New Therapies for Primary Hyperlipidaemia

Primary hyperlipidemias include a heterogeneous set of monogenic and polygenic conditions characterized by a strong family aggregation, severe forms of hypercholesterolemia and/or hypertriglyceridemia, appearance early on life and a high risk of cardiovascular events and/or recurrent pancreatitis. In real life, a small proportion of the primary hyperlipidemia cases is recognized and treated properly. Our goal is to present an update of current and upcoming therapies for patients with primary hyperlipidemia. Recently, new lipid lowering medications have obtained FDA and/or EMA authorization. These drugs target metabolic pathways, including (ATP)-citrate lyase (bempedoic acid), PCSK9 (inclisiran), apo CIII (volanesorsen) and ANGPTL3 (volanesorsen), that have additive effects with the actions of the currently available therapies (i.e. statins, ezetimibe or fibrates). We discuss the potential clinical indications for the novel medications. To conclude, the addition of these new medications to the therapeutic options for primary hyperlipidemia patients may increase the likelihood to achieve the treatment targets. Also, it could be a safer alternative for subjects with side effects for the currently available drugs.

P-EGS30 Audit of the management of patients presenting with gallstone pancreatitis during the COVID-19 pandemic

Background In the UK around 50% of cases of pancreatitis are caused by gallstones. BSG guidelines recommend ERCP is undertaken within 72h of onset of pain and patients should undergo definitive treatment with cholecystectomy if fit enough during the index admission or within two weeks of discharge to avoid the risk of potentially fatal recurrent pancreatitis. A national audit in 2015 showed that 34.2% of patients receive definitive treatment. During the first COVID-19 wave our surgical service was forced to modify practice including more conservative/non operative management potentially increasing the possibility of recurrent pancreatitis and thus complications. Methods We performed a retrospective audit of patients presenting to our unit with gallstone pancreatitis during the first wave of the COVID-19 pandemic from March to August 2020 (COVID) and compared this to the same period in 2019 (pre-COVID). Patients were filtered from a larger dataset of all admissions with an ICD-10 coding of any biliary disease. Patient demographics, admission details, investigations, surgical management and post-operative complications were recorded. This was then audited against the standards in the BSG guidelines for the management of pancreatitis. Results Conclusions There were significant differences in the management of the groups. Most significantly in the number of hot procedures and number of patients receiving definitive treatment, a consequence of the conservative approach during COVID. Our pre-COVID results are similar to our previous audit in 2016; 76% received definitive treatment. Those that didn’t have definitive treatment were generally due to frailty/co-morbidities. Majority of ERCP delays were due to weekend effect. Of the 40 patients who didn’t receive definitive treatment 16 have represented with biliary flares/pancreatitis in the year following the study period highlighting the importance of definitive treatment.

Improvement in Non-Pulmonary CFTR-Related Symptoms in a Patient With p.Phe508del/p.Arg117His (7T) Cystic Fibrosis Treated with Ivacaftor

Introduction: Diagnosis and management of CRMS/CFSPID and cystic fibrosis (CF) with mild phenotypes remains challenging, and this extends to expanding practice with the use of CFTR modulators. Case: We describe a case of an 18-year-old man with p.F508del/p.Arg117His(7T) initially presenting with CRMS/CFSPID. He went on to be diagnosed with pancreatic sufficient CF with minimal lung disease and no bronchiectasis. However, he has had significant CFTR-related symptoms with recurrent pancreatitis and chronic sinusitis. These non-pulmonary symptoms resolved following introduction of the CFTR modulator ivacaftor. Discussion/ Conclusion: Diagnosis and follow up of CRMS/CFSPID infants remains challenging, with most guidelines based on consensus opinion. Care for those with mild CF phenotypes, CRMS/CFSPID and those with CFTR-RD must be individualised, and open dialogue, education and patient centred care is necessary to ascertaining which patients might benefit from management in a multidisciplinary CF clinic and treatment. There may be a role for expanding the use of CFTR modulators to include non-pulmonary manifestations of CFTR dysfunction in some cases.

The Evaluation of Acute Pancreatitis into Acute Recurrent Pancreatitis in Children: The Impact of Etiological Factors

Background: The incidence of acute pancreatitis (AP), acute recurrent pancreatitis (ARP) and chronic pancreatitis (CP) in pediatric population is rising and becomes common clinical problem in gastroenterology. The assessment of morbidity risk factors is necessary to improve the quality of diagnosis, to determine further treatment and to identify groups with poor prognosis of the evolution of AP into ARP and CP. Objectives: The assessment of etiological factors in acute and acute recurrent pancreatitis in children. Material and methods: From January 2015 to November 2017, data on etiological factors responsible for the onset of AP and ARP were collected in a group of pediatric patients hospitalized at the Department of Paediatrics, Gastroenterology and Nutrition, Medical University of Wroclaw, Poland. The study group consisted of 39 patients (27 patients with AP, 11 patients with ARP and 1 with CP). Results: The potential etiological factor was established in 85.2% of children with AP and in 100% of children with ARP. Mutations in the SPINK1 gene were found in 44.4% of children from the ARP group, no mutations in the PRSS1 gene were found in this group. In all patients with a genetic predisposition (SPINK1 mutation) during the first episode of the ARP, coexistence of an additional predisposing factor was found. Conclusions: Patients with ARP require diagnostics towards mutations predisposing to the transition of AP into a chronic disease. The interaction of additional triggers plays a role in the development of pancreatitic inflammatory disease in genetically predisposed individuals.