SFEBES2021 Poster Presentations Metabolism, Obesity and Diabetes (78 abstracts)
1Liverpool University Hospitals Foundation Trust, Liverpool, United Kingdom; 2University of Liverpool, Liverpool, United Kingdom;
3Weill-Cornell Medicine, Ar-Rayyan, Qatar; 4University of Manchester, Manchester, United Kingdom; 5Manchester Royal Infirmary, Manchester, United Kingdom
A male in his 40s diagnosed with type 2 diabetes in 2011 (BMI:20.7kg/m2) was admitted with DKA (Dec 2018) after a period of poor glycaemic control on oral hypoglycaemic agents (Feb 2017: HbA1c-105mmol/mol, Nov 2018: HbA1c-115mmol/mol). There was dramatic improvement in glycaemic control after commencing him on subcutaneous insulin (April 2019: HbA1c-56mmol/mol). GAD65 antibodies were positive (24u/mL; normal<5u/mL) and a diagnosis of latent autoimmune diabetes (LADA) was made. After the initiation of insulin and rapid improvement in glycaemic control, the patient began to experience severe debilitating burning and shooting pain (10/10) across his abdomen, back, thighs and shins with hyperalgesia and allodynia. On examination the patient had normal strength in all limbs (MRC power grading 5/5), no muscle wasting, and no clinical large fibre deficits. He had an irritable nociceptor phenotype with mechanical brush stroke allodynia. Nerve conduction studies were at the lower end of the normal range (sural/peroneal nerve conduction velocity/amplitude: 42.9m/s; 7.5μV and 42.9m/s; 3.9m/s, respectively). MR brain imaging to rule out a central pain aetiology e.g. thalamic infarct was normal. However, corneal confocal microscopy (CCM), a measure of small sensory nerve fibre pathology was abnormal. Corneal nerve fibre length (CNFL) (6.0mm/mm2), fibre density (CNFD) (12.9/mm2) and branch density (CNBD) (6.7/mm2) were all markedly reduced indicative of small fibre degeneration (normative values CNFL:>12.5mm/mm2, CNFD:>20.6 no/mm2, CNBD:>22.7no/mm2). A diagnosis of treatment-induced neuropathy of diabetes (insulin neuritis) due to rapid improvement in glycaemic control was made based on sudden onset of neuropathic pain and objective evidence of small fibre degeneration. He received multidisciplinary support in the form of maximal dose anti-neuropathic drug therapy, psychological therapy and physiotherapy. After nine months, there was a significant improvement in pain (3-4/10), CCM measures of small nerve fibres showed regeneration (CNFL: 13.1mm/mm2; CNFD: 24.8/mm2; CNBD: 18.7/mm2) and he returned to work.