Gastrointestinal consequences of cancer treatment: evaluation of 10 years' experience at a tertiary UK centre.

OBJECTIVE: Up to 90% of patients treated for pelvic cancers experience chronic gastrointestinal (GI) symptoms. This study characterises this patient cohort at a single centre, addressing a paucity of publications reporting 'real-world' experiences. METHOD: Outpatient referrals, from oncology to the gastroenterology and nutrition services, at a tertiary London hospital from 2006 to 2016, were retrospectively identified. Patient characteristics, reported symptoms, investigations, diagnoses, response to therapeutics and follow-up were recorded. RESULTS: Of 269 patients referred, 81% were within the latter 5 years. A total of 260 patients had diagnoses of pelvic cancers (prostatic (52%), cervical (19%) and endometrial (19%)). Among 247 treated with radiotherapy, the median time from radiotherapy to symptom onset was 8 months. Common symptoms were rectal bleeding (51%), diarrhoea (32%), faecal urgency (19%) and pain (19%). Patients underwent a median of three investigations including lower GI endoscopy (86%), thyroid function tests (33%) and glucose hydrogen breath test (30%). Diagnoses included radiation proctopathy (39%), colonic polyps (16%), pelvic floor dysfunction (12%), bile acid malabsorption (BAM) (8%), small intestinal bacterial overgrowth (SIBO) (8%), vitamin D deficiency (7%) and iron deficiency (7%). Among 164 discharged patients, the time to discharge was 7 months, after a median of two appointments. CONCLUSIONS: This unique patient group reports a complex mix of symptoms and requires specialist review and consideration of often uninvestigated diagnoses (pelvic dysfunction, BAM, SIBO and nutritional deficiencies). Such patients are often overlooked, compared with those suffering many other chronic GI disorders. Further reports from non-dedicated centres treating patients with pelvic radiation disease will aid in understanding of secondary GI diagnoses and variation in practice.

Diagnosis of chronic anaemia in gastrointestinal disorders: A guideline by the Italian Association of Hospital Gastroenterologists and Endoscopists (AIGO) and the Italian Society of Paediatric Gastroenterology Hepatology and Nutrition (SIGENP).

Anaemia is a common pathologic condition, present in almost 5% of the adult population. Iron deficiency is the most common cause; other mechanisms can be involved, making anaemia a multi-factorial disorder in most cases. Anaemia being a frequent manifestation in the diseases of the gastrointestinal tract, patients are often referred to gastroenterologists. Furthermore, upper and lower endoscopy and enteroscopy are pivotal to the diagnostic roadmap of anaemia. In spite of its relevance in the daily clinical practice, there is a limited number of gastroenterological guidelines dedicated to the diagnosis of anaemia. For this reason, the Italian Association of Hospital Gastroenterologists and Endoscopists and the Italian Society of Paediatric Gastroenterology, Hepatology and Nutrition commissioned a panel of experts to prepare a specific guideline on anaemia and its diagnostic roadmap in the gastroenterological scenario. The panel also discussed about the potential involvement of gastroenterologists and endoscopists in the management of patients with anaemia, with particular attention to the correct use of investigations. The panel paid particular attention to practical issues with the aim to support gastroenterologists in their clinical practice when dealing with patients with anaemia.

Novel type of hepatitis B virus mutation: replacement mutation involving a hepatocyte nuclear factor 1 binding site tandem repeat in chronic hepatitis B virus genotype E.

The genetic diversity of hepatitis B virus (HBV) strains has evolved through mutations such as point mutations, deletions or insertions, and recombination. We identified and characterized a novel type of mutation which is a complex of external insertion, deletion, and internal duplication in sequences from one of six patients with chronic hepatitis B virus genotype E (HBV/E). We provisionally named this mutation a "replacement mutation"; the core promoter upstream regulatory sequence/basic core promoter was replaced with a part of the S1 promoter covering the hepatocyte nuclear factor 1 (HNF1) binding site, followed by a tandem repeat of the HNF1 site. A longitudinal analysis of the HBV population over 6 years showed the clonal change from wild-type HBV/E to replacement-mutant type, resulting in a lower hepatitis B (HB) e antigen titer, a high HBV DNA level in serum, and progression of liver fibrosis. In an in vitro study using a replication model, the replacement-mutant HBV showed higher replication levels than the wild-type HBV/E replicon, probably mediated by altered transcription factor binding. Additionally, this HNF1 site replacement mutation was associated with excessive HB nucleocapsid protein expression in hepatocytes, in both in vivo and in vitro studies. This novel mutation may be specific to HBV genotype E, and its prevalence requires further investigation.