Not all Pericarditis is Viral
1
MD ,
2
MD
Sital Singh
Edward Hearn
, Gabor Hertz
1University of California, Davis Medical Center; Sacramento, CA
2Kaiser Permanente Sacramento Medical Center; Sacramento, CA
LEARNING OBJECTIVES
• Recognize atypical presentations of AML
• Understand typical presentation of Acute Myelogenous
Leukemia (AML)
• Understand diagnosis of AML.
2
MD
CLINICAL COURSE
Figure 1. EKG
Patient was initially treated with colchicine and prednisone
for the pericarditis. He further improved with induction
chemotherapy and was discharged with close follow up.
After chemotherapy; AML showed remission even though
cytogenetics indicated poor prognosis (Fig. 5)
CASE PRESENTATION
37 year old man presented to ED complaining of shortness
of breath and midsternal chest pain for 1 week after lifting
weights. A bedside Echo in the ED showed no effusion. His
EKG showed ST elevations in anterior and inferior leads
and PR interval depression (Fig 1). His troponins were
negative. He was diagnosed with pericarditis and discharged
home with NSAIDS.
He returned two days later complaining of sharp, sternal
chest pain that was not tender to palpation and worsening
shortness of breath. Pain was worse when he slept on his
side, and relieved by ibuprofen. Echo showed small to
moderate pericardial effusion.
DISCUSSION
Figure 2. Bone Marrow Aspirate
Figure 4. Flow Cytometry
Trisomy is a rare cytogenetic abnormality in AML. Isolated
trisomies in AML are associated with an adverse outcome1.
Of these, trisomy 11 is one of the most rare isolated
abnormalities associated with AML2.
Monocytic AML is most likely to have extra myeloid
manifestation with gingival hyperplasia, skin changes, and
rarely acute pericarditis4.
ROS: positive for subjective fevers, fatigue/malaise, nonbloody vomiting and 10lb wt. loss. Negative for URI
symptoms, recent travel, TB, HIV.
PE: Vitals were unremarkable. Physical exam revealed no
JVD or rubs. Pulsus paradoxus was negative. No gingival
hyperplasia
DIAGNOSTIC STUDIES
CBC: WBC of 25.9, Hgb 9.1, PLT of 238, MCV of 102.
Differential:Monocytes 48(H). BLASTS 2(L), Myelocytes
1(H).
BMP: notable for Cr of 1.64 ESR: >120
Bone Marrow Aspiration - mononuclear large atypical
immature cells on smear and aspirate (Fig. 2).
Bone Marrow Biopsy - monotonous population of
immature myeloid cells (Fig. 3).
Flow Cytometry - a population of immature cells (90%)
with monocyte differentiation with markers indicating
monocytic AML (Fig. 4).
Karyotype - Trisomy 11
Acute Myelogenous Leukemia is an abnormal proliferation
of myeloid cells. Classically AML presents as:
• normocytic anemia with low or normal reticulocytes3.
• 75% of patients have PLT’s below 100,0004.
• Median leukocyte count is 15000.
• Smear usually shows myeloblasts3.
• Bone marrow biopsy usually reveals a hypercellular
marrow with cells of myeloid lineage3
• Diagnosis requires bone marrow infiltration with greater
than 20% of blasts or >20% from the peripheral blood4.
Figure 3. Bone Marrow Biopsy
Figure 5. Bone Marrow Biopsy
REFERENCES
1.)Farag SS, Archer KJ, Mrózek K, Vardiman JW, Carroll AJ, Pettenati MJ, Moore JO,
Kolitz JE, Mayer RJ, Stone RM, Larson RA, Bloomfield CD. Isolated trisomy of
chromosomes 8, 11, 13 and 21 is an adverse prognostic factor in adults with de novo
acute myeloid leukemia: results from Cancer and Leukemia Group B 8461. Int J Oncol.
2002;21:1041–1051.
2.)Heinonen K, Mrózek K, Lawrence D, Arthur DC, Pettenati MJ, Stamberg J,
Qumsiyeh MB, Verma RS, MacCallum J, Schiffer CA, Bloomfield CD. Clinical
characteristics of patients with de novo acute myeloid leukaemia and isolated trisomy 11:
a Cancer and Leukemia Group B study. Br J Haemaatol. 1998;101:513–520.
3.)Bob Lowenberg, M.D., James R. Downing, M.D., and Alan Burnett, M.D. Medical
Progress: Acute Myeloid Leukemia.N Engl J Med 1999; 341:1051-1062;September 30,
1999
4.)Verschurr C. Arnauld. Acute Monocytic Leukemia;Department of Pediatric Oncology.
University of Amsterdam.May 2004. Retrieved from Orpha.net on November 10,2012.