terlipressin
Sources réglementaires consultées
Indications approuvées
- Hémorragie digestive par rupture de varices œsogastriques et traitement urgent du syndrome hépatorénal de type 1.
Contre-indications
Absolues
- Grossesse ou hypersensibilité.
Mises en garde cliniques
- Mise en garde majeure · Peut provoquer une insuffisance respiratoire grave ou fatale, un œdème pulmonaire et une hypoxie. Surveiller la saturation en oxygène, la fréquence respiratoire et les signes de surcharge ; éviter en cas d’hypoxie ou d’aggravation respiratoire. — CIMA/AEMPS, ficha técnica 72359
- Mise en garde majeure · La vasoconstriction peut provoquer une ischémie myocardique, intestinale, périphérique ou cutanée, des arythmies et une nécrose. Surveiller pression, fréquence, ECG, électrolytes et perfusion ; utiliser uniquement par voie IV et éviter l’extravasation. — CIMA/AEMPS, ficha técnica 72359
- Mise en garde majeure · Dans le syndrome hépatorénal, éviter si la créatinine initiale est ≥5 mg/dl, en cas d’insuffisance hépatique aiguë sur chronique de grade 3 ou de MELD ≥39, sauf si le bénéfice l’emporte clairement sur le risque. — CIMA/AEMPS, ficha técnica 72359
Interactions médicamenteuses
- SévèreMédicaments provoquant une bradycardie
Mécanisme: Le propofol, le sufentanil et d’autres peuvent provoquer une bradycardie aiguë additive.
Recommandation: Surveiller la fréquence et l’ECG ; éviter les associations à haut risque.
CIMA/AEMPS, ficha técnica 72359https://cima.aemps.es/cima/dochtml/ft/72359/FT_72359.html
- SévèreMédicaments allongeant le QT ou diminuant potassium/magnésium
Mécanisme: Ils augmentent le risque d’arythmie ventriculaire et de torsade de pointes.
Recommandation: Corriger les électrolytes, surveiller l’ECG et éviter si possible.
CIMA/AEMPS, ficha técnica 72359https://cima.aemps.es/cima/dochtml/ft/72359/FT_72359.html
Effets indésirables
Communs (≥1%)
Douleur abdominale · Nausées, vomissements ou diarrhée · Pâleur · Dyspnée · Bradycardie · Hyponatrémie
Rares mais graves
Insuffisance respiratoire ou œdème pulmonaire · Ischémie myocardique ou intestinale · Arythmie ventriculaire de type torsade de pointes · Nécrose cutanée ou au site d’injection
Grossesse et allaitement
Contre-indiqué pendant la grossesse en raison des contractions utérines, de la diminution du débit utérin et du risque fœtal. Pendant l’allaitement, décider d’interrompre l’allaitement ou le traitement selon les bénéfices et les risques.
Bibliographie récente (PubMed)
Cirrhosis affects approximately 2.2 million adults in the US. From 2010 to 2021, the annual age-adjusted mortality of cirrhosis increased from 14.9 per 100 000 to 21.9 per 100 000 people. The most common causes of cirrhosis in the US, which can overlap, include alcohol use disorder (approximately 45% of all cases of cirrhosis), nonalcoholic fatty liver disease (26%), and hepatitis C (41%). Patients with cirrhosis experience symptoms including muscle cramps (approximately 64% prevalence), pruritus (39%), poor-quality sleep (63%), and sexual dysfunction (53%). Cirrhosis can be diagnosed by liver biopsy but may also be diagnosed noninvasively. Elastography, a noninvasive assessment of liver stiffness measured in kilopascals, can typically confirm cirrhosis at levels of 15 kPa or greater. Approximately 40% of people with cirrhosis are diagnosed when they present with complications such as hepatic encephalopathy or ascites. The median survival time following onset of hepatic encephalopathy and ascites is 0.92 and 1.1 years, respectively. Among people with ascites, the annual incidence of spontaneous bacterial peritonitis is 11% and of hepatorenal syndrome is 8%; the latter is associated with a median survival of less than 2 weeks. Approximately 1% to 4% of patients with cirrhosis develop hepatocellular carcinoma each year, which is associated with a 5-year survival of approximately 20%. In a 3-year randomized clinical trial of 201 patients with portal hypertension, nonselective β-blockers (carvedilol or propranolol) reduced the risk of decompensation or death compared with placebo (16% vs 27%). Compared with sequential initiation, combination aldosterone antagonist and loop diuretics were more likely to resolve ascites (76% vs 56%) with lower rates of hyperkalemia (4% vs 18%). In meta-analyses of randomized trials, lactulose was associated with reduced mortality relative to placebo (8.5% vs 14%) in randomized trials involving 705 patients and reduced risk of recurrent ov
Inotropes and vasopressors frequently are administered in critically ill and perioperative patients. However, clinical practice is highly variable across clinicians and institutions. The inotropic score and its upgrade "vasoactive-inotropic score" (VIS) can be used to objectively quantify the degree of hemodynamic support. Several studies demonstrated a correlation between high VIS and poor outcome. Furthermore, VIS can help compare different clinical and research experiences. Several recently developed scores include VIS in their model, although they still require independent validation. Conversely, VIS has several pitfalls, including the fact that a universally recognized version that includes all commonly used vasoactive drugs does not exist. In this review, the authors summarize all the VIS, VIS-related, and VIS-validating manuscripts, and suggest a new updated version of VIS that also includes terlipressin, methylene blue, and angiotensin II.
Patients with cirrhosis are prone to developing acute kidney injury (AKI), a complication associated with a markedly increased in-hospital morbidity and mortality, along with a risk of progression to chronic kidney disease. Whereas patients with cirrhosis are at increased risk of developing any phenotype of AKI, hepatorenal syndrome (HRS), a specific form of AKI (HRS-AKI) in patients with advanced cirrhosis and ascites, carries an especially high mortality risk. Early recognition of HRS-AKI is crucial since administration of splanchnic vasoconstrictors may reverse the AKI and serve as a bridge to liver transplantation, the only curative option. In 2023, a joint meeting of the International Club of Ascites (ICA) and the Acute Disease Quality Initiative (ADQI) was convened to develop new diagnostic criteria for HRS-AKI, to provide graded recommendations for the work-up, management and post-discharge follow-up of patients with cirrhosis and AKI, and to highlight priorities for further research.
Hepatorenal syndrome-acute kidney injury (HRS-AKI) occurs in the setting of advanced chronic liver disease, portal hypertension, and ascites. HRS-AKI is found in ∼20% of patients presenting to the hospital with AKI, but it may coexist with other causes of AKI and/or with preexisting chronic kidney disease, thereby making the diagnosis challenging. Novel biomarkers such as urinary neutrophil gelatinase-associated lipocalin may be useful. While HRS-AKI is a functional form of AKI related to circulatory and neurohormonal dysfunction, there is increasing recognition of the importance of systemic inflammation and the renal microenvironment. Early diagnosis and initiation of HRS-AKI-specific treatment can improve outcomes. The mainstay of therapy is a vasoconstrictor (terlipressin or norepinephrine) combined with albumin, which achieves resolution of HRS in 40-50% of cases. Liver transplantation is the only option for patients failing to respond to medical therapies.
Hepatorenal syndrome (HRS) is a form of kidney dysfunction that characteristically occurs in liver cirrhosis. It is characterized by a marked impairment of kidney function in response to circulatory and hemodynamic alterations that occur in advanced stages of liver cirrhosis, aggravated by systemic inflammation and bacterial translocation. The classical definitions of the types of HRS have been recently revisited and 2 forms of HRS have been redefined: the acute form, referred to as acute kidney injury (HRS-AKI), and the chronic form, referred to as chronic kidney disease. HRS-AKI is one of the most severe forms of AKI in patients with cirrhosis and it consists of an abrupt impairment of kidney function, frequently triggered by an infection, appearing in the setting of advanced decompensated cirrhosis. Differential diagnosis with other causes of AKI is crucial because HRS-AKI requires a specific treatment. Differential diagnosis with AKI-acute tubular necrosis may be challenging and kidney biomarkers may be useful in this setting. Treatment of HRS-AKI is based on the administration of vasoconstrictor drugs in combination with volume expansion with albumin. Prognosis of HRS-AKI is poor, and the ideal definitive treatment consists of liver transplantation or simultaneous liver-kidney transplantation. HRS-AKI has a big impact on patients' quality of life. Management of HRS-AKI remains challenging in specific situations such as alcohol-associated hepatitis or metabolic-associated steatotic liver disease cirrhosis. Developing preventive measures for HRS-AKI, improving its early identification, discovering new biomarkers for differential diagnosis, and improving the response to therapy are some of the unmet needs in the field of HRS-AKI.