IntroductionPain is a common and debilitating symptom in survivors of critical illness. The ‘Core Outcome Set for Survivors of Acute Respiratory Failure’ proposes that the pain and discomfort question of the EuroQol 5 Dimension 5 Level (EQ-5D-5L) could be used to assess pain in this group, however, it was recognised that further research is required to evaluate how this single question compares to other more detailed pain tools. This study aims to evaluate the relationship between the pain and discomfort question of the EQ-5D-5L and the Brief Pain Inventory (BPI) in survivors of critical illness.MethodsThis study retrospectively analysed paired EQ-5D-5L and BPI data extracted from a prospective, multicentre study evaluating the impact of a critical care recovery programme. 172 patients who received a complex recovery intervention and 108 patients who did not receive this intervention were included. Data were available for the intervention cohort at multiple time points, namely, baseline, 3 months and 12 months. While, data were available for the usual care cohort at a single time point (12 months). We assessed the correlation between the pain and discomfort question of the EQ-5D-5L and two separate components of the BPI: severity of pain and pain interference.ResultsCorrelation coefficients comparing the pain and discomfort question of the EQ-5D-5L and the BPI pain severity score ranged between 0.73 (95% CI 0.63 to 0.80) and 0.80 (95% CI 0.72 to 0.86). Correlation coefficients comparing the pain and discomfort question of the EQ-5D-5L and the BPI pain interference score ranged between 0.71 (95% CI 0.62 to 0.79) and 0.83 (95% CI 0.76 to 0.88) across the various time points.ConclusionsThe pain and discomfort question of the EQ-5D-5L correlates moderately well with a more detailed pain tool and may help to streamline assessments in survivorship studies. More in-depth tools may be of use where pain is the primary study outcome or a patient-reported concern.

Little has been published concerning the mechanism of action of deglycyrrhinized liquorice, although in rats it has been shown to reduce acute aspirin-induced gastric mucosal damage when given with aspirin (Rees et a1 1979; Bennett et a1 1980) and injury due to pyloric ligation (Anderson et al 1971, Aarsen 1973.A preparation (Caved S), combining deglycyrrhinized liquorice with antacids is of proven value in the healing of gastric ulceration and of equivalent efficacy in this respect to cimetidine and carbenoxalone (Morgan et a1 1978(Morgan et a1 , 1982.In this study we have determined the effect of pre-treatment of the gastric mucosa with deglycyrrhinized liquorice on aspirin-induced damage, the effect of deglycytrhinized liquorice on the bile acid potentiation of aspirin-induced injury and the effect of deglycyrrhinized liquorice on aspirin absorption in rats. Preliminary experiments determined that the dose of aspirin which produced haemorrhagic lesions in approximately 90% of the animals was 128 mg kg*. The dose of deglyrrhinized liquorice used was 2000 mg k g l , similar to that used by Rees et a1 (1979). Test solutions or suspensions were administered by intubation of the stomach through the mouth, using a syringe and olive-tipped needle. The design of study is shown in Table 1 and the volumes administered at time 0 and 30 min were 3.3 and 13.3 ml k g l respectively. Deglycyrrhinized liquorice suspended in water was given at time 0 in group 2 and contained in the aspirin suspension at 30 min in group 4. Aspirin consisted of acetylsalicylic acid (53.3 mmol litre-1, Evans Medical Co, Liverpool U.K.), dextrose (28 mmol litre-1) and sodium chloride (16.5 mmol litre-') in 0.5% carboxymethylcellulose. Materials and methodsFour hours after the final intubation, the rats were killed with ether, the stomachs removed, opened along the greater curvature and the mucosae washed under a constant stream of water. The observer, unaware of the rats grouping, examined the mucosa for haemorrhagic lesions and a scoring system was used to determine the amount of damage; lesions measuring 4, 1-2,2-3, or > 3 mm across scored 1, 2, 3 and 4 points respectively.The median lesion score with quartiles was calculated for each group and groups were compared using the Mann-Whitney U-test (2 tail). Deglycyrrhinized liquorice and aspirin plus bile acidinduced damage. The dose of aspirin was 64 mg k g l such as to cause haemorrhagic lesions in about 50% of the animals. The concentration of bile acid, taurodeoxycholic acid used was 5 mmol litre-' which is comparable with that found in post-prandial gastric aspirates of gastric ulcer patients (Rhodes et a1 1969) and, alone, does not cause significant damage in rats (Semple & Russell 1975). Aspirin was administered alone to group 5, and with taurodeoxycholic acid, deglycyrrhinized liquorice or both, to groups 6, 7 and 8 respectively ( Table 2). The volume of suspension administered was 13.3 ml k g l . Deglycyrrhinized liquorice and aspirin absorption. Two groups of rats (n = 7) were used, r...

SUMMARY The acetyl moiety in aspirin (acetyl salicylic acid: ASA) is considered to play a major part in the pathogenesis of ASA‐induced mucosal injury. At equivalent salicylate doses and pH values, the induction of acute gastric mucosal haemorrhagic erosions in rats by ASA and choline magnesium trisalicylate (CMT), a new non‐acetylated salicylate, with and without the potentiating damaging effect of taurodeoxycholic acid (TDCA) were compared. Test solutions were administered by per oral intubation to five groups of fasting Sprague–Dawley rats (n= 24). Gastric mucosa were examined after 4 hours and mucosal injury assessed by a lesion‐scoring system. The incidence and severity (median lesion scores with quartiles) of the lesions were 83% and 13 (7:20) respectively for ASA (128 mg kg−1) compared with 17% and 0 (0:0) for CMT (128 mg kg−1) (P < 0.001 and P < 0.001). TDCA increased mucosal damage to 100% and 29 (20:34) for ASA compared with 30% and 0 (0:4) for CMT (P < 0.001) and P < 0.001). Serum salicylate levels (median values of 1.4 for ASA and 1.5 mmol litre−1 for CMT) were not significantly different. It is concluded that replacing the acetyl moiety in ASA with choline and magnesium moieties reduces the ASA‐induced mucosal injury, without affecting blood salicylate concentrations.