While working on the hepatology ward as an internal medicine trainee, I looked after several patients with autoimmune hepatitis who developed steroid-induced hyperglycaemia. It quickly became clear how varied the glycaemic responses to steroids can be, and how differently hepatology and endocrinology services approach monitoring and management.
CASE PRESENTATIONS
'Hepatologists are excellent at managing immunosuppression, but glucose checks can be easily overlooked in non-diabetic patients, especially when fasting levels appear normal. On the other hand, endocrinologists may not always appreciate how complex glucose control can be in patients with liver disease, poor appetite, or fluctuating steroid doses.'
One case that stood out was a 54-year-old woman with newly diagnosed autoimmune hepatitis and chronic liver disease, though without cirrhosis. She had no previous history of diabetes, and her baseline glycated haemoglobin (HbA1c) was 37mmol/mol. Treatment began with intravenous methylprednisolone pulses, followed by high-dose oral prednisolone once daily.
Her glucose was checked four times daily from the start. While on intravenous methylprednisolone, she showed a steady rise in glucose across the day, with intermittent post-meal spikes. Once switched to oral prednisolone, her fasting levels remained normal, but she developed clear post-lunch and evening peaks – a pattern typical of morning prednisolone dosing.1,2,3
She was initially started on gliclazide, which gave partial improvement, but didn’t fully control her glucose. The diabetes outreach team were then involved and switched her to Humulin® I once daily in the morning, which helped cover the afternoon and evening peaks. As her course continued, her glucose rose again, and she was stepped up to biphasic insulin (NovoMix® 30). Later, as her steroids were tapered, her insulin requirements dropped quickly and she had mild hypoglycaemia, which resolved with dose reduction and close follow up.
Another patient on the ward, also with autoimmune hepatitis, was started on oral prednisolone, but only fasting glucose checks were done initially. These appeared reassuringly normal, and her hyperglycaemia wasn’t noticed until four-point testing was eventually introduced. Her post-lunch and evening readings were high, showing how easy it can be to miss steroid-induced hyperglycaemia if only fasting levels are monitored.2,4
DISCUSSION
'At present, there are no hepatology-specific guidelines for steroid-induced hyperglycaemia. A shared local protocol, developed by both teams, could help standardise practice and prevent cases from being missed.'
These cases highlighted a pattern I saw several times: glucose monitoring after starting steroids isn’t consistent on hepatology wards. Hepatologists are excellent at managing immunosuppression, but glucose checks can be easily overlooked in non-diabetic patients, especially when fasting levels appear normal. On the other hand, endocrinologists may not always appreciate how complex glucose control can be in patients with liver disease, poor appetite, or fluctuating steroid doses.
Guidelines from the Joint British Diabetes Societies for Inpatient Care (JBDS-IP)1 and the Endocrine Society4 recommend at least twice-daily glucose monitoring when starting high-dose glucocorticoids, moving to four-point testing if readings exceed 10–11mmol/l or if treatment is prolonged. Relying on fasting glucose alone can easily miss the afternoon and evening spikes typical of oral prednisolone.2,4
In patients with chronic liver disease, HbA1c can be misleadingly low due to anaemia and shortened red-cell lifespan, so capillary or continuous glucose monitoring gives a better reflection of true control.4,5 Tight glycaemic control should also be avoided: hypoglycaemia is particularly dangerous when hepatic glycogen stores and gluconeogenesis are impaired. The JBDS-IP suggest aiming for 6–10mmol/l, prioritising safety over perfection.1
Different steroid regimens produce distinct glycaemic patterns. Intravenous methylprednisolone and dexamethasone often cause a sustained rise in glucose throughout the day and night, while morning prednisolone tends to cause post-lunch and evening spikes. Recognising these patterns helps tailor insulin: morning intermediate-acting insulin (e.g. Humulin® I) for prednisolone, and basal–bolus or biphasic regimens for the more sustained rises seen with intravenous or long-acting steroids.1,2,3
In hepatology, practical barriers can add to the challenge. Nursing staff and resident doctors may be less familiar with insulin initiation, and there is often uncertainty about appropriate targets in liver disease. Early involvement of the diabetes outreach or endocrinology team can make a real difference by helping to spot hyperglycaemia early, choosing suitable regimens and safely reducing doses when steroids are tapered.
Overall, these cases reinforced the value of collaboration between hepatology and endocrinology. At present, there are no hepatology-specific guidelines for steroid-induced hyperglycaemia. A shared local protocol, developed by both teams, could help standardise practice and prevent cases from being missed.
- Steroid-induced hyperglycaemia can appear quickly, even in patients with normal HbA1c and no prior diabetes.
- HbA1c should not be relied upon to exclude dysglycaemia, particularly in liver disease, where it may underestimate glucose levels.
- Start with twice-daily glucose monitoring when initiating high-dose steroids, and move to four-point testing if readings exceed 10–11mmol/l or if treatment is prolonged.
- Different steroids produce different patterns: intravenous methylprednisolone and dexamethasone cause sustained rises, while morning prednisolone leads to afternoon and evening spikes; divided or evening doses can cause all-day hyperglycaemia.
- Select insulin regimes where the action profiles most closely match glycaemic patterns, but factor in the feasibility of implementation.
- Sulfonylureas can help in mild, short courses if oral intake is good, but should be avoided in advanced liver disease.
- Target glucose largely between 6–10mmol/l (up to 12mmol/l is acceptable) and personalise as needed.
- Early multidisciplinary collaboration between hepatology, endocrinology and nursing teams ensures safer, more consistent care.
MADIHA MIRZA
Internal Medicine Trainee, Addenbrooke’s Hospital, Cambridge
VISHAKHA BANSIYA
Consultant in Diabetes and Endocrinology, Addenbrooke’s Hospital, Cambridge
REFERENCES
1. JBDS-IP 2023 Management of Hyperglycaemia and Steroid (Glucocorticoid) Therapy edn 2 https://abcd.care/resource/current/jbds-08-management-hyperglycaemia-and-steroid-glucocorticoid-therapy.
2. Cho JH 2024 Endocrinology & Metabolism https://doi.org/10.3803/EnM.2024.1951.
3. Aberer F et al. 2021 Journal of Clinical Medicine https://doi.org/10.3390/jcm10102154.
4. Korytkowski MT et al. 2022 Journal of Clinical Endocrinology & Metabolism https://doi.org/10.1210/clinem/dgac278.
5. Barker HL et al. 2023 Diabetes Therapy https://doi.org/10.1007/s13300-023-01393-6.
