Endocrine Abstracts

Background: Gastric reduction duodenal switch involves restrictive and mal-absorptive aspect, removing approximately 70% of stomach and most of the duodenum. Surgical alteration leading to malabsorption of macronutrients is achieved with varying results of weight loss but resulting nutritional side effects are under-recognised. Issues in nutritional complication leading to neurological complications like peripheral neuropathy are increasingly recognised. We discuss a case of subacute common peroneal nerve palsy as a result of copper deficiency.

Aim: To recognise the key features of non-compressive nerve palsy in post-bariatric surgery as a result of copper deficiency.

Case Report: A 40-year old male presented post-operatively with unilateral lower leg pain and weakness made worse by a progressive sensory ataxia with occasional steatorrhea. Four months prior to this he underwent a gastric reduction duodenal switch surgery for severe obesity (pre-operative weight 155 kg and BMI of 55). Patient achieved a rapid weight loss of 79 kg. His comorbidities include type 2 diabetes mellitus in remission and obstructive sleep apnoea. On clinical examination, he had a unilateral foot drop with concurrent deficiency in serum copper and caeruloplasmin levels of 13 mg/dl (normal range 15–30 mg/dl). His other biochemical investigations including iron, zinc (12.8 mg/dl; range 11.5–18.5 mg/dl), calcium, vitamin B12 and vitamin D were all normal with good concordance to routine oral supplements. He denied exogenous excess zinc ingestion. Nerve conduction studies were unable to be performed as he was lost during follow-up.

Conclusion: Copper deficiency must be increasingly common as growing numbers of bariatric gastrointestinal surgery. Copper deficiency should be considered as a differential in investigating for non-compressive neuropathy with low serum copper and caeruloplasmin levels. Screening for copper should be considered for patients who undergo bariatric surgery.