Discussion
CML is a malignant neoplasm, which is characterized by the expansion of
the erythroid, myeloid, and platelets in the peripheral blood and
myeloid hyperplasia of the bone marrow. It is associated with the
BCR/ABL1 fusion gene. This gene encodes an abnormal protein which leads
to the constitutive activation of tyrosine kinase, which eventually
results in neoplastic proliferation(5). CML accounts for 15-20% of
leukemias in adults(6) and Ionization radiation exposure is the only
known risk factor(1, 7).
The average diagnostic age ranges from 60 to 65 years(8). About 50% of
cases are asymptomatic and are identified incidentally by routine
complete blood count tests(2). Anemia, splenomegaly, fatigue, weight
loss, and night sweats are the commonest initial manifestations(5).
Extramedullary involvement such as the lymph nodes, skin, and soft
tissues can be seen in patients with blast crises(9). very rarely, soft
tissue hematoma can be the first manifestation of CML. The soft tissue
hematoma may be explained by platelet dysfunction, acquired Von
Willebrand disease, or acquired Glanzmann’s thrombasthenia(3).
The clonal expansion of dysfunctional megakaryocytes can explain
platelet dysfunction in CML, which explains the anticipated improvement
in their function following the initiation of tyrosine kinase
inhibitors(3, 10-12).
The Morel‐Lavallée lesion is a closed traumatic soft‐tissue degloving
injury, first described by the French physician, Dr.
Victor‐Auguste‐François Morel‐Lavallée in 1863. This damage is the
result of the separation of the hypodermis from the fascial tissue due
to a shearing force. Hematoma collection forms due to disruption of the
soft tissue’s perforating blood and lymphatic vessels(3, 13). The
subcutaneous tissues beside the greater trochanter are the most
frequently affected areas by the Morel‐Lavallée lesion(13). We were able
to find three case reports in which the Morel Lavallee lesion was the
initial manifestation of CML. The first patient was a 16-year-old male
athlete who presented with swelling on his knee, confirmed to be CML
after investigation, and was managed both surgically and with a tyrosine
kinase inhibitor(14).
The second patient was a 55-year-old male who came with left thigh
swelling and was also diagnosed with CML after workup and treated with
imatinib and conservatively(4). The third case was a Morel Lavallee
lesion affecting the posterior chest wall, he was treated conservatively
and started on dasatinib(3). Our case is the fourth CML patient
presenting with Morel Lavallee lesion, and the first case that involved
the anterior abdominal wall. She was managed conservatively.
platelet dysfunction, acquired Glanzmann’s thrombasthenia, acquired Von
Willebrand deficiency, were attributed to the spontaneous hematoma in
the previous case reports(10-12).
Even though it’s not clear why this patient developed hematoma in
unusual site without any prior trauma, platelet dysfunction is the
likely etiology.