OPTICAL COHERENCE TOMOGRAPHY FINDINGS IN PRESUMED VETERINARY ANTHELMINTIC DRUG-INDUCED RETINAL TOXICITY: A Glimpse into Underlying Mechanism.

PURPOSE: To report optical coherence tomography findings of presumed veterinary anthelmintic drugs (VADs)-induced retinal toxicity that may aid in understanding potential pathogenic mechanisms. METHODS: This is a retrospective observational case series analysis of patients with vision abnormalities following the accidental or intentional consumption of veterinary anthelmintic drugs. All cases underwent a thorough ophthalmological examination. Moreover, medical records, as well as the initial and follow-up optical coherence tomography images, were thoroughly scrutinized. RESULTS: Four patients were identified (3 men; mean [range] age, 36.5 [22-52] years). Each patient overdosed on one or two of the following VADs: closantel, triclabendazole, praziquantel, pyrantel pamoate, and niclofolan. The most characteristic optical coherence tomography finding was diffuse, granular, hyperreflective lesions throughout the outer retina, which were initially identified in the ellipsoid zone in two cases. At follow-up, optical coherence tomography exhibited regression of hyperreflective lesions and extensive loss of the outer retinal elements in two patients. In addition, the subfoveal outer retinal layers may be partially preserved. CONCLUSION: Some veterinary anthelmintic drugs could be detrimental to the human retina if overdosed, resulting in visual disturbances. Optical coherence tomography revealed the mitochondria-enriched ellipsoid zone where outer retinal damage first appeared on, implying that these medications may harm the retina by inhibiting mitochondrial energy metabolism, as they do to eliminate parasites.

Study of the migration of Fasciola hepatica juveniles across the intestinal barrier of the host by quantitative proteomics in an ex vivo model.

Fasciola hepatica is a trematode parasite that infects animals and humans causing fasciolosis, a worldwide-distributed disease responsible for important economic losses and health problems. This disease is of growing public health concern since parasite isolates resistant to the current treatment (triclabendazole) have increasingly been described. F. hepatica infects its vertebrate host after ingestion of the encysted parasite (metacercariae), which are found in the water or attached to plants. Upon ingestion, newly excysted juveniles of F. hepatica (FhNEJ) emerge in the intestinal lumen and cross the intestinal barrier, reach the peritoneum and migrate to the biliary ducts, where adult worms fully develop. Despite the efforts made to develop new therapeutic and preventive tools, to date, protection against F. hepatica obtained in different animal models is far from optimal. Early events of host-FhNEJ interactions are of paramount importance for the infection progress in fasciolosis, especially those occurring at the host-parasite interface. Nevertheless, studies of FhNEJ responses to the changing host environment encountered during migration across host tissues are still scarce. Here, we set-up an ex vivo model coupled with quantitative SWATH-MS proteomics to study early host-parasite interaction events in fasciolosis. After comparing tegument and somatic fractions from control parasites and FhNEJ that managed to cross a mouse intestinal section ex vivo, a set of parasite proteins whose expression was statistically different were found. These included upregulation of cathepsins L3 and L4, proteolytic inhibitor Fh serpin 2, and a number of molecules linked with nutrient uptake and metabolism, including histone H4, H2A and H2B, low density lipoprotein receptor, tetraspanin, fatty acid binding protein a and glutathione-S-transferase. Downregulated proteins in FhNEJ after gut passage were more numerous than the upregulated ones, and included the heath shock proteins HSP90 and alpha crystallin, amongst others. This study brings new insights into early host-parasite interactions in fasciolosis and sheds light on the proteomic changes in FhNEJ triggered upon excystment and intestinal wall crossing, which could serve to define new targets for the prevention and treatment of this widespread parasitic disease.

Repositioning of the Anthelmintic Drugs Bithionol and Triclabendazole as Transthyretin Amyloidogenesis Inhibitors.

Transthyretin (TTR) is a causative protein of TTR amyloidosis (ATTR amyloidosis), a general term for diseases characterized by deposition of TTR amyloid fibrils in specific organs. ATTR amyloidosis can be ameliorated by stabilization of the TTR tetramer through the binding of small molecules. Here, we show that the clinical anthelmintic drugs bithionol (42) and triclabendazole (43) potently inhibit aggregation of the amyloidogenic variant V30M-TTR. A competitive binding assay using a fluorescence probe showed that the binding affinity of 42 with V30M-TTR was significantly higher than that of the first-in-class drug tafamidis (1), and the binding affinity of 43 was similar to that of 1. The crystallographic and thermodynamic analysis revealed that 42 efficiently occupied the halogen-binding grooves of TTR, resulting in the favorable binding entropy. Multifaceted in vitro studies of anthelmintic drugs have the potential to reposition these drugs as ATTR amyloidosis inhibitors.

[Hepatic tumor or giant liver fascciola?: case report]. / ¿Tumor hepático o Fasciola hepática gigante?: reporte de caso.

Hepatic Fasciola is a frequent disease in the Peruvian highlands. We present a case of hepatic Fasciola from the Andean zone of La Libertad, with symptoms of several months of evolution with pain in the right hypochondrium, jaundice and coluria. An abdominal CT scan was performed, demonstrating a liver mass probable neoplasm, and was referred to the Institute of Neoplastic Diseases. Laboratory tests were completed finding eosinophilia and variable increases in liver function tests. Fascioliasis was presented as a differential diagnosis and a Western Bloot examination was performed confirming its diagnosis. Treatment with 2 cycles of Triclabendazole was started, with a favorable clinical evolution.

Hepatic parasitic abscess resistant to traditional anthelmintics: difficulty of diagnosis and treatment of fascioliasis in the USA.

We report a case of human fascioliasis in the USA that encountered many diagnostic uncertainties. Numerous tests available for detection of fascioliasis were utilised but the diagnosis remained elusive. Confounders included three negative stool ova and parasite examinations, positive hepatitis A virus IgM antibody, cross-reactive false-positive Echinococcus IgG antibody, absence of characteristic image findings and unrevealing liver biopsy. Praziquantel was started as empiric treatment for helminth infections, but was ineffective. Due to the rarity of the disease in the USA, serologic testing and triclabendazole were only available from the Centers for Disease Control and Prevention, which led to a delay in diagnosis and treatment.

Zinc supplementation augments the suppressive effects of repurposed NF-κB inhibitors on ACE2 expression in human lung cell lines.

AIMS: Angiotensin-converting enzyme 2 (ACE2) is a key negative regulator of the renin-angiotensin system and also a major receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Here, we reveal a role for NF-κB in human lung cell expression of ACE2, and we further explore the potential utility of repurposing NF-κB inhibitors to downregulate ACE2. MAIN METHODS: Expression of ACE2 was assessed by Western blotting and RT-qPCR in multiple human lung cell lines with or without NF-κB inhibitor treatment. Surface ACE2 expression and intracellular reactive oxygen species (ROS) levels were measured with flow cytometry. p50 was knocked down with siRNA. Cytotoxicity was monitored by PARP cleavage and MTS assay. KEY FINDINGS: Pyrrolidine dithiocarbamate (PDTC), an NF-κB inhibitor, suppressed endogenous ACE2 mRNA and protein expression in H322M and Calu-3 cells. The ROS level in H322M cells was increased after PDTC treatment, and pretreatment with N-acetyl-cysteine (NAC) reversed PDTC-induced ACE2 suppression. Meanwhile, treatment with hydrogen peroxide augmented ACE2 suppression in H322M cells with p50 knockdown. Two repurposed NF-κB inhibitors, the anthelmintic drug triclabendazole and the antiprotozoal drug emetine, also reduced ACE2 mRNA and protein levels. Moreover, zinc supplementation augmented the suppressive effects of triclabendazole and emetine on ACE2 expression in H322M and Calu-3 cells. SIGNIFICANCE: These results suggest that ACE2 expression is modulated by ROS and NF-κB signaling in human lung cells, and the combination of zinc with triclabendazole or emetine shows promise for clinical treatment of ACE2-related disease.

Fasciola Hepatica Induced Hepatic Abscess Treated with Triclabendazole.

Fascioliasis is a zoonotic disease caused by Fasciola hepatica that infects mainly cattle, sheep, and goats. Humans can be infected by water or aquatic plants contaminated with metacercariae. The authors encountered two cases of F. hepatica infection. One patient reported abdominal discomfort with marked eosinophilia. The other patient had chest discomfort with marked eosinophilia. The abdominal CT images revealed hypodense lesions in the liver. The ultrasonography-guided liver biopsy findings in both patients were indicative of parasitic infections. Serological tests confirmed the definite diagnoses. Both patients were treated with a single dose of triclabendazole, which is the treatment of choice for fascioliasis. These findings suggest that a diagnosis of fascioliasis, particularly in the acute phase, should be considered in patients with abdominal pain, marked eosinophilia, and hypodense hepatic lesions on CT.

Immature Fasciola gigantica: Time-dependent ultrastructural changes following in vivo treatment with triclabendazole.

An in vivo study was carried out to investigate the ultrastructural effects of triclabendazole (TCBZ) on immature Fasciola gigantica in a goat model. Five goats were infected with an oral gavage of 150 metacercarial cysts of F. gigantica and anthelmintic treatment occurred at 4 weeks post infection with an oral dose of 10 mg/kg. They were euthanized at 0 (untreated), 24, 48, 72 and 96 h post treatment (h pt). Juvenile flukes were recovered from each of the goat's liver and processed for transmission electron microscopy (TEM). The untreated control flukes showed normal ultrastructure and no apparent changes were observed at 24 h pt. At 48 h pt, moderate levels of disruption were observed to the tegument and minor changes to the sub-tegument which included widespread blebbing and disruption of apical tegumental membrane, swollen mitochondria, reduced number of secretory bodies, swelling of basal infolds leading to severe vacuolation, and relatively mild disruption to the subtegumental muscle fibres, parenchyma and tegumental cells, whereas the gastrodermal cells appeared less affected. By 72 h pt, sloughing of the tegumental syncytium was evident leading to the exposure of the basal lamina and the disruption was severe in the subtegument too. At 96 h pt, the flukes were totally devoid of tegument and the disruption was extremely severe, distorting the ultrastructure of the entire fluke's body. The results of the present study revealed that the flukes showed time-dependent progressive disruption to the internal tissues which became increasingly severe over time pt. This is the first study to detail the time-scale and impacts on ultrastructural morphology of the in vivo TCBZ treatment of the immature tropical liver fluke, Fasciola gigantica.

Flukicide efficacy against Fasciola hepatica of Triclabendazole and Nitroxynil in cattle of the central valley of Chile / Avaliação da eficácia de triclabendazol e nitroxinil para o tratamento da infeção por Fasciola hepatica em bovinos do Vale Central do Chile

Abstract On a farm with permanent history of fasciolasis a study was performed aimed to know the efficacy of triclabendazole (TCBZ) and then to contrast with that of nitroxynil. Thirty-nine cattle naturally infected with Fasciola hepatica were randomly allocated into 4 experimental groups: Group 1 (control) was left untreated. Group 2 was treated with of 12 mg/kg body weight (bw) of TCBZ by oral route. Group 3 treated with 24 mg/kg bw TCBZ orally. Group 4 was treated with 10 mg/kg bw of nitroxynil subcutaneously. The anthelmintic efficacy was calculated as the percentage of reduction in faecal egg count (FEC) at 14 and 28 d post-treatment. Results indicated that there were no significant differences in the percentage of FEC reduction between control group and the groups treated with 12 or 24 mg/kg of TCBZ. On the contrary, the treatment with nitroxinyl significantly reduced the FEC and decreased the percentage of positive animals. In conclusion, Fasciola hepatica is reported for first time as resistant to TCBZ in Chile, which highlights the need of rotating drugs and assessing the efficacy of the administered drug in order to avoid the selection of resistant worms.

Resumo Em uma fazenda com histórico de fasciolose permanente, foi realizado um estudo com o objetivo de conhecer a eficácia do triclabendazol (TCBZ) e depois contrastar com o do nitroxinil. Trinta e nove bovinos naturalmente infectados com Fasciola hepatica foram distribuídos aleatoriamente em 4 grupos experimentais: Grupo 1 (controle), sem tratamento. O grupo 2 foi tratado com 12 mg/kg de peso vivo (PV) do TCBZ por via oral (VO). Grupo 3 tratado com 24 mg/kg de PV TCBZ por VO. O grupo 4 foi tratado com 10 mg /kg de PV Nitroxinil via subcutânea. A eficácia anti-helmíntica foi calculada comparando a percentagem de redução na contagem de ovos fecais (FEC) 14 e 28 dias pós tratamento. Não houve diferença significativa na porcentagem de redução FEC entre o grupo controle e os grupos tratados com 12 ou 24 mg/kg de TCBZ. Entretanto, o tratamento com nitroxinil reduziu significativamente o FEC e diminuiu a porcentagem de animais positivos. Em conclusão, a Fasciola hepatica é relatada pela primeira vez como resistente ao TCBZ no Chile, o que destaca a necessidade de realizar uma rotação em relação aos medicamentos anti-helmínticos e avaliar a eficácia do mesmo, a fim de evitar a seleção de vermes resistentes.

In Vitro Drug-Drug Interaction Potential of Sulfoxide and/or Sulfone Metabolites of Albendazole, Triclabendazole , Aldicarb, Methiocarb, Montelukast and Ziprasidone.

BACKGROUND: The use of polypharmacy in the present day clinical therapy has made the identification of clinical drug-drug interaction risk an important aspect of drug development process. Although many drugs can be metabolized to sulfoxide and/or sulfone metabolites, seldom is known on the CYP inhibition potential and/or the metabolic fate for such metabolites. OBJECTIVE: The key objectives were: a) to evaluate the in vitro CYP inhibition potential of selected parent drugs with sulfoxide/sulfone metabolites; b) to assess the in vitro metabolic fate of the same panel of parent drugs and metabolites. METHODS: In vitro drug-drug interaction potential of test compounds was investigated in two stages; 1) assessment of CYP450 inhibition potential of test compounds using human liver microsomes (HLM); and 2) assessment of test compounds as substrate of Phase I enzymes; including CYP450, FMO, AO and MAO using HLM, recombinant human CYP enzymes (rhCYP), Human Liver Cytosol (HLC) and Human Liver Mitochondrial (HLMit). All samples were analysed by LC-MS-MS method. RESULTS: CYP1A2 was inhibited by methiocarb, triclabendazole, triclabendazole sulfoxide, and ziprasidone sulfone with IC50 of 0.71 µM, 1.07 µM, 4.19 µM, and 17.14 µM, respectively. CYP2C8 was inhibited by montelukast, montelukast sulfoxide, montelukast sulfone, tribendazole, triclabendazole sulfoxide, and triclabendazole sulfone with IC50 of 0.08 µM, 0.05 µM, 0.02 µM, 3.31 µM, 8.95 µM, and 1.05 µM, respectively. CYP2C9 was inhibited by triclabendazole, triclabendazole sulfoxide, triclabendazole sulfone, montelukast, montelukast sulfoxide and montelukast sulfone with IC50 of 1.17 µM, 1.95 µM, 0.69 µM, 1.34 µM, 3.61 µM and 2.15 µM, respectively. CYP2C19 was inhibited by triclabendazole and triclabendazole sulfoxide with IC50 of 0.25 and 0.22, respectively. CYP3A4 was inhibited by montelukast sulfoxide and triclabendazole with IC50 of 9.33 and 15.11, respectively. Amongst the studied sulfoxide/sulfone substrates, the propensity of involvement of CY2C9 and CYP3A4 enzyme was high (approximately 56% of total) in the metabolic fate experiments. CONCLUSION: Based on the findings, a proper risk assessment strategy needs to be factored (i.e., perpetrator and/or victim drug) to overcome any imminent risk of potential clinical drug-drug interaction when sulfoxide/sulfone metabolite(s) generating drugs are coadministered in therapy.

Identification and characterization of the Fasciola hepatica sodium- and chloride-dependent taurine transporter.

The parasitic liver fluke Fasciola hepatica infests mainly ruminants, but it can also cause fasciolosis in people, who ingest the metacercariae encysted on plants. The drug of choice to treat fasciolosis is triclabendazole (TBZ), which has been on the market for several decades. This is also true for the other available drugs. Accordingly, drug-resistant flukes have been emerging at an increasing rate making it desirable to identify alternative drug targets. Here, we focused on the fact that adult F. hepatica persists in the hostile environment of the bile ducts of infected organisms. A common way to render bile acids less toxic is to conjugate them to taurine (2-aminoethanesulfonic acid). We cloned a transporter from the solute carrier-6 (SLC6) family, which was most closely related to the GABA-transporter-2 of other organisms. When heterologously expressed, this F. hepatica transporter supported the high-affinity cellular uptake of taurine (KM = 12.0 ± 0.5 µM) but not of GABA. Substrate uptake was dependent on Na+- and Cl- (calculated stoichiometry 2:1). Consistent with the low chloride concentration in mammalian bile, the F. hepatica transporter had a higher apparent affinity for Cl- (EC50 = 14±3 mM) than the human taurine transporter (EC50 = 55±7 mM). We incubated flukes with unconjugated bile acids in the presence and absence of taurine: taurine promoted survival of flukes; the taurine transporter inhibitor guanidinoethansulfonic acid abolished this protective effect of taurine. Based on these observations, we conclude that the taurine transporter is critical for the survival of liver flukes in the bile. Thus, the taurine transporter represents a candidate drug target.

"Liver fluke": conceptos actuales sobre fascioliasis / Liver fluke: update on fascioliasis

Fascioliasis is a parasitic disease produced mainly by the fluke Fasciola hepatica. The human infection is mainly due to the accidental intake of metacercariae present in watercress and/or contaminated water. The human disease is uncommon in Chile, despite the high prevalence of animal infection, which affects almost the entire national territory and determines high economic and productive impacts. Human fascioliasis can manifest like acute or chronic phase of the disease (in Chile, the majority in chronic phase) and its identification requires a high index of suspicion, in individuals with abdominal pain, hepatomegaly and eosinophilia, where the epidemiological background of watercress ingestion is usually present. Diagnosis usually requires the integration of egg visualization in stools, serology and imaging studies. The treatment of choice with triclabendazole is usually highly effective and safe.

La fascioliasis es una enfermedad parasitaria producida principalmente por el trematodo Fasciola hepática. La infección en el hombre, quien es un huésped accidental, se debe principalmente a la ingesta de metacercarias presentes en berros y/o aguas contaminadas. La enfermedad en humanos es infrecuente en Chile, a pesar de la alta prevalencia de infección animal, que afecta a casi todo el territorio nacional y determina un alto impacto económico y productivo. La fascioliasis humana puede manifestarse en fase aguda o crónica (en Chile, la mayoría en fase crónica) y su identificación requiere un alto índice de sospecha, en individuos con dolor abdominal, hepatomegalia y eosinofilia, donde el antecedente epidemiológico de ingesta de berros suele estar presente. El diagnóstico, habitualmente requiere la integración de la visualización directa de huevos en las deposiciones, estudios de serología e imágenes. El tratamiento de elección con triclabendazol, habitualmente es altamente efectivo y seguro.

Fascioliasis-a rare cause of hepatic nodules.

Fascioliasis is a zoonotic disease that can sometimes affect humans. It presents with non-specific signs and symptoms which makes it difficult to establish an early definitive diagnosis. This can be particularly true in non-endemic countries where a high degree of suspicion is needed to make the diagnosis. Another confounding factor is that many of the initial complains and findings are very similar to those of malignancy. We report a case of an otherwise healthy 47 year-old male presenting with abdominal pain, night-time sweating, anorexia, weight loss and loose stools that had several hepatic nodules visible in the abdominal CT scan. Although the initial hypothesis was hepatic malignancy or liver metastasis of unknown primary neoplasm, the workup performed led us to the correct diagnosis. He was treated successfully for hepatic fascioliasis, with a full recovery.

Fasciola hepatica-a "Diver" in the Biliary Tree.

Fasciola hepatica is an endemic trematode that affects millions of people worldwide. The human being can be an accidental host through consumption of contaminated food or water. The authors present a case of hepatic fascioliasis in a 69-year-old Portuguese woman who recently traveled from Egypt, Brazil, and India.

An Innovative High-Throughput Screening Approach for Discovery of Small Molecules That Inhibit TNF Receptors.

Tumor necrosis factor receptor 1 (TNFR1) is a transmembrane receptor that binds tumor necrosis factor or lymphotoxin-alpha and plays a critical role in regulating the inflammatory response. Upregulation of these ligands is associated with inflammatory and autoimmune diseases. Current treatments reduce symptoms by sequestering free ligands, but this can cause adverse side effects by unintentionally inhibiting ligand binding to off-target receptors. Hence, there is a need for new small molecules that specifically target the receptors, rather than the ligands. Here, we developed a TNFR1 FRET biosensor expressed in living cells to screen compounds from the NIH Clinical Collection. We used an innovative high-throughput fluorescence lifetime screening platform that has exquisite spatial and temporal resolution to identify two small-molecule compounds, zafirlukast and triclabendazole, that inhibit the TNFR1-induced IκBα degradation and NF-κB activation. Biochemical and computational docking methods were used to show that zafirlukast disrupts the interactions between TNFR1 pre-ligand assembly domain (PLAD), whereas triclabendazole acts allosterically. Importantly, neither compound inhibits ligand binding, proving for the first time that it is possible to inhibit receptor activation by targeting TNF receptor-receptor interactions. This strategy should be generally applicable to other members of the TNFR superfamily, as well as to oligomeric receptors in general.

DIAGNOSIS AND THERAPY OF LIVER FLUKE (FASCIOLOIDES MAGNA) INFECTION IN FALLOW DEER (DAMA DAMA) IN SERBIA.

Giant liver fluke ( Fascioloides magna ) infection is an important health problem of cervids in southeastern Europe. We measured the prevalence and intensity of infection with F. magna in a fenced area near the Danube River in the South Backa District of Serbia. Parasitologic, pathomorphologic, and histopathologic examinations were conducted from November 2007 to February 2008, beginning with a population of 127 adult fallow deer ( Dama dama ). After a positive diagnosis, therapy with triclabendazole-medicated corn was applied. Deer were treated at four baiting stations, using medicated feed providing triclabendazole at an estimated dose of 10-14 mg/kg of body weight per deer. Treatment lasted for 7 d in early February 2008 and an additional 7 d 2 wk later. For the complete success of pharmacotherapy it was necessary to prevent any contact of deer with the snail intermediate host ( Galba truncatula ). Intervention in the habitat, removing grass and low vegetation, and draining ponds reduces the possibility of contact. Six months after the treatment, livers of hunted deer were reddish, with fibrous tracks; pigmentation and cysts in the parenchyma were surrounded by a fibrous capsule and their fecal samples contained no eggs of F. magna . Over the following years, livers of hunted deer were negative, and the last control cull in March 2015 confirmed complete absence of infection. We reconfirmed the presence of giant liver flukes in fallow deer in Serbia, apparently the result of natural spread across the Danube from Hungary and Croatia. We also report that the treatment of deer with triclabendazole-medicated corn is an effective method for administration of therapeutic doses of drug in semicaptive deer. Interventions in the environment are necessary to prevent recontact of deer with habitats used by the snail intermediate host, and enable the success of the therapy.

North American paragonimiasis: epidemiology and diagnostic strategies.

Paragonimiasis is a zoonotic, food-borne trematode infection that affects around 23 million people in Asia, Africa and the Americas. North American paragonimiasis, caused by Paragonimus kellicotti, is a common infection of crustacean-feeding mammals in parts of the USA and Canada. Although infection rates in crayfish are very high in some areas, human infections are rare and depend on the consumption of raw or undercooked crayfish. Human infections can be easily prevented and treated, but proper diagnosis of paragonimiasis is a problem. Paragonimus lung flukes often cause serious disease symptoms before they produce eggs that may be detectable in sputum, bronchoalveolar lavage, stool or histological sections by microscopy or PCR. Antibodies against selected Paragonimus proteins are detectable as early as 2-3 weeks after infection. Therefore, antibody serology is the most promising diagnostic approach for paragonimiasis in North America and elsewhere.

Fasciola hepatica infection at a University Clinic in Turkey.

INTRODUCTION: We aimed to analyze the approaches to the diagnosis and treatment of patients with fascioliasis in light of current literature. METHODOLOGY: Thirty-nine patients with fascioliasis admitted to the Surgery Clinic of Dicle Medical Faculty (Turkey) were included in this study. The demographic, clinical, diagnostic, treatment and outcome data were analyzed retrospectively. RESULTS: Abdominal pain (n = 37; 95%) and eosinophilia (n = 31; 79%) were the most common findings. Twenty-seven patients were diagnosed by clinical and radiological findings. Patients were treated with triclabendazole. Thirty-six (92.4%) of the patients improved after medical treatment. CONCLUSIONS: The presence of typical clinical, laboratory and radiological findings is sufficient for diagnosis. Triclabendazole administration is often an effective treatment, with improvements occurring over the course of a few months.

[A case of fascioliasis in the intrahepatic duct with concurrent clonochiasis].

The main causes of biliary obstruction are stones and cancers. Fascioliasis is a very rare case which causes biliary obstruction. Fascioliasis is a zoonosis caused by Fasciola hepatica which infects herbivores like sheep and cattle. F. hepatica lives in the biliary system or the liver parenchyma of a host. In Korea, the occurrence of this infection in human is very rare and only few cases have been reported. A 32-year-old male presented with upper abdominal pain and jaundice. His laboratory finding revealed elevated liver transaminases. Abdomen CT scan showed mild left intrahepatic bile duct dilatation. On ERCP, adult F. hepatica worms were found and were thus removed. Concurrently, clonorchiasis was diagnosed by stool exam and serologic enzyme-linked immunosorbent assay test. Clonorchiasis was treated with praziquantel. Herein, we report a case of intrahepatic bile duct dilatation due to F. hepatica infection with concurrent Clonorchis sinensis infestation.

Severe iron deficiency anemia and marked eosinophilia in adolescent girls with the diagnosis of human fascioliasis.

Human fascioliasis (HF), caused by the common liver fluke Fasciola hepatica, is an endemic infection in many parts of tropical countries. HF can also be seen in some of the non-tropical countries. This report describes two girls with severe iron deficiency anemia and eosinophilia, who were diagnosed as HF. The infection was successfully eliminated with the administration of triclabendazole. No side effects or recurrence was observed after the treatment. It should be kept in mind that marked eosinophilia with severe iron deficiency anemia should alert pediatricians to the possibility of F. hepatica infection.