Background: Biological therapy is currently widely used to treat IBD. Infliximab, adalimumab and golimumab are currently licensed anti-TNF therapies. Biosimilar anti-TNF monoclonal antibodies are increasingly used. Anti-TNF therapies are widely used and their adverse effects are well characterised, and may cause significant morbidity and mortality in a small proportion of exposed patients. Gastroenterologists need to understand the mechanisms for these effects, recognise these swiftly and manage such events appropriately. Aim:To cover the range of potential adverse reactions as a result of biologic therapy and specifically management of these events. Methods: A Medline and Pubmed search was undertaken. Search terms includedwere "anti-TNF," "infliximab" or "adalimumab" or "golimumab" combined with the keywords "ulcerative colitis" or "Crohn's disease" or "inflammatory bowel disease" and then narrowed to articles containing the keywords "complications," "side effects" or "adverse events" or "safety profile." International guidelines were also reviewed where relevant.Results: Adverse events discussed in this review include infusion reactions, blood disorders and infections (including bacterial, viral, fungal and opportunistic infections) as well as autoimmune, dermatological disorders, cardiac and neurological conditions. Malignancies including solid organ, haematological and those linked to viral disease are discussed. Conclusions:Anti-TNF therapy has wide-ranging effects on the immune system resulting in a spectrum of potential adverse events in a small proportion of patients.Research advances are improving the understanding, recognition and management of these adverse events.

BackgroundPotassium ethylenediaminetetraacetic acid (EDTA) is a sample tube anticoagulant used for many laboratory analyses. Gross potassium EDTA contamination of blood samples is easily recognised by marked hyperkalaemia and hypocalcaemia (1-3). Subtle potassium EDTA contamination, however, is a relatively common often unrecognised erroneous cause of spurious hyperkalaemia (2). This has the potential to adversely affect patient care and waste healthcare resources (4,5).In addition to hyperkalaemia and hypocalcaemia, potassium EDTA contamination may also cause hypomagnesaemia (1,2) and hypozincaemia (2). There are, however, no data on the prevalence of EDTA contamination as a cause of hypocalcaemia, hypomagnesaemia and hypozincaemia. We therefore audited the prevalence of EDTA contamination as a cause of hypocalcaemia, hypomagnesaemia and hypozincaemia over a 1-month period. MethodsFollowing a recent service evaluation (2), we routinely measure EDTA in serum samples from patients with unexplained hyperkalaemia (serum potassium > 6.0 mmol ⁄ l).In addition, over a 1-month period EDTA concentrations were measured in hypocalcaemic (serum adjusted calcium < 2.0 mmol ⁄ l), hypomagnesaemic (serum magnesium < 0.7 mmol ⁄ l) and hypozincaemic (serum zinc < 11 lmol ⁄ l) serum samples.Blood samples for routine serum biochemistry, plasma glucose and routine haematology are respectively collected into Sarstedt serum ⁄ z4 gel tubes, S U M M A R YBackground: Potassium ethylenediaminetetraacetic acid (EDTA) is a sample tube anticoagulant used for many laboratory analyses. Gross potassium EDTA contamination of blood samples is easily recognised by marked hyperkalaemia and hypocalcaemia. However, subtle contamination is a relatively common, often unrecognised erroneous cause of spurious hyperkalaemia. Potassium EDTA contamination may also cause hypomagnesaemia and hypozincaemia. There are, however, no data on the prevalence of EDTA contamination as a cause of hypocalcaemia, hypomagnesaemia and hypozincaemia. Methods: Following a recent service evaluation, we measure EDTA in serum samples from patients with unexplained hyperkalaemia (serum potassium > 6.0 mmol ⁄ l). In addition, over a 1-month period EDTA concentrations were measured in hypocalcaemic (serum adjusted calcium < 2.0 mmol ⁄ l), hypomagnesaemic (serum magnesium < 0.7 mmol ⁄ l) and hypozincaemic (serum zinc < 11 lmol ⁄ l) serum samples. Results: Ethylenediaminetetraacetic acid contamination was detected in 31 samples, nine of which were detected by our routine screening programme. The remaining 22 samples represented 14.3% (19 ⁄ 133) of hypocalcaemic samples, 4.8% (5 ⁄ 104) of hypomagnesaemic samples and 1.4% (2 ⁄ 139) of hypozincaemic samples. A total of 25 ⁄ 31 (80.6%) of patients were re-bled, of which 23 ⁄ 25 (92%) results normalised. Conclusions: Factitious hyperkalaemia, hypocalcaemia and hypomagnesaemia caused by potassium EDTA contamination in our studies are relatively common, and if unrecognised may adversely affect patient care and waste scarce healthcare reso...

Background: Endoscopy within 24 h of admission (early endoscopy) is a quality standard in acute upper gastrointestinal bleeding (AUGIB). We aimed to audit time to endoscopy outcomes and identify factors affecting delayed endoscopy (>24 h of admission). Methods: This prospective multicentre audit enrolled patients admitted with AUGIB who underwent inpatient endoscopy between November and December 2017. Analyses were performed to identify factors associated with delayed endoscopy, and to compare patient outcomes, including length of stay and mortality rates, between early and delayed endoscopy groups. Results: Across 348 patients from 20 centres, the median time to endoscopy was 21.2 h (IQR 12.0-35.7), comprising median admission to referral and referral to endoscopy times of 8.1 h (IQR 3.7-18.1) and 6.7 h (IQR 3.0-23.1), respectively. Early endoscopy was achieved in 58.9%, although this varied by centre (range: 31.0-87.5%, p ¼ 0.002). On multivariable analysis, lower Glasgow-Blatchford score, delayed referral, admissions between 7:00 and 19:00 hours or via the emergency department were independent predictors of delayed endoscopy. Early endoscopy was associated with reduced length of stay (median difference 1 d; p ¼ 0.004), but not 30-d mortality (p ¼ 0.344). Conclusions: The majority of centres did not meet national standards for time to endoscopy. Strategic initiatives involving acute care services may be necessary to improve this outcome.

Serum calcium, 25-hydroxyvitamin D (25OHD) and parathyroid hormone (PTH) were measured in umbilical cord blood samples taken from 54 White and 22 South Asian babies born in the UK during the summer months. South Asians had lower serum calcium (p < 0.0027) and 25OHD (p < 0.0002) than Whites. Serum PTH was low in all subjects, but South Asians had relatively higher concentrations of serum PTH (p < 0.001) than Whites. The lower vitamin D and calcium in South Asian newborns is not associated with secondary hyperparathyroidism as previously reported but may still explain their increased prevalence of neonatal hypocalcaemia and rickets.

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