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Volume 83 - 2020 - Fasc.4 - Letters

Co-existence of eosinophilic esophagitis and Barrett’s esophagus: a possible association?

A 37-year-old female with no relevant previous medical history was referred to Gastroenterology consultation because of long-history of heartburn and dysphagia. She described frequent episodes of heartburn and dysphagia for solids and liquids since childhood and there was history of some episodes of food impaction. Esophagogastroduodenoscopy revealed reflux esopha- gitis and a circumferential segment of salmon-colored mucosa at distal esophagus from 27 to 34 cm from incisors, suggestive of Barrett’s esophagus (BE). This diagnosis was confirmed in biopsies of distal esophagus, which revealed intestinal metaplasia, focal papillomatosis and intra-epithelial eosinophilia with 80 eosinophils/ high-power field (HPF). Clinical and endoscopic findings were consistent with gastroesophageal reflux disease (GERD) and pantoprazole twice daily was started, with symptom improvement. After one year, esophagogastroduodenoscopy was repeated. In addition to the segment of BE previously identified from 27 to 34 cm from incisors (Figure 1A), concentric rings and longitudinal furrows were identified proximally from 20 to 27 cm (Figure 1B). Biopsies of distal esophagus expectedly demonstrated intestinal metaplasia without dysplasia (Figure 2A), whereas biopsies of proximal esophagus were remarkable for intra-epithelial eosino- philia with 15 eosinophils/HPF (despite treatment with pantoprazole) associated with acanthosis, spongiosis and basal cell hyperplasia (Figure 2B). These findings were consistent with simultaneous occurrence of eosinophilic esophagitis (EoE) and BE. Esophageal manometry did not reveal motor abnormalities. Despite symptomatic improvement with pantoprazole, occasional episodes of food impaction still occurred, most with spontaneous resolution. There was one, however, which required endoscopic resolution. Therapy with fluticasone was started with no more episodes of food impaction for several months.


Longstanding gastrointestinal symptoms after COVID-19

At present the world is engulfed by SARS-CoV-2 and while the situation is fairly controlled in some countries it is still spiralling out of control in many others. We are still learning about the short and long term impact of COVID 19 and its management. We observe that a portion of infected patients report gastrointestinal (GI) symptoms probably because enterocytes are (besides the lungs) rich in angiotensin converting enzyme (ACE)-2 receptors making them an important interaction site (1,2). I my clinical practice I noticed post COVID 19 patients consulting because of severe and persistent gastro-intestinal symptoms, two of which I will briefly describe to you.


Rituximab as second-line therapy after new direct antiviral agents in peripheral neuropathy Hepatitis C Virus related : always correct therapeutic approach?

Nowadays, Hepatitis C virus (HCV) infection remains a major public health problem in many countries (1). The cryoglobulinemic vasculitis HCV-related may involve small vessels of skin, kidney and peripheral nervous system. The treatment of peripheral neuropathy (PN) HCV related is based on corticosteroids, plasmapheresis, rituximab and new direct antiviral agents therapy (DAAs) (2). In May 2015, a male of 54-years old was referred to our Department for recurrent palpable purpura on legs, asthenia, arthralgias, sicca syndrome (dry mouth and eyes), paresthesias, burning and pain in all limbs. The clinical and laboratory parameters are reported in table 1. In peripheral blood, the cytometry detected monoclonal kB cells lymphocytes (MBL), CD20+, CD10-, CD38, CD23-, CD5+, CD22+, CD79b+, FMC7+, CD81+, CD200-. Computed tomography scan showed slight hepatomegaly, normal spleen, no lymphoadenophaties. The Electromyography (EMG) highlighted axonal motor-sensitive neuropathy to all limbs. From June to August 2015, therapy with sofosbuvir 400 mg/day, plus ribavirin 1000 mg/day started. After one month, HCV- RNA viremia was undetectable. At the end of therapy, clinical regression of purpura, asthenia and arthralgias were achieved. In August 2016 a complete immunological response has been reported (see table 2). However, in the peripheral blood MBL was still detectable and the EMG reported no remission of neuropathy.