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P28 Incidence of secondary adrenal suppression after prolonged use of Glucocorticoid therapy for children with inflammatory bowel disease
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  1. Virginia Chatzidaki1,
  2. Rebecca Renji Chungath2,
  3. Sarang Tamhne1,
  4. Marcus Auth1,
  5. Fiona Cameron1,
  6. Manjula Velayudhan Nair1,
  7. Jeng Haw Cheng1,
  8. Stephen Allen1,
  9. Elizabeth Renji1,
  10. Jo Blair1
  1. 1Alder Hey Children’s Hospital Trust
  2. 2Newcastle medical school

Abstract

Introduction Glucocorticoids (GCs) are used in all forms of paediatric inflammatory bowel disease (IBD) for their anti-inflammatory and immunosuppressive effect. Prolonged GC treatment may suppress the hypothalamic-pituitary-adrenal (HPA) axis causing secondary adrenal suppression (SAS), despite using a weaning regime, necessitating the use of hydrocortisone for replacement. The incidence and severity of SAS is poorly predictable and may be related to both the cumulative dose of GCs, but also to individual factors. Standard and low dose short Synacthen tests (SST, LDSST) are used to assess recovery of the HPA axis following a prolonged course of steroids.

Aims To report:

  1. the incidence of SAS following GC treatment for IBD in our centre

  2. the time to HPA axis recovery in patients with SAS

  3. risk factors for SAS

Patients and Methods 33 children with IBD (19M, 10–18 years) previously treated with GCs, who had been investigated for SAS from 01/01/2017 and 30/10/2020 were identified. Baseline information including age, sex, somatometric parameters, IBD diagnosis, age at diagnosis and maintenance treatment were collected. All their GC courses (n=47) in the defined period were reviewed, and those that led to SAS were compared for length and GC doses, previous exposure to GC, tests for HPA axis recovery and the requirement for hydrocortisone replacement therapy.

Results Of the 33 children, 15/33 (45.5%) had ulcerative colitis (UC), 10/33 (30.3%) had Crohn’s Disease (CD) and 8/33 (24.2%) were unclassified (IBDU). 10 children that were tested using non-standard tests for adrenal suppression were excluded.

23 children had their HPA axis recovery tested after 24 GC courses with LDSST (19/24, 79.2%) or SST (5/24, 20.8%). 16/23 children had steroid courses of ≥12 weeks, and 7/23 had a shorter course (<11 weeks) but had extended courses in the past (4/7) and/or high dose IV steroid (3/7). 14/23 (60.9%) children had suboptimal response with peak cortisol range 129–441 nmol/L (table 1). 8/14 retests were available in the study period, 5/8(62.5%) children recovered HPA axis function in a mean period of 6.83±SD2.4 months and 3/8 remained suppressed after a mean period of 4.6±SD2.7 months.

The mean duration of courses that induced SAS was 154± 86.8 days compared to 131.6±63 days in those without SAS, t=0.44, p=0.33, and the previous days of exposure were 219±95 days for those with SAS compared 316.5±154.2 days for those without SAS, t=-1.2, p=0.13.

High dose IV methylprednisolone (10–20 mg/kg) was used in 5/24 (20.8%) courses with 5/5 (100%) and 3/5 (60%) inducing HPA axis suppression on the first testing and retesting respectively. Standard dose (1.6 mg/kg) IV methylprednisolone followed by oral weaning GC course was used in 9/24 (37.5%) courses and 5/9 (55.6%) induced HPA axis suppression. Standard dose oral prednisolone (1–2 mg/kg) was used in 10/24 (41.7%) of the courses and 5/10 (50%) induced SAS.

Abstract P28 Table 1

Patients with inflammatory bowel disease tested with SSTs

Conclusion SAS was detected in 60.9% of our IBD patients who were tested after GCs therapy. Our data support previous reports that additional factors to the duration of treatment with GCs, as the use of high dose of intravenous GCs, may influence the risk of SAS.

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