Copper Deficiency Myelopathy After Upper Gastrointestinal Surgery

King, Dominic; Siau, Keith; Senthil, Latha; Kane, Katherine; Cooper, Sheldon C.

doi:10.1177/0884533617713955

Cited by 14 publications

(6 citation statements)

References 19 publications

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“…As an essential element of methionine synthase in the methylation cycle, the lack of serum copper leads to dysfunction of methionine synthase, which can cause demyelination that resembles SCD [ 24 , 25 ]. The pathological copper deficiency was usually caused by insufficient storage (preterm and infants), insufficient intakes or malabsorption (diet causes, chronic diarrhea, celiac disease, Crohn’s disease, long-time parenteral nutrition, intestinal surgery, and excessive zinc), increased demands (pregnancy, lactation and wound healing), increased losses (major burns and renal replacement therapy), or hereditary diseases (such as Menkes disease) [ 26 , 27 ]. As our cases had clear histories of N 2 O abuse and none of the above causes were involved, we suspected a possible link between the copper deficiency and N 2 O abuse.…”

Section: Discussionmentioning

confidence: 99%

Serum copper decrease and cerebellar atrophy in patients with nitrous oxide-induced subacute combined degeneration: two cases report

et al. 2021

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Background Subacute combined degeneration (SCD) is a neurological complication commonly associated with vitamin B12 deficiency. It can result from nitrous oxide (N2O) abuse and cause neuropsychiatric symptoms. However, there has been no literature regarding alterations of serum copper and cerebellum in SCD patients. Case presentation We reported two cases of young SCD patients with histories of N2O abuse. In these cases, elevated homocysteine, macrocytic anemia, spinal cord abnormalities, and peripheral nerve injuries were detected. In addition, decreased serum copper level and cerebellar atrophy were reported for the first time. The patients’ symptoms improved after withdrawal of N2O exposure and vitamin B12 supplements. Conclusion We reported two SCD cases with serum copper alteration and cerebellar atrophy after N2O abuse for the first time. These might be crucial complements to the diagnosis of SCD.

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Section: Discussionmentioning

confidence: 99%

Serum copper decrease and cerebellar atrophy in patients with nitrous oxide-induced subacute combined degeneration: two cases report

et al. 2021

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“…According to the World Health Organization, the normal serum copper ranges from 12.6 to 18.9 μmol/L. Multiple case reports of patients with CDM have reported serum copper values ranging from undetectable to 5.9 μmol/L 6 . Although serum copper levels are a good screening test for copper deficiency, it must be noted that during an inflammatory response, serum copper increases as a result of being transported by Cp 19 , an acute‐phase protein 4 .…”

Section: Discussionmentioning

confidence: 99%

Copper deficiency myelopathy and autism spectrum disorder

Pau

Westphalen

2020

J Paediatrics Child Health

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Copper deficiency is a rare cause of non-compressible myelopathy. 1 The clinical and radiological presentation closely mimics myelopathy caused by vitamin B12 deficiency. It typically presents with gait difficulties due to sensory ataxia but may also present with spasticity, paraesthesia and urinary symptoms.We report one of the youngest cases of copper deficiency myelopathy (CDM) documented in the literature.

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“…Copper deficiency has also been described in patients after Roux-en-Y gastric bypass surgery with incidence ranging from 12%–30% in the USA 14–17. Nutritional deficiencies are common following gastric bypass surgery as a large portion of the stomach and duodenum are bypassed.…”

Section: Discussionmentioning

confidence: 99%

Progressive myeloneuropathy with symptomatic anaemia

2019

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Hypocupremia is a rare and under-recognised cause of bone marrow dysplasia and myeloneuropathy. A 47-year-old Caucasian woman had progressive ascending peripheral neuropathy and gait ataxia over 3 months and fatigue, dyspnoea and unintentional weight loss over 8 months. She had profound macrocytic anaemia and neutropenia. Initial workup included normal serum vitamin B12. Bone marrow biopsy was suggestive of copper deficiency. Serum copper levels were later confirmed to be undetectable. The patient received oral copper repletion which resulted in complete normalisation of haematological abnormalities 16 weeks later. However, neurological deficits persisted. This case describes a delayed diagnosis of hypocupremia as initially suggested through invasive testing. Associating myeloneuropathy with cytopenia is imperative for accurate and prompt diagnosis of hypocupremia, which can be confirmed by serum analysis alone. Developing an accurate differential diagnosis can help prevent unnecessary procedures. Furthermore, initiating prompt copper repletion prevents further neurological impairment. Neurological deficits are often irreversible.

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Copper Deficiency Myelopathy After Upper Gastrointestinal Surgery

Cited by 14 publications

References 19 publications

Serum copper decrease and cerebellar atrophy in patients with nitrous oxide-induced subacute combined degeneration: two cases report

Serum copper decrease and cerebellar atrophy in patients with nitrous oxide-induced subacute combined degeneration: two cases report

Copper deficiency myelopathy and autism spectrum disorder

Progressive myeloneuropathy with symptomatic anaemia

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