CASE BASED REVIEW

Life-threatening spontaneous splenic rupture with systemiclupus erythematosus: case report and literature review

Jie Han & Ning Li & JiaYi Wang & JieRu Zhou & Jie Zhang

Received: 15 December 2011 /Accepted: 22 December 2011 /Published online: 11 February 2012# Clinical Rheumatology 2012

Abstract Although involvement of the reticuloendothelialsystem in systemic lupus erythematosus (SLE) is a well-recognised concomitant of the disease, spontaneous splenicrupture is an unusual occurrence. We observed a 54-year-oldwoman with SLE who had spontaneous splenic ruptureduring the late course of the disease and showed somechanges histopathologically. The courses and the clinicalcharacteristics of such patients are reviewed, and the diag-nosis and treatment of these cases are discussed. Earlyevaluation for SLE patients with spontaneous splenic rup-ture should be considered and included in the differentialdiagnosis of acute abdomen, as it may affect follow-up andtreatment, although the condition is rare.

Keywords Spleen . Spontaneous rupture . Systemic lupuserythematosus

Introduction

Splenic rupture in the absence of trauma called spontaneoussplenic rupture, which occurs suddenly or insidiously, wasfirst described by Aktinson and is a rare complication ofinfectious, haematological and neoplastic disorders [1, 2]. Ithas also been described in several rheumatic conditions [3].

Systemic lupus erythematosus (SLE) is a multisystemicautoimmune disease and the clinical manifestations of patients

with the disease vary depending on the organs involved.Although involvement of the reticuloendothelial system inSLE is a well-recognised concomitant of the disease, sponta-neous splenic rupture is an unusual occurrence.

We observed a 54-year-old woman with SLE who hadspontaneous splenic rupture during the late course of thedisease and showed some changes histopathologically. Thecourses and the clinical characteristics of such patients arereviewed.

Case report

The patient was a 54-year-old American woman. She pre-sented in 2000 at the age of 44 with fever, alopecia, arthral-gia and mucocutaneous lesions. Serological examinationdemonstrated leucopenia, positive antinuclear antibodies(titre>1:320 with a homogeneous pattern) and anti-double-stranded DNA antibodies. She was diagnosed as havingSLE in the United States and treated with prednisone, meth-otrexate and hydroxychloroquine in 2000. The disease wascontrolled gradually, and the steroid was tapered to predni-sone 10 mg/day. She was found to have bilateral femur headnecrosis and total hip replacement was performed in 2005.At the same time, she had a transient splenomegaly, butrecovered without specific treatment.

After she came to China in 2006, she was accepted forexamination at the clinic regularly, which demonstrated thedisease was stable, except for elevated anti-double-DNAantibody [114.3 IU/mL(<100)], decreased white bloodcells(3.9×109/L)and low complement 3 (C3) [0.193 g/L(0.22–0.34)] occasionally. Routine urine tests showed ele-vated white blood cells (1–5/HPF), but protein in urea wasnegative or trace. Erythrocyte sedimentation rate (ESR), C

J. Han (*) :N. Li : J. Wang : J. Zhou : J. ZhangDepartment of Rheumatology,Tong Ji University Affiliated Shanghai East Hospital,150 Ji Mo Road,Shanghai 200120, Chinae-mail: hjgj85528@126.com

Clin Rheumatol (2012) 31:1019–1025DOI 10.1007/s10067-011-1934-8

reactive protein (CRP), C4, liver and kidney functions aswell as electrolytes were always normal.

In March 2009, she was admitted to the local hospitalcomplaining of left epigastric discomfort, diarrhoea andfever. She had caught a “cold” 1 week previously. Onphysical examination, her temperature was 37.7°C, pulserate 82/min, respiratory rate 20/min, blood pressure 125/80 mmHg. She looked ill, but had no jaundice. The mainfindings were of epigastric tenderness, without guarding,spleen enlargement 1 cm below umbilicus, and the left kneewas slightly swollen. Admission laboratory data includedHGB of 101 g/L, MCV 88 fL, CRP 29 mg/L, anti-CCPantibody <25 U/L. X-ray of the left knee showed earlydegenerative change and osteopenia. Ultrasound of the ab-domen revealed (2009-3-2) MPV 10 mm, the spleen was79 mm in thickness and 147 mm in length, margin of spleeninferior extended to the left middle inferior belly, blood flowin the spleen was a little fast and the splenic vein was 7 mmin diameter.

Impression: splenomegaly The abdominal enhanced CTwas suggested to exclude ischaemia.

CT finding (2009-3-2) The size of the liver was not en-larged. The gall bladder was normal. The size of the spleenwas obviously enlarged. There were multiple small highshadow spots in the spleen area. There was a high spottedshadow under the spleen capsule. The spleen was not inten-sified after contrast media. There was a thinning change inthe middle and proximal segments of spleen artery. Thevessel wall was not smooth. There was a filling defect inthe spleen proximal vein, which was localised narrowingand thinning change, and the distal segment was developed.The pancreas was normal. Bilateral kidneys and adrenalglands were normal. There were no lymph nodes in hepaticportal and retroperitoneum.

Image diagnosis 1. Splenomegaly, blood supplement ofspleen was unwell. Spleen artery was thin, and there was afilling defect in the spleen vein. We have suggested that it iscaused by thrombosis of the spleen vein but not systemicdiseases (Fig. 1). 2. Spotty calcified change in spleen(Fig. 2a, b).

The patient was stable with spelomegaly. Fever, pain anddiarrhoea responded to symptomatic treatment, and thepatient’s syndromes were improved immediately afterward.Successive sonography (2009-3-4) revealed the regressionof splenic size, which was 38 mm in thickness and 102 mmin length. Diffuse dense echo spots could be observed inparenchyma, with no acoustic shadow posterior to it.

Splenic vein The splenic vein was 7 mm. The liver, gall-bladder, pancreas and kidneys were all normal.

After discharge, she still went to the clinic for exam-ination regularly, and routine blood and urine tests,ESR, liver and kidney functions were all normal. Thedisease was relatively stable. The medicines she hadbeen taking included prednisone 5 mg/day, methotrexate20 mg/week, hydroxychloroquine 300 mg/day, prilosec20 mg/day, alendronate sodium tablets (Fosamax)70 mg/week and folic acid 1 mg/day.

On February 5, 2010, she presented to our hospital withabdominal pain, diarrhoea, nausea, vomiting and syncope of3-h duration in emergency, with no history of trauma. Onexamination, her temperature was 37°C, pulse 90/min, res-piratory rate 25/min and blood pressure of 72/52 mmHg.She was apatheia and looked pale. Her abdomen was tense,tender with guarding to palpation. The spleen was palpable,but its definite size could not be determined because ofextreme abdominal tenderness and guarding. Non-clottedblood was extracted by peritoneocentesis. The EKG showedarrhythmia. Abdominal ultrasound (2010-2-5) revealed amarkedly enlarged spleen, measured at least 14.7×7.9 cm,with focal heterogeneous echo pattern and moderate amountof ascites. The inferior margin of the spleen was extended tothe mid to lower left abdomen.

Impression: splenomegaly Spontaneous splenic rupture wassuspected.

The patient was treated by fluid infusion and haemostasisimmediately. A laparotomy was performed on the day afteradmission as the blood pressure and hemoglobin (Hb) hadcontinued to fall down. Exploration confirmed haemoperi-toneum secondary to ruptured spleen with subcapsular hae-matoma. The spleen was mobilised and removed. Grossly, itwas 405 g, 120×100×30 mm. The surface was smooth andglossy, with two irregular lacerations on the anterior surface,20×10 mm and 70×5 mm, respectively. The cut surface wasbrunneus in colour. Part of the capsule was pale in colourand 28×10 mm in size, which boundary was obscure. Mi-croscopic examination (Fig. 3) failed to show any signifi-cant vascular lesion but revealed histiocytes proliferated,splenic follicle atropy with local haemosiderosis. Patholog-ical splenic rupture was diagnosed after combining grossappearance and clinical history. She made a good recoveryand was discharged from the hospital on the tenth day post-operation. A year after the event, the disease remains stable,and the patient is still on follow-up.

We have reviewed these cases in the current manuscript(Table 1). There are no case reports of SLE with splenicrupture in Chinese literature, and only five other cases arereported in English literature before our case is reported.Interestingly, there is one report almost every 10 years. Thecourses and the clinical characteristics of the reported casesare as follows:

1020 Clin Rheumatol (2012) 31:1019–1025

Case 1 [4] was a 61-year-old man who had splenectomywhen he presented with hypovolemic shock after minortrauma to the abdomen led to rupture of an enlarged spleen.

During subsequent investigations for 4 weeks, the diagnosisof SLE was established, and he responded well to cortico-steroids. Histopathology of the spleen was not done.

Fig. 1 CT scan showedsplenomegaly (indicated by thearrow)

Fig. 2 CT scan showed spotty calcified change in spleen (indicated by arrow)

Clin Rheumatol (2012) 31:1019–1025 1021

Case 2 [5] was a 31-year-old woman who had left upperquadrant pain and vomiting 4 years after a diagnosis of SLE.Laparotomy was done following aspiration of blood onparacentesis that confirmed splenic rupture. Interestingly,histopathologic examination of the spleen was normal ex-cept for irregular lacerations on the anterior surface and a4×4.2 cm subcapsular hematoma.

Case 3 [6] was a 35-year-old man with abdominalpain, who developed profound anaemia (Hb034 g/L)when he was hospitalised for atonic urinary bladder.He has been diagnosed as a SLE for one and a halfyears. Laparotomy was done after paracentesis, whichshowed dark bloody fluid. There was 2,200 mL ofclotted blood in the peritoneal cavity, and a splenectomywas done. Apart from the rupture site, the spleen lookednormal. The patient died of adult respiratory distresssyndrome.

Case 4 [7] was young, a 15-year-old girl, and had spon-taneous splenic rupture soon after the onset of SLE. She wasdiagnosed as SLE 3 months later. This was the first report ofa paediatric SLE patient who suffered with splenic rupture.

Abdominal computed tomographic scan with contrastrevealed a markedly enlarged spleen with haemoperito-neum. A laparotomy was performed, and exploration con-firmed haemoperitoneum. The symmetrically enlargedspleen had black areas which grossly appeared to beinfracted. Splenectomy was performed. Microscopic exam-ination revealed both large and small vessels necrotisingvasculitis associated with extensive multifocal white pulpnecrosis. The red pulp demonstrated marked congestion.Many of the involved vessels had intralumenal fibrin throm-bi; however, thrombosis was not seen in parenchyma out-side the areas of necrosis. Five months before herpresentation, SLE was highly suspected at another institu-tion, and 3 months after the presentation, the patient wasconfirmed SLE and treated with cyclophosphamide andcorticosteroids, and her clinical condition graduallyimproved.

Case 5 [8] is a 45-year-old woman. She presented at the ageof 26, with Raynaud’s phenomenon, polyarthritis and muco-cutaneous lesions. Serological investigation demonstratedlymphopenia, positive antinuclear antibodies (titre>1:5120

Fig. 3 H&E (a–f) and Masson (g–h) staining of the ruptured spleen.No significant vascular lesion was observed, but histiocytes proliferat-ed and splenic follicle atrophy with local haemosiderosis wererevealed. Characteristic “onion skin” appearance of the splenic centralartery can also be seen. a Splenic follicle atropy, b histiocytes

proliferated and splenic follicle atropy with local haemosiderosis, chistiocytes proliferated and local haemosiderosis, d subcapsular hae-morrhage, e focal haemosiderosis, f “onion skin” appearance of thesplenic central artery, g–h Masson staining showed green connectivetissue

1022 Clin Rheumatol (2012) 31:1019–1025

Tab

le1

Spo

ntaneous

splenicrupturein

system

iclupu

serythematosus

Author

Zim

merman-G

orskaet

al.

Krauser

Cheng-Chung

etal.

Tolaymat

etal.

Karassa

etal.

Present

patient

Year

1971

[4]

1976

[5]

1985

[6]

1995

[7]

2001

[8]

2011

Age/sex

61/M

31/F

35/M

15/F

45/F

54/F

SLEdiagnosisa

+4weeks

−4years

−1.5years

+3months

−19

years

−10

years

Major

SLE

features

Hepatom

egaly,splenomegaly,

lymphadenopathy,serositis,

anem

ia,polyarthritis,skin

rashes,cardiacandrenal

involvem

ent

Not

mentio

ned(no

splenomegaly)

Malar

rash,alopecia,

photosensitiv

ity,no

hepato-

splenomegaly,anem

ia

Arthralgia,renalinvolvem

ent,

splenomegaly,serositis,anem

ia,

lymphadenopathy,leukopenia

Polyarthritis,skin

rashes,mouth

ulcers,Raynaud

’sphenom

enon,

lymphadenopathy,CNS

involvem

ent,serositis,lymphopenia,

coronary

disease

Arthritis,splenomegaly,

alopecia,skinrashes,m

outh

ulcers,leukopenia

Auto-antib

odies

ANA

Not

mentio

ned

ANA

ANA,anti-Sm,anti-dsDNA

ANA,anti-dsDNA

ANA,anti-dsDNA

Treatmentb

None

Salicylates

Not

mentio

ned

None

Hydroxychloroquine,

azathioprine,

prenisone,CTX,salicylates

Prenisone,MTX,hydroxyl-

chloroquineAlendronate

sodium

Ultrosound

cNot

mentio

ned

Not

mentio

ned

Not

mentio

ned

Not

done

Moderateascites

Splenom

egaly,

moderate

ascites

CTc

Not

mentio

ned

Not

mentio

ned

Not

mentio

ned

Markedsplenomegaly,

Hem

operito

neum

Not

done

Not

done

Histopathological

exam

ination

Not

done

Irregularlaceratio

nson

theanterior

surface,

subcapsular

haem

atom

a,norm

alparenchyma

Subcapsular

haem

atom

a,norm

alparenchyma,no

vasculitis

Large

andsm

allvessel

necrotizing

vasculitis,extensivemultifocal

white

pulp

necrosis,redpulp

congestio

n,intralum

enal

fibrin

thrombi

inmanyof

theinvolved

vessels

Focal

haem

orrhage,occasional

reactiv

egerm

inal

centres,no

vasculitis,perivascular

sclerosis,

inflam

matorycellinfiltrateinto

the

capsuleadjacent

tothehaem

orrhage

Histio

cytesproliferated,

splenicfollicleatropy,local

haem

osiderosis

Prognosis

Splenectomyrecovered

Not

mentio

ned

Splenectomydied

Splenectomyrecovered

Splenectomyrecovered

Splenectomyrecovered

SLEsystem

iclupu

serythematosus,CNScentralnervou

ssystem

,ANAantin

uclear

antib

odies,ds-D

NAdo

uble-strandedDNA,CTXcyclop

hosphamide,MTXmetho

trexate,M

male,Ffemale

aSplenic

rupture0

time0

bTreatmentbefore

splenicrupture

cExaminationwhensplenicrupturehapp

ened

Clin Rheumatol (2012) 31:1019–1025 1023

with a homogeneous pattern) and anti-double-stranded DNAantibodies. She was diagnosed as SLE, and initially, she wastreated with hydroxychloroquine. Over the next decade, shehad a number of flares, characterised mainly by serositis andpolysynovitis, which were controlled with azathioprine andoccasionally with systemic corticosteroids. Sixteen years later,she had a complication with involvement in the central ner-vous system. Intravenous cyclophosphamide was started incombination with systemic corticosteroids, and the patient hada virtually complete recovery. Three years after that (19 yearsafter SLE onset), she was admitted to the local hospital com-plaining of abdominal pain and pain referred to the left shoul-der. The patient denied antecedent trauma. The ultrasound ofthe abdomen revealed a moderate amount of ascites. A lapa-rotomy was performed the day after admission as the Hb hadcontinued to fall. Exploration operation confirmed haemoper-itoneum secondary to ruptured spleen with subcapsular hae-matoma. The spleen was mobilised and removed.Microscopic examination failed to show any significant vas-cular lesion. She made a good recovery.

Case 6 is our report.

Discussion

Splenic rupture in the absence of trauma, called spontaneoussplenic rupture, is a rare complication of infectious, haema-tological and neoplastic disorders. Causes of atraumaticsplenic rupture can be divided into six main categories:infectious, neoplastic, inflammatory, congenital or structur-al, iatrogenic and finally idiopathic [9]. It complicates about0.2% of cases of infectious mononucleosis [10]. Other con-ditions reported in the paediatric age group include severemeningococcal septicaemia [11], congenital afibrinogene-mia [12] and malaria [13]. An increased risk for pathologicsplenic ruptures has also been reported in patients withsystemic vasculitis [14, 15] and several rheumatic condi-tions [3]. Many of these disorders lead to an altered organconsistency or enlargement, destroy the splenic capsule,alter local circulation or decrease fibrin stability, makingthe spleen more fragile or engendering a greater mass effectin decelerating trauma, thus, causing an increased risk andseverity of splenic injury, even after trivial traumata [16].

SLE is a multisystemic disease and the clinical manifes-tations of patients with the disease vary depending on theorgans involved. Involvement of the reticuloendothelial sys-tem manifested primarily with splenomegaly and lymphade-nopathy is a well-recognised feature of the disease. Itsreported frequency varies from 9 to 46% [3]. Althoughinvolvement of the reticuloendothelial system and hepato-splenomegaly in SLE are well-recognised concomitant ofthe disease, spontaneous splenic rupture is an unusualoccurrence.

Because of its rare occurrence, the clinical and patho-physiologic factors that may predispose the spleen to spon-taneous rupture have not been defined. In our literaturereview, we are able to identify five patients with SLE thathad reported to have had spontaneous rupture [4–8], and thecurrent report is the sixth case. In four of the six cases, theevent developed close to the onset of SLE. In contrast toprevious reports, Karassa et al. reported their patient hadspontaneous splenic rupture 19 years after the initial mani-festations of the disease, which is similar to our patient.Both patients had spontaneous splenic rupture in the stablecondition. Moreover, careful pathological sectioning of thespleen failed to show any definite explanation for the rup-ture, as vasculitis was not found, and other histopathologicalchanges were almost unremarkable. Interestingly, in two ofthe three previously reported cases in which the splenichistology was reported, apart from the rupture site, thespleen looked normal. Finally, while a variety of clottingabnormalities have been reported in SLE, mostly in thesetting of the antiphospholipid syndrome [17], platelet countand coagulation studies were normal in all patients at thetime of organ rupture. The absence of arterial thromboticvasculopathy [18] from the pathological examination whichcould lead to splenic infarction(s) with subsequent ruptureas well as the previously determined negative anticardiolipinantibodies also argue against the possibility of thrombosisrelated to these antibodies. Although two of the reportedpatients were taking salicylates at the time of the event, it isunlikely that this medication played a primary role in theinduction of this complication.

Contrast-enhanced CT is the modality of choice for eval-uation of splenic trauma and has been reported to be up to98% sensitive for detecting blunt splenic injury [19]. Fol-lowing rapid IV injection of contrast material, the spleenmay initially exhibit a heterogeneous pattern of parenchy-mal opacification, reflecting variable blood flow withindifferent compartments of the spleen. Care must be takennot to misinterpret this early post-injection heterogeneity asrepresenting splenic injury. In the questionable cases, repeatscans should be obtained following equilibration of thecontrast material. In normal cases, the splenic parenchymaachieves a uniform, homogeneous appearance with no sur-rounding haemorrhage. Injury to the spleen can take theform of laceration, intrasplenic haematoma, subcapsularhaematoma, or infarction. Splenic laceration typicallyappears as an irregular linear area of hypodensity oncontrast-enhanced CT. Intrasplenic haematoma appears asa broader area of hypodense, non-perfused splenic paren-chyma. The intraparenchymal haematoma may be homoge-neous or inhomogeneous and may contain a higherattenuation clot. Subcapsular haematomas appear as cres-centic or oval collections of fluid that flatten or indent theunderlying splenic parenchyma. Splenic infarcts may occur

1024 Clin Rheumatol (2012) 31:1019–1025

following injury to the splenic vasculature and appear aswedge-shaped areas of non-perfusion that extend to thesplenic capsule. Unenhancing portions of the spleen shouldsuggest injury or thrombosis of the artery of the affectedsegment, although perfusion defects may also be a result ofcontusion or may correspond to reversible local reactivehypoperfusion secondary to hypotension. In cases of severetrauma, the spleen may be shattered into multiple smallfragments. Multiple lacerations connecting opposed visceralsurfaces defines a shattered spleen.

Active bleeding can be identified on contrast-enhancedCT as intra- or extrasplenic areas of bright vascular enhance-ment with attenuation similar to or greater than that of theaorta or an adjacent major artery. The appearance may varywith the rate of haemorrhage and the CT technique used.With the introduction of faster MDCT protocols, earlier dataacquisition may allow smaller amounts of active haemor-rhage to be detected before the high density contrast mate-rial is diluted by surrounding haematoma, especially in aperisplenic location.

MRI is a valuable tool in the evaluation of the spleen andsurpasses CT imaging in many clinical settings. MRI isuseful in the further investigation of patients with a CTdiagnosis of splenomegaly to determine whether underlyingtumour infiltration is present [20].

Ultrasound is a simple and cheap method to examinesplenic rupture, which can reveal hypo/iso/hyperechoicblood-filled cleft within the spleen, loss of normal spleniccontour/fragmented spleen, generalised heterogeneous echopattern suggesting diffuse splenic injury [and] blood in theperisplenic tissue[21].

Once suspected splenic rupture is considered, diagnosticabdominal paracentesis should be taken first. If no clotblood was extracted, radiological and ultrasound examina-tions will reveal splenic rupture, and exploratory laparotomyshould be performed immediately. After splenectomy, thepatient could recover gradually. Among the six SLE patientswith splenic rupture reported, only one died of adult respi-ratory distress syndrome and the others recovered.

We conclude that spontaneous organ rupture should beincluded in the differential diagnosis of acute abdomen painin patients with SLE, and early evaluation for SLE patientswith spontaneous splenic rupture should be considered, as itmay affect follow-up and treatment [22]. Although the con-dition is rare, it is associated with high mortality.

Learning points

& Spontaneous splenic rupture is an unusual but importantoccurrence, which should be included in the differentialdiagnosis of acute abdomen pain in SLE patients.

& Spontaneous organ rupture can occur in the stable con-dition of SLE patients, which should be considered bythe physician.

Acknowledgements This work was partly funded by a ResearchGrant for Health Science and Technology development and innovationof Pudong New Area of Shanghai (Grant No. PKJ2011-Y06).

The authors thank Prof. SongGuo Zheng for his review of themanuscript and his insightful comments.

Disclosures None.

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