Vol:.(1234567890)
Obesity Surgery (2024) 34:4378–4384
https://doi.org/10.1007/s11695-024-07567-w
RESEARCH
Association of High‑Sensitivity C‑Reactive Protein (hs‑CRP) 
with Weight Loss After Sleeve Gastrectomy and Roux‑en‑Y Gastric 
Bypass at 10 Years: A Secondary Analysis of the SLEEVEPASS 
Randomized Clinical Trial
Ilmari Saarinen1,2 · Marjatta Strandberg3 · Saija Hurme1,3 · Sofia Grönroos1,2 · Anne Juuti4,5 · Mika Helmiö1,3 · 
Paulina Salminen1,3
Received: 12 August 2024 / Revised: 30 September 2024 / Accepted: 26 October 2024 / Published online: 7 November 2024 
© The Author(s) 2024
Abstract
Background Severe obesity is associated with a low-grade chronic inflammation, and high-sensitivity C-reactive protein 
(hs-CRP) is a marker that can be used to evaluate chronic inflammation status. Metabolic bariatric surgery (MBS) is shown 
to decrease hs-CRP level, but long-term results are scarce, and association with weight loss outcomes is undetermined. 
This study aims to evaluate chronic inflammation in patients with obesity using hs-CRP, and its association with long-term 
weight loss outcomes after laparoscopic sleeve gastrectomy (LSG) and laparoscopic Roux-en-Y gastric bypass (LRYGB).
Methods The long-term follow-up data of SLEEVEPASS (ClinicalTrials.gov NCT00793143) randomized clinical trial (RCT) 
was used. Hs-CRP was measured at baseline, and at 6 months, 1, 3, 5, 7, and 10 years after surgery, and the association with 
weight and weight loss outcomes were analyzed.
Results Hs-CRP at baseline was available for 59 out of 240 (24.6%) patients. In the whole study population, the nadir hs-CRP 
(mean estimate 1.14 mg/ml, 95% CI 0.87–1.49) was achieved at 3 years after surgery with a statistically significant difference 
to baseline (p = 0.003). No statistically significant difference was seen between LSG and LRYGB in hs-CRP change over 
time (operation*time interaction p = 0.540). Higher hs-CRP correlated with higher BMI at baseline (Spearman correlation 
0.282, p = 0.030) and at 10 years (Spearman correlation 0.490, p = 0.001). At 10 years, a greater percentage total weight 
loss (%TWL) correlated with lower hs-CRP level (Spearman correlation − 0.558, p < 0.001). Baseline hs-CRP (Spearman 
correlation − 0.152, p = 0.299) and hs-CRP change in first 6 months postoperatively (Spearman correlation 0.167, p = 0.254) 
did not correlate statistically significantly with %TWL at 10 years.
Conclusions MBS decreases hs-CRP also at long-term follow-up with weight loss as the driving force. Neither baseline 
hs-CRP nor hs-CRP change at 6 months were feasible as a predictive marker for long-term outcomes.
Keywords Metabolic bariatric surgery · Sleeve gastrectomy · Roux-en-Y gastric bypass · Severe obesity · Chronic 
inflammation · High-sensitivity CRP · Hs-CRP
Introduction
Obesity and its comorbidities such as type 2 diabetes 
(T2DM) and cardiovascular diseases (CVDs) are among 
the biggest global health threats [1]. Low-grade chronic 
inflammation is shown to be associated with obesity [2–5]. 
It has been suggested that adipose tissue activates and pro-
duces proinflammatory cytokines such as tumor necrosis 
factor alpha (TNF-α) and interleukin 6 (IL-6) [6, 7], and 
IL-6 in turn causes increased production of C-reactive pro-
tein (CRP), a commonly used inflammatory marker [8]. 
Key points
• MBS resulted in long-term decrease in hs-CRP at 10-year 
follow-up.
• No difference was seen between LSG and LRYGB in hs-CRP 
change over time.
• Greater %TWL correlated with lower hs-CRP at 10 years.
• Baseline hs-CRP or hs-CRP change in first 6 months 
postoperatively did not correlate with the outcome of surgery.
Extended author information available on the last page of the article
4379Obesity Surgery (2024) 34:4378–4384 
High-sensitivity CRP (hs-CRP) has been used to assess low-
grade inflammatory state in patients with metabolic diseases. 
Elevated hs-CRP levels have been reported in patients with 
obesity [9, 10]. Hs-CRP has predictive value in CVDs [11, 
12], and therefore The American Heart Association recom-
mends it for clinical use as one parameter of CVD risk [13]. 
Many studies have shown that elevated hs-CRP may also be 
an independent risk factor for worsening insulin resistance, 
increased mortality of patients with T2DM, and de novo 
T2DM [14–17]. However, there are also studies suggesting 
that obesity may be the link between elevated hs-CRP and 
metabolic diseases [18].
Metabolic bariatric surgery (MBS) is the most efficient 
treatment of severe obesity with good and sustainable weight 
loss and beneficial effects on obesity-related comorbidities 
[19–23]. MBS has also been shown to decrease hs-CRP 
levels [24]. A recent study suggests that hs-CRP correlates 
with preoperative weight and postoperative weight loss but 
not with remission of metabolic diseases [25]. Since 2014, 
laparoscopic sleeve gastrectomy (LSG) has been the most 
common bariatric procedure globally surpassing the gold 
standard, laparoscopic Roux-en-Y gastric bypass (LRYGB) 
in the number of performed operations [26]. Most of the 
studies examining MBS and hs-CRP focus on short-term 
results of LRYGB, and long-term results on the effects of 
LSG and both procedures on hs-CRP are lacking. The poten-
tial of hs-CRP as a predictive marker of MBS outcomes is 
yet to be determined [25].
To our knowledge, the SLEEVEPASS randomized 
clinical trial (RCT) is so far the largest RCT comparing 
the results of LSG and LRYGB with a 10-year follow-up 
[27]. The aims of this 10-year secondary analysis of the 
SLEEVEPASS trial were to assess the effect of MBS on 
hs-CRP at long-term follow-up and the association between 
weight loss and hs-CRP, to evaluate the potential predictive 
value of hs-CRP for MBS outcomes, and to compare the 
effects of LSG and LRYGB on hs-CRP.
Materials and Methods
The study design, rationale, and methods of the 
SLEEVEPASS trial have been reported previously [27]. 
Briefly, the SLEEVEPASS trial is a multicenter, multi-
surgeon, open label, randomized clinical equivalence 
trial conducted between March 2008, and June 2010 in 
three hospitals in Finland (Turku, Vaasa, and Helsinki), 
randomizing 240 patients with severe obesity to undergo 
either LSG or LRYGB. Eligibility criteria included body 
mass index (BMI; kg/m2) > 40 or > 35 with an obesity-
associated comorbidity, age 18 to 60 years, and a previous 
failed adequate conservative treatment. Exclusion criteria 
were BMI greater than 60, significant eating or psychiatric 
disorder, active alcohol or substance abuse, active gas-
tric ulcer disease, severe gastroesophageal reflux disease 
(GERD) with a large hiatal hernia, and previous bariatric 
surgery. The 10-year follow-up of the trial was completed 
in January 2021. The study protocol was approved by the 
ethics committees of each participating hospital (Turku, 
Helsinki, and Vaasa). The trial was designed in accord-
ance with the principles of the Declaration of Helsinki 
and registered at the clinical trials registry of the National 
Institutes of Health (ClinicalTrials.gov NCT00793143). 
All patients gave written informed consent.
CRP values were assayed with high-sensitivity CRP test 
(S-uCRP or S-hs-CRP) from blood samples collected from 
the trial patients preoperatively and at 6 months, 1, 3, 5, 7, 
and 10 years. All available hs-CRP values at all time points 
were included with the vast majority of the available values 
were from the patient cohort at Turku University hospital 
and a minority from Helsinki University Hospital. Hs-CRP 
tests were not included in the laboratory tests taken at Vaasa 
Central Hospital. All hs-CRP values ≥ 25 were considered 
as signs of an acute infection or autoimmune disease activa-
tion and were therefore excluded from the analyses. Weight 
loss was defined as percentage total weight loss (%TWL 
[preoperative weight − postoperative weight/preoperative 
weight × 100]).
Statistical Analyses
Continuous variables were characterized using means and 
standard deviations (SD) or medians with 25th and 75th per-
centiles (Q1, Q3) in case of non-normally distributed vari-
ables. For categorical variables, frequencies and percents 
were used.
Linear mixed models suitable for repeated measures 
were used to evaluate the differences between time-points 
and operations in hs-CRP. The final model included opera-
tion, time, BMI, and interaction of operation and time. The 
interaction of operation and time was not statistically sig-
nificant and therefore the results are presented using main 
effects of operation and time. The results were quantified 
using model-based estimates with 95% confidence intervals 
(95% CI). Values of hs-CRP were not normally distributed, 
and logarithmic transformation was used in the analyses, 
and estimates were transformed back to the original scale. 
Tukey–Kramer method was used to correct p values of pair-
wise comparisons of timepoints.
The correlations between continuous variables were eval-
uated using Spearman’s rank-order correlation coefficient. 
Two-tailed p values less than 0.05 were considered statisti-
cally significant. Statistical analyses were performed using 
SAS software, version 9.4 for Windows (SAS Institute Inc., 
Cary, NC, USA).
4380 Obesity Surgery (2024) 34:4378–4384
Results
The flow of the patients is presented in Fig. 1. Of the 240 
SLEEVEPASS study patients, 59 (24.6%) had baseline 
hs-CRP value available (56 patients at Turku University 
Hospital, 3 patients at Helsinki University hospital). Out 
of these 59 patients, 27 underwent LSG and 32 LRYGB. 
Baseline characteristics of the patients in this secondary 
analysis are described in Table 1.
Hs-CRP at all time points in the whole study population 
is presented in Fig. 2A, and hs-CRP levels by operation are 
presented in Fig. 2B. Hs-CRP was the highest at baseline 
(mean estimate 2.06, 95% CI 1.48–2.86). Postoperatively, 
a decrease was seen, and the nadir hs-CRP was achieved 
at 3 years (mean estimate 1.14 mg/L, 95% CI 0.87–1.49). 
There were statistically significant differences in hs-CRP 
Fig. 1  Flow of patients. Abbreviations: LSG, laparoscopic sleeve gastrectomy; LRYGB, laparoscopic Roux-en-Y gastric bypass; Hs-CRP, high-
sensitivity C-reactive protein
4381Obesity Surgery (2024) 34:4378–4384 
between timepoints (p < 0.001). Compared to baseline, there 
was a statistically significant difference in hs-CRP only at 
3 years (p = 0.043). After 3 years, hs-CRP increased until 
7 years (mean estimate 1.90 mg/L, 95% CI 1.42–2.56), but 
decreased again at 10 years (mean estimate 1.38 mg/L, 95% 
CI 1.05–1.81). There was no statistically significant differ-
ence between the operations in hs-CRP change over time 
(operation*time interaction p = 0.540). Hs-CRP decreased 
after both procedures, but it was higher through the whole 
10-year follow-up in LSG group (main effect of operation 
p < 0.001). Results were adjusted with BMI to enable the 
evaluation of the effect of operation. The results of the final 
model of Hs-CRP through 10-year follow-up are presented 
in Table 2.
A greater 10 year-%TWL correlated statistically signifi-
cantly with lower hs-CRP at 10 years (Spearman correla-
tion − 0.558, p < 0.001). The hs-CRP at baseline correlated 
statistically significantly with preoperative BMI (Spearman 
Table 1  Baseline patient characteristics
LSG laparoscopic sleeve gastrectomy, LRYGB laparoscopic Roux-en-Y gastric bypass, T2D type 2 diabetes mellitus, LDL low-density lipopro-
tein, CPAP continuous positive airway pressure, OSA obstructive sleep apnea, Hs-CRP high-sensitivity C-reactive protein
*Fisher’s exact test
†Analysis of variance
LSG LRYGB All included patients Excluded patients P comparing included 
and excluded patients
N 27 32 59 181 NA
Age (years), mean (SD) 46.7 (8.6) 47.2 (10.1) 47.0 (9.4) 48.9 (9.3) 0.945†
Female, frequency (%) 18/27 (66.7%) 20/32 (62.5%) 38/59 (64.4%) 129/181 (71.3%) 0.332*
Male, frequency (%) 9/27 (33.3%) 12/32 (37.5%) 21/59 (35.6%) 52/181 (28.7%) 0.332*
Body mass index, BMI (kg/m2), mean (SD) 47.3 (5.9) 48.9 (7.8) 48.2 (7.0) 47.8 (6.9) 0.896†
T2D, frequency (%) 13/27 (48.2%) 15/32 (46.9%) 28/59 (47.5%) 73/181 (40.3%) 0.364*
Blood pressure medication, frequency (%) 15/27 (55.6%) 24/32 (75.0%) 39/59 (66.1%) 131/181 (72.4%) 0.410*
High LDL/cholesterol medication, frequency 
(%)
7/27 (25.9%) 11/32 (34.4%) 18/59 (30.5%) 66/181 (36.5%) 0.436*
CPAP-treated OSA, frequency (%) 5/27 (18.5%) 10/32 (31.3%) 15/59 (25.4%) 48/181 (26.5%) 0.134*
Hs-CRP (mg/L), median  (Q1-Q3) 5.5 (2.7–8.2) 4.0 (2.8–5.5) 4.2 (2.8–7.0) NA NA
59 59 56 49 45 37 44
No. of patients:0
5
10
15
20
25
Baseline 6 months 1 years 3 years 5 years 7 years 10 years
H
s−
CR
P 
(m
g/m
L)
A  All study patients
27 27 27 21 19 14 2132 32 29 28 26 23 23
No. of patients:0
5
10
15
20
25
Baseline 6 months 1 years 3 years 5 years 7 years 10 years
H
s−
C
R
P
 (
m
g/
m
L)
LSG
LRYGB
B  Divided by operation 
Fig. 2  Hs-CRP through a 10-year follow-up. A All study patients. 
B Divided by operation. The lower and upper hinges correspond 
to the first and third quartiles (the 25th and 75th percentiles), and 
whiskers indicate smallest observation greater than or equal to lower 
hinge—1.5 * IQR and largest observation less than or equal to upper 
hinge + 1.5 * IQR. Dots indicate outliers. Abbreviations: LSG, lapa-
roscopic sleeve gastrectomy; LRYGB, laparoscopic Roux-en-Y gas-
tric bypass; Hs-CRP, high-sensitivity C-reactive protein
4382 Obesity Surgery (2024) 34:4378–4384
correlation 0.282, p = 0.030). Also at 10 years, hs-CRP cor-
related statistically significantly with present BMI (Spear-
man correlation 0.490, p = 0.001). No statistically signifi-
cant correlation was seen between baseline hs-CRP level 
and %TWL at 10  years (Spearman correlation − 0.152, 
p = 0.299). Similarly, hs-CRP change in first 6 months post-
operatively (Spearman correlation 0.167, p = 0.254) did not 
correlate statistically significantly with %TWL at 10 years.
Discussion
In this secondary analysis of the SLEEVEPASS trial, meta-
bolic bariatric surgery resulted in sustainable improvement 
on chronic inflammation evaluated by decreased postopera-
tive hs-CRP levels up to 10 years postoperatively with both 
the nadir and statistically significant difference at 3 years. 
Between LSG and LRYGB, there was no statistically signifi-
cant difference in hs-CRP change over time. Hs-CRP cor-
related statistically significantly with BMI at baseline and at 
10 years. In addition, greater %TWL correlated statistically 
significantly with lower hs-CRP at 10 years. Preoperative 
hs-CRP and hs-CRP change in first 6 months postopera-
tively did not correlate statistically significantly with 10-year 
%TWL outcomes.
To our knowledge, this is the first RCT comparing LSG 
and LRYGB to assess post-bariatric hs-CRP decrease with a 
10-year follow-up. Other studies have also reported sustain-
able improvement in hs-CRP level at 7 years with a slight 
increase from the lowest point at 3 years to 7 years [28, 29]. 
This is in line with this study having the nadir hs-CRP at 
3 years and other studies reporting lowest hs-CRP levels at 
2 years postoperatively followed by a minor increase [28, 
29]. Our results indicate and corroborate a strong correla-
tion between hs-CRP and BMI pre- and postoperatively. 
Weight loss seems to be the driving force behind the hs-CRP 
decrease after MBS [25, 28, 30]. These findings support the 
hypothesis that the amount of adipose tissue in obesity is 
the key determinant of the grade of chronic inflammation 
[4, 18].
In this study, baseline hs-CRP was not a predictive fac-
tor of %TWL at 10 years. In a previous study [25], higher 
baseline hs-CRP was associated with greater weight loss 
at 3 years postoperatively. However, this correlation was 
low and not considered to have clinical utility [25]. We also 
examined whether hs-CRP change during the first 6 months 
after surgery had predictive value over long-term outcome 
of surgery as the majority of the MBS-induced weight loss is 
achieved during this time, but the change in hs-CRP during 
the first 6 months did not correlate statistically significantly 
with long-term outcomes. The applicability of baseline hs-
CRP as a prognostic tool after MBS is very limited based 
on the results of this study, but this serum biomarker should 
be included in future trials to further assess the clinical 
applicability.
In this RCT, baseline hs-CRP was higher in LSG 
group, and this difference persisted through the follow-
up to 10 years. When adjusted for BMI, operation*time 
interaction was not statistically significant. Our results are 
in line with a retrospective study [28] showing no differ-
ences in hs-CRP between the two procedures. In a recent 
study comparing serum biomarkers between laparoscopic 
Table 2  Mean hs-CRP at follow-up points and effects of operation and time
LSG laparoscopic sleeve gastrectomy, LRYGB laparoscopic Roux-en-Y gastric bypass, Hs-CRP high-sensitivity C-reactive protein
*Linear mixed models were used. Results were adjusted for BMI. Logarithmic transformation was used in the analyses, and estimates were 
transformed back to the original scale
†Tukey–Kramer method
All study patients
Follow-up point Hs-CRP (mg/mL), 
mean estimate (95% 
CI)*
P compared to baseline† P compared to 3 years†
Baseline 2.06 (1.48–2.86) NA 0.043
6 months 1.92 (1.49–2.48) 0.999 0.002
1 year 1.42 (1.09–1.85) 0.518 0.680
3 years 1.14 (0.87–1.49) 0.043 NA
5 years 1.81 (1.38–2.38) 0.994 0.026
7 years 1.90 (1.42–2.56) 0.999 0.023
10 years 1.38 (1.05–1.81) 0.286 0.858
Operation comparison
Main effect of operation* Main effect of time* Operation*time interaction*
LSG 2.5 (1.48–3.4)  < 0.001 0.001 0.540
LRYGB 1.0 (0.8–1.4)
4383Obesity Surgery (2024) 34:4378–4384 
adjustable banding and LRYGB [25], the hs-CRP decrease 
independent of weight loss was greater after LRYGB, 
highlighting the potential impact of performed anatomi-
cal modifications.
Our study has several limitations. Firstly, our major limi-
tation is the small number of patients with available hs-CRP 
values at baseline and at all follow-up time points. This is 
mainly due to the fact of missing laboratory tests due to 
human error at two of the participating study hospitals as 
Vaasa has no hs-CRP values, and in Helsinki, only three 
patients have available hs-CRP values available. However, as 
this is based on the simple error of not including the hs-CRP 
in the follow-up, selection bias is very unlikely. All of the 
results may be naturally influenced by the small number of 
patients. However, out of the 80 patients at Turku University 
Hospital, 53 (66%) patients had available hs-CRP values. 
Secondly, our small sample size did not allow assessment of 
potential association between hs-CRP and secondary end-
points of MBS, such as resolution of comorbidities and mor-
tality. Thirdly, the higher baseline hs-CRP in the LSG group 
may be and most likely is caused by the small sample size 
in this randomized data. Fourthly, only the 3-year hs-CRP 
differed statistically significantly from baseline and other 
follow-up points, and this may also be attributable to the 
sample size. However, our results form a similar hs-CRP tra-
jectory compared with other studies [28, 29]. The fifth limi-
tation is that this study consists of patients with Caucasian 
ethnic background potentially limiting the generalizability of 
the results. Further research in larger prospective cohorts is 
needed to evaluate the potential association between hs-CRP 
and MBS outcomes.
In summary, our findings indicate that MBS decreases 
hs-CRP also at long-term follow-up with weight loss as the 
driving force demonstrating a long-term enhancement in 
chronic inflammation after both LSG and LRYGB. Neither 
hs-CRP at baseline nor hs-CRP change during the first 
6 months after surgery was feasible as a predictive marker 
for long-term outcomes of MBS.
Acknowledgements The authors give their thanks to all trial patients. 
We thank all the collaborators in original trials: P. Peromaa-Haavisto, 
J. Ovaska, M. Leivonen and M. Soinio. They also express thanks to 
M. Victorzon (Department of Surgery, University of Turku, and Vaasa 
Central Hospital, Vaasa, Finland) who was involved in this trial, but 
passed away before this work was submitted.
Author Contribution I.S., M.S., and P.S. had full access to all the data 
in the study and take full responsibility for the integrity of the data 
and the accuracy of the data analyses. P.S. had the final responsibility 
for the decision to submit the manuscript for publication. Concept and 
design: I.S., S.H., M.S., and P.S. Acquisition, analysis, or interpreta-
tion of data: I.S., S.H., S.G., A.J., M.H., M.S., and P.S. Drafting of the 
manuscript: I.S., S.H., M.S., and P.S. Critical revision of the manu-
script: I.S., S.H., S.G., A.J., M.H., M.S., and P.S. Statistical analyses: 
I.S., S.H., M.S., and P.S. Administrative, technical, or material support: 
I.S., S.H., M.S., and P.S.
Funding Open Access funding provided by University of Turku 
(including Turku University Central Hospital). The SLEEVEPASS trial 
was supported by the Mary and Georg C. Ehrnrooth Foundation, by a 
government research grant from the EVO Foundation awarded to Turku 
University Hospital and by Finnish Cultural Foundation, Satakunta 
Regional fund.
Role of the Funder/Sponsor
The study funders had no role in the design and conduct of the 
study; collection, management, analysis, and interpretation of the data; 
preparation, review, or approval of the manuscript; or decision to sub-
mit the manuscript for publication.
Data Availability The data will be made available by reasonable request 
from the corresponding author.
Declarations 
Competing Interests The authors declare no competing interests.
Open Access This article is licensed under a Creative Commons Attri-
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need to obtain permission directly from the copyright holder. To view a 
copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
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Publisher's Note Springer Nature remains neutral with regard to 
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Authors and Affiliations
Ilmari Saarinen1,2 · Marjatta Strandberg3 · Saija Hurme1,3 · Sofia Grönroos1,2 · Anne Juuti4,5 · Mika Helmiö1,3 · 
Paulina Salminen1,3
 * Paulina Salminen 
 paulina.salminen@tyks.fi
 Ilmari Saarinen 
 itksaa@utu.fi
 Marjatta Strandberg 
 marjatta.strandberg@tyks.fi
 Saija Hurme 
 saija.hurme@utu.fi
 Sofia Grönroos 
 sapgro@utu.fi
 Anne Juuti 
 anne.juuti@hus.fi
 Mika Helmiö 
 mika.helmio@tyks.fi
1 University of Turku, Turku, Finland
2 Satasairaala Central Hospital, Pori, Finland
3 Turku University Hospital, Turku, Finland
4 Helsinki University Hospital, Helsinki, Finland
5 University of Helsinki, Helsinki, Finland