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DOI:10.2214/AJR.05.0716
AJR 2006; 187:W236-W237
© American Roentgen Ray Society

Central Hepatic Involvement in Paragonimiasis: Appearance on CT and MRI

Alice Yao, Nancy Hammond, Rameez Alasadi and Paul Nikolaidis

University of Iowa College of Medicine Iowa City, IA 52242
Northwestern University Feinberg School of Medicine Chicago, IL 60611

A 61-year-old woman presented to her primary care physician with cough and shortness breath. The patient had no abdominal pain, diarrhea, urticaria, or jaundice and no recent travel history. After treatment for presumed bronchitis, the patient's presenting symptoms persisted and she developed chest pain. A contrast-enhanced CT of the chest showed a left pleural-based consolidation with loculated left pleural fluid. In addition to the pulmonary findings, the CT examination showed nonspecific hepatic lesions. A subsequent triple-phase liver CT further delineated these lesions as branching, grouped, hypodense tubular structures within the central portion of the right and left lobes of the liver (Fig. 6A). MRI of the abdomen was then performed, which showed low-signal-intensity structures with peripheral enhancement (Fig. 6B). Lesions were barely conspicuous on T2-HASTE sequences, demonstrating only faint hyperintensity. MR cholangiopancreatography (MRCP), including RARE, thin-section HASTE, and navigator-triggered 2D PACE (prospective acquisition correction) sequences, showed that the lesions did not clearly communicate with the biliary tree (Fig. 6C).


Figure 1
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Fig. 6A 61-year-old woman presenting with cough and shortness of breath with ill-defined hepatic abnormalities on chest CT. Patient subsequently underwent triplephase liver CT and MRI/MR cholangiopancreatography (MRCP). Contrast-enhanced axial CT image obtained during portal venous phase shows centrally located hypodense tubular structures in right and left hepatic lobes (arrows). Based on CT, it was uncertain if structures communicated with biliary tract, so MRI/MRCP was subsequently performed.

 

Figure 2
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Fig. 6B 61-year-old woman presenting with cough and shortness of breath with ill-defined hepatic abnormalities on chest CT. Patient subsequently underwent triplephase liver CT and MRI/MR cholangiopancreatography (MRCP). Axial T1-weighted fat-saturated gradient-echo gadolinium-enhanced sequences show centrally located low-signal-intensity structures with peripheral enhancement (arrows) involving right and left hepatic lobes.

 

Figure 3
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Fig. 6C 61-year-old woman presenting with cough and shortness of breath with ill-defined hepatic abnormalities on chest CT. Patient subsequently underwent triplephase liver CT and MRI/MR cholangiopancreatography (MRCP). Navigator-triggered 2D PACE (prospective acquisition correction) sequences show no communication of hepatic abnormalities with biliary tree.

 
Diagnostic sonography-guided thoracentesis was performed showing a high proportion of eosinophils in the pleural fluid. Further laboratory tests showed a normal WBC with 31% eosinophils and normal transaminase, alkaline phosphatase, and bilirubin levels. Serology was positive for Paragonimus IgG antibodies.

The patient was treated uneventfully for paragonimiasis with a standard course of praziquantel. The patient's pretherapy brain MRI was unremarkable for cerebral involvement. Follow-up CT at 4 weeks showed significant reduction in the centrally located abnormal, branching hypodense structures.

Paragonimiasis is a parasitic infectious disease caused by the Paragonimus genus, a lung fluke. It is found worldwide but is endemic in areas of Asia as the result of consumption of raw freshwater crab or crayfish. Human infection in the United States is rare [1]. Paragonimiasis classically presents with pulmonary manifestations caused by the migration pattern of the juvenile worms [2]. Ectopic infection may occur and most commonly involves the brain and subcutaneous tissue. Involvement of the liver is rare.

Symptoms of paragonimiasis correspond to parasitic migration and maturation. Pulmonary involvement produces cough, hemoptysis, and chest pain. Ectopic infection patterns include cutaneous manifestations due to migration into the skin or cerebral manifestations due to migration to the brain. Rare migration from the abdominal cavity into the liver causes hepatic damage.

Definitive diagnosis is achieved by the detection of parasitic eggs in the sputum or feces. The serologic quantification of Paragonimus-specific antibodies employs the enzyme-linked immunosorbent assay (ELISA) test and is widely used for the diagnosis of paragonimiasis. The measurement of antibody titers is also useful in assessing response to therapy.

CT findings of hepatic paragonimiasis have been documented in two case reports in the English literature. One case showed a cystic lesion with internal septations proven to be a parasitic granuloma [3]. The second case showed multiple small, low-attenuating lesions representing eosinophilic abscesses [4]. MRI findings were documented in one case report in the Korean literature. This case revealed cystic lesions with low signal intensity on T1- and high signal intensity on T2-weighted images [5]. The hepatic lesions in these cases were located peripherally, suggesting capsular invasion by the parasites [5, 6]. This case shows unusual involvement of the central portion of the liver.

The differential diagnosis of low-attenuating, tubular lesions with peripheral enhancement in the liver includes cholangitis, pyogenic abscess, cholangiocarcinoma, and primary sclerosing cholangitis. In the setting of the patient with eosinophilia or risk factors for parasitic infection or both, additional considerations include hepatic involvement by fascioliasis, clonorchiasis, and paragonimiasis.

This case is an unusual presentation of paragonimiasis involving the central aspect of the liver with imaging characteristics differing from the few other reported cases to date.


References
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References
 

  1. DeFrain M, Hooker R. North American paragonimiasis: case report of a severe clinical infection. Chest 2002;121 : 1368-1372[Abstract/Free Full Text]
  2. Yokagawa M. Paragonimus and paragonimiasis. Adv Parasitol 1965; 3:99 -158[Medline]
  3. Rha SE, Ha HK, Kim JG, et al. CT features of intraperitoneal manifestations of parasitic infestation. AJR1999; 172:1289 -1292[Abstract/Free Full Text]
  4. Singcharoen T, Rawd-Aree P, Baddeley H. Computed tomography findings in disseminated paragonimiasis. Br J Radiol1988; 61:83 -86[Medline]
  5. Kim EA, Juhng SK, Kim HW, et al. Imaging findings of hepatic paragonimiasis: a case report. J Korean Med Sci2004; 19:759 -762[Medline]
  6. Hu X, Feng R, Zheng Z, et al. Hepatic damage in experimental and clinical paragonimiasis. Am J Trop Med Hyg1982; 31:1148 -1155[Abstract/Free Full Text]

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