Correlation between body mass index and disease activity in patients with systemic lupus erythematosus from China

doi:10.21203/rs.3.rs-5645855/v1

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Correlation between body mass index and disease activity in patients with systemic lupus erythematosus from China

https://doi.org/10.21203/rs.3.rs-5645855/v1

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Objective

To assess the association between clinical indicators (primarily Body Mass Index, BMI) and disease activity in systemic lupus erythematosus (SLE) populations in a large population-based cohort.

Methods

Four hundred consecutive patients with SLE were studied to determine the relation among clinical features, inflammatory and biochemical indicators, and parameters of disease activity. Significance values have been adjusted by Bonferroni correction for multiple tests, then differences between continuous variables were analysed by Kruskal Wallis tests. Multivariate analyses were carried out by multiple linear regression models.

Results

Four hundred SLE patients were included in the study, including 375 women and 25 men. 61 patients (15.25%) were underweight (BMI<18.5 kg/m²), 267 patients (66.75%) had a normal BMI (18.5 kg/m²≤BMI<25 kg/m²), and 72 (18.00%) were overweight (BMI ≥ 25kg/m²). BMI was negatively correlated with SLE disease activity index (SLEDAI) score (ρ=-0.11, P = 0.02) and positively correlated with inflammatory index complement component 3 (C3, ρ = 0.19, P = 1.16x10^-4). Patients in underweight group had the highest proportion (14.8%) of moderate to severe disease activity (SLEDAI ≥ 10) compared to normal weight (3.4%) and overweight (1.4%) patients. SLEDAI score, Anti-dsDNA, C3, WBC count, ALT, NEUT and HGB were significantly different between the underweight group and the other two groups.

Conclusions

These findings suggest that SLE patients with low BMI have higher disease activity, which means low BMI exerted a negative impact on disease activity in SLE patients. Causal relation between disease activity and BMI requires further investigation.

Systemic lupus erythematosus

Body mass index

Systemic lupus erythematosus disease activity index

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that forms pathogenic autoantibodies and immune complexes and mediates organ and tissue damage[1, 2]. The global SLE incidence and newly diagnosed population were estimated to be 5.14 (1.4 to 15.13) per 100 000 person-years and 0.40 million annually, respectively[3]. The pathogenesis of SLE is not complete clear, genetic factors and hormone levels are known causes, the latter of which make SLE more likely to occur in women, with a ratio of about 9 women to 1 man[2, 4]. Environmental factors are considered be related to pathogenesis and disease activity. Specific or cumulative environmental exposures can lead to disruption of immune tolerance, eventually leading to the formation of autoantibodies and subsequent clinical manifestations over time.

As a common environmental factor, abnormal body weight is associated with various diseases. Body mass index (BMI) is the one of most commonly used body weight indices in clinical practice. Many previous studies have focused on the adverse effects of obesity on disease, including SLE[5]. Obese women have a higher risk of SLE compared to women with a normal BMI[6]. Obese patients with SLE exhibited higher SLE Disease Activity Index (SLEDAI) scores, lower complement component 3 (C3) levels, and elevated inflammatory biomarkers compared to patients with a normal BMI[7]. This may be attributed to dysregulated endocrine function and abnormal secretion of inflammatory factors in adipose tissue[7]. Like high BMI, although the mechanism may not be clear, low BMI also has a bad effect on some diseases. [8, 9]. However, there is limited research focusing on the risk of underweight in SLE.

In this cross-sectional observational study, the relationship between BMI, disease activity, inflammatory markers, biochemical indices, and immune cell counts in individuals with SLE were analysis. Furthermore, SLEDAI and other clinical variables were stratified by BMI categories (underweight, normal weight, and overweight) among SLE patients. The results suggest that low BMI may be a risk factor for SLE disease activity. This conclusion may be able to guide the weight management of SLE patients in clinical work.

Participants

This is a cross-sectional study that enrolled consecutive 400 adult patients (18 years or older) with SLE (375 female and 25 male) from December 2020 to December 2022 outpatients or inpatients in department of rheumatology and immunology, First Affiliated Hospital of Xi’an Jiaotong University, Shaanxi, China. All patients fulfilled the American College of Rheumatology (ACR) revised criteria for the SLE classification [10]. Exclusion criteria were not being able to read, understand and/or sign the informed consent; pregnancy, pleural effusion, ascites, or other conditions in which BMI cannot be measured; complicated with severe organ damage or other diseases affecting the study. This study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of First Affiliated Hospital, School of Medicine, Xi’an Jiaotong University (No. XJTU1AF2020LSK-278). Detailed information about the aims and study procedures was given to all the participants, who signed informed consent before being included in the study.

Data collection

Clinical features, including age, disease duration, BMI, and medication use, as well as inflammatory and biochemical indicators such as C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), immunoglobulin A (IgA), immunoglobulin M (IgM), immunoglobulin G (IgG), C3, C4, hemoglobin (HGB), aspartate aminotransferase (AST), alanine aminotransferase (ALT), albumin (ALB), blood urea nitrogen (BUN), creatinine (CRE), uric acid (UA), 24-hour urine protein, blood cell analysis, anti-dsDNA, SLEDAI were obtained from clinical records.

BMI categories

The BMI was calculated by Weight(kg)/Height²(m²), and in accordance with the World Health Organization (WHO) BMI category classification, patients were considered underweight (BMI < 18.5), normal weight (18.5 kg/m²≤BMI<25 kg/m²), and overweight (BMI ≥ 25kg/m²)[11].

Statistical Analyses

SPSS (version 16.0, IBM) or Prism (version 6.0, GraphPad Software) were used to analyze the statistical significance of data generated from the current study. Data were presented as mean ± standard deviation (SD), median (interquartile range) or n(%), as appropriate. Multiple comparisons were performed using one-way ANOVA test followed by Tuckey Kramer test for post hoc analysis. The unpaired two-tailed Student’s test was used to compare the difference between the two groups. Normal distribution of the data was assessed by Shapiro-Wilk test with P > 0.05. Pearson correlation coefficient was used to analyze the correlations between two variables and P values < 0.05 were considered as statistically significant.

Patient characteristics

Demographics, clinical characteristics and use of medicine of the study participants are presented in Table 1. In total, 400 patients were enrolled. Of these, 375 patients (93.75%) were female and 25 patients (6.25%) were male. The mean age was 40.86 ± 12.91 years, and the median disease course was 74.00 ± 73.06 months. A total of 373 patients (93.25%) received glucocorticoid, with an average daily dose of 13.24 ± 14.10mg/d (equivalent to prednisone), an average duration of administration of 14.61 ± 22.49 months, and an average total dose of 3.84 ± 4.86g (equivalent to prednisone). Immunosuppressants used included hydroxychloroquine (n = 310, 77.5%), leflunomide (n = 38, 9.50%), Cyclophosphamide (n = 37, 9.25%), mycophenolate mofetil (n = 116, 29.00%), azathioprine (n = 1, 0.25%), cyclosporine (n = 43, 10.75%), tacrolimus (n = 37, 9.25%), methotrexate (n = 10, 2.50%), irammod (n = 22, 5.50%) and thalidomide (n = 8, 2.00%). Patients were divided into three groups: 61 patients (15.25%) with underweight patients, 267 patients (66.75%) with normal weight, and 72 patients (18.00%) with overweight. There is only one patient (BMI ≥ 30 kg/m²) and no morbidly obese (BMI ≥ 40 kg/m²) patient in overweight group. Therefore, the overweight group did not to be further stratified into overweight, obese and morbidly obese groups. There was no statistical difference in age, disease duration, and the duration and dosage of prednisone or Immunosuppressant use among the three groups.

Table 1

Demographics and clinical data of the entire study population and different BMI groups
	Underweight (n = 61)	Normal weight (n = 267)	Overweight (n = 72)	Total (n = 400)
Age	40.03 ± 13.78	40.82 ± 12.90	41.74 ± 12.31	40.86 ± 12.91
Sex
Male	5(8.20%)	13(4.87%)	7(9.72%)	25(6.25%)
Female	56(91.80%)	254(95.13%)	65(90.28%)	375(93.75%)
Disease duration (m)	62.69 ± 64.86	76.83 ± 73.11	73.08 ± 79.18	74.00 ± 73.06
BMI (kg/m²)	17.33 ± 0.86	21.12 ± 1.47	25.90 ± 1.81	21.40 ± 2.90
Prednisone use	60(98.36%)	24(90.37%)	68(94.44%)	152(38.00%)
Duration of Prenisone (m)	17.53 ± 20.39	15.36 ± 24.39	15.59 ± 19.30	14.61 ± 22.49
Prednisone DDD (mg/d)	12.62 ± 12.99	14.35 ± 13.57	14.98 ± 16.72	13.24 ± 14.10
Prednisone NTD (g)	3.95 ± 3.22	4.26 ± 5.49	4.09 ± 4.01	3.84 ± 4.86
Immunosuppressant
HCQ	47(77.05%)	205(76.78%)	58(80.56%)	310(77.50%)
HCQ DDD (g)	0.31 ± 0.11	0.31 ± 0.11	0.35 ± 0.09	0.28 ± 0.14
LEF	4(6.56%)	25(9.36%)	9(12.50%)	38(9.50%)
CTX	5(8.20%)	28(10.49%)	4(5.56%)	37(9.25%)
MMF	21(34.43%)	68(25.47%)	27(37.50%)	116(29.00%)
Azathioprine	0	1(0.37%)	0	1(0.25%)
Cyclosporine	8(13.11%)	28(10.49%)	7(9.72%)	43(10.75%)
Tacrolimus	7(11.48%)	24(8.99%)	6(8.33%)	37(9.25%)
Methotrexate	2(3.28%)	6(2.25%)	2(2.78%)	10(2.50%)
Irammod	3(4.92%)	14(5.24%)	5(6.94%)	22(5.50%)
Thalidomide	0	6(2.25%)	2(2.78%)	8(2.00%)
Biotherapies
Rituximab	2(3.28%)	3(1.12%)	1(1.39%)	6(1.50%)
belimumab	7(11.47%)	24(8.99%)	8(11.11%)	39(9.75%)
Four hundred patients with SLE (375 women and 25 men) were studied. Their mean ± SD age was 40.86 ± 12.91 years, the mean ± SD duration of disease was 74.00 ± 73.06 months, and the mean ± SD BMI of the patients was 21.40 ± 2.90 kg/m². 61 patients (15.25%) were underweight (BMI<18.5 kg/m²), 267 patients (66.75%) had a normal BMI (18.5 kg/m²≤BMI<25 kg/m²), and 72 (18.00%) were overweight (BMI ≥ 25kg/m²). There were no significant difference in age, sex, disease duration, duration of glucocorticoids, NTD and DDD of glucocorticoids among three gourps.
NTD, Normalized Total Dose. DDD, Daily Defined Dose. HCQ, Hydroxychloroquine. LEF, Leflunomide. CTX, Cyclophosphamide. MMF, Mycophenolate mofetil.

Relation between BMI and clinical variables

To investigate multicollinearity among the four clinical feature aspects, including clinical, inflammatory, biochemical indices and immune cells, we selected variables for Spearman correlation tests (some data did not conform to a normal distribution), as depicted in Fig. 1. Subsequently, we compared clinical indicators among the underweight, normal weight, and overweight groups. The results are presented in Figs. 2 and 3.

First, Fig. 1 demonstrates a negative correlation between BMI and SLEDAI score (ρ = -0.11, P = 0.02). The underweight group exhibited the highest SLEDAI score (Fig. 2A). Significant differences in SLEDAI score were observed between the underweight group and the normal weight group (P = 8.70 × 10^-4), as well as between the underweight group and the overweight group (P = 5.79 × 10^-4). However, no significant differences were found between the normal weight group and the overweight group (P = 1.00). Subsequently, we analyzed the distribution of SLEDAI scores within each of the three groups separately, as depicted in Fig. 2B. The underweight group had the lowest proportion of SLEDAI scores between 0 and 4 (indicating disease inactivity) at 55.7%, whereas the overweight group had the highest proportion at 77.8%. Conversely, the underweight group showed the highest proportion of SLEDAI scores ≥ 10 (indicating moderate to high disease activity) at 1.4%, whereas the overweight group had the lowest proportion at 14.8%. These results are consistent with those presented in Fig. 1, illustrating that individuals with lower BMI tend to have higher SLEDAI scores, indicative of more significant disease activity.

Kidney is one of the most representative organs involved in systemic lupus erythematosus. There was no significant difference in the rate of renal involvement or the positive rate of 24-hour urinary protein quantitation among the three groups. At the same time, the 24-hour urinary protein quantitative value of patients with low body weight and renal involvement was lower than that of the other two groups, but there was no significant difference. This data is shown in Supplementary Fig. 1.

As important immunological indices for evaluating disease activity in SLE, anti-dsDNA antibodies, complement levels and IgG were further analyzed. The level of anti-dsDNA antibodies (Fig. 3A) was found to be significantly higher in the underweight group compared to the normal weight group (P = 0.04). Furthermore, a positive correlation was observed between BMI and C3 levels (ρ = 0.19, P = 1.16 × 10^-4), as depicted in Fig. 1. Additionally, C3 levels (Fig. 3B) exhibited significant variation among the three different BMI groups (underweight vs. normal weight, P = 3.80 × 10^-3; underweight vs. overweight, P = 1.50 × 10^-5; normal weight vs. overweight, P = 0.03), with the lowest mean C3 level observed in the underweight group. C4 and IgG, which were also commonly used in disease activity assessment, were showed no significant statistical difference among the three groups and are therefore not shown.

In biochemical and blood tests, a lower ALT, HGB, counts of WBC, LYM, NEYT, MONO (Fig. 3C-H) were showed in underweight group, compared to normal weight group, overweight group, or both normal weight group and overweight group. Studies have shown that high body weight people mean higher ALT level[12]. Therefore, it is not surprising that low body recombination has lower ALT. Additionally, other immune cell counts were also collected, including NK cell, helper T cell and killer T cell. Those cells count showed no significant correlation with BMI (Fig. 1) and no significant different in different BMI groups (data not shown).

Furthermore, BMI shows positive correlations with specific metabolic indicators: uric acid (UA, ρ = 0.17, P = 7.32 x 10^-4), total cholesterol (TC, ρ = 0.16, P = 1.83 x 10^-3), and triglycerides (TG, ρ = 0.19, P = 4.01 x 10^-3). Reasonably, UA and the other two lipid metabolism-related parameters in the underweight group were significantly lower compared to the other two groups (Fig. 3I-K).

The relationship between body weight and diseases has always been a hot topic of clinical research, especially in recent years, with obesity becoming a global public health concern garnering even more attention. It has been shown that the general population has elevated concentrations of inflammatory markers and mediators such as CRP and interleukin-6 (IL-6) in the context of obesity[13, 14], which means high body weight and obesity are independent contributors to systemic low-grade inflammatory status[15]. At the same time, SLE is an autoimmune disease characterized by a chronic low-grade inflammatory state that is independent of the disease activity[16]. Therefore, with the addition of these two factors, obese SLE patients will present with a higher systemic inflammatory status than normal weight. It has been reported in the literature that obesity is considered to be one of the unfavorable factors for the activity of SLE[7] and other autoimmune diseases[5]. However, the potential harms of low BMI on diseases have received less attention. Previous studies reported some negative effects of low BMI on SLE. Wietske Lambers' findings showed that among patients who were diagnosed with SLE after long-term follow-up, they presented more with low BMI before diagnosis[4]. Underweight also contributed to adverse mental health-related quality of life (HRQoL) outcome in SLE patients[17]. These studies suggest that low BMI may have a negative impact on SLE. These studies suggest that low BMI may have a negative impact on SLE. However, whether low BMI has a negative impact on SLE disease activity has not been reported.

This study investigated the relation between BMI and disease activity in SLE patients. We demonstrated for the first time that SLE patients who were underweight (BMI<18.5 kg/m²) had higher SLEDAI scores, i.e., higher disease activity, compared to normal weight and overweight SLE patients. The lowest proportion of moderate/severe disease activity (SLEDAI ≥ 10 points) in the entire study population was documented for overweight patients (1.4%) and the highest for underweight (14.8%). High dsDNA values, low C3 values and low blood cells are the characteristics of SLE patients in the underweight group, suggesting high disease activity.

Prior to our study, there was evidence that body weight was associated with systemic inflammatory status and disease activity, including SLE[7, 18]. A study from Spain explored the relationship between BMI and disease activity in 276 patients with SLE[18].The results suggested obese SLE patients have more severe disease activity and organ damage and higher levels of inflammatory markers hs-CRP and C3 complement compared to overweight or normal weight SLE patients[18]. A reasonable explanation for this conclusion is that adipose tissue itself is involved in inflammation[18]. There have been sufficient results to prove that adipose tissue has endocrine function and can secrete complement and pro-inflammatory factors ^{13, 14}. Consistent with the licture from Spain, complement C3 was positively correlated with BMI in our study. However, our study also has unique or inconsistent results. The most obvious finding is that a worse SLEDAI was showed in underweight patient but not overweight/obese patient in our study. We analyzed some possible reasons for this result. Firstly, previous studies did not include underweight SLE patients. Body weight distribution in Asian SLE patient populations has not been documented. However, the prevalence of overweight and obesity in China might still be lower than in other developed nations[19]. Thus there were not enough obese people to compare in our study population. Relatively speaking, in their study, the underweight population was also not included in the grouping. Secondly, as our study is a cross-sectional study, another possible explanation for the higher disease activity in patients with low BMI is that at the cut-off point of our statistical information, patients have developed or received treatment, and high disease activity puts the whole body in a state of high inflammatory consumption, causing a decrease in body weight and BMI. This needs to be further confirmed by rigorous clinical trials or long-term cohort studies. Another difference from previous studies[7, 18] is that inflammatory markers such as CRP did not show a significant increase in the overweight group than normal weight group. The reasons are still being considered to be related to the uniqueness of the study population. In our study, the mean BMI of patients in overweight group was just 25.90 ± 1.81 kg/m², slightly above the overweight standard (BMI ≥ 25kg/m²),, and much lower compared to the obese group in other studies[7, 18]. This may have led to the lack of difference in CRP levels between the groups in our study.

Although this study is a large population cohort, there are some limitations. Most importantly, this is a cross-sectional study and we cannot address the causal relation between low BMI and high SLE disease activity through this study. Longer follow- up of this cohort is necessary to show the predictive value of the BMI in combination with other promising variables like autoantibodies in a SLE population- based cohort. As mentioned above, obese patients were missing in our study population, so differences between obese and underweight patient populations could not be observed. Thirdly, It has been shown that BMI is not currently the best indicator for assessing obesity[20], some BMI metrics have been suggested as more accurate surrogates of adiposity, such as percent of the BMI 95th percentile (%BMIp95), percent of the BMI median (%BMIp50), triponderal mass index (TMI, weight/height3), and absolute BMI[21, 22]. But there is no clear conclusion whether BMI is best for evaluating underweight population. In future in-depth studies, we will supplement more effective relevant indicators to assess the patient 's weight. However, further investigation of this association in future studies has merit. This study supports the usefulness of further prediction and screening for highly active disease in the SLE patient population by providing insight into BMI values in SLE patients. This may help to develop a stepwise approach for earlier control of SLE.

Weight and health management of SLE patients has always been a hot issue discussed by rheumatologists. We expect to find the ideal body weight of SLE patients through research to achieve the purpose of reducing the activity of the disease, predicting severe lupus or disease relapse, and guiding medication. As the independent risk factor for the development of cardiovascular events[23–26], overweight or obesity is has been used clinically as a risk of cardiovascular disease in lupus[27]. We showed for the first time that SLE patients with low BMI had higher disease activity and lower levels of complement and blood cells. This may mean that for SLE patients, low body weight is also unfavorable for disease control. It enriches the understanding of rheumatologists and has a certain reference role for us to determine the condition of newly diagnosed patients and predict the prognosis. Therefore, it is of interest to test BMI in SLE population, in relation to other characteristics including biochemical values.

Together, underweight exerted a negative impact on disease activity. This conclusion gives us some more understanding of the indicators that are associated with SLE disease activity and facilitates our further understanding and research of SLE in the future.

SLE	Systemic Lupus Erythematosus
BMI	Body Mass Index
CRP	C-reactive Protein
IL-6	Interleukin-6
SLEDAI	Systemic Lupus Erythematosus Disease Activity Index
C3	Complement component 3
C4	Complement component 4
HGB	Hemoglobin
AST	Aspartate Aminotransferase
ALT	Alanine Aminotransferase
ALB	Albumin
BUN	Blood Urea Nitrogen
CRE	Creatinine
UA	Uric Acid
WBC	White Blood Cells
LYM	Lymphocyte
NEYT	Neutrophil
MONO	Monocyte
NK cell	Natural Killer Cell
IgA	Immunoglobulin A
IgM	Immunoglobulin M
IgG	Immunoglobulin G
hs-CRP	High-Sensitivity C-reactive Protein
TMI	Triponderal Mass Index
ACR	American College of Rheumatology

Ethics approval and consent to participate

This was a retrospectively study, and all data were from another cohort study (ClinicalTrials. Gov identifier: NCT04893161). The study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of First Affiliated Hospital, School of Medicine, Xi’an Jiaotong University (No. XJTU1AF2020LSK-278). Informed consent was obtained from all patients before participation.

Consent for publication

Not applicable.

Availability of data and materials

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Competing interests

The authors declare they have no competing interests.

Funding

The study was supported by the Shaanxi Province Natural Science Foundation (No. 2023-JC-YB-754 and No. 2023-JC-YB-774), Shaanxi Province key research and development plan project (No. 2023-ZDLSF-11) and First Affiliated Hospital of Xi’an JiaoTong University Foundation (No. 2022MS-04).

Authors' contributions

HL and XD analyzed data and drafted the paper. XL, ZH LH collected data. LH designed the presented study. XL, ZH LH were responsible for patient management. All authors discussed the results and contributed to the final manuscript.

Acknowledgements

We thank Dr. Jun Wang (Institute of Gene and Cell Therapy of Xi’an JiaoTong University) for technical assistance.

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Correlation between body mass index and disease activity in patients with systemic lupus erythematosus from China

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