ECE2023 Poster Presentations Diabetes, Obesity, Metabolism and Nutrition (159 abstracts)
1Department of Medicine, University Hospital Llandough,, Endocrinology and Diabetes, Llandough, United Kingdom; 2Department of Medicine, University Hospital Llandough, Department of Endocrinology and diabetes, Llandough, United Kingdom; 2Department of Medicine, University Hospital Llandough,, Department of Endocrinology and diabetes, Llandough, United Kingdom
Background: Bruns Garlands syndrome is a rare disorder in people living with diabetes, manifesting as unilateral or bilateral muscle pain, weakness and atrophy in the proximal region of the lower limbs. Herein, we present the case of a patient with Bruns-Garland syndrome caused by sodium/glucose co-transporter 2 inhibitors (SGLT2i).
Case description: A 55-year-old male with background of type 2 diabetes for 5 years, and currently on oral therapy, presented to the emergency admissions unit with ketosis, acidosis and borderline hyperglycaemia (ketones 6 mmol/l, pH 7.21 and blood glucose of 11 mmol/l, respectively). On further questioning, his diabetes control was suboptimal with some mild tingling sensation in his lower limbs first noticed a year ago; Empagliflozin was added to his therapy at that time, resulting in significant weight loss of about 8 kgs over 6 weeks and a substantial reduction in HbA1c from 103 to 48 mmol/mol in less than 6 months. On examination, he had widespread vitiligo, and proximal muscle wasting with bilateral lower limb weakness, reduced reflexes and paraesthesia, suggestive of peripheral neuropathy. Baseline myopathy screening was negative. Imaging studies were negative for sinister causes of weight loss. MRI spine was inconclusive, suggesting mild degenerative changes with multifocal disc prolapses and nerve root impingements, but no spinal canal stenosis. Nerve conduction studies of upper and lower limbs revealed a moderately severe, length dependent sensorimotor axonal neuropathy. This was confirmed with electromyography indicating an axonal peripheral neuropathy, with superimposed bilateral lumbar plexopathy/femoral neuropathy, suggestive of acute on ongoing neurogenic changes in bilateral lower limbs distally and proximally. Despite HbA1c improvement, his symptoms further progressed to debilitating proximal myopathy, with severe paraesthesia and burning sensation over his thighs in the next few months, despite Vitamin B12 levels replacement therapy.
Conclusion: Rapid improvement of HbA1c with SGLT2i or a direct effect of SGLT2i can significantly worsen background neuropathic changes leading to Bruns-Garland type diabetic amyotrophy. With the widespread use of SGLT2i, it is important that physicians treating patients with diabetes recognise these symptoms and consider this association in patients developing fatigue and weakness.