Cognitive Impairment in SLE May Be Predicted by Vitamin D Deficiency

Patricia Inacio, PhD avatar

by Patricia Inacio, PhD |

Share this article:

Share article via email
vitamin D and systemic lupus erythematosus

Deficiency of a specific form of vitamin D (25(OH)D3) is associated with and independently predicts worse cognitive function in systemic lupus erythematosus (SLE) patients, according to a study in the journal PLOS One. The report is titled “25-Hydroxyvitamin D3 Deficiency Independently Predicts Cognitive Impairment in Patients with Systemic Lupus Erythematosus.

SLE is a chronic, systemic autoimmune disease whose etiology is unknown. A frequent manifestation in SLE patients is the occurrence of neurologic and psychiatric syndromes, collectively known as neuropsychiatric systemic lupus erythematosus (NPSLE). Cognitive dysfunction is the most prevalent manifestation of NPSLE in SLE patients (with incidence of up to 80%), the American College of Rheumatology (ACR) Ad Hoc Committee on Neuropsychiatric Lupus Nomenclature states.

Recent epidemiological reports within the general population showed that vitamin D deficiency is a potential risk factor for cognitive impairment. Notably, studies on SLE identified vitamin D deficiency as a contributor towards disease activity and patient morbidity.

Researchers investigated the relationship between vitamin D and cognitive dysfunction, recruiting a total of 61 adult SLE patients attending outpatient clinics of National University Hospital, Singapore, (all patients fulfilled at least four of the American College of Rheumatology 1997 Revised Classification Criteria) and 61 gender-matched healthy controls. Cognitive function on both groups was determined by the Automated Neuropsychological Assessment Metrics (ANAM), self-administered computer tests that include simple reaction time, as well as tests for learning and recall, visual perception and mental rotation, among others.

The study’s primary outcome was the total throughput score (TTS) for each of the eight ANAM tests. The team defined cognitive dysfunction as TTS lower than 1.5 SD of the mean of healthy controls. To correlate cognitive levels and vitamin D, researchers measured 25-hydroxyvitamin D [25(OH)D2 + 25(OH)D3]  levels, the two most useful markers for vitamin D.

While SLE patients’ TTS was significantly lower than that of healthy controls, no differences in 25(OH)D3 levels, total 25(OH)D levels, and total 25(OH)D deficiency between both groups was observed. However, SLE patients presented 25(OH)D3 deficiency more commonly when compared to controls.

“The association between 25(OH)D3 deficiency and cognitive impairment in SLE is novel and may provide further insights into the pathophysiological impact of vitamin D on cognitive dysfunction. Further prospective studies are warranted to clarify if SLE patients with 25(OH)D3 deficiency are more likely to experience cognitive dysfunction and whether the correction of 25(OH)D3deficiency with vitamin D3 supplementation could improve or even prevent the process of cognitive dysfunction amongst SLE patients,” the authors conclude.