Fasciola hepatica: The Difficult Process From Clinical Suspicion to Diagnosis, From Diagnosis to Treatment

To the Editor: Fasciola hepatica (FH) should be considered in the differential diagnosis of eosinophilia, especially in areas with inadequate health services and limited access to healthcare. This parasite is a cause of severe liver and biliary disease, so suspect it in areas with contaminated water and plants.1,2 A 14-year-old male patient living in an area with poor sanitary conditions near a stream presented with abdominal pain, nausea and fever. Physical examination revealed tenderness in the right upper quadrant and palpation of the liver. Laboratory results showed that liver enzymes were elevated aspartate aminotransferase 138 U/L, alanine aminotransferase 210 U/L, while gamma-glutamyl transferase and bilirubin levels were normal. Complete blood count revealed a WBC count of 24.030/mm³, eosinophil rate of 64%, C-reactive protein 50 mg/L and erythrocyte sedimentation rate of 70 mm/hour. Abdominal ultrasonography showed a hydropic gallbladder with a thickened, edematous wall and small fluid in the pericholecystic area. The patient was referred to the pediatric gastroenterology service with a presumptive diagnosis of eosinophilic cholecystitis and started on empirical cefotaxime-metronidazole. Stool samples were negative for parasites. Follow-up ultrasonography showed heterogeneous liver parenchyma with peripheral hypoechoic areas, increased periportal echogenicity, and 7–8 enlarged lymph nodes. Tests for FH, Schistosoma, Strongyloides, Trichinella, Ascaris, Toxocara, hydatid cyst, ameba, and brucella were performed due to eosinophilia. Although the patient’s acute phase reactants improved and she had no active complaints, the leukocytosis and eosinophilia persisted. The FH IgG (indirect hemagglutination) test was positive at 1/640. A diagnosis of acute FH (hepatic phase) was made and metronidazole was started as triclobendazole was not available locally. After obtaining triclobendazole from abroad, treatment was started at a dose of 10 mg/kg/day. The eosinophilia resolved by the third month, and the abdominal ultrasound findings normalized by the sixth month. The family screening showed elevated eosinophil levels in the sister, though she had no symptoms. The FH IgG (indirect hemagglutination) test result was 1/1280; triclobendazole was prescribed. The differential diagnosis of fascioliasis includes cholecystitis, cholangitis, ruptured hydatid cyst, liver abscess, malignancy, viral hepatitis, toxocariasis, schistosomiasis, ascariasis and strongyloidiasis. The diagnosis of fascioliasis may often be overlooked due to multiple differential diagnostic options, nonspecific findings and low incidence of infection and the diagnosis is usually delayed.3 In our case, although the necessary investigations were performed on the 5th day of the patient’s hospitalization, the diagnosis and treatment process took approximately 45 days due to practical obstacles such as serologic test results and obtaining the necessary drugs for treatment. Furthermore, the patient’s distance from the hospital and limited access to healthcare services further prolonged the treatment process. This illustrates how challenging and time-consuming the diagnostic process for endemic parasitic diseases such as fascioliasis can be. It can be even longer when clinical awareness is inadequate and diagnostic methods are not applied in a timely manner. Therefore, detailed questioning of patients’ dietary habits and environmental risk factors should increase the suspicion of fascioliasis with findings such as eosinophilia and serologic tests should be performed at the earliest possible period.