atients with pancreatitis may develop extrapancreaticmanifestations. Lobular panniculitis, which appearsin 2 to 3% of patients, may predate the identification
f pancreatitis by days or several weeks (1). More rarely, theseatients can also develop arthritis with intraosseous fat ne-
Staff Physician, Department of Rheumatology, Hospital Universitario de Bellvitge-DIBELL, Barcelona, Spain.
†Resident, Department of Rheumatology, Hospital Universitario de Bellvitge-DIBELL, Barcelona, Spain.
‡Staff Physician, Department of Internal Medicine, Hospital Universitario deellvitge-IDIBELL, Barcelona, Spain.§Staff Physician, Department of Radiology, Hospital Universitario de Bellvitge-
DIBELL, Barcelona, Spain.¶Head of Department, Department of Rheumatology, Hospital Universitario de
ellvitge-IDIBELL, Barcelona, Spain.Address reprint requests to Francisco Javier Narváez García, MD, PhD, Department of
bheumatology (planta 10-2), Hospital Universitario de Bellvitge, Feixa Llarga s/n. 08907,=Hospitalet de Llobregat, Barcelona, Spain. E-mail: [email protected].
rosis, thus forming the triad of pancreatitis, panniculitis,nd polyarthritis, referred to in the literature as the PPP syn-rome (2-24). The absence or mild nature of the abdominalymptoms raises the risk of misdiagnosis of the pancreaticisease (3,5-9,12-15,21,22). In addition, in some of theseatients the arthritis follows a chronic course with a pooresponse to treatment and the rapid development of radio-raphic lesions (6,7,9,16,22,23).
We report a case of the PPP syndrome with evidence ofxtensive intraosseous fat necrosis in the involved joints,s revealed by magnetic resonance imaging (MRI). Welso review the available literature and summarize thelinical characteristics of patients with this condition.
ETHODS
n addition to our case, a literature search (PubMed data-
ase, National Library of Medicine, Bethesda, MD) for
rticles published between January 1970 and February008 was performed using the Medline subheadings andey words “pancreatitis” or “pancreatic disease,” “pannic-litis,” “arthritis,” and “intraosseous fat necrosis.” Onlynglish-, French-, and Spanish-language reports were se-
ected for review. The references of the studies obtainedere then examined to identify additional reports. We
ncluded only those cases that were sufficiently detailed toe analyzed individually.
ESULTS
ase Report
45-year-old man with a 30-year history of heavy alcoholbuse was admitted to our center for alcohol detoxifica-ion. On admission, the patient reported that he had ex-erienced mild upper abdominal pain, without nausea oromiting, for 1 week.
On physical examination the abdomen was soft, tendern the epigastrium and left hypochondrium, with non-ender hepatomegaly; joint and skin examination at thatime were normal. Laboratory examination revealed anlevated erythrocyte sedimentation rate (84 mm/h), C-re-ctive protein of 254 mg/L (normal, �5), hemoglobin of0.9 g/dL, mean corpuscular volume of 102, white bloodells of 16.5 � 109/L (82% neutrophils), platelet count of43 � 109/L, serum amylase of 83 U/L (normal, �1.32),
ipase of 64.5 ukat/L (normal, �1), aspartate transami-ase of 0.7 ukat/L (normal, �0.5), alkaline phosphatasef 2.8 ukat/L (normal, �1.5), and gamma glutamylranspeptidase of 5.7 ukat/L (normal, �1.16). Bilirubin,lanine aminotransferase, albumin, total proteins, choles-erol, triglycerides, serum calcium, and renal function testere all normal. Amylasuria was 409 UI/24 hours (nor-al, �6.68). Prothrombin ratio and activated partial
hromboplastin time, antithrombin, protein C, and pro-ein S were also normal; antiphospholipid antibodies wereegative. Screening for hepatitis B and C was negative and1-antitrypsin was normal.Computed tomography of the abdomen confirmed the
uspicion of acute pancreatitis and revealed segmental in-ammation of the uncinate process of the pancreas, with
rregular contour and obliteration of peripancreatic fat andartial thrombosis of the portal vein. There was no evidencef pseudocysts, biliary stone disease, or pancreatic stones.he patient was initially treated with bowel rest and nutri-
ional support, analgesia (meperidine), and anticoagulationherapy (initially heparin followed by acenocumarol), withrogressive resolution of the abdominal pain.
However, 3 days after admission the patient developedultiple painful erythematous nodules of 1 to 3 cm in
iameter on both legs. Biopsy of the skin nodules showedubcutaneous fat necrosis consistent with a nodular pan-iculitis. Over the next 5 days he also developed pain andarked swelling involving the left ankle, both wrists, and
everal small joints of both hands. Joint examination re-
ealed diffuse swelling, redness, and tenderness over both b
rists and all metacarpophalangeal (MCP) joints. The leftnkle was tender, warm, grossly swollen, and fluctuant.rthrocentesis of the left ankle revealed a thick, yellowish,reamy fluid. Leukocyte and differential cell counts couldot be performed accurately in this fluid because of theigh viscosity. Sudan and oil-red-O stains of the synovialuid were positive, indicating high lipid content. Cul-ures were sterile and no microcrystals were found. Plainadiographs of hands, wrists, and ankles revealed onlyoft-tissue swelling. Rheumatoid factor and antinuclearntibodies were negative.
Treatment with 30 mg/d of prednisone and nonsteroi-al anti-inflammatory drugs (NSAID) was started, withomplete resolution of the panniculitis lesions but with-ut apparent improvement of the joint symptoms. Overhe next few days the right wrist and, subsequently, theeft ankle and left wrist began to drain spontaneously.hese joints were incised with evacuation of abundant
reamy yellowish material. Histopathological examina-ion showed necrotic fat and connective tissue with lowevels of lymphocyte and macrophage infiltration. Gramtaining and serial cultures of this material were negative.
RI of the involved joints (hands and left ankle) showedultiple foci of abnormal signal, with ill-defined low sig-
al intensity on T1-weighted images and high signal in-ensity on fat-suppressed T2-weighted and short tau in-ersion recovery (STIR) images, within the marrow of theffected bones (distal radius, scaphoid, base of the meta-arpals, distal tibia, peroneal malleolus, calcaneus and ta-us), compatible with the diagnosis of fat necrosis andccompanying marrow edema. These bone lesionshowed diffuse contrast enhancement. Other MRI fea-ures were concomitant synovitis, more pronounced inhe right wrist, and panniculitis of periarticular soft tissuesidentified as thickening and signal intensity alteration ofhe subcutaneous fat) (Fig. 1).
During subsequent follow-up, with topical therapydaily wound cleaning using saline followed by the ap-lication of iodine), NSAID (diclofenac), and analge-ics, the surgical incisions healed and the joint inflam-ation subsided over the next 8 weeks without
elapses. A new computed tomography of the abdomenhowed resolution of the portal thrombosis andarked improvement of the inflammatory changes,ithout evidence of pancreatic pseudocyst or phleg-ons/abscesses. On day 28 of hospitalization, the pan-
reatic enzyme levels normalized. Although remainingystemically well, the patient continued to suffer per-istent mechanical joint pain and functional sequelae,ffecting the right wrist in particular. A radiographerformed 5 weeks after the onset of arthritis showedhe rapid development of joint damage in both wristsparticularly the right) and left ankle, with loss of jointpace and multiple osteolytic lesions, with a pattern of
one destruction and endosteal erosion (Fig. 2).
L
Ist
wnoh
i(c2latetomasil
agT
Ftitecsignal intensity of the radial soft tissues (short white arrows).
Fsrbcm
J. Narváez et al. 419
iterature Review
n addition to our case, 24 well-documented cases of PPPyndrome were identified in the literature (3,5-23). De-ails of these patients are summarized in Table 1.
Of the 25 patients, 17 (68%) were men and 8 (32%) wereomen (male:female ratio of 2.1) with a mean age at diag-osis of 51 � 16 years (range, 13-76 years). Fifty-six percentf patients were younger than 50 years, and 64% (16/25)ad a history of alcohol abuse (past or present).
The underlying pancreatic disease was acute pancreatitisn 60% (15/25) of the cases and chronic pancreatitis in 40%10/25); in 36% (9/25) of the cases pancreatitis was compli-ated by the development of a pancreatic pseudocyst. Only8% (7/25) of the patients had severe upper abdominal pain
eading to the clinical suspicion of pancreatitis; in the rest,bdominal symptoms were absent or mild. The clinical pic-ure of pancreatic panniculitis consisted of tender or painlessrythematous nodules usually located in the distal parts ofhe lower extremities (around the ankles and pretibial regionsf the legs) and occasionally on the arms and trunk. In theajority of the cases panniculitis resolved without ulcer-
tion; in 24% (6/25) of the patients the nodules evolved intoterile necrotic abscesses that ulcerated spontaneously, exud-ng a thick creamy purulent-appearing oily material, due toiquefaction fat necrosis.
Peripheral joint involvement consisted of symmetric orsymmetric polyarthritis in 88% (22/25) of the cases, oli-oarthritis in 8% (2/25), and monoarthritis in 4% (1/25).
igure 2 Posteroanterior radiograph of the hand demon-trates multiple ill-defined osteolytic lesions in the distaladius, with a pathologic fracture of the lateral corticalorder and minimal periosteal reaction. Note similarhanges in the scaphoid bone, and base of fourth and fifthetacarpals.
igure 1 (A and B) Consecutive coronal STIR MR images ofhe right wrist show multiple foci with ill-defined high signalntensity (long white arrows) corresponding to areas of in-ramedullary fat necrosis and accompanying bone marrowdema. Note also carpal synovitis (black arrows), andhanges of panniculitis with thickening and ill-defined high
he most commonly affected joints were the ankles,
kih1ctah
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nt1w(a4prwerwi
DIP, di
420 PPP syndrome
nees, wrists, and MCP joints; less frequently, proximalnterphalangeal and distal interphalangeal joints of theands, elbows, and small joints of feet were involved. In/3 of patients the joint symptoms predated the identifi-ation of pancreatic disease; in the remaining patientshey coincided with or followed the diagnosis of pancre-titis. Synovial fluid was analyzed in 2 cases, showing aigh lipid content and the presence of liquid lipid crystals.Uniformly present laboratory findings included ele-
ated pancreatic enzyme levels in the serum and/or urine,nd high acute phase reactants. Peripheral blood eosino-hilia may also be present.Six of the 25 patients (24%) died during the first days
r weeks after admission due to complications of pancre-
Table 1 Clinical Characteristics and Outcome of Reported
titis. The underlying pancreatic disease was misdiag- c
osed in most of these patients, leading to a delay inreatment. Data on long-term follow-up were available in6 of the remaining 19 patients; in all of them the arthritisas treated with NSAID and/or corticosteroids. In 56%
9/16) of these patients joint symptoms were transientnd cured without sequelae, whereas in the remaining4% (7/16) the arthritis followed a chronic course with aoor response to treatment and the rapid development ofadiographic lesions. The earliest radiographic changesere multiple ill-defined osteolytic lesions and moth-
aten bone destruction, loss of joint space, and periostealeaction (the latter present only in few cases). The changesere usually observed 3 to 6 weeks after the peak of clin-
cal pancreatitis. Several months later, features of osteone-
of PPP Syndrome
ase Abdominal Symptoms
lism Absenteudocyst, Mild anorexia
eudocyst, Absent
pseudocyst, Absent
Nausea and vomiting
lism Minimal abdominal tendernesslism Absent
Intermittent bouts of abdominal painlism Not reportedlism (abstinent Absent
pseudocyst, Absent
Painless obstructive jaundiceAbsent
eudocyst, Mild abdominal pain and vomiting
pseudocyst Absentudocyst Absent
Severe abdominal pain and vomiting
pseudocyst Abdominal pain and distensionnic Abdominal pain, nausea and vomiting
Abdominal painholism Chronic Abdominal pain and vomiting
m Mild abdominal painholism Absent
lism Recurrent abdominal pain
lism Mild abdominal pain
stal interphalangeal joints; MTP, metatarsophalangeal joints.
Cases
ic Dise
lcohoith ps
ith ps
with
lcoholcoho
lcoholcoho
with
ith ps
withd pse
withChro
, alco
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rosis were found with resulting bone sclerosis, often pro-
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J. Narváez et al. 421
ressing to fragmentation and subsequent subarticularone collapse.Six patients were studied with MRI. The main MRI
ndings included the presence of multiple areas of in-ramedullary fat necrosis and accompanying bone mar-ow edema, along with synovitis and changes of pan-iculitis in the periarticular soft tissues.
ISCUSSION
obular panniculitis, together with arthritis and/or boneecrosis, may complicate pancreatic disease. This triadas been described mainly in patients with acute or
Table 1 Continued
Arthritis (Involved Joints)Evidence of Intr
Techniqu
MCP and PIPWrists, elbows, knees, ankles, and most
finger jointsAnkles, PIP, knees, and several toes
Ankles, knee, wrists, MCP, and PIP
Ankles
Wrists and MTPAnkles, knees, wrist, MCP, and PIP
Ankles and right little fingerAnkles, elbow, and MCPAnkles, knees, wrists, and MCP
Knee, MCP, and PIP
Wrists, MCP, and PIPAnkles and small joints of hands and feetAnkles, knee, wrists, PIP, and DIP
Ankles and small joints of handsAnkles, knees, and wristsAnkles, knees, elbows, and wrists
Ankles, knees, and elbowsAnkles, knees, elbows, wrists, PIP, and
DIPAnkles, knees, wristsAnkle
Hip, ankle, and kneeAnkle and small joints of hands and feet
Ankles, knee, and small joints of handsand feet
Ankle, wrists, MCP, and PIP
hronic pancreatitis (2-24), as well as in a few cases of t
ancreatic tumors (25,26) and ischemic pancreatic dis-ase (27). The acronym PPP syndrome is not widely usednd is not entirely accurate as the arthritis is not alwaysolyarticular.Although this syndrome may appear at any age, the
ypical patient with this syndrome is a middle-aged manith a history of heavy alcohol abuse (3,5,6,9,11,12,9,21-23). It is important to stress that in almost 2/3 ofatients abdominal symptoms are absent or mild, whichay lead to misdiagnosis (3,5-9,12-15,21,22). Our pa-
ient had few abdominal symptoms, despite high serumevels of pancreatic enzymes, as reported elsewhere in theiterature. The delay in diagnosis and specific treatment of
s Fat Necrosis by Imagingthological Fractures
Outcome of JointInvolvement
es/Yes Not reportedo/No Died 3 months after
admissiones/Yes Evolution to chronicity,
functional sequelaeo/No Recovered
es/Yes Evolution to chronicity,functional sequelae
o/No Died 10 days after admissiones/No Evolution to chronicity,
functional sequelaees/No Recoveredo/No Died 22 days after admissiono/No Died several days after
admission Recoveredo/No Not reported
o/No Recoveredes/No Recoveredes/Yes
o/No Recoveredo/No Recoveredes/Yes Evolution to chronicity,
functional sequelaees/Yes Recoveredo/No Died 15 days after admission
es/No Not reportedes/No Died 4 months after
admissiono/No Recoveredes/Yes Evolution to chronicity,
functional sequelaees/Yes Evolution to chronicity,
functional sequelaees/No Evolution to chronicity,
functional sequelae
aosseues/Pa
YN
Y
N
Y
NY
YNN
N
NYY
NNY
YN
YY
NY
Y
Y
he underlying pancreatitis worsens the prognosis of this
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422 PPP syndrome
ondition, which has a mortality rate as high as 24%5,8,11,12,18,20).
The skin lesions of panniculitis in the PPP syndromeegin as erythematous nodules in the subcutaneous tis-ues; they may or may not be tender and typically eruptver the lower extremities (1). Lesions range in size from aew millimeters to approximately 5 cm. They must beifferentiated from erythema nodosum, lupus profundus,utaneous polyarteritis nodosa, and Weber–Christian dis-ase, which may have a similar appearance. The differen-iation from erythema nodosum is made based on loca-ion and histology. Unlike erythema nodosum, the skinesions in PPP syndrome may migrate proximally over therms and trunk (1). Histologically, areas of fat necrosisharacteristically contain ghost-like fat cells, a feature notresent in other causes of panniculitis (1,11,28). Sterilebscess formation with spontaneous drainage may occurn some cases, releasing a thick, creamy purulent-appear-ng material that is rich in lipids (11,12,14,23). Theseeatures can be a valuable clue for directing attention to annderlying pancreatic disorder.Peripheral joint involvement in PPP syndrome usually
resents as symmetric or asymmetric polyarthritis involv-ng the small and large joints, although a few cases ofligoarthritis or monoarthritis have also been described7,20,21). The most commonly affected joints are thenkles, knees, wrists, and MCP joints, although any jointan be involved. Septic arthritis, gout, and early rheuma-oid arthritis all enter the differential diagnosis. Synovialuid contains a high lipid content, and the presence of
iquid lipid crystals (seen under polarized light as stronglyositive birefringent microspherules with a Maltese crossppearance) has been described in a few cases (8,18).nce triggered, the arthritis follows its own course, inde-
endent of the pancreatitis; the arthritis may persist andvolve even after serum pancreatic enzyme levels return toormal, as was the case in our patient. In most patients
oint symptoms are transient, but evolution to chronicityay occur in some cases, with the development of radio-
raphic joint damage (6,7,9,16,22,23). Unfortunately,here is no objective means of identifying which of theseatients will have a chronic course. While persistentlyigh pancreatic enzyme levels appear to correspond withhe subsequent progression of fat necrosis, serum amylasend lipase levels usually correlate poorly with joint diseaseeverity. The development of a pancreatic pseudocyst haseen documented in some of these patients (6,9,23).Characteristic radiological findings are multiple osteo-
ytic lesions and moth-eaten bone destruction, loss ofoint space, and periostitis (although the periosteal reac-ion is not always present) (6,7,9,16,22,23,27,29-31).hese changes occur both in the long bones and in the
mall bones of the hands and feet. The joint damage de-elops over several weeks to several months and seems toorrelate pathologically with areas of extensive intramed-llary fat necrosis and trabecular bone destruction, as
emonstrated with MRI (9,10,19,20,22-24,30,31). Over
ime, diagnostic features of osteonecrosis and bone scle-osis develop, often progressing to fragmentation andubsequent subarticular bone collapse (3,6,7,9,10,13,4,16,17,19,20,22,23,29-30). MRI is more sensitive thanadiography for the detection of the fatty marrow abnormal-ties, which seem to precede necrosis and may add early di-gnostic information (9,10,20,22-24,26,29,30).
The pathogenesis of the PPP syndrome is still unclear,lthough the most widely accepted hypothesis suggestshat the release of pancreatic enzymes (including lipase,mylase, trypsin, and phospholipase A) from a diseasedancreas into the systemic circulation leads to lipolysisnd secondary inflammation in distant visceral and soft-issue sites, including the synovium and bone marrow2,9,10,12,23). Histopathological findings of fat necrosisn biopsies of skin lesions and periarticular tissue fromnvolved joints lend credence to this notion (1,11,12), asoes the demonstration of extensive intramedullary fatecrosis in MRI studies (9,10,20,22-24,26,29,30). Someuthors believe that the arthritis associated with pancre-tic disease is caused by locally high levels of free fattycids: lipolytic pancreatic enzymes bind to adipose cellembranes (such as those in periarticular or bone marrow
issues) and initiate hydrolysis of triglycerides to free fattycids. Free fatty acids may then be released into the jointnd cause acute arthritis (18).
Treatment of patients with the PPP syndrome shoulde directed at the underlying pancreatic disease. Earlydentification of complications that may contribute to
aintaining high circulating levels of pancreatic enzymes,uch as stenosis of Wirsung’s duct or the development ofseudocysts, is important since the massive release of pan-reatic enzymes into the bloodstream is a factor in trigger-ng and perpetuating subcutaneous fat necrosis and ar-hritis. In addition, because of the high incidence of sepsisnd associated mortality, it is important to be alert to theossibility of secondary infection and to treat it promptly.ther treatment options that can potentially reduce pan-
reatic secretory stimulation (such as subcutaneous oc-eotride) (21) or plasmapheresis (11) have also been useds adjunctive treatment in some cases, but the experienceith these therapies is anecdotal. Management of the skin
esions and arthritis with corticosteroids and NSAID issually ineffective, since they can only alleviate symp-oms, and there is no evidence that they reduce the dura-ion of the disease (2-24).
EFERENCES
1. Dahl R, Su WP, Cullimore C, Dicken H. Pancreatic panniculitis.J Am Acad Dermatol 1995;33:413-7.
2. Fine RM. Subcutaneous fat necrosis, pancreatitis, and arthropa-thy. Int J Dermatol 1983;22:575-6.
3. Boswell SH, Baylin GJ. Metastatic fat necrosis and lytic bonelesions in a patient with painless acute pancreatitis. Radiology1973;106:85-6.
4. Phillips RM, Sulser RE, Songcharoen S. Inflammatory arthritisand subcutaneous fat necrosis associated with acute and chronic
pancreatitis. Arthritis Rheum 1980;23:355-60.
1
1
1
1
1
1
1
1
1
1
2
2
2
2
2
2
2
2
2
2
3
3
J. Narváez et al. 423
5. Wilson HA, Askari AD, Neiderhiser DH, Johnson AM, AndrewsBS, Hoskins LC. Pancreatitis with arthropathy and subcutaneousfat necrosis: evidence for the pathogenicity of lipolytic enzymes.Arthritis Rheum 1983;26:121-6.
7. Baron M, Paltiel H, Lander P. Aseptic necrosis of the talus andcalcaneal insufficiency fractures in a patient with pancreatitis, sub-cutaneous fat necrosis, and arthritis. Arthritis Rheum 1984;27:1309-13.
8. Saag KG, Niemann TH, Warner CA, Naides SJ. Subcutaneouspancreatic fat necrosis associated with acute arthritis. J Rheumatol1992;19:630-2.
0. Watts RA, Kelly S, Hacking JC, Lomas D, Hazleman BL. Fatnecrosis: an unusual cause of polyarthritis. J Rheumatol 1993;20:1432-5.
1. Francombe J, Kingsnorth AN, Tunn E. Panniculitis, arthritis andpancreatitis. Br J Rheumatol 1995;34:680-3.
2. Shbeeb MI, Duffy J, Bjornsson J, Ashby AM, Matteson EL. Sub-cutaneous fat necrosis and polyarthritis associated with pancreaticdisease. Arthritis Rheum 1996;39:1922-5.
3. Rodriguez M, López GL, Prieto P, Fernandez L, Willisch A, ArceM. Massive subcutaneous and intraosseous fat necrosis associatedwith pancreatitis: natural evolution of the radiographic picture.Clin Rheumatol 1997;16:199-203.
4. Ordás Calvo C, Jirout Casillas F, Cerrato Rodriguez ME, BallinaGarcía FJ, Rodriguez Pérez A. Nodular lesions and arthritis asso-ciated with chronic alcoholism. Rev Clin Esp 1998;198:619-20.
5. López A, García-Estañ J, Marras C, Castaño M, Rojas MJ, Garre C,et al. Pancreatitis associated with pleural-mediastinal pseudocyst,panniculitis and polyarthritis. Clin Rheumatol 1998;17:335-9.
6. Karasick D, Schweitzer ME. Case 4: intraosseous fat necrosis as-sociated with pancreatitis. Radiology 1998;209:521-4.
7. Menon P, Kulshreshta R. Pancreatitis with panniculitis and ar-thritis: a rare association. Pediatr Surg Int 2004;20:161-2.
8. Ferrari R, Wendelboe M, Ford PM, Corbett WEN, AnastassiadesTP. Pancreatitis arthritis with periarticular fat necrosis. J Rheu-
matol 1993;20:1436-7.
9. L=Hirondel JL, Fournier L, Fretille A, Denizet D, Loyau G. In-traosseous fat necrosis and metaphyseal osteonecrosis in a patientwith chronic pancreatitis: MR imaging and CT scanning. ClinExp Rheumatol 1994;12:191-4.
0. Kotilainen P, Saario R, Mattila K, Nylamo E, Aho H. Intraosse-ous fat necrosis simulating septic arthritis and osteomyelitis in apatient with chronic pancreatitis. Arch Orthop Trauma Surg1998;118:174-5.
1. Mourad FH, Hannoush HM, Bahlawan M, Uthman I, UthmanS. Panniculitis and arthritis as the presenting manifestation ofchronic pancreatitis. J Clin Gastroenterol 2001;32:259-61.
2. Morita O, Ogose A, Hotta T, Kawashima H, Higuchi T, SuzukiK, et al. Pathological fractures due to intraosseous fat necrosisassociated with pancreatitis. Rheumatology 2003;42:394-6.
3. Price-Forbes AN, Filer A, Udeshi UL, Rai A. Progression of im-aging in pancreatitis panniculitis polyarthritis (PPP) syndrome.Scand J Rheumatol 2006;35:72-4.
4. Fesler P, Ambrozkiewicz M, du Cailar G, Mimran A, Ribstein J.Pancreatic panniculitis with polyarthritis and pathological frac-ture. Presse Med 2005;34:1109-10.
5. Tannenbaum H, Anderson LG, Schur PH. Association of poly-arthritis, subcutaneous nodules and pancreatic disease. J Rheuma-tol 1975;2:14-20.
6. Radin D, Colletti P, Forrester D, Tang W. Pancreatic acinar cellcarcinoma with subcutaneous and intraosseous fat necrosis. Radi-ology 1986;158:67-8.
7. Smukler NM, Schumacher HR, Pascual E, Brown S, Ryan WE,Sadeghian MR. Synovial fat necrosis associated with ischemicpancreatic disease. Arthritis Rheum 1979;22:547-53.
8. Dhawan SS, Jimenez-Acosta F, Poppiti RJ Jr, Barkin JS. Subcu-taneous fat necrosis associated with pancreatitis: histochemicaland electron microscopic findgins. Am J Gastroenterol 1990;85:1025-8.
9. Bayo F 3rd, Massie JD, Sebes J. Intraosseous fat necrosis andinfarction associated with pancreatitis. Clin Nucl Med 1993;18:837-9.
0. Tolin BS, Esterhai JL, Allan DA, Furth EE, Schumacher HR.Pancreatic osteoarthropathy with unusually destructive sequelae.Orthopaedics 1993;16:473-7.
1. Ahn BC, Lee J, Suh KJ, Chun KA, Sohn SK, Lee K, et al. In-tramedullary fat necrosis of multiple bones associated with pan-
