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

Introduction: Wilson’s disease is a rare inherited liver disorder caused by copper metabolism dysfunction,whereas Crohn’s disease is a chronic inflammatory bowel condition.The co-occurrence of both conditions in an adolescent is extremely rare and becomes particularly noteworthy when associated with severe complications.
Case presentation: We report a 17-year-old male with cirrhotic Wilson’s disease,stable on D-penicillamine, who developed severe anal pain and bloody diarrhea.On proctologic examination,he had hemorrhoids, a s crotal fissure,and a non-draining anal fistula.
Laboratory investigations revealed severe anemia (Hb 4.4 g/dL),leukopenia,and elevated C-reactive protein. Colonoscopy showed multiple ileocolic ulcers on edematous mucosa, suggestive of active Crohn’s disease, confirmed by histopathological examination of biopsies. Pelvic MRI identified a grade II active, intersphincteric, abscessed perianal fistula. Antibiotic therapy was initiated accordingly. The patient was treated with high-dose intravenous corticosteroids for three weeks, followed by oral tapering, leading to significant clinical and laboratory improvement. However, during hospitalization, he developed disseminated intravascular coagulation (DIC) with thrombotic microangiopathy, requiring transfusion of fresh frozen plasma.His condition improved favorably thereafter
Discussion: The coexistence of Wilson’s and Crohn’s diseases is extremely rare. This case stands out for the onset of severe Crohn’s in a patient with chronic liver disease, a complex perianal fistula needing multidisciplinary care,and DIC with thrombotic microangiopathy—likely from systemic inflammation. It highlights the diagnostic and therapeutic challenges in adolescents with multiple chronic illnesses

Conclusion: The association between Wilson’s disease and Crohn’s disease is exceedingly rare. This case emphasizes the need for a multidisciplinary approach in managing complex patients, particularly when faced with severe complications.

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

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

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

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.