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Objectives To determine the age-standardised prevalence of inflammatory bowel disease (IBD) in a metropolitan area of Sydney, with a focus on its prevalence among older people. Design, setting Population-based epidemiological study of people with IBD in the City of Canada Bay, a local government area in the inner west of Sydney, during 1 March 2016 - 10 November 2016. Participants Patients diagnosed with confirmed IBD according to the Copenhagen or revised Porto criteria. Main outcome measures Crude prevalence of IBD, including Crohn disease and ulcerative colitis; age-standardised prevalence of IBD, based on the World Health Organization standard population; prevalence rates among people aged 65 years or more. Results The median age of 364 people with IBD was 47 years (IQR, 34-62 years); 185 were women (50.8%). The crude IBD prevalence rate was 414 cases (95% CI, 371-456 cases) per 100 000 population; the age-standardised rate was 348 cases (95% CI, 312-385 cases) per 100 000 population. The age-standardised rate for Crohn disease was 166 cases (95% CI, 141-192 cases) per 100 000 population; for ulcerative colitis, 148 cases (95% CI, 124-171 cases) per 100 000 population. The IBD prevalence rate in people aged 65 years or more was 612 cases (95% CI, 564-660 cases) per 100 000, and for those aged 85 years or more, 891 cases (95% CI, 833-949 cases) per 100 000; for people under 65, the rate was 380 cases (95% CI, 342-418 cases) per 100 000. Conclusions We found that the prevalence of confirmed IBD in a metropolitan sample was highest among older people. Challenges for managing older patients with IBD include higher rates of comorbid conditions, polypharmacy, and cognitive decline, and the immunosuppressive nature of standard therapies for IBD.

Background Knowledge of Inflammatory Bowel Disease (IBD) prevalence allows health care administrators to understand disease burden and appropriately plan for research and medical care. Young IBD subjects often migrate from rural to urban areas for education and work opportunities, necessitating metropolitan prevalence studies to reduce under-representation. Also, the impact of urbanisation on IBD prevalence requires further exploration. Unlike IBD incidence, where young age-groups dominate, we hypothesised that the elderly age-groups would have the highest IBD prevalence given mortality rates being equivalent to the general population. We aimed to determine the first IBD prevalence rates for New South Wales, Australia. Methods This was an observational, population-based epidemiological study which captured disease information of people living with IBD within the metropolitan City of Canada Bay Local Government Area on the 1st of January 2016. The diagnosis was according to the Copenhagen Criteria. Age-standardisation was according to the WHO Standard Population. Results We identified 330 cases of IBD (49.1% male, median age 47, IQR=27, crude point prevalence rate of 371.5 per 100,000). Full diagnostic confirmation was achieved in 100%. The age-standardised point prevalence rate was 359.2 per 1 00 000. The crude point prevalence rates were 167.8, 158.8 and 45.0 per 1 00 000 for Crohn’s disease (CD), ulcerative colitis (UC) and IBD Unspecified (IBDU), respectively. The age-standardised rates were 171.6, 148.1 and 39.5 per 1 00 000 for CD, UC, and IBDU respectively. IBD prevalence steadily increased with age, peaking at 1061 per 1 00 000 in patients older than 85 years. A trend was observed between prevalence and socioeconomic status between suburbs. Conclusions Sydney exhibited the highest prevalence of IBD in Australasia. The extrapolated estimate for Australia was 89 000 people with IBD. Higher socioeconomic status and urbanisation may be contributing factors. The ageing IBD population accounts for the highest prevalence, peaking at greater than 1000 per 1 00 000. Safer therapies, cancer screening strategies and greater attention towards comorbidities are therefore of increasing importance in managing IBD patients.

Epstein Barr virus (EBV) positive mucocutaneous ulcers (EBVMCU) form part of a spectrum of EBV-associated lymphoproliferative disease. They have been reported in the setting of immunosenescence and iatrogenic immunosuppression, affecting the oropharyngeal mucosa, skin and gastrointestinal tract (GIT). Case reports and series to date suggest a benign natural history responding to conservative management, particularly in the GIT. We report an unusual case of EBVMCU in the colon, arising in the setting of immunosuppression in the treatment of Crohn's disease, with progression to Hodgkin lymphoma 18 mo after cessation of infliximab. The patient presented with multiple areas of segmental colonic ulceration, histologically showing a polymorphous infiltrate with EBV positive Reed-Sternberg-like cells. A diagnosis of EBVMCU was made. The ulcers failed to regress upon cessation of infliximab and methotrexate for 18 mo. Following commencement of prednisolone for her Crohn's disease, the patient developed widespread Hodgkin lymphoma which ultimately presented as a life-threatening lower GIT bleed requiring emergency colectomy. This is the first report of progression of EBVMCU to Hodgkin lymphoma, in the setting of ongoing iatrogenic immunosuppression and inflammatory bowel disease.

Gastric acid secretion has been considered to decline with increasing age but this view is being re-evaluated as the importance of Helicobacter pylori infection emerges. This study aimed to determine the effect of age, H pylori, and gastritis with atrophy on the serum gastrin concentration, gastric secretory volumes, and acid output in healthy, asymptomatic men. Young men (mean (SD) age 22.9 (0.6) years; n = 22) were compared with old men (72.9 (1.2) years; n = 28) in respect of basal serum gastrin and basal, sham fed, pentagastrin stimulated maximal and peak acid secretion. Antral, corpus, and fundal biopsy specimens were taken for histology and H pylori status (histology, culture, and rapid urease test). H pylori associated gastritis was present in three of 22 young (13.6%) and 16 of 28 old (57.1%) men. Gastritis with atrophy was present in 11 old subjects, 10 of whom were H pylori positive. These subjects had higher mean (SD) serum gastrin concentrations than old subjects without atrophy and young subjects (61.8 (9.2); 40.0 (2.9); 36.8 (2.3) pmol/l respectively; p < 0.001). H pylori infected subjects had higher gastrin values than uninfected subjects, overall (55.3 (5.9); 36.0 (1.8) pmol/l; p < 0.001) and in subjects without atrophy (45.3 (4.2); 36.0 (1.8) pmol/l; p < 0.03). In subjects without H pylori infection, gastrin values did not differ with age (old 37.1 (1.7); young 35.4 (2.1) pmol/l). The maximal gastric secretory volume was lower in old subjects with atrophy. Acid output (mmol/h) in subjects with atrophy was lower than in subjects with no atrophy (basal: 3.0(1.1); 5.1(0.7); p=NS; sham led: 5.4 (1.4); 9.3 (0.8); p

Cytokine gene expression was analysed by reverse transcriptase-polymerase chain reaction (RT-PCR) amplification of RNA from 27 human liver allograft specimens diagnosed as acute (n=19) or chronic (n=8) rejection and from 12 normal human livers. In initial screening experiments, mRNA for cytokines interleukin (IL)-1β, IL-6, IL-10 and gamma-interferon (IFN-γ) was expressed in all normal livers and almost all allograft specimens tested. IL-2 mRNA was expressed at barely detectable levels in four of 12 normal livers screened and in 20 of 26 liver allograft specimens with rejection. This constitutive expression of cytokine mRNA required semiquantitative PCR analysis to differentiate levels of cytokine mRNA expression between specimens. Titration of cDNA prior to PCR amplification was initially used and showed significantly more IL-2 (p=0.02) and IFN-γ (p=0.03) in acute rejection compared to normal liver. There was also significantly less IL-10 in chronic rejection compared to acute rejection (p=0.02) or normal liver (p=0.01) and less IL-6 in acute rejection compared to chronically rejecting liver (p=0.05). IL-1β (p=0.04) and IL-6 (p=0.01) were reduced in acute rejection compared to normal liver. The slight increase of IL-2 in acute rejection and the slight decrease of IL-10 in chronic rejection was confirmed by a second semiquantitative analysis which involved removal of aliquots of PCR reaction at successive cycles followed by dot-blotting and hybridization. In conclusion, the changes in cytokine mRNA levels with rejection were slight and only barely detectable with the methods used, suggesting that monitoring mRNA expression of these cytokines will be of little use for diagnosis of rejection. The increase in IL-2 mRNA observed with acute rejection and decrease in IL-10 mRNA in chronic rejection is consistent with their ability to respectively promote and inhibit delayed-type hypersensitivity reactions such as rejection.