Background: Data on patients with inflammatory bowel diseases (IBD) who have had 2019 novel coronavirus (SARS-CoV-2) disease (COVID-19) are needed.Aim: To report the clinical characteristics, including gastrointestinal symptoms, of COVID-19 in IBD patients, and to assess the risk of COVID-19 in IBD. Methods:This case series included consecutive IBD patients with laboratory-confirmed COVID-19. Age-adjusted cumulative incidences were compared with the general population in the Madrid region.Results: Through April 8, 12 of 1918 IBD patients were diagnosed with COVID-19. The average age was 52 years, 75% of the patients were female and 58.3% had Crohn's disease. Seven patients (58%) were on maintenance treatment with immunomodulators/biologics, of these four with combined therapy (33%). Eight patients (66%) required hospitalisation (one intensive care unit admission, and two deaths), and four patients were isolated at home. Nine patients had diarrhoea ranging between 4 and 10 loose stools per day (mean 5.4, SD 1.6). In five patients (42%) diarrhoea was a presenting symptom. In two patients, diarrhoea was the only symptom at debut. Cumulative incidence of COVID-19 was 6.2 per 1000 IBD patients. IBD patients had a lower adjusted incidence ratio of COVID-19 (OR 0.74, 95% CI 0.70-0.77; P < 0.001), and a similar associated mortality ratio (OR 0.95, 95% CI: 0.84-1.06; P = 0.36), compared with the general population.Conclusions: IBD patients do not have an increased risk of COVID-19 and associated mortality compared with the general population. In many IBD patients, diarrhoea was a presenting symptom, and sometimes, was the only symptom at onset of COVID-19. IMM treatment, n (%) 559 (29.1) Azathioprine, n (%) 353 (63.1) Mercaptopurine, n (%) 105 (18.8) Methotrexate, n (%) 90 (16.1) Tofacitinib*, n (%) 6 (1.1) Tacrolimus, n (%) 2 (0.3) Mycophenolate, n (%) 3 (0.5) Biological treatment, n (%) 301 (15.7) Infliximab, n (%) 110 (36.5) Adalimumab, n (%) 119 (39.5) Golimumab, n (%) 31 (10.3) Vedolizumab, n (%) 18 (6.0) Ustekinumab, n (%) 23 (7.6) Biological + IMM treatment, n (%) 157 (8.2) IMM alone, n (%) 402 (20.9) Biologics alone n (%) 144 (7.5) Disease location (L): L1 terminal ileum, L2 colon, L3 ileocolon, L4 upper gastrointestinal tract; Disease behaviour (B): B1 nonstricturing nonpenetrating; B2 stricturing, B3 penetrating. IMM: immunomodulator; Tofacitinib* is a JAKinase inhibitor not similar to conventional IMM. Abbreviations: IQR, interquartile range; Montreal classification' of Crohn's disease (CD); SD, standard deviation; UC, ulcerative colitis.

Memantine, a partial antagonist of N-methyl-D-aspartate receptor (NMDAR), approved for moderate to severe Alzheimer’s disease (AD) treatment within the US and Europe under brand name Namenda (Forest), Axura and Akatinol (Merz), and Ebixa and Abixa (Lundbeck), may have potential in alleviating additional neurological conditions, such as vascular dementia (VD) and Parkinson’s disease (PD). In various animal models, memantine has been reported to be a neuroprotective agent that positively impacts both neurodegenerative and vascular processes. While excessive levels of glutamate result in neurotoxicity, in part through the over-activation of NMDARs, memantine—as a partial NMDAR antagonist, blocks the NMDA glutamate receptors to normalize the glutamatergic system and ameliorate cognitive and memory deficits. The key to memantine’s therapeutic action lies in its uncompetitive binding to the NMDAR through which low affinity and rapid off-rate kinetics of memantine at the level of the NMDAR-channel preserves the physiological function of the receptor, underpinning memantine’s tolerability and low adverse event profile. As the biochemical pathways evoked by NMDAR antagonism also play a role in PD and since no other drug is sufficiently effective to substitute for the first-line treatment of L-dopa despite its side effects, memantine may be useful in PD treatment with possibly fewer side effects. In spite of the relative modest nature of its adverse effects, memantine has been shown to provide only a moderate decrease in clinical deterioration in AD and VD, and hence efforts are being undertaken in the design of new and more potent memantine-based drugs to hopefully provide greater efficacy.

In this real-life cohort of patients with UC, golimumab therapy was effective for inducing and maintaining clinical response. Although anti-TNF-naive patients had better outcomes, golimumab was also effective in anti-TNF-experienced patients. Only the patients given golimumab after previous failure of 2 anti-TNF agents had significantly worse outcomes. Golimumab dose escalation was beneficial and safe.