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com

547

CONCISE REPORT

Acute abdominal pain in systemic lupus erythematosus:

focus on lupus enteritis (gastrointestinal vasculitis)
C-K Lee, M S Ahn, E Y Lee, J H Shin, Y-S Cho, H K Ha, B Yoo, H-B Moon
.............................................................................................................................

Ann Rheum Dis 2002;61:547–550

challenging diagnostic and therapeutic problem. Evaluation of

Objective: To determine the causes of acute abdominal abdominal pain in patients with SLE is complicated by the
pain in systemic lupus erythematosus (SLE) and to compare disease itself and by concomitant disease. The side effects of
the clinical and laboratory data, especially antiphospho- drugs are also often a problem in evaluation.
lipid antibodies and the SLE Disease Activity Index The presence of the antiphospholipid antibody (aPL) is
(SLEDAI), between lupus enteritis (gastrointestinal vasculi- more likely to be associated with thrombosis or chronic fetal
tis) and acute abdominal pain without lupus enteritis in miscarriages.1 To the best of our knowledge, the relation
patients with SLE. between reversible ischaemic bowel disease in SLE and aPL
Methods: A retrospective study was carried out for all has not been adequately investigated.
patients admitted with SLE from 1993 to March 2001. The In the hope of detecting variables for predicting the occur-
SLEDAI and laboratory data were collected at the time of rence of lupus enteritis, we performed a retrospective
diagnosis of SLE and at the time of acute abdominal pain. case-control study to examine clinical and laboratory vari-
Lupus enteritis (gastrointestinal vasculitis) was diagnosed ables, particularly aPL and the systemic lupus Disease Activity
by clinical investigation and abdominal computed tomo- Index (SLEDAI).2
graphic findings.
Results: Chart review identified 175 patients (20 male, PATIENTS AND METHODS
155 female) who had been admitted with SLE. Of these Patients
patients, 38 (22%) presented with acute abdominal pain. We reviewed the records of patients with SLE who had been
Lupus enteritis was the most common cause of acute admitted to our hospital from 1993 to March 2001 and we
abdominal pain. Patients were divided into three groups: identified patients who had presented with acute abdominal
group 1: lupus enteritis (n=17), group 2: acute abdominal pain. All the patients fulfilled the 1982 revised American
pain without lupus enteritis (n=21), and group 3: SLE with- Rheumatism Association criteria for the classification of
out acute abdominal pain (n=137). There was no SLE.3 During this eight year period, 175 patients (20 male, 155
difference in age and sex among the three groups. female) were studied. Of these patients, 38 (22%) presented
Antiphospholipid, anti-RNP, anti-Sm, anti-Ro, and anti-La with acute abdominal pain. Patients were divided into three
antibodies did not differ among the three groups. There groups. Lupus enteritis (n=17) (group 1) was diagnosed if at
was no difference in the SLEDAI at the time of diagnosis least three of the following signs were seen on a computed
and at the time of acute abdominal pain between groups tomographic (CT) scan: bowel wall thickening, target sign,
1 and 2. Complement, erythrocyte sedimentation rate, C dilatation of intestinal segments, engorgement of mesenteric
reactive protein, and anti-dsDNA measured at the time of vessels, and increased attenuation of mesenteric fat.4 Two con-
acute abdominal pain did not differ between groups 1 and trol groups were selected. The first control group (n=21)
2. A drop in the white blood cell count at the time of (group 2) comprised patients with acute abdominal pain
abdominal pain was more prominent in group 1 than without lupus enteritis. The second control group (n=137)
group 2. In lupus enteritis, the jejunum and ileum were the (group 3) consisted of patients with SLE without acute
sites most commonly affected. Rectal involvement was rare. abdominal pain.
Even though four patients relapsed, all the patients with
lupus enteritis, including those who relapsed, responded Clinical features and laboratory data
well to corticosteroid. The demographic data of the patients (sex, age, duration of
Conclusion: Lupus enteritis is the most common cause of disease, and duration of abdominal pain) were recorded.
acute abdominal pain in SLE. All patients with lupus enteri- SLEDAI was calculated at the time of diagnosis of SLE and at
tis responded well to a high dose of a corticosteroid with- the time of acute abdominal pain. The laboratory data, includ-
out surgical intervention. The SLEDAI and laboratory data, ing the white blood cell (WBC) count, haemoglobin, platelets,
except leucopenia, do not correlate with the occurrence of complement, erythrocyte sedimentation rate (ESR), C reactive
lupus enteritis. protein (CRP), anti-dsDNA, aPL, anti-Sm antibody, anti-
ribonucleoprotein (anti-RNP) antibody, anti-Ro antibody, and
anti-La antibody, were measured at the time of diagnosis of
SLE. The WBC count, haemoglobin, platelets, complement,

S
ystemic lupus erythematosus (SLE) is a multifactorial ESR, CRP, and anti-dsDNA were measured at the time of acute
autoimmune disease that mostly affects young women,
resulting in significant morbidity and mortality. Lupus .............................................................
enteritis, with or without infarction, is one of the most serious
complications of SLE. Lupus enteritis may contribute to Abbreviations: aPL, antiphospholipid antibody; β2GPI, β2-glycoprotein I;
CRP, C reactive protein; CT, computed tomographic (scan); ELISA,
greater morbidity and mortality, and early recognition and enzyme linked immunosorbent assay; ESR, erythrocyte sedimentation
treatment are important if long term survival is to be rate; GI, gastrointestinal; SLE, systemic lupus erythematosus; SLEDAI, SLE
improved. The occurrence of acute abdominal pain in SLE is a Disease Activity Index; WBC, white blood cell

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548 Lee, Ahn, Lee, et al

Table 1 Autoantibody profile

Group 1 Group 2 Group 3
(n=17) (n=21) (n=137) p Value

aPL 7/16 10/18 45/83 0.72

LAC 1/15 4/17 20/76 0.26
aCL (IgG/IgM) 6/15 9/17 32/65 0.75
β2GPI (IgG/IgM) 2/13 2/11 4/28 0.41
Anti-RNP 4/14 4/19 29/94 0.69
Anti-Sm 2/15 4/19 15/95 0.81
Anti-Ro 7/14 5/17 43/93 0.39
Anti-La 1/14 1/17 12/92 0.60

Group 1, lupus enteritis; group 2, acute abdominal pain without lupus enteritis; group 3, SLE without acute
abdominal pain; aPL, antiphospholipid antibody; LAC, lupus anticoagulant; aCL, anticardiolipin antibody;
β2GPI, β2-glycoprotein I.

abdominal pain and were compared with levels calculated at SLEDAI between two episodes were also measured. A drop in
the time of diagnosis of SLE. CRP was measured quantitatively the WBC count at the time of abdominal pain was much more
by immunonephelometry (N Latex CRP mono, Behring Diag- prominent in group 1. Other laboratory indices (haemoglobin,
nostics, San Jose, California, USA) (normal 0–6 mg/l). ESR, anti-dsDNA, CRP, C3, and C4) were no different between
Complements 3 and 4 were calculated by nephelometry groups 1 and 2. Thus, only the fall in the WBC count,
(Beckman Array System, Beckman Instruments, Brea, Califor- correlated with the occurrence of lupus enteritis. The SLEDAI
nia, USA) (normal 880–2010 mg/l and 160–407 mg/l, calculated at the time of diagnosis of SLE (mean 13.7 (range
respectively). Anti-dsDNA antibody was detected by radioim- 6–28) v 17.0 (range 2–42)) and at the time of acute abdominal
munometric assay (anti-dsDNA kit, Ortho-Clinical Diagnos- pain (mean 10.3 (range 2–28) v 12.5 (range 2–26)) did not
tics, Rochester, NY, USA) (normal 0–7 IU/ml). A lupus anti- differ between groups 1 and 2. At the time of diagnosis, the
coagulant test was performed using dilute Russell viper clinical involvement defined in the SLEDAI did not differ
venom time reagent (STAgo compact, Diagnostica STAGO, among the three groups: the kidney (12/17, 15/21, 85/137,
France). Anticardiolipin antibody (IgG/IgM) was detected by p=0.59), central nervous system (0/17, 4/21, 19/137, p=0.19),
the enzyme linked immunosorbent assay (ELISA) (Varelisa skin/mucosa (10/17, 16/21, 92/137, p=0.52), blood (4/17,
cardiolipin antibody kit, Pharmacia and Upjohn Diagnostics, 12/21, 53/137, p=0.10), and musculoskeletal system involve-
Freiburg, Germany). Anti-β2-glycoprotein I (anti-β2GPI) anti- ment (3/17, 10/21, 57/137, p=0.12). Also, the clinical involve-
body (IgG/IgM) was detected by ELISA (anti- β2GPI-QUANTA ment did not differ between groups 1 and 2 at the time of
Lite Kit, INOVA Diagnostics, San Diego, USA). acute abdominal pain. As for most of the laboratory indices,
Four patients with lupus enteritis (n=17) relapsed. For the the SLEDAI did not correlate with the occurrence of lupus
21 episodes of lupus enteritis, CT scanning recorded the sites enteritis.
affected and the characteristic findings. Of 21 episodes of lupus enteritis, including relapsed cases
(n=4), all had bowel wall thickening. Target sign (fig 1) was
Statistical methods seen in 14 cases (67%). The jejunum and the ileum were the
Laboratory indices and the SLEDAI were tested by the Mann- sites most commonly affected, being involved in 17 (80%) and
Whitney test, Kruskal-Wallis test, and the χ2 test. A p value of 18 (85%) cases, respectively. Rectal involvement was rare,
<0.05 was considered significant. occurring in only three (14%) cases. Nineteen of 21 cases had
bowel involvement in multiple vascular territories not
RESULTS confined in one vascular territory. Of 21 cases, none had
There were no differences in sex (male/female: 2/15, 3/18, mesenteric vascular thrombosis on abdominal CT scans.
15/122, p=0.90) and age (mean (SD): 34 (12.5), 36 (11.6), 38 Patients were treated with intravenous high dose methyl-
(12.2), p=0.29) among the three groups. The average duration prednisolone (1 mg/kg/day) and all responded well. Subse-
(months) between SLE diagnosis and acute abdominal pain quently, intravenous methylprednisolone was switched to oral
was no different between groups 1 and 2 (36 (44.0), 28.8 prednisolone (median 5 days, range 1–34 days) and tapered.
(33.4), p=0.26). The duration (days) of acute abdominal pain Four patients relapsed when the steroid treatment was
symptoms before admission to hospital was no different tapered. However, the patients who relapsed responded well to
between groups 1 and 2 (6.3 (7.4), 8.9 (8.9), p=0.26). Lupus intravenous methylprednisolone without the addition of other
enteritis was the initial manifestation of SLE in 6/17 cases. immunosuppressive agents. Surgical intervention was not
Lupus enteritis was the most common cause of acute abdomi- needed during the follow up of lupus enteritis (median 29
nal pain in our data, occurring in 17/38 (45%) patients. months, range 2–87 months).
Urinary tract infection occurred in 6 (16%), acute gastroen-
teritis in 5 (13%), pancreatitis in 2 (5%), infectious diarrhoea DISCUSSION
in 2 (5%), haemorrhagic gastritis in 2 (5%), serositis in 1 (3%), Gastrointestinal vasculitis, with or without infarction, is one
cholecystitis in 1 (3%), IVC thrombosis in 1 (3%), and gastric of the most serious complications of SLE. The prevalence of
ulcer in 1 (3%). The frequencies of autoantibodies were com- intestinal vasculitis in patients with SLE has been reported to
pared among the three groups (table 1). The presence of aPL range from 0.2 to 53%.6 7 Although the underlying lesion in
was determined if one of the following three tests was positive most cases of gastrointestinal (GI) vasculitis in SLE is a small
on two occasions, at least six weeks apart: lupus anticoagulant vessel arteritis or venulitis, vasculitis is not found in all cases.
test, anticardiolipin antibody, and anti-β2GPI antibody.5 There Therefore, we applied the term “lupus enteritis” rather than
was no difference in the positivity of aPL among the three GI vasculitis to GI tract lesions in our patients with SLE.
groups. The frequencies of anti-RNP, anti-Sm, anti-Ro, and Medina et al looked at the aetiology of abdominal pain in 51
anti-La were no different among the three groups. patients with active and inactive SLE using the SLEDAI.6
Table 2 describes the laboratory indices and the SLEDAI cal- Patients with gastrointestinal vasculitis (19 cases) or throm-
culated at the time of diagnosis of SLE and at the time of acute bosis (three cases) had higher SLEDAI scores than 14 active
abdominal pain. Differences of laboratory indices and the patients with SLE with non-SLE related acute abdomen. In

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Acute abdominal pain in SLE 549

Table 2 Laboratory data and SLEDAI. Results shown as mean (SD)

Group 1 Group 2 Group 3
(n=17) (n=21) (n=137) p Value

WBC (×10 9/l)

Dx 7.56 (3.79) 4.80 (4.19) 5.44 (3.69) 0.00*
AA 6.79 (3.95) 6.84 (4.54) 0.70
∆(AA-Dx) −0.78 (3.58) 2.04 (3.88) 0.01*
Hb (g/l)
Dx 109 (21) 104 (25) 99 (27) 0.39
AA 115 (17) 109 (19) 0.22
∆(AA-Dx) 6 (16) 4 (14) 0.98
PLT (×10 9/l)
Dx 270.9 (112.0) 139.7 (92.8) 181.4 (101.3) 0.00*
AA 273.4 (97.6) 151.7 (91.6) 0.00*
∆(AA-Dx) 2.4 (78.4) 11.9 (61.1) 0.91
C3 (mg/l)
Dx 528 (183) 415 (201) 528 (183) 0.21
AA 562 (201) 551 (352) 0.38
∆(AA-Dx) 51 (209) 137 (299) 0.35
C4 (mg/l)
Dx 153 (73) 139 (89) 155 (104) 0.62
AA 135 (65) 174 (109) 0.63
∆(AA-Dx) −7.7 (63) 35 (75) 0.25
ESR (mm/1st h)
Dx 45.6 (32.1) 59.3 (43.7) 59.8 (37.6) 0.39
AA 47.6 (23.7) 59.0 (45.2) 0.65
∆(AA-Dx) 1.6 (24.5) −0.28 (20.3) 0.85
Anti-ds DNA (IU/ml)
Dx 98.9 (140.0) 889.4 (1840.2) 292.1 (675.9) 0.57
AA 243.5 (379.8) 107.9 (208.5) 0.48
∆(AA-Dx) 115.8 (312.3) −778.4 (1835.1) 0.10
CRP (mg/l)
Dx 20 (26) 22 (44) 18 (29) 0.43
AA 23 (28) 32 (48) 0.81
∆(AA-Dx) 1 (24) 8 (29) 0.60
SLEDAI
Dx 13.7 (5.9) 17.0 (8.6) 14.2 (6.8) 0.36
AA 10.3 (5.98) 12.5 (8.1) 0.36
∆(AA-Dx) −3.4 (4.6) −4.5 (9.7) 0.67

*Statistically significant using Kruskal-Wallis test or Mann-Whitney test.

Group 1, lupus enteritis; group 2, acute abdominal pain without lupus enteritis; group 3, SLE without acute
abdominal pain; WBC, white blood cells; Hb, haemoglobin; PLT, platelets; Dx, at diagnosis of SLE; AA,
acute abdominal pain; ∆(AA-Dx), difference between acute abdominal pain and at diagnosis of SLE.

prominent in group 1 than in group 2. Therefore, the SLEDAI

and laboratory indices, except leucopenia, did not correlate
with the occurrence of lupus enteritis.
In SLE and SLE-like conditions, a prevalence of aPL of
between 18% and 61% has been reported.1 8 Several reports
have described an association between intestinal infarction
and aPL.6 9 Although mesenteric vascular thrombosis was not
found on abdominal CT scans in our series, we compared the
incidence of aPL among the three groups, but no differences
were found. Therefore, autoantibodies, including aPL, did not
correlate with the occurrence of lupus enteritis.
The diagnosis of bowel ischaemia is often difficult to make
Figure 1 Abdominal CT scan showing circumferential wall
on the basis of plain radiography and barium studies. The
thickening and target sign in small and large bowels. Mesenteric
change is also noted with engorged mesenteric vessels and common CT findings in mesenteric ischaemia include dilated
haziness. bowel, focal or diffuse bowel wall thickening, abnormal bowel
wall enhancement (double halo or target sign), mesenteric
oedema, engorged mesenteric vessel, and ascites.10 However,
our data, lupus enteritis (45%) was the most common cause of the lack of specificity of these signs is a limitation of CT
acute abdominal pain and the incidence was comparable with because they can also be seen in patients with pancreatitis,
the previous report.6 Contrary to the previous report of
mechanical bowel obstruction, peritonitis, or inflammatory
Medina et al,6 the SLEDAI was similar at the time of diagnosis
bowel disease, all of which may mimic intestinal ischaemia.10
of SLE among the three groups and at the time of acute
abdominal pain between groups 1 and 2. In addition, the In the present series, the jejunum and ileum were the sites
SLEDAI calculated at the time of acute abdominal pain was most commonly affected. The segments of bowel thickening
lower than that at the time of diagnosis of SLE in both groups were multifocal and not confined to a single vascular territory
1 and 2. Thus, it implies that acute abdominal pain, including in 19/21 cases with bowel wall thickening because mesenteric
lupus enteritis, might occur in patients whose disease vasculitis may affect several vessels simultaneously.11 It
activities had been under control. Only a drop in the WBC seemed that rectal involvement was rare owing to the rich and
count at the time of acute abdominal pain was much more multiple blood supply of the rectum. Therefore, in the clinical

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550 Lee, Ahn, Lee, et al

investigation of abdominal pain in SLE, involvement of multi- Department of Internal Medicine, University of Ulsan College of
ple vascular territories on CT scans, in addition to improve- Medicine, Asan Medical Center, 388-1 Pungnap-dong, Songpa-gu,
Seoul 138-736, Korea; [email protected]
ment after intravenous prednisolone treatment, may favour a
diagnosis of reversible ischaemic bowel disease. Accepted 18 December 2001
Because of the paucity of cases of lupus enteritis, no
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Acute abdominal pain in systemic lupus

erythematosus: focus on lupus enteritis
(gastrointestinal vasculitis)
C-K Lee, M S Ahn, E Y Lee, J H Shin, Y-S Cho, H K Ha, B Yoo and H-B
Moon

Ann Rheum Dis2002 61: 547-550

doi: 10.1136/ard.61.6.547

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