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PubMed2004

Cutaneous leukaemic infiltrations in a patient with previously undiagnosed myelodysplastic syndrome.

We report the rare case of a patient with leukaemia cutis first presenting only on the hand and fingers and then subsequently spreading over the trunk and face. The lesions heralded the transformation of a previously undiagnosed myelodysplastic syndrome type RAEB (refractory anaemia with blast excess) into frank myeloid leukaemia. The haematological disease was first detected by the dermatohistopathologist. This case underlines the need to look meticulously for skin changes and perform early skin biopsies in haematological patients, as the skin can reveal the first clinical signs of an otherwise not evident bone marrow disorder. Leukaemia cutis as the initial clinical presentation of a transforming myelodysplastic syndrome type RAEB into acute myeloid leukaemia has been reported only very rarely.

Aged↗
PubMed1993

Granulocytic sarcoma of the larynx preceding chronic myeloid leukemia.

The authors report one case of granulocytic sarcoma infiltrating the larynx and cervical lymph nodes in a 50-year-old smoking patient. At the time of diagnosis there was no clinical and laboratory evidence of acute myeloid leukemia or chronic myeloproliferative disease. Four months after diagnosis, bone marrow morphology was consistent with chronic myeloid leukemia, accelerated phase. Cytogenetic abnormalities (Ph 1 chromosome, t(1; 12) (p36; p13), and trisomy of chromosome 20) were also found in hemopoetic cells. Granulocytic sarcoma preceding installation of chronic myeloid leukemia, as described here, seems to be a rare clinical event.

Humans↗
PubMed1995

[A new case of congenital leukemia with leukemia cutis].

Congenital leukaemia is a condition occurring very rarely. In a recent review in 1993, 175 cases are reported, 25-30% of them being well documented as leukaemia cutis. We reported a new case of congenital leukaemia diagnosed as an acute non lymphoblastic leukaemia M4 (FAB) and diagnosed at birth. It involves a newborn female at 42 weeks of gestational age. The most relevant clinical features were hepatomegaly and cutaneous petechial lesions along with a generalized distribution of nodules. From the blood peripheral count, leukocytosis is observed (177 x 10(9)/L) with 48% blasts of myeloid immunophenotype. The coagulation studies were consistent with a disseminated intravascular coagulation syndrome. A biopsy carried out on a cutaneous nodule, revealed diffuse dermoepidermic infiltration by immature cells of myeloid lineage, with cellularity and count similar to that of bone marrow and peripheral blood. The karyotype in the peripheral blood was normal. Infectious and immune causes were excluded as well as constitutional illnesses associated with unstable haematopoiesis. The family rejected treatment with chemotherapy and the baby died on day 53 of life due to progressive leukocytosis and concurrent infection. Our case, like 80% of the cases reported, is of myeloid origin and confirms the fatal evolution of untreated congenital leukaemia.

Diagnosis, Differential↗
PubMed1997

[Bilateral isolated infiltration in the epididymis and sperm cord as first sign of chronic lymphatic leukemia].

OBJECTIVE: Involvement of extralymphatic tissue in chronic lymphocytic leukemia (CLL) is uncommon and that of the epididymis and spermatic cord is rare. This paper describes an unusual case with metastasis to both epididymis and the spermatic cord as the first sign of reactivation of CLL. METHODS/RESULTS: A patient with CLL is described. The first sign of disease progression was the involvement of both epididymis and the spermatic cord. The literature on tumors of the epididymis and spermatic cord and CLL is briefly reviewed. CONCLUSION: Metastatic tumors of the epididymis and spermatic cord are rare. The importance of the pathological findings in making the diagnosis is underscored.

Epididymis↗
PubMed2001

Extramedullary infiltrates at diagnosis have no prognostic significance in children with acute myeloid leukaemia.

This retrospective study was designed to review the relative frequency and prognostic significance of extramedullary infiltrates in children with acute myeloid leukaemia (AML). The registration data and initial discharge summaries were reviewed for all children diagnosed with AML, and registered by the Dutch Childhood Leukaemia Study Group (DCLSG). Between 1972 and 1998, 477 children were diagnosed with AML. Of these patients, 120 (25.1%) had extramedullary leukaemia (EML) at diagnosis. Four categories of EML were found: skin, soft tissue or bone, gingival infiltration and central nervous system (CNS) involvement. Patients who presented with gingival infiltrates, were older than those without EML or those in the other EML subgroups, had a high initial WBC count and a high proportion of M4/M5 morphological variants. This type of presentation could indicate a special biological entity. Univariate analysis of prognostic factors in patients treated after 1985 with intensive protocols showed that initial WBC count and the presence of favourable cytogenetic findings were significant. The presence of EML at diagnosis had no significant effect on event-free survival. In a stepwise multiple regression analysis only favourable cytogenetic findings remained significant.

Acute Disease↗
PubMed2006

Myeloid sarcoma of the maxillary bone.

Myeloid sarcoma (MS) is a malignant tumour of myeloblasts rarely occurring in the maxillary bone. The tumour may precede or be concurrent with leukaemic infiltration of the bone marrow or herald blastic transformation of a myelodysplastic syndrome or a chronic myeloproliferative disorder. Myeloid sarcoma is uncommon in the oral cavity, but it can involve the palate, gingiva, extraction socket, and cheek. Recognition and diagnosis of myeloid sarcoma involving the soft tissues of the oral cavity in an otherwise asymptomatic patient is important and mandates an appropriate haematological diagnostic workup. We herein report on a new case without any evidence of haematological disorders. We discuss the pathological diagnosis and the therapeutical approaches.

Aged, 80 and over↗
PubMed1993

Central nervous system involvement of adult T-cell leukemia-lymphoma with multinucleated giant cells in the brain, skin, and kidney.

BACKGROUND: A case of central nervous system (CNS) involvement in a patient with adult T-cell leukemia-lymphoma (ATLL) with multinucleated giant cells (MNGC) is presented. METHODS: A 48-year-old woman with human T-lymphotropic virus type I (HTLV-I) antibody titer had multiple focal brain symptoms and skin eruptions without lymphadenopathy, hepatosplenomegaly, or increased abnormal lymphocytes in the peripheral blood. No spastic paraparesis of the lower limbs was found. The encephalopathy was progressive, and she died 5 months later despite repeated intrathecal administration of methotrexate, cytosine arabinoside, and prednisolone and monthly systemic chemotherapy with doxorubicin, cyclophosphamide, vincristine, and prednisolone. RESULTS: Postmortem examinations identified unusual ATLL lesions composed of marked infiltrations of atypical mononuclear cells and bizarre MNGC with histiocytic granulomatous reactions in the leptomeninges, brain tissues along the Virchow-Robin spaces, skin, and kidney. Immunohistochemical stains confirmed the T-cell nature of such mononuclear cells and partially T-cell and partially macrophage nature of the MNGC, although no evidence of HTLV-I expression was found. CONCLUSIONS: ATLL presenting with CNS symptoms is rare. It was assumed that the direct cytopathic effects of HTLV-I were responsible for the formation of the MNGC after considering the similarity with MNGC in encephalopathy caused by the human immunodeficiency virus.

Brain↗
PubMed2003

Chronic lymphocytic leukemia and multiple myeloma in the same patient: case report.

We hereby report the occurrence of a non-secreting multiple myeloma (MM) during the course of chronic lymphocytic leukemia (CLL). A 73-year-old patient developed a non-secreting MM 7 years after the diagnosis of CD5 (+) B cell CLL. He received intermittent chlorambucil and prednisolone therapy. The occurrence of tumors in the frontal bone led to resection of the tissue and histopathologic examination revealed neoplastic plasma cell islands within the CLL infiltration. There was no immunoglobulin or light chain accumulation in the serum. Clonal relationship between these diseases has been shown by comparing the isotypes and idiotype of both the heavy and light chains. In our case, the MM was of non-secreting type and thus we could not establish any relation between the 2 disorders. Such a case has not been reported until now in the literature. CLL and MM in the same patient is a rare occurence and investigation of the transformation event at the molecular level will contribute to our understanding of B-cell ontogenesis.

Aged↗
PubMed2004

Ophthalmic manifestations of acute leukaemias: the ophthalmologist's role.

With evolving diagnostic and therapeutic advances, the survival of patients with acute leukaemia has considerably improved. This has led to an increase in the variability of ocular presentations in the form of side effects of the treatment and the ways leukaemic relapses are being first identified as an ocular presentation. Leukaemia may involve many ocular tissues either by direct infiltration, haemorrhage, ischaemia, or toxicity due to various chemotherapeutic agents. Ocular involvement may also be seen in graft-versus-host reaction in patients undergoing allogeneic bone marrow transplantation, or simply as increased susceptibility to infections as a result of immunosuppression that these patients undergo. This can range from simple bacterial conjunctivitis to an endophthalmitis. Leukaemia can present as pathology in the adnexae, conjunctiva, sclera, cornea, anterior chamber, iris, lens, vitreous, retina, choroid, and optic nerve. Recognition of the varied ocular presentations is also important in assessing the course and prognosis of leukaemia. We have presented a systematic approach taking each part of the eye in turn and outlining how leukaemia has been shown to affect it.

Acute Disease↗
PubMed2000

Clinicopathological features of aggressive large granular lymphocyte leukaemia resemble Fas ligand transgenic mice.

Fas ligand triggers cell death after interaction with its receptor Fas. Altered expression of Fas has been associated with lymphoproliferation and autoimmune disorders in both mice and man. Apoptosis of lung and liver tissue is seen in Fas ligand transgenic mice. It is not known whether constitutive expression of Fas ligand can cause a similar human disease. Four patients with aggressive large granular lymphocyte (LGL) leukaemia involving lung and liver were studied. All four patients were severely ill with pulmonary involvement. Two patients presented with hypoxia and were oxygen dependent; the other two patients had severe pulmonary hypertension. Lung biopsies showed interstitial infiltration by leukaemic LGL. The infiltrating lymphocytes expressed both Fas and Fas ligand, whereas normal pneumocytes expressed only Fas. Similar findings were observed in liver biopsies from these patients. Features mimicking the pathological changes of graft-versus-host disease were observed, including pneumocyte apoptosis. All four patients had high levels of circulating Fas ligand. Successful treatment with oral methotrexate or 2-chlorodeoxyadenosine was associated with disappearance or marked reduction of circulating Fas ligand. These results suggest that dysregulated expression of Fas ligand can lead to human disease with pathological features resembling graft-versus-host disease.

Adult↗
PubMed2005

Repressible transgenic model of NRAS oncogene-driven mast cell disease in the mouse.

To create a model in which to study the effects of RAS dysregulation in hematopoietic disease, we developed separate founder lines of transgenic mice, with the tetracycline transactivator (tTA) driven by the Vav hematopoietic promoter in one line and NRASV12 driven by the tetracycline responsive element (TRE2) in the other. When these lines are crossed, doubly transgenic animals uniformly develop a disease similar to human aggressive systemic mastocytosis (ASM) or mast cell leukemia (MCL) when they are between 2 and 4 months of age. Disease is characterized by tissue infiltrates of large, well-differentiated mast cells in the spleen, liver, skin, lung, and thymus. Analysis of bone sections shows small to large foci of similarly well-differentiated mast cells. Results also show that transgene expression and diseases are repressible through the administration of doxycycline in the drinking water of affected animals, indicating that NRASV12 expression is required to initiate and maintain disease in doubly transgenic mice. Our inducible system of transgenes, developed as a model of mutant NRASV12 oncogene-driven myeloid disease, will be useful for studying the role of RAS dysregulation in hematopoietic disease in general and in discrete human diseases, specifically ASM and MCL.

Animals↗
PubMed1984

Spontaneous and induced leukemias of myeloid origin in recombinant inbred BXH mice.

BXH-2 recombinant inbred (RI) mice produce high titers of B-ecotropic murine leukemia virus beginning early in life and have a high incidence of non-T-cell leukemias that occur before 1 year of age. The leukemias that develop are in some cases associated with hind limb paralysis. In addition, a dualtropic mink cell focus-forming virus has been isolated from leukemic cells of BXH-2 mice. Immunological and cytochemical characterization of the BXH-2 leukemias showed that they are of the myeloid lineage. To assess the oncogenicity of the BXH-2 viruses, newborn mice of several BXH RI strains were inoculated at birth with biologically cloned B-ecotropic or mink cell focus-forming murine leukemia virus. These studies demonstrated that the B-ecotropic virus can induce myeloid leukemias in other BXH RI strains, whereas the dualtropic mink cell focus-forming isolates were nononcogenic in the strains tested. DNA-DNA reassociation analysis indicated that the organotropism of the B-ecotropic murine leukemia virus is confined to lymphoid tissues. Southern analysis of tumor DNAs showed that there was amplification of ecotropic virus-specific sequences in BXH-2 myeloid tumors and in all leukemias induced in other BXH RI strains by inoculation of the BXH-2 B-ecotropic virus. Although B-ecotropic virus is expressed in central nervous tissues of paralyzed BXH-2 mice, we were unable to induce the disorder in several BXH RI strains inoculated intracranially at birth with either the B-ecotropic or dualtropic virus. These results suggest that the paralysis that occurs in BXH-2 mice is due to the infiltration of leukemic cells into the central nervous system.

Animals↗
PubMed2002

Translocation t(9;22) (p23;q11) in atypical chronic myeloid leukemia (aCML) presenting osteolytic lesions.

A 58-year-old man with a 4-month history of atypical chronic myeloid leukemia (aCML), treated with INF-alpha and hydroxyurea, presented with severe localized bone pain with involvement of upper limbs on July 17, 2000. Cytogenetic analysis of peripheral blood cells showed 46,XY,t(9;22)(p23;q11) and no BCR-ABL fusion gene was detected by fluorescence in situ hybridization (FISH). On October 30,2000, x-rays revealed extended destruction of the bilateral proximal upper limbs; pain in the femoral bones appeared in December, and the patient couldn't walk. Roentgenograms taken on January 4, 2001, showed diffuse lytic changes in bilateral femoral bones. On January 23, 2001, fixation of pending fractures in the bilateral femoral bones with an intramedullary rod had produced good results. The infiltration of immature myeloid cells was diagnosed by the histological findings of a bone specimen from the right femur. Because the serum levels of parathyroid hormone (PTH), PTH related protein, and calcitonin were normal, we considered that the bone destruction was caused by the invasion of immature myeloid cells. Four months later, the patient showed a marked increase in peripheral immature granulocytes. A bone marrow specimen showed blastic marrow, and he died of a brain hemorrhage. This report suggests that aCML might cause destructive bone lesions prior to the disease progression. To our knowledge, this is the first published case of aCML in which the chromosomal abnormality t(9;22)(p23;ql 1) was detected.

Cerebral Hemorrhage↗
PubMed2003

Early detection of meningeal localization in acute promyelocytic leukaemia patients with high presenting leucocyte count.

Extramedullary relapse occurs infrequently in acute promyelocytic leukaemia (APL) but has been increasingly reported after the advent of all-trans retinoic acid (ATRA) treatment, probably as a consequence of improved patient survival. We describe our single centre experience of six APL patients who had disease localization in the central nervous system (CNS). In three patients, clinical symptoms (headache and/or nausea) that presented during follow-up led to the performance of a lumbar puncture and detection of overt CNS infiltration. Two of these patients had simultaneous haematological relapse and one was in molecular remission when CNS leukaemia was documented. One patient with no local symptoms showed CNS infiltration at the time of molecular relapse. Following the introduction of routine lumbar puncture, carried out after front-line induction in all newly diagnosed patients with white blood cell count (WBC) greater than 10 x 109/l, two additional patients in molecular remission with no local symptoms were found to have initial APL localization in the CNS. Presenting features included in 6/6 patients an elevated WBC count (> 10 x 109/l) and a predominance of the PML/RAR bcr3 type (5/6 patients) and of microgranular morphology (5/6 patients). Our findings highlight the importance of carrying out lumbar puncture in APL patients presenting with high-risk features.

Adult↗
PubMed1993

Specific skin manifestations in acute leukemia with monocytic differentiation. A morphologic and immunohistochemical study of 11 cases.

BACKGROUND: Monocytic differentiation is present in the myelomonocytic (M4) and monocytic (M5) type of acute myeloblastic leukemia. Infiltration of the skin in acute myelomonocytic leukemia occurs in 10-20% of patients, the skin lesions occasionally being the first symptom, even preceding monocytosis. METHODS: Eleven patients with myelomonocytic (n = 2) and monocytic leukemia (n = 9) were studied who had skin manifestations. RESULTS AND CONCLUSIONS: Clinically, all patients showed disseminated papules or nodules that corresponded histologically to nodular or diffuse infiltrates of monocytoid cells, occasionally displaying a whorled pattern. The currently available antibodies for paraffin-embedded sections (lysozyme, elastase, leukocyte common antigen (CD45), MT1 (CD43), Leu-M1 (CD15), LN2 (CD74), MB2, MB1 (CD45RA), LN1 (w75), Mac387, L26 (CD20), UCHL1 (CDR0), MT2 (CD45RA), and KP-1 (CD68)) and chloracetate-esterase are not more helpful in diagnosis than are the histologic findings. By contrast, the antibodies used on frozen sections (Leu-4 (CD3), Leu-3a (CD4), BA1 (CD24), B4 (CD19), Leu-M5 (CD11c), Vim12 (CD11b), VimD5 (CD15), KiM6 (CD68), KIM7 (CD68), My7 (CD13), and My9 (CD33) allow the definition of a reaction pattern that is diagnostic for acute myeloid leukemia with monocytic differentiation.

Adult↗
PubMed2005

Efficient engraftment of primary adult T-cell leukemia cells in newborn NOD/SCID/beta2-microglobulin(null) mice.

Adult T-cell leukemia (ATL) develops via multiple oncogenic steps in human T-cell leukemia virus type I (HTLV-I) carriers. To better understand pathogenesis of ATL, we developed a novel xenogeneic engraftment model in which primary ATL cells are intravenously transplanted into neonatal nonobese diabetic (NOD)/severe-combined immunodeficiency (SCID)/beta2-microglobulin(null) (NOD/SCID/beta2m(null)) mice. Acute-type ATL cells engrafted in the peripheral blood and in the lymph nodes of recipients at a high efficiency. Engrafted ATL cells were dually positive for human CD4 and CD25, and displayed patterns of HTLV-I integration identical to those of donors by Southern blot analysis. These cells infiltrated into recipients' liver, and formed nodular lesions, recapitulating the clinical feature of each patient. In contrast, in smoldering-type ATL cases, multiple clones of ATL cells engrafted efficiently in NOD/SCID/beta2m(null) mice. When smoldering-type ATL cells were retransplanted into secondary NOD/SCID/beta2m(null) recipients, single HTLV-I-infected clones became predominant, suggesting that clones with dominant proliferative activity can be competitively selected in this xenogeneic system. Taken together, the NOD/SCID/beta2m(null) newborn system is useful to understand kinetics, metastasis, and disease progression of ATL in vivo.

Anemia, Refractory, with Excess of Blasts↗
PubMed2002

Precursor T-cell acute lymphoblastic leukemia/lymphoma involving the uterine cervix, myometrium, endometrium, and appendix.

This report presents a case of precursor T-cell acute lymphoblastic leukemia/lymphoma (ALL) involving the uterine cervix, myometrium, endometrium, and appendix. The patient was a 38-year-old woman with a history of ALL who had been in remission for 4 years following chemotherapy. The malignant lymphoid infiltrate was characterized by blasts, showing scant cytoplasm, irregular hyperchromatic nuclei, and occasional prominent nucleoli. They were immunoreactive for CD45RB, CD3, CD43, CD34, and focally for TdT. Curiously, the blasts replaced the endometrial stroma and spared the associated epithelium. The patient was again treated with chemotherapy but her disease did not respond. She succumbed to her disease approximately 10 months after her initial evaluation for symptoms related to ALL relapse. Precursor T-cell ALL most commonly presents as a mediastinal mass in adolescent males. Although any organ may be affected, involvement of the female reproductive organs is rare. This case shows some of the varied manifestations of precursor T-cell ALL and highlights the necessity of considering the female reproductive tract as a possible location of relapsing disease.

Adult↗
PubMed1999

[Leptomeningeal dissemination of chronic lymphatic leukemia. Molecular genetic detection in cerebrospinal fluid].

The diagnosis of leptomeningeal dissemination of chronic lymphatic leukemia (CLL) by conventional cytology is unreliable because cytomorphologic criteria of malignancy are often lacking. Immunophenotyping of leukocyte differentiation antigens may also be of limited diagnostic value due to the small number of cells in cerebrospinal fluid (CSF) samples. Molecular methods may support the specific diagnosis of leptomeningeal infiltration of CLL. We present an 54 old patient who was diagnosed with CLL five years ago. Despite clinical signs of leptomeningeal involvement neither magnetic resonance imaging (MRI) nor conventional CSF analysis were suggestive of lymphomatous meningitis. Using PCR we selectively amplified the highly variable and clone-specific CDR3 region of the locus encoding the immunoglobulin heavy chain (IgH) in DNA obtained from both CSF and peripheral blood cells. Analysis of PCR products by high resolution gel electrophoresis revealed a single DNA fragment respectively indicating the presence of a monoclonal cell population in both compartments. DNA sequence analysis of the amplified CDR3 segments confirmed the clonal identity of cells and the leptomeningeal dissemination of CLL.

B-Lymphocytes↗