No serum or radiological findings are specific of WD. Sometimes endoscopy show erosive bulbitis or duodenitis. Immunohistochemistry allows the detection of Tropheryma whipplei in different bodily samples. Differential diagnosis includes rheumatic disease, coeliac disease, sarcoidosis, lymphoma, Addison’s disease and neurologic disorders. Disease identification is essential to avoid immunosuppressive therapy which has been observed to be associated with a rapid clinical deterioration in WD. Our case confirms that WD should be considered as differential diagnosis in patients with gastrointestinal symptoms and arthropathy, especially in middle-aged

men. In contrast with CT suggesting lymphoproliferative CDK inhibitor disease, US showed images consistent with

fat deposits, a feature typically described in Whipple’s disease. Findings of low density, highly fatty lymph nodes with a marked hyperechoic pattern in the mesentery and retroperitoneum may be associated with WD. An appropriate therapy can obtain clinical remission. However, it is well known that clinical relapse after treatment discontinuation may occur in 2-33% of cases after an average time of 5 years. Presently, optimal duration of the antibacterial mTOR inhibitor treatment and follow up strategies are not yet well established. Further studies are needed to clarify these unresolved issues. “
“E. M. Brunt illustrated in her article focusing on nonalcoholic fatty liver disease (NAFLD) the difficulty in giving names to complex entities which are not, or cannot be, fully characterized, particularly when it comes to the combination of pathological/clinical and prognostic

criteria.1 Here, we discuss another issue illustrating the confusion of terms. This concern is minor in terms of public health, but a source of diagnostic problem for liver specialists SB-3CT and important for patients who develop benign hepatocellular nodules. Focal nodular hyperplasia (FNH) is believed to be a nonspecific response to locally increased blood flow. In 1989, Wanless et al. described an entity they called telangiectatic focal nodular hyperplasia (TFNH) occurring in the multiple FNH syndrome as well as in a minority of patients with solitary FNH.2 They mentioned without detail that at the microscopic level, lesions were similar to those observed in hereditary hemorrhagic telangiectasia (HHT). Ten years later, Nguyen et al. described lesions classified as FNH of telangiectatic form.3 At the microscopic scale, the hepatic plates were separated by sinusoidal dilatation, sometimes alternating with areas of marked ectasia. In 2004, Paradis et al. showed that the molecular profile of the TFNH at the DNA, gene, and protein expression level was more similar to that of hepatocellular adenomas (HCAs) than that of typical FNH. Telangiectasia was defined at the microscopic level as areas of sinusoidal dilatation, congestion, and peliosis.