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Early purulent meningococcal pericarditis due to an unusual strain of Neisseria meningitidis
Pathology (2002 ) 34, pp. 289– 298
CORRESPONDENCE
Early purulent meningococcal pericarditis due to an unusual strain of Neisseria meningitidis Sir, Herrick first described pericarditis due to Neisseria meningitidis in 1918. 1 Two forms, early and late, have been described. Early purulent pericarditis (often described in the literature as primary meningococcal pericarditis) is thought to be caused by meningococci invading the pericardium, and is rarely described in the literature. Twenty cases have been previously described in the English language literature.2,3 Late meningococcal pericarditis is thought to be immunological in aetiology and much more common. We describe a case of early purulent pericarditis which was diagnosed using DNA polymerase chain reaction ( PCR). Early purulent meningococcal pericarditis is usually associated with serogroup C meningococci, 2 and the strain described here belonged to sequence type ( ST) 11 which had previously been reported to be characteristic of ET-37 complex meningococci.4,5 In addition, the isolate’s phenotype was unusual, being C:2a:P1.4 and, on sequencing, the porA gene was found to be P1.7b,4. A previously well 41-year-old man presented with fever and chest pain. He was in shock and exhibited a purpuric
rash. There was no meningism or other neurological signs. Antibiotics were commenced. The jugular venous pressure was raised to the angle of the jaw, the apex beat was impalpable, the heart sounds were faint and no rub was audible. The chest X-ray showed a small, globular heart, and the electrocardiogram showed widespread ST elevation, consistent with pericarditis. Echocardiography revealed a pericardial effusion. Neisseria meningitidis was identified from blood cultures taken on admission. A sample of EDTA blood from the date of admission demonstrated the presence of Neisseria meningitidis serogroup C by PCR, detecting IS1106 and ctrA as previously described.6 The patient developed bilateral pleural effusions. Culture and PCR of pleural fluid for Neisseria meningitidis were negative. On day 4, the patient developed signs of tamponade, confirmed on echocardiography. Pericardiocentesis yielded 830 ml of straw-coloured fluid. The pericardial fluid failed to grow bacteria, but PCR was positive for Neisseria meningitidis serogroup C. Fevers and neutrophilia persisted. CT scan of the thorax (Fig. 1) and transthoracic echocardiogram showed large pleural and pericardial effusions. Pericardectomy was performed on day 19. The pericardium was 3 cm thick and contained buttery exudate, which was excised with the pericardium. Culture of
Fig. 1 CT scan of thorax showing massive pericardial and moderate bilateral pleural effusions.
ISSN 0031–3025 printed/ISSN 1465– 3931 online/02/030289 – 10 © 2002 Royal College of Pathologists of Australasia DOI:10.1080/00313020220131390
290
CORRESPONDENCE
pericardium and exudate were negative. The patient made a complete recovery and returned to work. Determination of serogroup, serotype ( which determines either the class 2 or 3 outer membrane protein) and serosubtype ( which determines the class 1 outer membrane protein) was performed as previously described using monoclonal antibodies ( National Institute of Biological Standards and Control, UK).7 This strain gave the phenotype serogroup C, serotype 2a and serosubtype P1.4, which is written as C:2a:P1.4. PCR products, amplified from the porA gene ( which encodes for the class 1 outer membrane protein), were sequenced and a segment of the porA gene starting five codons from the signal peptide was analysed as described previously.8 The porA genotype was found to be P1.7b,4. The sequence of the porA gene for this isolate has been given GeneBank accession number AF244935. PCR products used for multilocus sequence typing ( MLST) were obtained using primers and cycling conditions as previously described.4,5 The ST was determined by submitting the seven allele consensus sequences to the MLST database.5 fumC allele PCR products were additionally sequenced to ascertain if this strain was ET-15 using a primer as described previously.9 The blood culture isolate had the following MLST allele numbers: abcZ 2, adk 3, aroE 4, fumC 3, gdh 8, pdhC 4 and pgm 6. This allelic profile was confirmed by MLST analysis to belong to ST-11, which had previously been reported to be characteristic of ET-37 complex meningococci.4,5 The sequence upstream from the MLST fumC sequencing primers revealed that the fumC gene of this strain had a point mutation at position 640, indicative of ET-15, as described previously.9 Early purulent pericarditis is commonly termed primary meningococcal pericarditis. This is defined as purulent pericarditis without initial clinical evidence of meningococcaemia, meningitis or other foci of meningococcal infection.2,3 Most cases of primary meningococcal pericarditis reported in the English language literature indeed had clinical evidence of meningococcal infection elsewhere at presentation or prior to the symptoms of pericardial infection.2,3 Finkelstein et al., have suggested three classifications for meningococcal pericarditis: pericarditis as a local manifestation of disseminated meningococcal disease ( DMP); isolated meningococcal pericarditis ( IMP); and reactive meningococcal pericarditis ( RMP).10 The patient described in this present report had features common to both the DMP and IMP classifications as suggested above. Therefore, it is less confusing to define pericarditis related to meningococcal infection as either early purulent pericarditis or late immunological. Blaser et al., in 1984 similarly grouped the two entities, classifying them as infectious or immunological.2 Early purulent pericarditis is thought to develop from direct invasion of the pericardium by Neisseria meningitidis. Late pericarditis develops in the course of adequately treated meningococcal disease, representing an immune complex phenomenon. Analysis of 20 reported cases has been reviewed and published previously.2,3 Most patients were adolescents and adults. Serogroup C was disproportionately associated. Cardiac tamponade occurred in most cases. The diagnosis was derived from pericardial fluid cultures in previous cases and blood cultures were positive in 44%
Pathology ( 2002 ), 34, June
of these cases. Despite rapid progression of complications, all cases previously described have survived. Our case demonstrated the utility of a serogroup specific PCR for the diagnosis of meningococcal disease. PCR on EDTA blood and CSF is very sensitive and specific for this diagnosis.6 The positive result on the pericardial fluid was consistent with the clinical picture of purulent meningococcal pericarditis, as it denotes the presence of DNA and thus the organism in the pericardial sac. PCR was useful in confirming the presence of the organism in the pericardium, as the administration of antibiotics several days before pericardial fluid was obtained would nearly always result in negative cultures. We also used a number of DNA-based techniques to further characterise this isolate. Only limited data, at most the serogroup, had been reported for previous cases.2,3 The DNA-based approach to population genetics, known as multilocus sequence typing ( MLST), has been used for population studies,5 and has also proved useful in the investigation of an outbreak of meningococcal disease.4 The strain we have described here belonged to ST-11, which is analogous to the ET-37 complex as defined by multilocus enzyme electrophoresis ( MLEE). The molecular basis for the distinction of ET-15 from other ET-37 complex meningococci has been elucidated,9 and our strain was found to belong to ET-15. Over the past decade, ET-15 meningococci have been associated with clusters of meningococcal disease both locally and internationally.7,8,11 The porA gene of our strain was sequenced as we only detected a partial PorA phenotype. The monoclonal antibody-based typing scheme currently used is not comprehensive and many isolates, such as the one described here, could only be partially typed.8 Sequencing revealed a porA P1.7b,4 genotype, which has commonly been associated with meningococci belonging to Lineage III.11,12 porA variation within the period of 13 years since the origin of ET-15 was thought to involve only related variable regions.8 The unusual phenotype of this strain, found also to belong to the ET-15 clone, presents further evidence of porA gene mosaic structure which could only have arisen through recombination events. Diversification or micro-evolution such as this has been evidenced in other clonal groups. Examination of meningococci belonging to the ET-5 complex, first described in 1986, suggested that recombination of whole genes of porB ( which encodes either the class 2 or 3 outer membrane protein) and porA had occurred and, due to the chromosomal location of these two genes, must have arisen due to two separate genetic events.12 So whilst these events are not unique to the ET-15 clone, it appears to be only a recently apparent phenomenon within this clone.8 Meningococci belonging to the ET-15 clone of the ET-37 complex was responsible for increased meningococcal disease within the Sydney region of New South Wales, Australia, in 1996–1998, and the phenotype generally associated with these strains was C:2a:P1.5.7,8 This is the first occasion that meningococci with the phenotype C:2a:P1.4 have been associated with the ET-37 complex in New South Wales, Australia. Our case of purulent pericarditis due to Neisseria meningitidis adds to the literature on this rare entity, and demonstrates the need to classify the type of pericarditis correctly so that the required treatment, drainage, be
CORRESPONDENCE
instituted. The case also demonstrates the utility of PCR in diagnosing purulent meningococcal pericarditis after antibiotics are given. The unusual clinical presentation associated with this strain is of concern because meningococci belonging to the ET-15 clone of the ST-11/ET-37 complex have been associated with higher morbidity and mortality. Jane Jelfs*† Brian R. Hughes*‡ Iain B. Gosbell*§ * Department of Microbiology and Infectious Diseases, South Western Area Pathology Service, Liverpool, and §School of Pathology, Faculty of Medicine, University of New South Wales, Kensington, New South Wales, Australia. Present affiliations: †CSL Vaccines, CSL Limited, North Ryde, and ‡Department of Clinical Services, Albion Street Centre, Surry Hills, New South Wales, Australia
1. Herrick WW. Meningococcic pericarditis, with report of 12 cases. Medical service of the base hospital, Camp Jackson, S.C. Med Clin North Am 1918; 2: 411– 26. 2. Blaser MJ, Reingold AL, Alsever RN, Hightower A. Primary meningococcal pericarditis: a disease of adults associated with serogroup C Neisseria meningitidis. Rev Infect Dis 1984; 6: 625– 32. 3. Baevsky RH. Primary meningococcal pericarditis. Clin Infect Dis 1999; 29: 213–5. 4. Feavers I, Gray S, Urwin R, et al. Multilocus sequence typing and antigen sequencing in the investigation of a meningococcal disease outbreak. J Clin Microbiol 1999; 37: 3883–7. 5. Maiden MC, Bygraves JA, Feil E, et al. Multilocus sequence typing: a portable approach to the identification of clones within populations of pathogenic microorganisms. Proc Natl Acad Sci USA 1998; 95: 3140– 5. 6. Porritt RJ, Mercer JL, Munro R. Detection and serogroup determination of Neisseria meningitidis in CSF by polymerase chain reaction ( PCR). Pathology 2000; 32: 42–5.
A
291
7. Jelfs J, Jalaludin B, Munro R, et al. A cluster of meningococcal disease in western Sydney, Australia initially associated with a nightclub. Epidemiol Infect 1998; 120: 263–70. 8. Jelfs J, Munro R, Wedege E, Caugant DA. Sequence variation in the porA gene of clone of Neisseria meningitidis during epidemic spread. Clin Diagn Lab Immunol 2000; 7: 390– 5. 9. Vogel U, Claus H, Frosch M, Caugant DA. Molecular basis for distinction of the ET-15 Clone within the ET-37 complex of Neisseria meningitidis. J Clin Microbiol 2000; 38: 941–2. 10. Finkelstein Y, Adler Y, Nussinovitch M, Varsano I, Amir J. A new classification for pericarditis associated with meningococcal infection. Eur J Pediatr 1997; 156: 585– 8. 11. Caugant DA. Population genetics and molecular epidemiology of Neisseria meningitidis. APMIS 1998; 106: 505– 25. 12. Martin DR, Walker SJ, Baker MG, Lennon DR. New Zealand epidemic of meningococcal disease identified by a strain with phenotype B:4:P1.4. J Infect Dis 1998; 177: 497– 500.
Soft tissue amyloidoma Sir, Deposition of amyloid is usually a systemic disease. Sometimes localised amyloid deposits are present, limited to a single organ or tissue. Nodular masses of amyloid known as amyloidomas have been reported as occurring in the nasal sinus, larynx,1 lung, 2 spleen, eyelid, skin, lower urinary tract,3,4 lymph node,5,6 tongue, gastrointestinal tract, breast,6 bone,6–10 brain, and rarely in the soft tissue.5,6,11,12 This report describes a case of soft tissue amyloidoma involving the anteromedial left pelvis. A 40-year-old Malay man presented with a painless swelling over the left hip. For 11 months he had been aware of the swelling which had progressively enlarged. Physical examination revealed a firm mass measuring 10 cm in diameter over the left hip. The hip function was normal and there was no lymphadenopathy. Plain radiographs showed a soft tissue swelling with no involvement of the skeletal structures. The full blood count, blood urea and electrolytes levels were normal. MRI ( Fig. 1) shows a lobulated mass, measuring 10 ´ 5 ´ 14 cm with well-circumscribed margins in the anteromedial left pelvis. There was clear fat-plane between
B
Fig. 1 ( A) Transverse MRI and ( B) coronal MRI of pelvis showing a soft tissue lobulated mass measuring 10 pelvis. No bone involvement was noted.
´ 5 ´ 14 cm in the anteromedial left
CORRESPONDENCE
Early purulent meningococcal pericarditis due to an unusual strain of Neisseria meningitidis Sir, Herrick first described pericarditis due to Neisseria meningitidis in 1918. 1 Two forms, early and late, have been described. Early purulent pericarditis (often described in the literature as primary meningococcal pericarditis) is thought to be caused by meningococci invading the pericardium, and is rarely described in the literature. Twenty cases have been previously described in the English language literature.2,3 Late meningococcal pericarditis is thought to be immunological in aetiology and much more common. We describe a case of early purulent pericarditis which was diagnosed using DNA polymerase chain reaction ( PCR). Early purulent meningococcal pericarditis is usually associated with serogroup C meningococci, 2 and the strain described here belonged to sequence type ( ST) 11 which had previously been reported to be characteristic of ET-37 complex meningococci.4,5 In addition, the isolate’s phenotype was unusual, being C:2a:P1.4 and, on sequencing, the porA gene was found to be P1.7b,4. A previously well 41-year-old man presented with fever and chest pain. He was in shock and exhibited a purpuric
rash. There was no meningism or other neurological signs. Antibiotics were commenced. The jugular venous pressure was raised to the angle of the jaw, the apex beat was impalpable, the heart sounds were faint and no rub was audible. The chest X-ray showed a small, globular heart, and the electrocardiogram showed widespread ST elevation, consistent with pericarditis. Echocardiography revealed a pericardial effusion. Neisseria meningitidis was identified from blood cultures taken on admission. A sample of EDTA blood from the date of admission demonstrated the presence of Neisseria meningitidis serogroup C by PCR, detecting IS1106 and ctrA as previously described.6 The patient developed bilateral pleural effusions. Culture and PCR of pleural fluid for Neisseria meningitidis were negative. On day 4, the patient developed signs of tamponade, confirmed on echocardiography. Pericardiocentesis yielded 830 ml of straw-coloured fluid. The pericardial fluid failed to grow bacteria, but PCR was positive for Neisseria meningitidis serogroup C. Fevers and neutrophilia persisted. CT scan of the thorax (Fig. 1) and transthoracic echocardiogram showed large pleural and pericardial effusions. Pericardectomy was performed on day 19. The pericardium was 3 cm thick and contained buttery exudate, which was excised with the pericardium. Culture of
Fig. 1 CT scan of thorax showing massive pericardial and moderate bilateral pleural effusions.
ISSN 0031–3025 printed/ISSN 1465– 3931 online/02/030289 – 10 © 2002 Royal College of Pathologists of Australasia DOI:10.1080/00313020220131390
290
CORRESPONDENCE
pericardium and exudate were negative. The patient made a complete recovery and returned to work. Determination of serogroup, serotype ( which determines either the class 2 or 3 outer membrane protein) and serosubtype ( which determines the class 1 outer membrane protein) was performed as previously described using monoclonal antibodies ( National Institute of Biological Standards and Control, UK).7 This strain gave the phenotype serogroup C, serotype 2a and serosubtype P1.4, which is written as C:2a:P1.4. PCR products, amplified from the porA gene ( which encodes for the class 1 outer membrane protein), were sequenced and a segment of the porA gene starting five codons from the signal peptide was analysed as described previously.8 The porA genotype was found to be P1.7b,4. The sequence of the porA gene for this isolate has been given GeneBank accession number AF244935. PCR products used for multilocus sequence typing ( MLST) were obtained using primers and cycling conditions as previously described.4,5 The ST was determined by submitting the seven allele consensus sequences to the MLST database.5 fumC allele PCR products were additionally sequenced to ascertain if this strain was ET-15 using a primer as described previously.9 The blood culture isolate had the following MLST allele numbers: abcZ 2, adk 3, aroE 4, fumC 3, gdh 8, pdhC 4 and pgm 6. This allelic profile was confirmed by MLST analysis to belong to ST-11, which had previously been reported to be characteristic of ET-37 complex meningococci.4,5 The sequence upstream from the MLST fumC sequencing primers revealed that the fumC gene of this strain had a point mutation at position 640, indicative of ET-15, as described previously.9 Early purulent pericarditis is commonly termed primary meningococcal pericarditis. This is defined as purulent pericarditis without initial clinical evidence of meningococcaemia, meningitis or other foci of meningococcal infection.2,3 Most cases of primary meningococcal pericarditis reported in the English language literature indeed had clinical evidence of meningococcal infection elsewhere at presentation or prior to the symptoms of pericardial infection.2,3 Finkelstein et al., have suggested three classifications for meningococcal pericarditis: pericarditis as a local manifestation of disseminated meningococcal disease ( DMP); isolated meningococcal pericarditis ( IMP); and reactive meningococcal pericarditis ( RMP).10 The patient described in this present report had features common to both the DMP and IMP classifications as suggested above. Therefore, it is less confusing to define pericarditis related to meningococcal infection as either early purulent pericarditis or late immunological. Blaser et al., in 1984 similarly grouped the two entities, classifying them as infectious or immunological.2 Early purulent pericarditis is thought to develop from direct invasion of the pericardium by Neisseria meningitidis. Late pericarditis develops in the course of adequately treated meningococcal disease, representing an immune complex phenomenon. Analysis of 20 reported cases has been reviewed and published previously.2,3 Most patients were adolescents and adults. Serogroup C was disproportionately associated. Cardiac tamponade occurred in most cases. The diagnosis was derived from pericardial fluid cultures in previous cases and blood cultures were positive in 44%
Pathology ( 2002 ), 34, June
of these cases. Despite rapid progression of complications, all cases previously described have survived. Our case demonstrated the utility of a serogroup specific PCR for the diagnosis of meningococcal disease. PCR on EDTA blood and CSF is very sensitive and specific for this diagnosis.6 The positive result on the pericardial fluid was consistent with the clinical picture of purulent meningococcal pericarditis, as it denotes the presence of DNA and thus the organism in the pericardial sac. PCR was useful in confirming the presence of the organism in the pericardium, as the administration of antibiotics several days before pericardial fluid was obtained would nearly always result in negative cultures. We also used a number of DNA-based techniques to further characterise this isolate. Only limited data, at most the serogroup, had been reported for previous cases.2,3 The DNA-based approach to population genetics, known as multilocus sequence typing ( MLST), has been used for population studies,5 and has also proved useful in the investigation of an outbreak of meningococcal disease.4 The strain we have described here belonged to ST-11, which is analogous to the ET-37 complex as defined by multilocus enzyme electrophoresis ( MLEE). The molecular basis for the distinction of ET-15 from other ET-37 complex meningococci has been elucidated,9 and our strain was found to belong to ET-15. Over the past decade, ET-15 meningococci have been associated with clusters of meningococcal disease both locally and internationally.7,8,11 The porA gene of our strain was sequenced as we only detected a partial PorA phenotype. The monoclonal antibody-based typing scheme currently used is not comprehensive and many isolates, such as the one described here, could only be partially typed.8 Sequencing revealed a porA P1.7b,4 genotype, which has commonly been associated with meningococci belonging to Lineage III.11,12 porA variation within the period of 13 years since the origin of ET-15 was thought to involve only related variable regions.8 The unusual phenotype of this strain, found also to belong to the ET-15 clone, presents further evidence of porA gene mosaic structure which could only have arisen through recombination events. Diversification or micro-evolution such as this has been evidenced in other clonal groups. Examination of meningococci belonging to the ET-5 complex, first described in 1986, suggested that recombination of whole genes of porB ( which encodes either the class 2 or 3 outer membrane protein) and porA had occurred and, due to the chromosomal location of these two genes, must have arisen due to two separate genetic events.12 So whilst these events are not unique to the ET-15 clone, it appears to be only a recently apparent phenomenon within this clone.8 Meningococci belonging to the ET-15 clone of the ET-37 complex was responsible for increased meningococcal disease within the Sydney region of New South Wales, Australia, in 1996–1998, and the phenotype generally associated with these strains was C:2a:P1.5.7,8 This is the first occasion that meningococci with the phenotype C:2a:P1.4 have been associated with the ET-37 complex in New South Wales, Australia. Our case of purulent pericarditis due to Neisseria meningitidis adds to the literature on this rare entity, and demonstrates the need to classify the type of pericarditis correctly so that the required treatment, drainage, be
CORRESPONDENCE
instituted. The case also demonstrates the utility of PCR in diagnosing purulent meningococcal pericarditis after antibiotics are given. The unusual clinical presentation associated with this strain is of concern because meningococci belonging to the ET-15 clone of the ST-11/ET-37 complex have been associated with higher morbidity and mortality. Jane Jelfs*† Brian R. Hughes*‡ Iain B. Gosbell*§ * Department of Microbiology and Infectious Diseases, South Western Area Pathology Service, Liverpool, and §School of Pathology, Faculty of Medicine, University of New South Wales, Kensington, New South Wales, Australia. Present affiliations: †CSL Vaccines, CSL Limited, North Ryde, and ‡Department of Clinical Services, Albion Street Centre, Surry Hills, New South Wales, Australia
1. Herrick WW. Meningococcic pericarditis, with report of 12 cases. Medical service of the base hospital, Camp Jackson, S.C. Med Clin North Am 1918; 2: 411– 26. 2. Blaser MJ, Reingold AL, Alsever RN, Hightower A. Primary meningococcal pericarditis: a disease of adults associated with serogroup C Neisseria meningitidis. Rev Infect Dis 1984; 6: 625– 32. 3. Baevsky RH. Primary meningococcal pericarditis. Clin Infect Dis 1999; 29: 213–5. 4. Feavers I, Gray S, Urwin R, et al. Multilocus sequence typing and antigen sequencing in the investigation of a meningococcal disease outbreak. J Clin Microbiol 1999; 37: 3883–7. 5. Maiden MC, Bygraves JA, Feil E, et al. Multilocus sequence typing: a portable approach to the identification of clones within populations of pathogenic microorganisms. Proc Natl Acad Sci USA 1998; 95: 3140– 5. 6. Porritt RJ, Mercer JL, Munro R. Detection and serogroup determination of Neisseria meningitidis in CSF by polymerase chain reaction ( PCR). Pathology 2000; 32: 42–5.
A
291
7. Jelfs J, Jalaludin B, Munro R, et al. A cluster of meningococcal disease in western Sydney, Australia initially associated with a nightclub. Epidemiol Infect 1998; 120: 263–70. 8. Jelfs J, Munro R, Wedege E, Caugant DA. Sequence variation in the porA gene of clone of Neisseria meningitidis during epidemic spread. Clin Diagn Lab Immunol 2000; 7: 390– 5. 9. Vogel U, Claus H, Frosch M, Caugant DA. Molecular basis for distinction of the ET-15 Clone within the ET-37 complex of Neisseria meningitidis. J Clin Microbiol 2000; 38: 941–2. 10. Finkelstein Y, Adler Y, Nussinovitch M, Varsano I, Amir J. A new classification for pericarditis associated with meningococcal infection. Eur J Pediatr 1997; 156: 585– 8. 11. Caugant DA. Population genetics and molecular epidemiology of Neisseria meningitidis. APMIS 1998; 106: 505– 25. 12. Martin DR, Walker SJ, Baker MG, Lennon DR. New Zealand epidemic of meningococcal disease identified by a strain with phenotype B:4:P1.4. J Infect Dis 1998; 177: 497– 500.
Soft tissue amyloidoma Sir, Deposition of amyloid is usually a systemic disease. Sometimes localised amyloid deposits are present, limited to a single organ or tissue. Nodular masses of amyloid known as amyloidomas have been reported as occurring in the nasal sinus, larynx,1 lung, 2 spleen, eyelid, skin, lower urinary tract,3,4 lymph node,5,6 tongue, gastrointestinal tract, breast,6 bone,6–10 brain, and rarely in the soft tissue.5,6,11,12 This report describes a case of soft tissue amyloidoma involving the anteromedial left pelvis. A 40-year-old Malay man presented with a painless swelling over the left hip. For 11 months he had been aware of the swelling which had progressively enlarged. Physical examination revealed a firm mass measuring 10 cm in diameter over the left hip. The hip function was normal and there was no lymphadenopathy. Plain radiographs showed a soft tissue swelling with no involvement of the skeletal structures. The full blood count, blood urea and electrolytes levels were normal. MRI ( Fig. 1) shows a lobulated mass, measuring 10 ´ 5 ´ 14 cm with well-circumscribed margins in the anteromedial left pelvis. There was clear fat-plane between
B
Fig. 1 ( A) Transverse MRI and ( B) coronal MRI of pelvis showing a soft tissue lobulated mass measuring 10 pelvis. No bone involvement was noted.
´ 5 ´ 14 cm in the anteromedial left