Introduction

Exocrine pancreatic insufficiency (EPI) is defined as a reduction in the exocrine pancreatic secretion and/or intraluminal activity of pancreatic enzymes below the level that allows normal digestion of nutrients. Currently, diagnosing EPI presents challenges: the most accurate method requires collecting faecal samples for several days to measure faecal fat excretion following a specific diet, while faecal elastase test, although simpler, has a high incidence of false positives.
The study assesses whether measuring lipase in blood, following the ingestion of a standard high-fat meal could provide a more accessible diagnosis of EPI. The hypothesis is that blood lipase increases proportionally to pancreatic secretion in individuals without EPI, allowing differentiation between patients with and without insufficiency.

Aims & Methods

The study's main objective was to investigate whether blood levels of lipase increase after a fatty meal in normal subjects. If blood lipase and lipase secreted by the pancreas have a correlation, by calculating the area under the curve of several determinations of blood lipase in healthy subjects, we could set a normal pattern of lipase secretion. In the future, this pattern can be compared to patients with EPI to test if it can be a screening tool for EPI.
For the study, 10 healthy volunteers were tested. All participants fasted before receiving a test meal designed to stimulate lipase secretion. Blood samples were then taken every 30 minutes for six hours to measure lipase blood levels and calculate the area under the curve (AUC) using the trapezoid method.

Results

The mean (standard deviation) of the maximum and minimum lipase blood levels was 24 (9) and 19 (8) U/L, respectively. The mean percentage change in lipase was 31% (standard deviation 16%). The area under the curve of blood lipase levels between the baseline sample and the sample at 360 minutes had a mean of 7749 (standard deviation 3129) units per litre per hour. The median time to peak lipase was 0 minutes, meaning that the expected peak in blood lipase did not occur after the test meal: in 60% of cases, the highest peak of all measurements was the baseline measurement, with no clear peak in response to the meal in the remaining cases, in contrast with pancreatic secretion into the duodenum.

Conclusion

According to our patient sample, lipase does not increase in the blood after stimulation with a test meal, as occurs in pancreatic lipase secretion into the duodenum. Lipasemia is, therefore, independent of pancreatic secretion and does not seem to be a promising parameter for screening exocrine pancreatic insufficiency.

References

1. Sastre J, Sabater L, Aparisi L. [Physiology of pancreatic secretion]. Gastroenterol Hepatol. 2005;28 Suppl 1:3-9.
2. Gonzalez-Sanchez V, Amrani R, Gonzalez V, Trigo C, Pico A, de-Madaria E. Diagnosis of exocrine pancreatic insufficiency in chronic pancreatitis: (13)C-Mixed Triglyceride Breath Test versus Fecal Elastase. Pancreatology. 2017;17(4):580-5.
3. Sabater L, Ausania F, Bakker OJ, Boadas J, Dominguez-Munoz JE, Falconi M, et al. Evidence-based Guidelines for the Management of Exocrine Pancreatic Insufficiency After Pancreatic Surgery. Ann Surg. 2016.
4. Lohr JM, Dominguez-Munoz E, Rosendahl J, Besselink M, Mayerle J, Lerch MM, et al. United European Gastroenterology evidence-based guidelines for the diagnosis and therapy of chronic pancreatitis (HaPanEU). United European Gastroenterol J. 2017;5(2):153-99.
5. Lundh G. Pancreatic exocrine function in neoplastic and inflammatory disease; a simple and reliable new test. Gastroenterology. 1962;42:275-80.

Clinical Case Summary

Cryptosporidiosis is a gastrointestinal infection caused by the protozoan Cryptosporidium spp. It is typically self-limited in immunocompetent patients. However, in immunocompromised individuals, it can lead to moderate to severe diarrhea and significant morbidity and mortality.¹
We present the case of a 31-year-old woman with a history of Crohn’s disease in remission, who presented with a one-week history of diarrhea (up to 10 bowel movements daily), abdominal pain, and fever (38°C). Laboratory tests revealed an elevated C-reactive protein (CRP), and intestinal ultrasound showed bowel wall thickening, hyperemia and wall disruption, suggestive of an active flare. However, routine stool culture isolated Cryptosporidium, and based on her clinical background, oral paromomycin and azithromycin were initiated, resulting in complete clinical remission.
Cryptosporidiosis is a common parasitic cause of diarrhea, particularly affecting immunocompromised patients, such as those with HIV, cancer or solid organ transplants.²
Although few cases have been described in inflammatory bowel disease (IBD), the immunosuppressive state of these patients may increase the risk of infection. Diagnosing cryptosporidiosis in this population can be challenging, as stool tests detect only about 30% of cases, and the clinical presentation often mimics an IBD flare.³
Treatment is generally supportive and reserved for severe or refractory cases. Nitazoxanide is the drug of choice, and in non-responders, it can be combined with fluoroquinolones or azithromycin. In IBD patients, the decision to initiate specific antiparasitic treatment depends on the degree of immunosuppression and the clinical scenario.⁴
A clear association between IBD and cryptosporidiosis has not been established, but it is crucial to rule out opportunistic gastrointestinal infections in suspected flare-ups before starting specific therapies.
image "Bowel wall thickening, hyperemia, and disruption of the normal layer pattern."

References

(1) Janssen B, Snowden J. Cryptosporidiosis. 2023 Jul 10. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. PMID: 28846353.
(2) Liu B, Schnider A, DeArmond M, Banach DB, Haubrich BA. Cryptosporidiosis in individuals with inflammatory bowel disease: a scoping review protocol. BMJ Open. 2024 Oct 15;14(10):e086529. doi: 10.1136/bmjopen-2024-086529. PMID: 39414295; PMCID: PMC11481120.
(3) Ferreira J, Baden R, Magge S, Cheifetz A. Cryptosporidiosis masquerading as a Crohn's flare. Inflamm Bowel Dis. 2011 Oct;17(10):E133-4. doi: 10.1002/ibd.21811. Epub 2011 Jul 7. PMID: 21739536.
(4) Manthey MW, Ross AB, Soergel KH. Cryptosporidiosis and inflammatory bowel disease. Dig Dis Sci 1997;42:1580–6.

Introduction

Appropriate knowledge of surface features of colorectal polyps is necessary for their adequate management. Data are limited regarding the diagnostic value of surface pattern-based prediction of histology.

Aims & Methods

This nationwide observational cohort study aimed to compare the optical diagnosis based on Kudo’s pit pattern and the histologic result in case of colorectal polyps endoscopically removed during screening colonoscopies.
Data regarding Kudo’s pit pattern of the lesions (Kudo I-V), and the final histological results were obtained from clinical records of screening colonoscopies which were prospectively collected in the registry of Hungarian National Public Health Institute. The level of agreement was characterized by Cohen’s kappa coefficient. The feasibility of optical diagnostics to differentiate neoplastic and non-neoplastic lesions, as well as to identify submucosally invasive cancer (SMIC) were investigated. The potential effects of polyp size and location (left/right colon), and that of timing of colonoscopy (1st period between 2019 and 2021, and 2nd period between 2022 and 2023) were also evaluated.

Results

A total of 8289 polyps removed during screening colonoscopy were registered in the database between 2019 and 2023, from these 7187 were neoplastic (439 SMIC) and 1102 were non-neoplastic. Out of the 1095 serrated polyps 171 contained dysplasia. Non-neoplastic polyps had Kudo I pattern in 7.7%, Kudo II in 48.1%, Kudo III in 40.9%, Kudo IV in 3.2%, and Kudo V in 0.1% of the cases. Neoplastic lesions without submucosal invasion had Kudo I surface pattern in 2.0%, Kudo II in 7.5%, Kudo III in 71.2%, Kudo IV in 17.4%, and Kudo V in 1.7% of the cases, while in case of SMIC, the surface pattern was Kudo I in 0.2%, Kudo II in 0.7%, Kudo III in 15.7%, Kudo IV in 8.9%, and Kudo V in 74.5% of the cases.
Kudo I-II category showed moderate agreement with non-neoplastic lesions (κ=0.440), irrespective of lesion size and location, and timing of screening colonoscopy. The level of agreement was only slight for serrated lesions (κ=0.168). Kudo V category demonstrated substantial agreement (κ=0.722) with SMIC, irrespective of lesion size, location, and timing. SMICs could be identified based on Kudo V category with 74.5% sensitivity, 98.5% specificity, 73.0% positive and 98.6% negative predictive value.

Conclusion

This is the first real-world data obtained from screening colonoscopies of the Hungarian national colorectal screening program. Optical diagnosis might support the differentiation of neoplastic and non-neoplastic lesions and can be especially helpful in identifying SMICs that might require a different management approach.

Clinical Case Summary

Hydatid cyst disease, caused by the Echinococcus parasite, is a zoonotic infection that typically targets the liver, lungs, and nervous system. It commonly occurs in regions such as the Maghreb countries, where it presents a significant health concern. While hydatid cysts in the liver are usually asymptomatic, complications such as cyst rupture, infection, or obstruction can arise, with portal vein involvement being particularly rare. This case report describes a 56-year-old male with a history of surgery for hydatid liver cyst, who presented with portal vein invasion mimicking portal vein thrombosis. Diagnostic imaging, including Color Doppler ultrasound and MRI, revealed a multiloculated cyst in the fourth liver segment with communication to the portal vein, leading to thrombosis and cavernous transformation of the portal vein. Despite the rupture of the hydatid cyst into the portal vein, no anaphylactic shock occurred. Portal vein thrombosis and cavernous transformation due to hydatid cysts represent an exceptional and complex complication of echinococcosis, highlighting the importance of early recognition and appropriate management. Treatment strategies should address both the hydatid liver cyst and associated portal hypertension, with surgical intervention being the cornerstone, including hepatectomies and laparoscopic approaches. This case highlights the necessity of heightened clinical awareness in endemic regions for managing this rare, potentially life-threatening complication.