49f0-9472-4dbeeb408f39
Interactions médicamenteuses
- SévèreCiclosporine
Mécanisme: L’octréotide peut réduire son absorption et sa concentration.
Recommandation: Surveiller les concentrations et ajuster la ciclosporine pour éviter la perte du greffon.
DailyMed, set_id 4e2c9856-1836-49f0-9472-4dbeeb408f39
- ModéréeInsuline et antidiabétiques
Mécanisme: L’inhibition de l’insuline et du glucagon peut provoquer une hypo- ou hyperglycémie.
Recommandation: Surveiller la glycémie lors de l’instauration ou de la modification de l’octréotide et adapter le traitement antidiabétique.
DailyMed, set_id 4e2c9856-1836-49f0-9472-4dbeeb408f39
- SévèreDotatate de lutétium-177
Mécanisme: Les analogues de la somatostatine peuvent interférer avec la liaison au récepteur pendant la thérapie radionucléide.
Recommandation: Arrêter l’octréotide au moins 24 heures avant chaque dose de dotatate de lutétium-177.
DailyMed, set_id 4e2c9856-1836-49f0-9472-4dbeeb408f39
- ModéréeBêtabloquants et autres médicaments bradycardisants
Mécanisme: L’effet bradycardisant peut être augmenté.
Recommandation: Surveiller la fréquence et la conduction cardiaques et adapter le traitement concomitant si nécessaire.
DailyMed, set_id 4e2c9856-1836-49f0-9472-4dbeeb408f39
- ModéréeBromocriptine
Mécanisme: L’octréotide peut augmenter sa biodisponibilité.
Recommandation: Surveiller les effets indésirables et ajuster si nécessaire.
DailyMed, set_id 4e2c9856-1836-49f0-9472-4dbeeb408f39
Effets indésirables
Communs (≥1%)
Diarrhée, selles molles, nausées, douleur abdominale, anomalies biliaires, bradycardie, hyperglycémie et hypothyroïdie
Rares mais graves
Bloc auriculo-ventriculaire complet, pancréatite et réaction anaphylactique
Grossesse et allaitement
Les données pendant la grossesse sont limitées ; n’utiliser qu’en cas de nécessité manifeste. Le passage dans le lait maternel est inconnu ; la décision doit être individualisée.
Bibliographie récente (PubMed)
There are currently no standard first-line treatment options for patients with higher grade 2-3, well-differentiated, advanced, gastroenteropancreatic neuroendocrine tumours. We aimed to investigate the efficacy and safety of first-line [177Lu]Lu-DOTA-TATE (177Lu-Dotatate) treatment. NETTER-2 was an open-label, randomised, parallel-group, superiority, phase 3 trial. We enrolled patients (aged ≥15 years) with newly diagnosed higher grade 2 (Ki67 ≥10% and ≤20%) and grade 3 (Ki67 >20% and ≤55%), somatostatin receptor-positive (in all target lesions), advanced gastroenteropancreatic neuroendocrine tumours from 45 centres across nine countries in North America, Europe, and Asia. We used interactive response technologies to randomly assign (2:1) patients to receive four cycles (cycle interval was 8 weeks ± 1 week) of intravenous 177Lu-Dotatate plus intramuscular octreotide 30 mg long-acting repeatable (LAR) then octreotide 30 mg LAR every 4 weeks (177Lu-Dotatate group) or high-dose octreotide 60 mg LAR every 4 weeks (control group), stratified by neuroendocrine tumour grade (2 vs 3) and origin (pancreas vs other). Tumour assessments were done at baseline, week 16, and week 24, and then every 12 weeks until disease progression or death. The primary endpoint was progression-free survival by blinded, independent, central radiology assessment. We did the primary analysis at 101 progression-free survival events as the final progression-free survival analysis. NETTER-2 is registered with ClinicalTrials.gov, NCT03972488, and is active and not recruiting. Between Jan 22, 2020, and Oct 13, 2022, we screened 261 patients, 35 (13%) of whom were excluded. We randomly assigned 226 (87%) patients (121 [54%] male and 105 [46%] female) to the 177Lu-Dotatate group (n=151 [67%]) and control group (n=75 [33%]). Median progression-free survival was 8·5 months (95% CI 7·7-13·8) in the control group and 22·8 months (19·4-not estimated) in the 177Lu-Dotatate group (stratified hazard ratio 0·276
Chylothorax in neonates results from leakage of lymph from thoracic lymphatic ducts and is mainly congenital or posttraumatic. The clinical course of the effusion is heterogeneous, and consensus on treatment, timing, and modalities of measures has not yet been established. This review aims to present, along with levels of evidence and recommendation grades, all current therapeutic possibilities for the treatment of chylothorax in neonates. An extensive search of publications between 1970 and 2020 was performed in the PubMed, Cochrane Database of Systematic Reviews, and UpToDate databases. A stepwise approach algorithm was proposed for both congenital and traumatic conditions to guide the clinician in a rational and systematic way for approaching the treatment of neonates with chylothorax. The treatment strategy for neonatal chylothorax generally involves supportive care and includes drainage and procedures to reduce chyle flow. A stepwise approach starting with the least invasive method is advocated. Progression in the invasiveness of treatment options is determined by the response to previous treatments. A practical stepwise approach algorithm is proposed for both, congenital and traumatic chylothoraces.
1: ESGE recommends that patients with compensated advanced chronic liver disease (ACLD; due to viruses, alcohol, and/or nonobese [BMI < 30 kg/m2] nonalcoholic steatohepatitis) and clinically significant portal hypertension (hepatic venous pressure gradient [HVPG] > 10 mmHg and/or liver stiffness by transient elastography > 25 kPa) should receive, if no contraindications, nonselective beta blocker (NSBB) therapy (preferably carvedilol) to prevent the development of variceal bleeding.Strong recommendation, moderate quality evidence. 2: ESGE recommends that in those patients unable to receive NSBB therapy with a screening upper gastrointestinal (GI) endoscopy that demonstrates high risk esophageal varices, endoscopic band ligation (EBL) is the endoscopic prophylactic treatment of choice. EBL should be repeated every 2-4 weeks until variceal eradication is achieved. Thereafter, surveillance EGD should be performed every 3-6 months in the first year following eradication.Strong recommendation, moderate quality evidence. 3: ESGE recommends, in hemodynamically stable patients with acute upper GI hemorrhage (UGIH) and no history of cardiovascular disease, a restrictive red blood cell (RBC) transfusion strategy, with a hemoglobin threshold of ≤ 70 g/L prompting RBC transfusion. A post-transfusion target hemoglobin of 70-90 g/L is desired.Strong recommendation, moderate quality evidence. 4 : ESGE recommends that patients with ACLD presenting with suspected acute variceal bleeding be risk stratified according to the Child-Pugh score and MELD score, and by documentation of active/inactive bleeding at the time of upper GI endoscopy.Strong recommendation, high quality of evidence. 5 : ESGE recommends the vasoactive agents terlipressin, octreotide, or somatostatin be initiated at the time of presentation in patients with suspected acute variceal bleeding and be continued for a duration of up to 5 days.Strong recommendation, high quality evidence. 6 : ESGE recommends antibiotic pro
Hepatorenal syndrome (HRS) is a primarily functional form of acute kidney injury (AKI) that develops in patients with decompensated cirrhosis. The pathophysiologic cascade that leads to HRS begins with pooling of blood in the splanchnic system, resulting in a decrease in effective circulating arterial volume. The definitive treatment of HRS is liver transplantation. When this is not possible, HRS is treated with a combination of vasoconstrictor agents and intravenous albumin. Although the combination of midodrine and octreotide is used in the United States, the recently approved terlipressin, an analog of vasopressin, is likely to become the first-line standard of care.
Cirrhosis is a major cause of morbidity and mortality in the United States and worldwide. It consists of compensated, decompensated, and further decompensated stages; median survival is more than 15 years, 2 years, and 9 months for each stage, respectively. With each stage, there is progressive worsening of portal hypertension and the vasodilatory-hyperdynamic circulatory state, resulting in a progressive decrease in effective arterial blood volume and renal perfusion. Vasoconstrictors reduce portal pressure via splanchnic vasoconstriction and are used in the management of variceal hemorrhage. Intravenous (IV) albumin increases effective arterial blood volume and is used in the prevention of acute kidney injury (AKI) and death after large-volume paracentesis and in patients with spontaneous bacterial peritonitis (SBP). The combination of vasoconstrictors and albumin is used in the reversal of hepatorenal syndrome (HRS-AKI), the most lethal complication of cirrhosis. Because a potent vasoconstrictor, terlipressin, was recently approved by the US Food and Drug Administration, and because recent trials have explored use of IV albumin in other settings, it was considered that a best practice update would be relevant regarding the use of vasoactive drugs and IV albumin in the following 3 specific scenarios: variceal hemorrhage, ascites and SBP, and HRS. This expert review was commissioned and approved by the American Gastroenterological Association (AGA) Institute Clinical Practice Updates Committee and the AGA Governing Board to provide timely guidance on a topic of high clinical importance to the AGA membership. It underwent internal peer review through standard procedures of Gastroenterology. These Best Practice Advice statements were drawn from a review of the published literature and from expert opinion. Some of the statements are unchanged from published guidelines because of lack of new evidence in the literature. Because systematic reviews were not performed, the