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Abstract Number: 2653

Clinical Features in Patients with Anti-Triosephosphate Isomerase Antibody-Positive Neuropsychiatric Systemic Lupus Erythematosus

Shuzo Sato1, Hiroshi Watanabe2, Tomoyuki Asano2, Hiroko Kobayashi3, Hiromasa Ohira2 and Makiko Yashiro2, 1Gastroenterology and Immunology, Fukushima Medical University School of Medicine, Fukushima, Japan, 2Gastroenterology and Rheumatology, Fukushima Medical University School of Medicine, Fukushima, Japan, 3Gastroenterlogy and Rheumatology, Fukushima Medical University School of Medicine, Fukushima, Japan

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: CNS Lupus and autoantibodies

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Session Information

Title: Systemic Lupus Erythematosus - Clinical Aspects and Treatment: Epidemiology, Women's Health, Cardiovascular and CNS

Session Type: Abstract Submissions (ACR)

Background/Purpose: Although several autoantibodies of Neuropsychiatric Systemic Lupus Erythematosus (NPSLE) have been reported, none of these autoantibodies were conclusively established as pathogenic. We have reported that autoantibodies to triosephosphate isomerase (TPI), which is an important glycolytic enzyme in red blood cells or neuronal cells, are associated with NPSLE pathogenesis. We have detected the presence of anti-TPI antibodies in sera of human NPSLE patients. However, clinical features regarding anti-TPI antibody-positive NPSLE patients are not known. The aim of this study was to determine the clinical features of anti-TPI antibody-positive NPSLE patients.

Methods: Clinical data was retrospectively collected from 24 NPSLE patients (mean age: 26.41 ± 8.93 years old, 4 males and 20 females). NPSLE manifestations were determined according to the ACR case definitions for NPSLE. NPSLE patients were divided into 2 groups (anti-TPI antibody-positive or negative), and compared clinical features as follows: age, sex, disease duration, NPSLE manifestation, other SLE manifestations, SLEDAI, and laboratory data. Serum samples collected from all NPSLE patients were analyzed by Western blotting to detect anti-TPI antibodies using rabbit muscle TPI protein.

Results: 7 of 24 NPSLE patients were positive for anti-TPI antibodies (29.1%). Age, the rate of female, and SLEDAI were not significantly different between 2 groups. In Laboratory data, the platelet count was significantly elevated in anti-TPI positive NPSLE patients (221,800 vs 158,300  /μl, p = 0.047). In NPSLE manifestation, Lupus headache was more frequently observed in anti-TPI antibody-positive NPSLE patients (28.5% vs 0%, p= 0.012) (Table). The frequency of Seizure, Organic Brain Syndrome and Psychosis was similar in both groups in this study. Myelopathy and aseptic meningitis were observed only in anti-TPI antibody-negative NPSLE patients.

Conclusion: General clinical features were similar between anti-TPI antibody-positive NPSLE patients and negative patients, however, anti-TPI antibody-positive patients may have higher platelet count and higher frequency of lupus headache, compared to anti-TPI antibody-negative NPSLE patients.

Table. Clinical features of anti-TPI antibody-positive NPSLE patients.

 

Clinical items

Anti-TPI positive

Anti-TPI negative

p

number

7

17

–

Age (years old)

30.85 ± 9.7

24.58 ± 8.2

0.16

Sex (female %)

100%

76.5%

0.08

SLEDAI

16.42 ± 7.82

15.41 ± 6.51

0.76

Laboratory Data

 

 

 

WBC /μL

7857 ± 7054

6688 ± 3905

0.69

Hemoglobin g/dL

11.17 ± 3.25

11.17 ± 2.40

0.99

Platelet /μL

22.18 ± 6.05

15.83 ± 7.49

0.04

C3mg/dL

67.71 ± 44.8

56.11 ± 26.98

0.54

C4mg/dL

15.14 ± 14.95

13.76 ± 9.29

0.82

NPSLE manifestation

 

 

 

Seizure

42.8%

23.5%

0.17

OBS

14.3%

23.5%

0.31

Psychosis

28.5%

17.6%

0.27

Headache

28.5%

0%

0.01


Disclosure:

S. Sato,
None;

H. Watanabe,
None;

T. Asano,
None;

H. Kobayashi,
None;

H. Ohira,
None;

M. Yashiro,
None.

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