This cohort from across the UK is older than other multicentre AIH cohorts. One-fifth had decompensation or MELD >15. Diagnosis was delayed in 19%, diagnostic testing was incomplete in one-third and rosettes and emperipolesis were infrequently reported.

Background and AimAcute gastrointestinal bleeding carries poor outcomes unless prompt endoscopic hemostasis is achieved. Mortality in these patients remains significant. Hemospray is a novel intervention that creates a mechanical barrier over bleeding sites. We report the largest dataset of patient outcomes after treatment with Hemospray from an international multicenter registry.Patients and MethodsProspective data (Jan 2016–May 2018) from 12 centers across Europe were collected. Immediate hemostasis was defined as endoscopic cessation of bleeding within 5 min after application of Hemospray. Rebleeding was defined as subsequent drop in hemoglobin, hematemesis, persistent melena with hemodynamic compromise post‐therapy.ResultsThree hundred and fourteen cases were recruited worldwide (231 males, 83 females). Median pretreatment Blatchford score was 11 (IQR: 8–14) and median complete Rockall score (RS) was 7 (IQR: 6–8) for all patients. Peptic ulcer disease (PUD) was the most common pathology (167/314 = 53%) and Forrest Ib the most common bleed type in PUD (100/167 = 60%). 281 patients (89.5%) achieved immediate hemostasis after successful endoscopic therapy with Hemospray. Rebleeding occurred in 29 (10.3%) of the 281 patients who achieved immediate hemostasis. Seven‐day and 30‐day all‐cause mortality were 11.5% (36/314) and 20.1% (63/314), respectively (lower than the predicted rates as per the RS). Similar hemostasis rates were noted in the Hemospray monotherapy (92.4%), combination therapy (88.7%) and rescue therapy (85.5%) groups.ConclusionsThese data show high rates of immediate hemostasis overall and in all subgroups. Rebleeding and mortality rates were in keeping/lower than predicted rates.

Background With few data regarding treatment and outcome of patients with AIH outside of large centres we present such a study of patients with AIH in 28 UK hospitals of varying size and facilities. Methods Patients with AIH were identified in 14 University and 14 District General hospitals; incident cases during 2007–2015 and prevalent cases, presenting 2000–2015. Treatment and outcomes were analysed. Results In 1267 patients with AIH, followed up for 3.8 (0–15) years, 5‐ and 10‐year death/transplant rates were 7.1 ± 0.8% and 10.1 ± 1.3% (all‐cause) and 4.0 ± 0.6% and 5.9 ± 1% (liver related) respectively. Baseline parameters independently associated with death/transplantation for all causes were: older age, vascular/respiratory co‐morbidity, cirrhosis, decompensation, platelet count, attending transplant centre and for liver related: the last four of these and peak bilirubin. All‐cause and liver‐related death/transplantation was independently associated with: non‐treatment with corticosteroids, non‐treatment with a steroid‐sparing agent (SSA), non‐treatment of asymptomatic or non‐cirrhotic patients and initial dose of Prednisolone >35 mg/0.5 mg/kg/day (all‐cause only), but not with type of steroid (Prednisolone vs. Budesonide) or steroid duration beyond 12 months. Subsequent all‐cause and liver‐death/transplant rates showed independent associations with smaller percentage fall in serum ALT after 1 and 3 months, but not with failure to normalise levels over 12 months. Conclusions We observed higher death/transplant rates in patients with AIH who were untreated with steroids (including asymptomatic or non‐cirrhotic subgroups), those receiving higher Prednisolone doses and those who did not receive an SSA. Similar death/transplant rates were seen in those receiving Prednisolone or Budesonide, those continuing steroids after 12 months and patients attaining normal ALT within 12 months versus not.

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