INTRODUCTION
Postural hypotension is a debilitating manifestation of diabetic autonomic neuropathy that is difficult to treat. It’s thought to be secondary to damaged sympathetic fibres and poor baroreceptor response1. We report a case of postural hypotension successfully managed with erythropoietin in a young woman with type 1 diabetes mellitus.
CASE
A 24-year-old woman with symptomatic postural hypotension on a background of type 1 diabetes for 17 years presents to Endocrinology clinic for evaluation. Whilst past glucose control had not always been ideal (HbA1c up to 12%), more recent reports were commonly <7.0%. Diabetes complications included retinopathy, painful peripheral neuropathy, and gastroparesis.
Onset of postural hypotension was relatively abrupt and prompted hospitalisation in May 2019. Supine BP 121/84 dropped to 80/64 upon standing, improving to 98/73mmHg after 5mins. Complete blood count, serum electrolytes, renal and liver function tests, inflammatory markers, cortisol, and ACTH were unremarkable.
She trialled multiple different agents including: fluodrocortisone, dothiepin, bethahistine, caffeine, midodrine, and octreotide. Compression stockings as recommended by vascular occupational therapist were inappropriate due to exacerbation of painful peripheral neuropathy.
Nerve conduction studies in July 2019 and May 2020 confirmed a length-dependent axonal sensorimotor large fibre peripheral neuropathy without demyelination.
In February 2021, she commenced weekly erythropoietin 6000U. She did not have anaemia (Hb 126 [ref: 115-160]) or renal impairment (creatinine 62). Her symptoms had significantly improved on subsequent review, with resolution of postural drop (sitting BP 129/89; standing BP 125/87; 3min standing BP 124/89). Follow up Hb was 156.
CONCLUSION
This case report is an example of erythropoietin successfully managing postural hypotension secondary to diabetic autonomic neuropathy. There is sparse literature on this topic, with postulation that erythropoietin’s pressor effect is from increased blood viscosity with increased haemoglobin production2, or increased nitric oxide binding reducing vasodilatation of vasculature3. Further research is required into this phenomenon.