Clinical Case Summary

Drug-induced liver injury is an adverse effect of many pharmaceutical agents. Alverine citrate, an antispasmodic agent found in the fixed-dose combination Meteospasmyl (alverine citrate and simethicone), is widely used in functional gastrointestinal disorders. To date, only three cases are published in the literature. We report a case, with strong evidence, including a rechallenge confirming the causality.
Patient Observation: A 43-year-old woman presented with biliary-type abdominal pain. Her medical history was limited to hypertension treated with bisoprolol with no alcohol use or recent medication. Abdominal ultrasound revealed uncomplicated cholelithiasis; liver tests were normal. Alverine citrate was prescribed for symptomatic relief. Within two weeks, she developed jaundice and fatigue with a normal clinical examination. Blood tests showed severe hepatocellular injury: ALT and AST were 22× and 39× ULN, bilirubin was 274 µmol/L, and GGT/ALP were mildly elevated. Viral and autoimmune panels were negative. Imaging excluded biliary obstruction. Liver biopsy revealed portal inflammation with eosinophilic infiltrates, suggestive of immunoallergic hepatitis. The discontinuation of the drug led to normalization of liver enzymes. 3 years later, the patient was inadvertently re-exposed to alverine citrate, triggering a reproducible episode of acute hepatitis, thereby confirming causality. Diagnostic probability was assessed with the RUCAM score (12, "highly probable") and Naranjo scale (8, "probable"). Only three prior cases of alverine citrate-induced hepatitis, none of which reported a confirmed rechallenge. Although liver biopsy is not routinely required in DILI, it was essential here for diagnostic clarification.
Alverine citrate should be recognized as a rare cause of acute hepatitis. This case confirms its hepatotoxic potential and underscores the importance of early recognition and drug withdrawal to prevent recurrence.

References

1. RUCAM Scale: https://clincasequest.hospital/rucam-scale/
2. Naranjo Scale: https://proeurodilinet.eu/wp-content/uploads/2019/03/Causality-assessment-training-course-15-MARCH-.pdf
3. Couzigou P et al. Hepatitis and Alverine Citrate. J Hepatol. 1997. https://www.sciencedirect.com/science/article/abs/pii/S0168827897801870
4. Turkish case report. Turk J Gastroenterol. 2004. https://pubmed.ncbi.nlm.nih.gov/15259090/
5. Korean case report. Korean J Hepatol. 2010. https://pubmed.ncbi.nlm.nih.gov/20375645/
6. Simethicone safety review. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033443/
7. Zhang X et al. Histopathologic Manifestations of Drug-induced Hepatotoxicity. Clin Liver Dis. 2013.

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.

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.

Clinical Case Summary

A 72-year-old patient with a history of atrial fibrillation on treatment and cirrhosis, presented with subjective fevers and abdominal distention for 2 months. An initial laboratory work-up showed an inflammatory syndrome and a prothrombin level of 40 %. The rest of the work-up was unremarkable. A computed tomography (CT) scan of the abdomen showed dysmorphic liver with signs of portal hypertension and abundant ascites with micronodular infiltration of the greater omentum.
Paracentesis showed ascitic fluid (AF) with total nucleated cells 2400 with 5% neutrophils and 87% lymphocytes and protein levels at 40. Cytology was negative for malignancy.
Initially, the patient was considered for diagnostic laparoscopy to investigate the persistent abdominal symptoms. However, in light of the current epidemiological context, marked by a heightened incidence of tuberculosis in the region, a systematic workup for tuberculosis was prioritized. Direct examination and culture for acid-fast bacilli (AFB) were negative, however Xpert Mtb/Rif was positive. standard chest X-ray showed a normal parenchyma with a small right pleural effusions. Thoracentesis was done and pleural fluid AFB culture was negative.
He was started on isoniazid, rifampin, pyrazinamide and ethambutol and was discharged with a close follow up.

Introduction

EUS-guided Gallbladder Drainage (EUS-GBD) with Lumen Apposing Metal Stent (LAMS) is a standard treatment for management of acute cholecystitis (AC) in unfit-for-surgery patients. Gallbladder Perforation is standardly considered as a contraindication to EUS-GBD.

Aims & Methods

This series aims at exploring outcomes of EUS-GBD in patients with AC and contained perforation (cp-AC).
All consecutive patients undergoing EUS-GBD in a single tertiary institution between 2020 and 2024 were enrolled in a prospective registry (PROTECT, ClinicalTrials.gov NCT04813055). Patients with cp-AC were included in this series, when presenting gallbladder wall rupture with adjacent encapsulated fluid collections. Baseline demographics and technical details were registered together with Technical success, Clinical success, Adverse Events (AEs), Recurrence and Survival evaluated every 60 days.

Results

From a prospective cohort of 48 EUS-GBD, 19 patients presented with cp-AC (median age 71 [62-78], male 42.1%, Charlson Comorbidity Index of 8 [7-9.8]). Acute cholecystitis was iatrogenic in 79% of these cases (ERCP with metal stenting in 14 and TACE in 1). Reason to avoid surgery was underlying malignancy in 89.5% and comorbidities in 15.8%. Amongst underlying malignancies, the most frequent one was Pancreatic Adenocarcinoma.
Ascites was present in 26.3% of cases. All procedures were performed transduodenally, with an operative luminal space of 31 [25 – 36] mm and a median tract thickness of 6 [5-8] mm.
A 10 mm Hot Axios LAMS was used in 95% of cases, and the release was free-hand in 89% and over-the-wire after former distention in 11% of cases. Antibiotic prophylaxis and coaxial double-pigtail plastic stents were adopted in 95% of cases.
Technical success was 100%. Clinical success was 94.7%, with a statistically significant 7-days reduction of white blood cells (p=0.0017 ) and C Reactive Protein (p=0.0067) .
AEs were registered in 21% of cases, severe/fatal in 11%.
Of note, 2 AEs (1 fatal) were related to additional attempts of draining liver abscesses adjacent to the GBD.
Five patients (27%) underwent additional endoscopic procedures for peroral cholecystoscopy, GBD clearance and LAMS removal, while 2 (11%) patients experienced uneventful LAMS migration.
Median hospital stay was 8 [6-13] days and median time to chemotherapy was 26 [19-56] days for those who were candidate to oncological treatment (N=10).
After a median follow-up of 254 [56-454] days, no AC recurrence was registered.

Conclusion

In the context of AC, contained perforation with adjacent collections does not seem to represent a contraindication to EUS-GBD with LAMS, despite the additional complexity related to a thicker interluminal distance. Management of large adjacent abscesses should involve multidisciplinary management and might require percutaneous drainage.

Clinical Case Summary

Introduction: Pancreatic involvement in non-Hodgkin lymphomas is rare and often mimics pancreatic adenocarcinoma. We report a case in which endoscopic ultrasound (EUS) was pivotal in establishing the correct diagnosis.
Case Presentation: A 39-year-old male, a chronic smoker, presented with jaundice, anorexia, and fever. Laboratory findings revealed hepatocellular injury and cholestasis (total bilirubin: 15 mg/dL; GGT: 868 U/L; ALP: 679 U/L). CT imaging (Figure 1) demonstrated a large retroperitoneal mass infiltrating both the pancreas and adjacent vascular structures, associated with ascites and omental thickening. EUS (Figure 2) revealed a hypoechoic, poorly defined mass in the head and body of the pancreas (65×55 mm), with evidence of vascular invasion. A fine-needle biopsy (22G) was performed. Endoscopic Retrograde Cholangiopancreatography (ERCP) confirmed malignant duodenal stenosis. Histopathology was consistent with diffuse large B-cell lymphoma (DLBCL). The patient was initiated on R-CHOP chemotherapy (Rituximab, Cyclophosphamide, Hydroxydaunorubicin, Oncovin, Prednisone) after baseline staging. Eight months later, follow-up EUS (Figure 3) showed no residual pancreatic mass.
Discussion: In atypical pancreatic masses—especially in younger patients with systemic symptoms—EUS is essential for tissue acquisition and accurate differential diagnosis. Unlike adenocarcinoma, pancreatic lymphomas respond well to chemotherapy.
Conclusion: Early use of EUS in atypical pancreatic masses can prevent misdiagnosis, reduce time to treatment, and avoid unnecessary surgical interventions.

References

Figure 1 - retroperitoneal mass infiltrating pancreas and vascular structures
Figure 2 - hypoechoic, poorly defined mass in the head and body of the pancreas
Figure 3 - no residual pancreatic mass