Fasciola Hepatica Mimicking Malignancy on 18F-Fluorodeoxyglucose-Positron Emission Tomography/Computed Tomography.

A 48-year-old female with complaints of gastrointestinal symptoms such as abdominal pain, fatigue, vomiting, nausea, and weight loss was diagnosed with neuroendocrine tumor after removal of a 2 mm lesion from the stomach with endoscopic biopsy. Her magnetic resonance imaging that was performed due to on-going symptoms showed multiple linear hypointense lesions in the liver. Positron emission tomography/computed tomography (PET/CT) scan was performed for differential diagnosis, which showed high fluorodeoxyglucose (FDG) uptake in these lesions. Clinical and laboratory findings revealed the final diagnosis as Fasciola hepatica. The imaging features of this case is presented to aid in differentiating this infectious disease from malignancy and avoid misdiagnosis on FDG-PET/CT.

Alveolar echinococcosis of the liver: a single center experience.

INTRODUCTION: In humans, alveolar echinococcosis (AE) of the liver is caused by canine tapeworm called Echinococcus multilocularis. The disease is most prevalent in the northern hemisphere and in the eastern part of Turkey. OBJECTIVES: The aim of the study was to review the natural history of AE and its clinical and radiological features. PATIENTS AND METHODS: The retrospective study involved 23 patients (10 men, 13 women), aged 34-75 years with AE who had been referred to our liver disease clinic in the past 4 years. Only patients with pathologically proven AE were included in the study. The sociodemographic, clinical, and radiological features of AE were also evaluated. RESULTS: The main laboratory characteristics of AE included mild eosinophilic leukocytosis with hypergammaglobulinemia, elevated C-reactive protein levels, near-normal liver transaminases, and increased levels of cholestatic enzymes and immunoglobulin E. Eight patients (35%) had hepatitis B e antigen-negative hepatitis B infection. Budd-Chiari syndrome was identified in 3 of 23 patients (13%). Eighty-three percent of the patients had a seropositive test result for AE, and approximately one-third of the patients had distant metastasis. Surgical treatment was administered in 4 patients. Four patients died due to complications during follow-up. CONCLUSIONS: Patients with AE have numerous complications and advanced disease at the time of diagnosis. The clinical picture of AE comprises a number of hepatic and extrahepatic disturbances related both to destructive and mass effects of the tapeworm.

Peripheral lymphocyte DNA damage and oxidative status after eradication therapy in patients infected with Helicobacter pylori.

INTRODUCTION: Helicobacter pylori infection has been shown to cause inflammation, increased production of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. However, the effect of eradication treatment on DNA damage in patients infected with H. pylori is unclear. OBJECTIVES: The objective of this study was to investigate the effect of eradication treatment on peripheral DNA damage and oxidative status in patients wth H. pylori infection. PATIENTS AND METHODS: The study involved 42 patients positive for H. pylori (Hp+) and 25 patients negative for H. pylori (Hp-). Peripheral lymphocyte DNA damage was assessed using the alkaline comet assay and plasma oxidative status was determined. Measurements were conducted at baseline and 2 weeks after eradication treatment. RESULTS: The total antioxidant status (TAS) was lower in Hp+ patients than in Hp- patients (P <0.05), while the total oxidant status (TOS), oxidative stress index (OSI), and peripheral lymphocyte DNA damage were higher (P <0.001 for all parameters). TOS, OSI, and peripheral lymphocyte DNA damage were significantly lower after eradication treatment (P <0.001 for all parameters), while TAS was significantly higher (P <0.05). There was no correlation between TOS, OSI, peripheral lymphocyte DNA damage, and TAS and the histopathological degree of antral gastric inflammation in the Hp+ group (P >0.05). CONCLUSIONS: Our results suggest that H. pylori eradication significantly decreases peripheral lymphocyte DNA damage and oxidative stress. Eradication treatment might help prevent the development of gastric cancer in patients with H. pylori infection.

Peripheral lymphocyte DNA damage and oxidative stress in patients with ulcerative colitis.

INTRODUCTION: Ulcerative colitis (UC) is a fairly common chronic inflammatory disorder. Chronic inflammation may contribute to the risk of colorectal cancer through the accumulation of specific products resulting from DNA damage. Previous studies reported that DNA damage and oxidative stress play a significant role in the pathophysiology of UC, but the results are inconsistent. OBJECTIVES: In the present study, we investigated peripheral DNA damage and oxidative stress in patients with UC. PATIENTS AND METHODS: The study included 20 patients with UC and 20 controls. Peripheral lymphocyte DNA damage was measured using the alkaline comet assay. Plasma total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were determined. RESULTS: DNA damage levels, TOS, and OSI were significantly higher in patients with UC than in controls (P <0.001 for all parameters), while TAC was significantly lower (P <0.001). DNA damage was significantly correlated with TOS, TAC, and OSI (r = 0.604, P <0.001; r = -0.593, P <0.001; and r = 0.716, P <0.001, respectively). Moreover, TAC levels were significantly correlated with TOS and OSI (r = 0.604, P <0.001; r = -0.399, P <0.05; and r = -0.513, P <0.05, respectively). CONCLUSIONS: Our results show that increased peripheral DNA damage and oxidative stress seem to be associated with decreased antioxidant levels and thus may in part contribute to the development of colorectal cancer associated with UC.