Diagnosis Of Acute Myelomonocytic Leukemia Research Articles

Leukemia-induced Gingival Overgrowth as an Early Manifestation in Pregnancy: A Case Report

Leukemia is a neoplastic disease with early oral and periodontal manifestations such as ulceration, infection, bleeding and gingival hyperplasia. This paper describes a 39-year-old pregnant woman with a diagnosis of acute myelomonocytic leukemia (AML), with gingival enlargement in the upper and lower jaws. A gingival biopsy was performed, followed by a complete blood count and peripheral blood smear. From a histopathological view, infiltration of the neoplastic (myelomonocytoblastic) cells was observed and many immature lymphoid cells were revealed by the hematologic tests. The interesting clinical finding about this case was the absence of spontaneous bleeding and profuse bleeding on probing. This case is reported to emphasize the leukemia-induced gingival enlargement in pregnancy and the early diagnosis of AML by dentists, which results in immediate treatment and management of the patient.

G-CSF Induced Atypical Monocytic Proliferation Mimicking Acute Myelomonocytic Leukemia in Post-Induction Chemotherapy AML Patient

Abstract 4283 Introduction:Granulocyte colony-stimulating factor (G-CSF) is a major hematopoietic cytokine involved in control of neutrophil production, proliferation and survival.1 Nowadays, recombinant G-CSF is widely used in patients with hematopoietic malignanies receiving chemotherapy to increase leukocyte count.2 Studies have showed that G-CSF use in these settings is safe and does not increase relapse rate.3,4 However, A phenomena called transient atypical monocytosis, or pseudoleukemia, induced by G-CSF administration in AML patients with chemotherapy have been reported.5,6 This entity mimics recurrent/relapsed acute leukemia and causes confusion in pathologic diagnosis and potential problems in clinical management. The case presented in this report is an example of this entity. Pathology:A 55-year old male patient presented with leukocytosis and anemia. Peripheral blood smear examination revealed a blast population and monocytosis. Flow cytometry on the blood sample showed 37% blasts with expression of CD33, CD13, CD117, HLA-DR, CD34, CD14, CD15 and CD64. FISH study revealed a chromosomal abnormality of inversion 16. A diagnosis of acute myelomonocytic leukemia was established. The patient was treated with induction chemotherapy and was given Neupogen from day 6 through day 20. Bone marrow examination on the day 14th showed an aplastic marrow. However, examination of the patient's day 21 bone marrow revealed marked hypercellularity with sheets of large atypical monocytic cells and brisk mitotic figures. These cells showed round to ovoid nuclei, basophilic cytoplasm and prominent nucleoli, morphologically indistinguishable from blastic cells. Immunohistochemical studies confirmed that most of these atypical cells were lysozyme, CD163 and CD68 positive monocytes, some of them were positive for CD117. These findings raised concerns of recurrent/relapsed AML. However, FISH study was negative for inversion 16. These results indicate that the findings in the patient's day 21 marrow were most likely G-CSF-induced changes. The Neupogen was discontinued soon after. The patient was followed-up with periodic bone marrow examination and FISH study, which showed negative results. Currently, the patient is in complete remission. Discussion:We report one case of G-CSF induced atypical monocytic proliferation in an AML patient with induction chemotherapy. The findings could have created diagnostic problems if FISH study data had not available since those atypical cells were morphologically indistinguishable from blastic cells. Studies have shown that administration of recombinant G-CSF induces a rapid and sustained elevation in absolute peripheral neutrophil counts, and its use in leukemic patients during or after induction chemotherapy is safe and does not increase relapse rates.4 G-CSF shortens the transit time of developing granulocytes in bone marrow and accelerates the release of neutrophils that have undergone recent cell division.1 Our case of transient atypical monocytosis and a few similar cases reported in literatures showed an unusual response to G-CSF. This phenomenon was mostly seen in AML-M4, AML-M5 and AML-M3 cases7 and the mechanism is not entirely clear. A possible explanation is that G-CSF does not only act on neutrophils but also acts on progenitor hematopoietic cells including monocytes.8 One problem is that this entity can mimic recurrent AML causing confusion or potential misdiagnosis if clinical information or cytogenetic studies are not available. Therefore, it is important that both clinicians and pathologists be aware of this phenomenon in hematology/oncology settings. Appropriate discontinuation of G-CSF and following-up these patients with morphologic examination and cytogenetic studies is necessary. Meanwhile, a thorough understanding of exogenous G-CSF effects in cancer patients is essential to reduce any potential risks caused by its administration. Disclosures:No relevant conflicts of interest to declare.

Detection of a novel CBFB/MYH11 variant fusion transcript (K-type) showing partial insertion of exon 6 of CBFB gene using two commercially available multiplex RT-PCR kits

We report on a 20-year-old man with acute myeloid leukemia (AML) showing a distinct novel CBFB/MYH11 variant fusion transcript. Initial results of bone marrow, chromosome, and flow cytometric analyses were not in accordance with the diagnosis of acute myelomonocytic leukemia with eosinophilia (AML-M4Eo) or AML with a CBFB/MYH11 rearrangement. However, results from 2 commercially available multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) tests repeatedly showed an unusual PCR product from his bone marrow specimen. Not only does this case show a partial insertion of exon 6 of the CBFB (ENSG00000067955) gene, but it also involves novel breakpoints within both exon 6 of the CBFB gene and exon 28 (previously exon 7) of the MYH11 (ENSG00000133392) gene, which is regarded as a previously non-reported, new type (K-type) of CBFB/MYH11 fusion transcript. In addition, our study result was in agreement with the recent report of Schnittger et al. that rare fusion transcripts of CBFB/MYH11 are correlated with an atypical cytomorphology and other aberrant characteristics. Therefore, multiplex RT-PCR and sequence analysis of these atypical products should be performed to diagnose atypical AML with CBFB/MYH11 rearrangement, to predict prognosis of these patients as well as to elucidate the molecular mechanism.

Systemic mastocytosis with acute myelomonocytic leukemia: a case report

Bone marrow mastocytosis may be associated with many clonal non mast cell hematological neoplasms and its association with acute myeloid leukemia especially with t (8; 21) has been described. We describe an interesting case of coexistence of systemic mastocytosis with acute myelomonocytic leukemia in a young child. Diagnosis of acute myelomonocytic leukemia was based on bone marrow aspirate findings coupled with cytochemistry. Systemic mastocytosis was diagnosed on the basis of bone marrow biopsy findings showing blasts as well as multifocal dense mast cell infiltrates with spindling and atypical morphology which was confirmed on toluidine blue staining.

SIMULTANEOUS OCCURRENCE OF ADVANCED NEUROBLASTOMA AND ACUTE MYELOID LEUKEMIA

The authors report the case of a 4-year-old boy with a diagnosis of stage IV neuroblastoma (NB), who had been treated with 6 cycles of cyclophosphamide, doxorubicin, cisplatin, and etoposide for 12 months. The patient reached partial remission and presented a diagnosis of acute myelomonocytic leukemia (M4 AML), confirmed by immunophenotyping. After 2 months of therapy for leukemia, the child died with both malignancies in activity. A necropsy histologically confirmed the simultaneity of the two diseases. The authors review the possibilities of this association. The review leads to the conclusion that AML can occur as a secondary malignancy after the onset of the neuroblastoma, or be suggested by a misdiagnosis. The simultaneous occurrence of both as described here is not, however, found in the literature, to the best of the authors' knowledge.

Facial heliotrope rash as the initial manifestation of acute myelomonocytic leukemia

The association of leukocytoclastic vasculitis or dermatomyositis with malignancies has been reported. We describe a patient who developed a skin rash, histologically compatible with dermatomyositis, which during the course of the disease switched to leukocytoclastic vasculitis, which was accompanied with peripheral blood pancytopenia in the absence of any specific pathological manifestation from the bone marrow three years prior to the diagnosis of acute myelomonocytic leukemia (AMML).

Acute myelomonocytic leukemia revealed by a chickenpox-like rash

An unusual case of leukemia cutis is presented. A 42-year-old man presented with a vesicular skin rash mimicking chickenpox. Skin biopsy firmly ruled out the diagnosis of varicella and revealed an infiltration of the superficial derma by myeloblasts. Bone marrow aspirates confirmed the diagnosis of acute myelomonocytic leukemia (type M4).

Acute myelomonocytic leukemia revealed by a chickenpox‐like rash

AbstractAn unusual case of leukemia cutis is presented. A 42‐year‐old man presented with a vesicular skin rash mimicking chickenpox. Skin biopsy firmly ruled out the diagnosis of varicella and revealed an infiltration of the superficial derma by myeloblasts. Bone marrow aspirates confirmed the diagnosis of acute myelomonocytic leukemia (type M4).

Atypical (7;19) translocation in acute myelomonocytic leukemia

Chromosome studies were carried out after a 24-hour harvest of unstimulated bone marrow aspirate cell cultures from a 75-year-old male with a clinical diagnosis of acute myelomonocytic leukemia (FAB M4). Analysis of nine cells after trypsin-Giemsa banding (GTG) revealed two cell lines with a mosaic chromosome pattern, 46,XY/46,XY,t(7;19)(q22;p13.3). A review of the recent literature reveals one case of childhood ALL with a 46,XY/46,XY,t(7;19)(q11;q13) chromosome pattern [1] and a 46,XY,t(3q;11q),t(7q;19p),t(15;17)(q26;q22) in one patient with ANLL (FAB M3) [2]. The t(7;19)(q22;p13.3) seen in our case has not been reported as the sole specific clonal chromosome rearrangement in myeloid neoplasia. Interestingly, the plasminogen activator inhibitor type I, multi-drug resistance, and erythropoietin genes are located at band 7q22 and the insulin receptor gene is located at band 19p13.3. Both sites contain fragile site loci. The possible role of these fragile sites, genes, or other genes in the rearrangement can only be surmised.

Acute Myelomonocytic Leukemia Presenting as a Benign-Appearing Cutaneous Eruption

Aleukemic leukemia cutis is a rare condition in which patients have skin lesions containing leukemic cells before evidence of leukemia can be detected in the peripheral blood. There are only 23 cases of this phenomenon documented in the English literature. We describe a 62-year-old woman who developed a diffuse, clinically benign-appearing cutaneous eruption, which histologically showed an atypical infiltrate of cells, 4 months before leukemic cells were found in her peripheral blood and the diagnosis of acute myelomonocytic leukemia was made by bone marrow aspiration. This case illustrates the difficulty in diagnosing leukemia cutis from examination of routine histologic sections and the importance of specialized marker studies in determining the cause of an atypical cellular infiltrate of the skin. It also illustrates how leukemia cutis can masquerade as a clinically benign-appearing cutaneous eruption in a seemingly healthy patient with normal blood parameters.

Acute myelomonocytic leukemia presenting as a benign-appearing cutaneous eruption

Aleukemic leukemia cutis is a rare condition in which patients have skin lesions containing leukemic cells before evidence of leukemia can be detected in the peripheral blood. There are only 23 cases of this phenomenon documented in the English literature. We describe a 62-year-old woman who developed a diffuse, clinically benign-appearing cutaneous eruption, which histologically showed an atypical infiltrate of cells, 4 months before leukemic cells were found in her peripheral blood and the diagnosis of acute myelomonocytic leukemia was made by bone marrow aspiration. This case illustrates the difficulty in diagnosing leukemia cutis from examination of routine histologic sections and the importance of specialized marker studies in determining the cause of an atypical cellular infiltrate of the skin. It also illustrates how leukemia cutis can masquerade as a clinically benign-appearing cutaneous eruption in a seemingly healthy patient with normal blood parameters.

Primary Gingival Enlargement as a Diagnostic Indicator in Acute Myelomonocytic Leukemia

A 25-YEAR-OLD CHINESE FEMALE, five months pregnant, came to our dental clinic with a chief complaint of slight gingival inflammation. A diagnosis of pregnancy gingivitis was made. One week later, there was a sudden onset of extremely generalized gingival enlargement and very high WBC count (144,000/cmm) was noted. Physical, laboratory, and microscopic examination led to the diagnosis of acute myelomonocytic leukemia. The observations of good oral hygiene and clinical course suggested that leukemic cell infiltration was the major cause of sudden onset of gingival enlargement. This article emphasizes the importance of primary gingival enlargement in the initial diagnosis of leukemia.

Marked Hypophosphatemia Associated With Acute Myelomonocytic Leukemia

A 51-year-man was seen with the diagnosis of acute myelomonocytic leukemia. The WBC count was 380,000/microL at presentation. The serum phosphorus concentration was 0.4 mg/dL and 0.2 mg/dL prior to any phosphorus replacement. Urinary phosphorus excretion was too low to be measured. The patient did not demonstrate any of the usual causes of profound hypophosphatemia with hypophosphaturia. The parathyroid glands were normal at necropsy. Reasons for believing the profound hypophosphatemia was due to phosphorus uptake by the leukemic cells are discussed.

Acute myelomonocytic leukemia in a dog.

An adult female Collie with anorexia, lethargy, posterior limb ataxia, and enterorrhagia had severe leukemia. In the peripheral blood were granulocytes, monocytes and cells with characteristics of both (myelomonocytic intermediates). The dog died within 17 days of the onset of illness. There were widely disseminated green-yellow foci of leukocytes of the same types as in the peripheral blood. A diagnosis of acute myelomonocytic leukemia was made.

Cytologic expressions of spontaneous tumor-specific immunity in an untreated myelomonocytic leukemia. Sustained, complete remission following minimal immunosuppressive therapy.

A monocytosis of about 40% had been persistently described for several months in a 49-year-old Caucasian female during examination for benign upper respiratory and gastrointestinal viral-type infections. Finally, a persistent low-grade fever, asthenia and abdominal discomfort led to the hematological diagnosis of acute myelomonocytic leukemia. The past history revealed multiple atopies. In the peripheral blood there were different kinds of lymphocytes with predominance of small, round agranular ones and moderate eosinophilia; the leukemic cells were large monocytoid elements with bizarre poly-lobulated nuclei of fine chromatin mesh, pale blue, agranular cytoplasm with many large vacuoles. The remarkable feature was that the monocytoid elements were in spherical clusters of 5–50 or more cells and that these clusters always contained a few small lymphocytes. These clusters were not broken by the smearing on the slide and because of their mass they rolled to the edges of the smear. The length of the smoldering, asymptomatic disease with ‘monocytosis’, the abundance of small lymphocytes and the clustering or rosetting of monocytoid-lymphocytic elements were taken as indications of autoimmune leukemic cytolysis which entertained a partial spontaneous remission or at least a prolonged host-tumor symbiosis. In recognition of these expressions of host-resistance a minimal immunosuppressive therapy (MIST) program was tried. A complete, sustained (40 weeks) remission was obtained since.