Introduction

Acute pancreatitis (AP) is one of the most common gastroenterological diseases requiring admission to the hospital. The main etiological factors of AP are gallstones and excessive alcohol consumption, but rarer causes, such as hypercalcemia, should keep on mind. Only few cases are reported in the literature, and the severity of hypercalcaemia-induced acute pancreatitis is not known.

Aims & Methods

We aim to assess the occurrence and severity of hypercalcaemia-induced AP and compare it with the clinical characteristics of AP caused by other etiological factors. We collected patients from the Hungarian Acute Pancreatitis Registry, Hungarian GOULASH study and the Europe-wide EASY study, who had AP and had a serum calcium level above 2.6 mmol/l. Patients were divided into three groups: hypercalcemia-induced AP, where no other etiology than hypercalcemia were present, mixed etiology group, where both hypercalcemia and other etiologies were revealed and the control group with normal serum calcium level. Propensity score matching adjusted by age, sex, diabetes, lipid disorder, previous pancreatic disease was made and several outcome parameters were analyzed during the statistical analysis. Hypercalcemic cases were divided into 3 subgroups based on the level of serum calcium: mild (2.6< >3.0 mmol/l), moderate (3.0 < >3.5 mmol/l) or severe hypercalcemia (>3.5 mmol/l).

Results

1.02% of our AP patients (19/1867) had clear hypercalcemic etiology and 3.75 % (70/1867) of the patients had mixed etiology, 1778 patients were in the control group. There was no difference in the mean ages of the patients in the three groups (57.3± 16.3 and 56.1 ± 20.1 vs. 55.1 ± 14.6 years). Severe AP was significantly more frequent in patients with hypercalcemia-induced AP compared to the control group [21.05% (4/19) vs 6.13% (109/1778); odds ratio: 4.08 (95% CI, 1.08-15.38)]. Renal failure was more frequent in hypercalcemic etiology compared to AP patients with normal serum calcium level [27.27% (3/11) vs 5.35% (95/1776); odds ratio: 6.63, (95% CI, 1.36-32.35)]. There was no significant difference in CRP, amylase, lipase, WBC, creatinine, length of hospital stay, mortality, intensive care admission, the presence of pancreatic necrosis, pseudocysts, and other organ failure between the hypercalcemic or mixed etiology and the control groups. There was no significant difference in the severity of AP between the mixed etiology and normal serum calcium groups. The outcome of acute pancreatitis was not influenced by the severity of hypercalcemia within the hypercalcemic group.

Conclusion

Hypercalcemia-induced AP has a higher risk for developing into severe AP and renal failure compared to other etiology.

Introduction

Hepatic encephalopathy (HE) after Transjugular Intrahepatic Portosystemic Shunt (TIPS) affect 35-50% of patients. The use of prophylactic agents (Lactulose and Rifaximin) to prevent post-TIPS HE remains controversial and currently not recommended by professional guidelines. Our aim was to assess real world practice and identify potential predictors for post-TIPS HE and benefit from post-TIPS prophylaxis.

Aims & Methods

Retrospective cohort study of patients undergoing TIPS at the Tel-Aviv Medical Center (2016-2024). The primary outcome was overt HE, with secondary outcomes of liver transplantation (LT) and mortality.

Results

Seventy-nine patients underwent TIPS, median age was 60 years and 52% were male. Primary liver disease was metabolic dysfunction-associated steatohepatitis (MASH) in 34%, viral (20%), and alcohol-related liver disease (ALD) (16.5%). Indications for TIPS were variceal bleeding (52%) and refractory ascites (38%). Prior to the procedure 31% had ≥ 1 episodes of HE, 21.5% were treated with Lactulose and/or Rifaximin, and 58% were on betablocker treatment. At the time of the procedure, the patient's Child-Pugh score was A/B/C in 19%/66%/11% respectively, with a median MELD-Na of 10.9. Median follow up was 22.75 months. Overall, 22 patients died during follow-up and 8 underwent liver transplantation. 45 patients (57%) developed post-TIPS HE, 60% of them during the first three months. Early post-TIPS HE treatment was given to 49%: 10% Lactulose, 5% Rifaximin, and 34% both. Among those patients, 44% were previously (pre-TIPS) on HE treatment. Development of HE was not predicted by pre-or post-TIPS MELD-Na or Child-Pugh score, TIPS diameter, postTIPS gradient, or post-procedure ammonia levels. Rates of HE also did not differ according to initial prophylaxis treatment (59% with treatment, 56% without, p=1). Pre-TIPS AST and albumin were associated with post-TIPS HE (36.6U/L vs. 60.44 U/L, p=0.03; 34.6g/dl vs. 31.8g/dl, p = 0.05). Prior beta-blocker treatment was associated with post-TIPS HE (14% vs 32%, p = 0.01) but not varices as the indication for TIPS. Mortality rate was not affected by the occurrence of post-TIPS HE (28% among those who developed HE vs. 26% among those who didn't, p = 1).

Conclusion

Early post-TIPS preventive treatment was mostly given to patients previously treated with Lactulose/Rifaximin, however it did not affect the rate of post-TIPS HE. Development of HE did not increase mortality.

References

1. Wolfgang el al. ASSLD practice Guidance, Hepatology (2024)
2. Yao el al.J Gastrointestin Liver Dis (2015)