NMOSD Could Drive Vitamin B12 Deficiency

Case Report Suggests Testing for NMOSD When SCD Signs Are Present

Lindsey Shapiro, PhD avatar

by Lindsey Shapiro, PhD |

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This illustration shows a person under a magnifying glass, and flanked by two healthcare workers.

Researchers have identified a rare case of co-existing neuromyelitis optica spectrum disorder (NMOSD) and subacute combined degeneration (SCD) — two distinct disorders marked by nerve damage in the brain or spinal cord.

The case highlights the possibility that NMOSD may be the underlying driver of the vitamin B12 deficiency that causes SCD, emphasizing the importance of testing for NMOSD when signs of SCD are present, according to the researchers.

Adding immunotherapy — the standard treatment for NMOSD — to vitamin B12 supplementation may be the optimal therapeutic approach for such  patients.

The study, “Neuromyelitis optica spectrum disease coexisting with subacute combined degeneration: a case report,” was published in the journal BMC Neurology.

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This illustration of a person's central nervous system (CNS) accompanies a story about neuromyelitis optic spectrum disorder (NMOSD).

High Incidence of Pain in NMOSD Is Mostly Nerve-related

NMOSD is an autoimmune disease primarily marked by inflammation in the central nervous system (CNS), comprised of the brain and spinal cord. It’s a demyelinating disease, meaning that the loss of myelin. a fatty substance that surrounds and protects nerve cells, is evident.

Like NMOSD, SCD is a demyelinating disease affecting the CNS. In this condition, lack of vitamin B12 leads to demyelination that mainly affects the spinal cord and causes progressive nerve damage.

Although both are marked by myelin loss, and with some overlapping symptoms like inflammation, weakness, or vision loss, there have been few reports of the conditions co-existing.

The 61-year-old woman described in the case report first came to the community clinic with complaints of numbness and weakness in her extremities that had lasted for more than two months, She then was treated with oral vitamin B12 supplements.

While she initially improved slightly, her symptoms began to worsen again and interfered with her daily life.

In the neurology department at the researchers’ hospital in China, it was revealed the woman had a history of an autoimmune thyroid disorder called Hashimoto’s thyroiditis and of high blood pressure, but was compliant taking her blood pressure medication. She also had a good diet and didn’t use alcohol or cigarettes.

During a neurological exam, the clinicians found the woman to have weakness and impaired sensations, as well as signs of mild cognitive impairment. She also had signs of macrocytic anemia, a condition marked by abnormally large red blood cells, as well as an ongoing vitamin B12 deficiency despite the supplements.

Abnormalities consistent with SCD were observed on her spinal cord with MRI imaging, with no brain abnormalities observed. She was diagnosed with SCD of unknown cause and continued treatment with injectable vitamin B12 supplementation.

At the same time, a test came back positive for aquaporin-4 (AQP4) antibodies, the most common type of NMOSD-causing antibodies, leading the clinicians to add NMOSD to her SCD diagnosis.

The woman was subsequently treated with into-the-vein methylprednisolone, a standard treatment to push NMOSD into remission. Her symptoms of weakness eased, and she was switched to oral prednisolone for six months in addition to B12 supplementation.

Six months later, her symptoms had resolved completely and MRI abnormalities had reduced.

According to the researchers, it is possible that NMOSD was the underlying cause of the B12 deficiency that drove SCD in the patient.

A previous study found that nearly half of NMOSD patients with AQP4 antibodies also had low vitamin B12 levels. This relationship may be due to that fact that certain cells in the stomach responsible for absorbing vitamins like B12 also express AQP4, the team noted.

Inability to absorb vitamin B12

Essentially, it’s possible that when AQP4 is attacked in NMOSD, it damages those cells, impairing the body’s ability to absorb vitamin B12.

“Even if it is easy to diagnose SCD by detecting vitamin B12 levels and by utilizing spinal cord MRI, it is usually difficult to determine the real pathogeny of vitamin B12 deficiency,” the researchers wrote.

The team added that this can lead to delays in appropriate treatments that address the underlying driver of the vitamin B12 deficiency that causes SCD — treatments that may be critical if vitamin B12 supplements aren’t sufficient to ease symptoms.

To prevent such a delay, “AQP4 antibody examination is suggested for SCD patients with no obvious cause and poor effects of routine treatment,” the researchers wrote, adding that immunotherapy is necessary for such patients.