Long-term outcomes and adverse effects of teduglutide in patients with short bowel syndrome: Highlighting hyperamylasemia and hyperlipasemia.

PURPOSE: Short bowel syndrome is a malabsorptive condition that occurs due to surgical removal or a congenital absence of a significant portion of the small intestine. Patients with short bowel syndrome often rely on parenteral support for extended periods or even their entire lives. Teduglutide, a glucagon-like peptide-2 analog, has shown promising results in reducing dependency on parenteral support in these patients by promoting intestinal adaptation and enhancing nutrient absorption. However, the long-term safety of teduglutide remains a concern, particularly with respect to its potential for the development of hyperamylasemia and hyperlipasemia. METHODS: This study involved patients who received teduglutide from December 2012 to December 2022 at Boston Medical Center. We evaluated outcomes and adverse events, focusing on hyperamylasemia and hyperlipasemia, through chart review. RESULTS: Thirteen eligible patients were identified who had used teduglutide. Of these, the majority (84.6%) experienced a reduction in parenteral support. A high incidence (72.7%) of nonpathological pancreatic enzyme elevation was observed in patients treated with teduglutide. These elevations were often dose dependent and were not associated with any clinical signs of acute pancreatitis or abnormal imaging findings. CONCLUSION: This study highlights the need for further investigations into the long-term safety of teduglutide and the importance of closely monitoring amylase and lipase levels in patients undergoing treatment with teduglutide.

High-dose intravenous glucocorticoid induces hyperamylasemia: a case series.

BACKGROUND: Glucocorticoids have many side effects, and high-dose intravenous application may cause rare adverse reactions such as hyperamylasemia. The aim of this study is to explore the clinical characteristics, treatment, and prognosis of hyperamylasemia induced by high-dose intravenous glucocorticoids. CASE PRESENTATION: Four Asian female patients, aged between 26 and 71 years, were diagnosed with hyperamylasemia after intravenous administration of high-dose glucocorticoid. Amylase levels were elevated to varying degrees in all patients, but the peaks were below three times the upper limit of normal, and imaging showed no significant pancreatic abnormalities. Two patients developed abdominal pain, which was resolved by inhibition of pancreatic secretion, while the other patients were asymptomatic. Two patients were discharged after a significant decrease in amylase levels, while the other two were discharged after improvement of the primary disease. CONCLUSION: High-dose intravenous glucocorticoid can cause hyperamylasemia, which should be given enough attention by clinicians. Etiological differentiation of hyperamylasemia should be emphasized in clinical practice, especially when the diagnosis of acute pancreatitis is not clear.

Brigatinib Dose Rationale in Anaplastic Lymphoma Kinase-Positive Non-Small Cell Lung Cancer: Exposure-Response Analyses of Pivotal ALTA Study.

Brigatinib is a kinase inhibitor indicated for patients with advanced anaplastic lymphoma kinase-positive non-small cell lung cancer who progressed on or are intolerant to crizotinib. Approval was based on results from a randomized, dose-ranging phase II study (ALK in Lung Cancer Trial of AP26113 (ALTA)). Despite an apparent dose-response relationship for efficacy in ALTA, an exposure-response relationship was not discernable using static models driven by time-averaged exposure. However, exposure-response modeling using daily time-varying area under the concentration curve as the predictor in time-to-event models predicted that increasing the dose of brigatinib (range, 30 mg once daily (q.d.) to 240 mg q.d.) would result in clinically meaningful improvements in progression-free survival (PFS), intracranial PFS, and overall survival. Grade ≥ 2 rash and amylase elevation were predicted to significantly increase with brigatinib exposure. These results provided support for a favorable benefit-risk profile with the approved dosing regimen (180 mg q.d. with 7-day lead-in at 90 mg) versus 90 mg q.d.

Acute pancreatitis associated with lamivudine therapy for chronic B hepatitis.

Hyperamylasemia is a common complication during lamivudine use. We report a case of a pancreatitis following lamivudine therapy. A careful monitoring of amylase levels during treatment with lamivudine is discussed, mainly in the first weeks, considering the cost of this exam and further complication.

Acute pancreatitis associated with lamivudine therapy for chronic B hepatitis

Hyperamylasemia is a common complication during lamivudine use. We report a case of a pancreatitis following lamivudine therapy. A careful monitoring of amylase levels during treatment with lamivudine is discussed, mainly in the first weeks, considering the cost of this exam and further complication.

Propofol-induced hyperamylasaemia in a general intensive care unit.

This study examined the incidence of hyperamylasaemia, in the absence of other plausible causes of pancreatic dysfunction, in intensive care unit (ICU) patients who received propofol. One-hundred-and-seventy-two consecutive patients of a general ICU who stayed for more than 24 hours were studied. Patients with a diagnosis consistent with elevated serum amylase levels at admission were excluded from the study, as were patients who had received medications known to raise serum amylase levels. Forty-four patients 53 +/- 20 years of age and median duration of ICU stay of five days (range two to 55) were eligible. Thirty of those, aged 54 +/- 21 years and median duration of ICU stay of five days (range two to 27) received continuous infusion of propofol for sedation (maximum dose 45 microg/kg/min). Of the 30 patients who received propofol, 16 (53%) developed hyperamylasaemia (125 to 466 IU/l) after two to nine days of continuous infusion. Liver and kidney function remained normal throughout the observation period. Of the 14 patients who did not receive propofol (aged 51 +/- 18 years), only two (14%) developed hyperamylasaemia, a significantly lower incidence (P = 0.021). Propofol infusion is associated with biochemical evidence of pancreatic injury. Amylase levels monitoring of propofol-sedated patients is warranted.

Hyperamylasemia and acute pancreatitis following anticholinesterase poisoning.

A prospective study was undertaken to find the incidence of hyperamylasemia and acute pancreatitis in patients with anticholinesterase poisoning. This was done by serial estimation of total serum amylase and pancreatic imaging by ultrasonography and confirmed, if necessary, by computerized tomography. Anticholinesterase poisoning was caused by either ingestion or accidental exposure to organophosphates or carbamates; it was diagnosed when patients presented with features of cholinergic crisis, depressed serum butyrylcholinesterase activity of >50% and showed improvement following administration of atropine alone or atropine and 2-PAM. All the patients admitted with anticholinesterase poisoning between July 2001 and June 2005 were prospectively studied for elevated serum amylase. The serum amylase levels were estimated daily up to 10 days in survivors and in nonsurvivors till they survived. Ultrasonography of the abdomen was carried out in all to find swelling of the pancreas. Computerized tomography was undertaken in those who had a swollen pancreas or whose serum amylase levels were elevated significantly (> or =800 S.U). Of the 86 patients enrolled, 79 were taken up for analysis as data were incomplete in 7. Of the 79 patients, serum amylase was found to be elevated that is, >200 S.U. in 37 patients (46.95%). In three patients it was 800 S.U. One of them showed swollen pancreas on ultrasonography, which was confirmed by computerized tomography. This patient had ingested propoxyfur. In the other two patients, evidence of acute pancreatitis was not observed (on autopsy in one who died and on imaging in the other who survived). They had ingested chlorpyrifos. There was no significant correlation between the nature of the compounds (organophosphate or carbamates), inhibition of serum BUChE at admission, duration and severity of cholinergic syndrome and increase and time course of increase in serum amylase. Except for fenthion, significant persistent increase in serum amylase was not observed with individual compounds. The other associated abnormalities were polymorphonuclear leukocytosis (TLC >11,000/cumm) in all 37 patients who had elevated amylase, hyperglycemia (6/37) and, elevated transaminases (6/37). Mild elevation of serum amylase is common in patients with anticholinesterase poisoning. However, acute pancreatitis is rare.

Hyperamylasaemia and acute pancreatitis in paracetamol poisoning.

BACKGROUND: Hyperamylasaemia and even acute pancreatitis have been reported in patients with paracetamol poisoning. AIMS: To describe the incidence, clinical characteristics, and prognostic implications of hyperamylasaemia in paracetamol poisoning. PATIENTS: Six hundred and two patients transferred to a specialized unit with severe paracetamol poisoning and 212 unselected patients admitted from the local region. METHODS: Retrospective study based on hospital charts. The optimum threshold of serum amylase to discriminate non-survivors was identified. RESULTS: An elevated serum amylase (>100 U/L) occurred in 28 of the unselected patients (13%), in 218 of the transferred patients (36%), and in 118 of 148 patients (80%) with fulminant hepatic failure. Only 33 cases of paracetamol-associated acute pancreatitis were diagnosed. A threshold serum amylase of 150 U/L to discriminate non-survivors had sensitivity 76%, specificity 85%, positive predictive value 33%, and negative predictive value 97%. In a logistic regression analysis, a serum amylase > 150 U/L was associated with an excess mortality (odds ratio 5.0, 2.6-9.7). CONCLUSIONS: Hyperamylasaemia is frequent in patients with paracetamol poisoning, whereas clinical acute pancreatitis occurs rarely. The incidence of hyperamylasaemia increases with the degree of hepatic dysfunction. A serum amylase exceeding 1.5 times the upper normal limit indicates a poor prognosis.